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THE FEDERATION OF EUROPEAN


COMPANION ANIMAL
VETERINARY ASSOCIATIONS

SOCIET CULTURALE ITALIANA


VETERINARI PER
ANIMALI DA COMPAGNIA

55

55

55

5 55

555

4 CONGRESSO

FECAVA SCIVAC
EUROPEO

BOLOGNA

18-21

GIUGNO

PROGRAMMA DEFINITIVO
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Ter 15

1998

Con il patrocinio di

Facolt di Veterinaria dellUniversit di Bologna


FNOVI, Federazione Nazionale Ordini Veterinari Italiani
Provincia di Bologna
Comune di Bologna
Ambiente, Sviluppo Sostenibile, Politiche Giovanili,
Protezione Civile
Comune di Bologna
Politiche Sociali, Sanit e Sicurezza
In collaborazione con
A.I.V.P.A Associazione Italiana Veterinari Piccoli Animali

Circolo Veterinario Bolognese

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5

THE FEDERATION OF EUROPEAN COMPANION


ANIMAL VETERINARY ASSOCIATIONS

SCIVAC

SOCIET CULTURALE ITALIANA VETERINARI


PER ANIMALI DA COMPAGNIA

PALAZZO

TRECCHI

26100

CREMONA

TEL. 0372 460440 FAX 0372 457091 - email: info.scivac@softeam.it

THE

FEDERATION OF EUROPEAN COMPANION


ANIMAL VETERINARY ASSOCIATIONS

Caro Collega,
sono veramente onorato di presentare il 4 Congresso Europeo della FECAVA che si
terr a Bologna dal 18 al 21 Giugno 1998. Limportanza di questo evento assume molteplici significati. Innanzitutto viene riconosciuta alla Medicina Veterinaria Italiana la crescita compiuta in questi anni che lha portata a qualificarsi a livello europeo in una posizione di tutto rispetto. Contemporaneamente, laver affidato a SCIVAC lorganizzazione congressuale
testimonia il ruolo che la nostra Associazione ha assunto nellambito FECAVA, e questo ci rende giustamente orgogliosi.
Queste le cifre del 4 Congresso FECAVA che dimostrano di quale portata sar questo congresso: un pre-congress day con otto gruppi specialistici, dodici ore di discussione interattiva di casi
clinici, tre giorni interi con un programma scientifico eccellente, sei sale con relazioni in contemporanea, relazioni dal livello base a quello avanzato, undici relazioni sullo stato dellarte dei vari settori
della clinica e della chirurgia, oltre quaranta relatori invitati, tredici argomenti trattati. In quattro giorni
verranno trattati argomenti che spazieranno dalla clinica alla chirurgia, dalla medicina felina a quella degli animali esotici, dalla cardiologia alloftalmologia senza tralasciare alcun argomento che possa
interessare la clinica degli animali da compagnia. I relatori invitati sono stati selezionati tra i migliori
dEuropa e degli Stati Uniti, con la presenza di un buon gruppo di Colleghi italiani.
A questo congresso si sono completamente dedicati una Commissione Scientifica di altissimo livello, che ha lavoratto per oltre due anni al programma, e uno staff tecnico che render levento unico
per la sua organizzazione. Ritengo quindi di poter dire che per molto tempo sar difficile avere unaltra occasione di questa portata per fare il punto sui traguardi e sulle nuove indicazioni terapeutiche
nella clinica degli animali da compagnia.
La sede congressuale sar la meravigliosa citt di Bologna, ricca di storia e di tradizione. Sita in una
delle pi belle regioni dItalia la citt far certamente da degna cornice ad un evento cos importante.
Mi preme ringraziare fin dora il Consiglio Direttivo della FECAVA che ha voluto accordarci la sua
fiducia, dando mandato a SCIVAC di organizzare questo congresso. Devo inoltre un doveroso ringraziamento al Consiglio Direttivo e alla Commissione Scientifica della SCIVAC per il lavoro svolto ed infine a tutti gli Sponsor che hanno voluto sostenere questa importante iniziativa.
In attesa di incontrarTi a Bologna Ti porgo i pi cordiali saluti.
Carlo Scotti
Presidente SCIVAC

scivac

Presidente
CARLO SCOTTI

Presidente Senior
GIORGIO ROMANELLI

SOCIET CULTURALE ITALIANA VETERINARI


Vice Presidente
PIERMARIO PIGA

Segretario
UGO LOTTI

PER

Tesoriere
GILDO BARONI

ANIMALI

DA

Consigliere
MARCO CALDIN

COMPAGNIA
Consigliere
MATTEO SPALLAROSSA

Uffici: Palazzo Trecchi - 26100 Cremona - Tel. O (0372) 460440 - Telefax (0372) 457091 - E MAIL: info.scivac@softeam.it - Partita I.V.A. 00861330199

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5

ANIMAL VETERINARY ASSOCIATIONS

THE FEDERATION OF EUROPEAN COMPANION

________ FECAVA _______

Cari Colleghi,
a nome dei componenti del Direttivo della Federazione Europea delle Associazioni
Veterinarie per Animali da Compagnia, ho il piacere di invitarvi al 4 Congresso
Europeo FECAVA SCIVAC che si terr in una delle pi belle citt dEuropa: Bologna.
LAssociazione organizzatrice, la SCIVAC - Societ Culturale Italiana Veterinari per
Animali da Compagnia - il cui numero di iscritti il pi alto fra tutte le Societ aderenti alla FECAVA - vi offre lopportunit di prendere parte ad un evento unico per la vostra crescita professionale che unisce laggiornamento scientifico allesperienza di una delle aree storico-geografiche che
pi hanno concorso alla formazione della civilt moderna occidentale.
La decisione del Direttivo FECAVA di aderire unanimemente e con entusiasmo alla proposta
della SCIVAC di organizzare il 4 Congresso Europeo e di eleggere Bologna a sede congressuale
ha un particolare significato.
Abbiamo cos voluto onorare la SCIVAC, Associazione fondatrice della Federazione attivamente impegnata a sostenerne i progetti e le iniziative, e rendere omaggio alla straordinaria bellezza della citt di Bologna, alla sua felice collocazione geografica e al contributo che ha saputo
dare allo sviluppo della vita artistica, culturale e spirituale dEuropa.
Nessun altro Continente pu paragonare il proprio passato a quello lunghissimo e affascinante che lEuropa ha conosciuto, sia per gli aspetti culturali e scientifici che per il sentimento damicizia maturato fra le sue popolazioni. LEuropa da sempre la pietra di paragone di ogni progresso dellumanit.
sulla base di questa concezione e di questorgoglio europeisti che qualche anno fa nata la
nostra Federazione. Allora, nessuno avrebbe potuto immaginare limpatto e linfluenza che la
FECAVA avrebbe ottenuto sulla professione veterinaria per animali da compagnia.
La nascita della FECAVA stata ufficialmente sancita il 12 maggio 1990, alla presenza di tredici Associazioni fondatrici; adesso, la FECAVA conta ventisei societ aderenti, per un totale di
circa venticinquemila soci effettivi e dieci Societ Specialistiche veterinarie europee, in qualit di
membri associati.
I congressi europei fino ad ora realizzati si sono rivelati tra i principali eventi scientifici
dEuropa. Anche in questa occasione, stata rispettata la consuetudine di mantenere il programma scientifico ad alti livelli di qualit e successo come nei precedenti congressi europei e quindi
offrire ai partecipanti conoscenze consolidate, aggiornamenti ed elementi di valutazione critica
degli stessi, nellintento di promuovere lo scambio e il confronto culturale.
Lottimo programma scientifico, linvitante programma sociale e la citt di Bologna, con la sua
storia e i suoi paesaggi mirabili, sono elementi ideali combinati con la tradizionale ospitalit italiana, i vini e la cucina dItalia. Sar felice di vedervi numerosi, da tutti i Paesi dEuropa, e sono certo
che ricorderete questa occasione come degna e importante.
Dr. Ben Albalas
Presidente FECAVA

RELATORIALCONG
DAVID AUCOIN
DVM, Dip ACVCP
Vets Choice
Santa Monica, California
USA

MARCO CALDIN
Med Vet
Libero Professionista,
Padova

ELLEN BJERKAS
DVM, PhD, Dipl ECVO
Dept of SA Clin Sciences
Norwegian College of
Vet Med
NORVEGIA

MARIO CANIATTI
DVM
Universit di Milano
Istituto di Anatomia
Patologica Veterinaria

CLAUDIO BROVIDA
Med Vet
Libero Professionista,
Torino

DIDIER CARLOTTI
DVM, Dipl ECVD
Les Places Sainte Eulalie
FRANCIA

LEONARDO BRUNETTI
Med Vet
Libero Professionista,
Pistoia

DANIELE COTTO
Med Vet
Libero Professionista, Torino

PAOLO BURACCO
Med Vet
Universit di Torino
Dipartimento di Patologia
Animale

GUILLERMO COUTO
DVM, Dipl ACVIM
The Ohio State University
Columbus, Ohio
USA

CLAUDIO BUSSADORI
Med Vet, Dipl ECVIM
Libero Professionista,
Milano
6

GRESSO
LORENZO CROSTA
Med Vet
Libero Professionista,
Milano

STEPHEN DIVERS
Bsc, C Biol, M.I. Biol,
B.Vet. Med, MRCVS
Exotic Animal Center, Essex
GRAN BRETAGNA

BERNARD F. FELDMAN
DVM, PhD, Dipl ACVIM
College of Vet Medicine
Blacksburg, Virginia - USA
LUIS FERRER
DVM, Dipl ECVD
Universitat Autonoma de
Barcelona - Barcelona
SPAGNA
ANTONIO FERRETTI
Med Vet, Dipl ECVS
Libero Professionista,
Milano

CORINNE FOURNEL-FLEURY
DVM, PhD
Ecole Nat Vet de Lyon
Marcy lEtoile - FRANCIA
TOMMASO FURLANELLO
Med Vet

Libero Professionista,
Padova

ADOLFO GUANDALINI
Med Vet
Libero Professionista,
Roma

HERMAN A. W. HAZEWINKEL
DVM, PhD, Dipl ECVS
State University of Utrecht
OLANDA
DOMINIQUE HERIPRET
DVM, Dipl ECVD
Clinique Veterinaire Fregis
Arcueil - Paris - FRANCIA

RICHARD LeCOUTEUR
VMD, PhD, Dipl ACVIM
University of California
Davis, California - USA

CHRISTOPHE LOMBARD
DVM, Dipl ACVIM,
Dipl ECVIM
Universitat Bern
SVIZZERA
GEORGE LUBAS
Med Vet
7
Universit di Pisa, Istituto di Pat

RELATORIALCONG
GIUSEPPE MOSCONI
Med Vet,
Libero Professionista,
Ozzano Emilia

Speciale e Clin Med


Veterinaria
LUCA MECHELLI
Med Vet
Universit di Perugia
Istituto di Anatomia
Patologica

GERT NIEBAUER
Med Vet, PhD,
MS, Dipl ECVS
Libero Professionista,
Orbetello

DENNY MEYER
DVM, Dipl ACVP,
Dipl ACVIM
Boulder, Colorado - USA

CLAUDIO PERUCCIO
Med Vet, Dipl ECVO
Universit di Torino
Dipartimento di Patologia
Animale

AR MICHELL
Dsc, MRCVS
Animal Health Trust
Newmarket Suffolk
GRAN BRETAGNA

S.M. PETERSEN-JONES
DVO, Dipl ECVO, MRCVS
University of Cambridge
Cambridge
GRAN BRETAGNA

MASSIMO MILLEFANTI
Med Vet
Libero Professionista, Milano

STEFANO PIZZIRANI
Med Vet, Dipl ECVS
Libero Professionista,
Firenze

PIERRE M. MONTAVON
DVM
Veterinar-Chirurgische
Klinik der Universitat Zurich
SVIZZERA

AD RIJNBERK
DVM PhD
University of Utrecht
OLANDA

GRESSO
GIORGIO ROMANELLI
Med Vet, Dipl ECVS
Libero Professionista,
Milano

MATTEO TOMMASINI
Med Vet, Dipl ECVS
Libero Professionista,
Roma

GIANLUCA ROVESTI
Med Vet, Dipl ECVS
Libero Professionista,
Reggio Emilia

ALDO VEZZONI
Med Vet, Dipl ECVS
Libero Professionista,
Cremona

ROBERTO SANTILLI
Med Vet
Libero Professionista,
Milano

FRANK VERSTRAETE
DVM, Dipl AVDC,
Dipl ECVS
University of California
Davis, California, USA

KARSTEN SCHOBER
DVM
University of Leipzig
GERMANIA

C. VON WERTHERN
DVM, Dipl ECVS
Veterinar-Chirurgische Klinik
der Universitat Zurich
SVIZZERA

PETER W. SCOTT
Msc, BVSc, FRCVS
Zoo & Aquatic Vet Group
Winchester
GRAN BRETAGNA

SIMON WHEELER
BVSc, PhD, Dipl ECVN
The Royal Veterinary College
University of London
GRAN BRETAGNA

DANIEL D. SMEAK
DVM, Dipl ACVS
The Ohio State University
Columbus, Ohio
USA

RICHARD A.S. WHITE


PhD, DVR, FRCVS, Dipl
ACVS, Dipl ECVS
University of Cambridge
GRAN BRETAGNA
9

SEMINARI PRE-C
S

8,30

A
R

L
E

A
G

D
S

I
T R

SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

HOLIDAY INN 250

ESFM
MEDICINA FELINA

SIDEV
DERMATOLOGIA

ESVO - ECVO - SOVI


OFTALMOLOGIA

ESCG
GASTROENTEROLOGIA

Approccio diagnostico
alle malattie cutanee su
base autoimmune nel
cane e nel gatto (30)
Dominique Heripret (F)

PALPEBRE E TERZA PALPEBRA


Tecnica di cantoplastica laterale per la
correzione della macro fessura palpebrale nel cane - P. Bedford (UK)

Tecniche per il
trattamento dei tumori colorettali nel cane:
valutazione critica (30)
R.A.S. White (UK)

9,30 Alterazioni ematiche


(1a parte)
Neutropenia e
piressia nel gatto (60)

Gioved Mattina 18 Giugno 1998

10,00

Pemfigo e pemfigoide
nel cane e nel gatto
(1a parte)
(30)

Guillermo Couto (USA) e


Bernard Feldman (USA)
10,30

Luis Ferrer (E)

11,00 Alterazioni ematiche


(2a parte)
Il gatto anemico:
modalit pratiche di
valutazione (60)

Pemfigo e pemfigoide
nel cane e nel gatto
(2a parte)
(30)

Luis Ferrer (E)


11,30

Guillermo Couto (USA) e


Bernard Feldman (USA)

Lupus discoideo e
lupus sistemico (60)

Aspetto ultrasonografico e con


Risonanza Magnetica dell'adenite eosinofilica della ghiandola della nittitante in
un cane - S.M. Turner (UK)

Prolasso ed iperplasia della ghiandola


della membrana nel coniglio
P. Boydell (UK)

ORBITA
Un caso di miosite eosinofilica unilaterale in un cane - M. Bandini (I)

Fisiopatologia della
ritenzione degli acidi
biliari (30)

D. Meyer (USA)

CORNEA
Un caso di ulcera bilaterale simmetrica
e stagionale cortico-responsiva in un
coniglio nano - P. Anfray, C. Bonetti (I)
Individuazione con microscopio elettronico a trasmissione di particelle citoplasmatiche simil-virali nelle cornee e congiuntive di cani con panno (cheratite
superficiale cronica - Uberreiter)
F. Rapp (A)
Cheratoplastica lamellare per la cura del
sequestro corneale nel gatto
M.T. Pena Gimenez (E)
Uso di collanti tissutali per la cura dell'erosione corneale cronica nel gatto
A.C. Leber (D)
Applicazioni cliniche di lembi tarso-congiuntivali isolati nel cane e nel gatto:
risultati in 40 casi - N. D'Anna (I)

L Helicobacter
gastrico nel cane
e nel gatto (30)

G.Cattoli (I)
Telediagnostica,
telechirurgia e
teleinsegnamento
(30)
J. Uson (E)
R

12,00
Discussione (30)

12,30

Alterazioni ematiche
(3a parte)
Il gatto anemico:
approccio terapeutico
pratico (60)

Altre malattie cutanee


immunomediate
(1a parte) (30)

Luis Ferrer (E)

TERAPIA
Penetrazione corneale, congiuntivale e
intraoculare dell'acido fusidico per uso
topico nel cane - G. J. McLellan (UK)

Dominique Heripret (F)

Guillermo Couto (USA) e


Bernard Feldman (USA)
13,00

GLAUCOMA
La crioterapia per la cura del glaucoma.
Risultati con l'azoto liquido - B. Clerc (F)
Glaucoma secondario a difetti oculari
multipli in un Gatto Inglese a pelo corto
R. Elks (UK)
Displasia del legamento pettinato nel
Siberian Husky. Studio clinico, biometrico e istopatologico
G. Chaudieu (F)

18

CONGRESSUALI
E S S O
O N E

8,30

SALA AZZURRA 150

SALA BIANCA 200

IEWG
ORTOPEDIA

SIMESC
ESVC
MEDICINA SPORTIVA CARDIOLOGIA

INTRODUCTION
Fisiopatologia
Who is IEWG? What are the aims of the
dellallenamento (15)
IEWG?
Dominique Grandjean (F)
Flckiger (Zurich - CH)

Diagnostic accurracy
of high resolution radiography and
arthroscopy
of elbows in growing dogs
Kramers (Zurich - CH)

Tecniche di allenamento
(1a parte) (25)
Dominique Grandjean (F)

PATHOPHYSIOLOGY OF ED
Pathophysiology of bony changes in
the dysplastic elbow joint
Poulos (Davis - USA)
Role of nutrition on the skeletal development
Hazewinkel/Nap (Utrecht/Eindhoven - NL)
EPIDEMIOLOGY/PREVENTION
CONCEPTS
Incidence of developmental articular
malformation in the Labrador Retriever
Wind (Davis - USA)
Effect of breed animal selection on the
incidence of ED in German Shepherd
dogs
Lavelle (Melbourne - AUS)
Prevalence and incidence of ED in a
colony of Labrador Retrievers
Lang/Ohlert (Bern - Switzerland)
open
Swenson (Uppsala - Sweden)
Predictability of FCPM in Dutch
Labrador Retrievers and Bernese
Mountain dogs
Ubbink (Utrecht - The Netherlands)
Breed value estimation in the dog.
Impact on the incidence of heritable
diseases
Beuing (Giessen - Germany)
PREVENTION CONCEPTS (continued)
The German ED prevention protocol;
preliminary results in selected breeds
Tellhelm (Giessen - Germany)
The British ED protocol
Pead (London - England)
Incidence of canine ED in Italy and clinical approach by veterinary profession
Mortellaro (Milano - Italy)
The WSAVA Hereditary Defects
Committee: Current activities and goals
Hedhammar/Bedford (Sweden/London)

Anestesia degli uccelli


da gabbia e da voliera
(60)

L.P. Tilley (USA)

Tecniche di allenamento
(2a parte) (20)
Dominique Grandjean (F)

Peter Scott (UK)

Fisioterapia e riabilitazione nel


cane sportivo (20)

Recenti acquisizioni
nei risultati clinici dellimpiego degli ACE inibitori in medicina per
piccoli animali (40)
J.L. Pouchelon (F)

Problemi ortopedici di
metacarpo, metatarso e falangi
nel cane sportivo (20)
Alessandro Piras (I) e Brian Jones
(IRL)

Aggiornamenti in tema
di patologie valvolari
acquisite nel cane (40)
J. Haggstrom (S)

Trattamento delle fratture delle


ossa lunghe nel cane atleta (20)

Problemi riproduttivi nei cani


sportivi (20)
Giovanni Majolino (I)

Le pi frequenti malattie virali dei pappagalli


(50)
Claudio Peccati (I)

10,30
11,00

11,30

Tecniche diagnostiche
impiegabili in medicina
aviare (50)
Peter Scott (UK)

11,50
12,00

Difetti del setto interventricolare nel cane


(40)
G. DAgnolo (I)
12,30
Indagine sulla flora residen- 12,40
te nelle prime vie respiratorie degli psittacidi (20)

Linseminazione artificiale con


seme fresco e congelato: che
cosa c di nuovo (20)
Stefano Romagnoli (I)

9,30

10,00

Incongruenze articolari del gomito: un problema emergente nelle


razze sportive (15)

*
Hills

Gruppo di Studio
ANIMALI ESOTICI

Il prontuario
farmaceutico
cardiologico Tilley
per il veterinario
pratico (60)

DIAGNOSIS OF ELBOW DYSPLASIA (ED)


Radiographic technique and film interpretation for ED screening
Lang (Bern - CH)

SALA SMERALDO 100

SALA BLU 150

Sandra De Oliveira (UK)

E
13,00

19

4 C O N G R E S S O F E C AVA S C I VA C

N G R
A Z I

Gioved Mattina 18 Giugno 1998

SEMINARI PRE-C
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

HOLIDAY INN 250

ESFM
MEDICINA FELINA

SIDEV
DERMATOLOGIA

ESVO - ECVO - SOVI


OFTALMOLOGIA

ESCG
GASTROENTEROLOGIA

14,00 Biochimica
clinica felina:
i gatti non sono cani
piccoli da un punto di
vista biochimico !!! (60)

Altre malattie cutanee


immunomediate
(2a parte) (30)

LENTE
Controllo del diabete del cane e cataratta
diabetica
D. Salgado ( CH)

Luis Ferrer (E)

UVEA
Uveite pigmentaria nel Golden Retriever:
43 casi
J.S. Sapienza (USA)

Il trattamento endoscopico nella palliazione dei tumori gastrointestinali nelluomo (30)


E. Meroni (I)

14,30

Diagnosi clinica
differenziale delle
patologie cutanee
autoimmuni (45)

Denny Meyer (USA)

Sindrome uveodermatologica in un cane


V.J. Babo (BRA)
L'uveite felina: riscontri sierologici e clinici in 44 casi
M. Roze (F)

Il linfoma
gastrointestinale del
cane e del gatto (30)

G.Couto (USA)

Gioved Pomeriggio 18 Giugno 1998

15,00

Alterazioni vestibolari
nel gatto (60)

15,15

Dominique Heripret (F)

Valutazione immunoistochimica della


risposta immune in un caso di uveite
ricorrente nel cavallo
L. Mertel (I)

Diagnosi istologica
differenziale delle
patologie cutanee
autoimmuni (45)

RETINA
La retina normale nella Phoca vitulina,
riscontri elettroretinografici e morfologici
E. Bjerkas (N)

Approccio nutrizionale al paziente


gastrectomizzato e\o
enterectomizzato (30)
B. Stanley (USA)
Discussione (30)

Aspetti elettroretinografici dell'onda d nel


gatto normale e distrofico
B. Ekesten (S)

Rick LeCouteur (USA)


Luis Ferrer (E)
16,00

16,30 Patologie spinali nel


gatto (60)

OTTICA E TECNICHE DIAGNOSTICHE


Risultati della cheratometria e della
schiascopia pre e post operatoria in 1000
cani di razze diverse - W. Neumann (D)

Protocolli terapeutici
(e nuove terapie) delle
malattie cutanee
autoimmuni (60)

Studio biometrico dell'occhio del cane


mediante ultrasonografia - S. Schoofs (B)
Indagine ultrasonografica dei nervi ottici
in cani colpiti da cecit improvvisa
P. Boydell (UK)

Rick LeCouteur (USA)

Fabbisogno dietetico
nel cane con patologia epatica (30)

H. Meyer (NL)
Discussione (30)

ANIMALI ESOTICI
Anomalie dello sviluppo oculare in una
tigre del Bengala - T. Grimes (UK)

Dominique Heripret (F)

Tonometria negli erbivori selvatici


R. Ofri (ISR)

17,30
Disordini
neuromuscolari nel
gatto (60)

Discussione (60)

OCULOPATIE EREDITARIE
Oculopatie ereditarie: il punto di vista
Italiano - C. Peruccio (I)
Oculopatie ereditarie: risultati preliminari
in alcune razze in Italia
E. Barbasso (I)
Per le presunte malattie oculari ereditarie: note sulle procedure adottate
dall'ECVO (relazione del Comitato
Malattie Genetiche dell'ECVO)
F.C. Stades (NL)

18,30 Rick LeCouteur (USA)

20

CONGRESSUALI

SALA AZZURRA 150

SALA BIANCA 200

IEWG
ORTOPEDIA

SIMESC
ESVC
MEDICINA SPORTIVA CARDIOLOGIA

TREATMENT
Arthroscopic approach in dogs
with ED
Meyer-Lindenberg, Hannover (D)
Results of ulna ostectomy
as a treatment for UAP
Vezzoni (Cremona - I)

Doping nel cane sportivo: vecchi


e nuovi concetti (20)
Dominique Grandjean (F)

SALA SMERALDO 100

SALA BLU 150

Rottura LCA: diagnosi,


ricostruzione e follow-up (30)
Immunoprofilassi
dallevamento:
organizzazione di un
programma vaccinale (20)
Swanneke D. Hendriks (NL)

Gruppo di Studio
ANIMALI ESOTICI

Ipertensione: diagnosi e Tecniche


trattamento (40)
anestesiologiche e
L.P. Tilley (USA)
patologie
chirurgiche nei rettili
(60)

14,00

14,30
Aggiornamenti in tema
di cardiomiopatia
dilatativa nel cane (40)
M. Borgarelli (I)

Distocie dei rettili (60)

Rottura del gastrocnemio nei


cani da caccia e da corsa (20)
Gianluca Rovesti (I)

15,15

Stress ossidativo indotto dallesercizio nel cane


sportivo e conseguenze sui fabbisogni nutrizionali di sostanze
anti-ossidanti (30)

Nuovi concetti nel


trattamento della
cardiomiopatia
dilatativa del cane e
terapie alternative (40)
C. Amberger (CH)

Comunicazioni libere

Discussion of the
seminar films

Integrazione
nutrizionale ergogenica nel
cane atleta (15)
D. Grandjean (F)

Workshop di
ecocardiografia (90)
C. Bussadori (I) e
C. Lombard (CH)

*
Hills
La zoppia di spalla nel cane
atleta: diagnosi e trattamento (15)
M. Olivieri (I)

Miopatia dei muscoli gracile e


semitendinoso (15)
A. Piras (I)

Tecniche diagnostiche
impiegabili nei rettili
(50)
Stephen Divers (UK)

16,00
16,30

17,00

17,20
Utilizzo della miscela
anestetica ZKX in pic17,30
coli animali esotici e
selvatici (20)
Amerio Croce (I)
Le pi comuni
patologie dei ricci: un
problema veramente
spinoso (50)
Rosanna Trossarello (I)

Patologie articolari degenerative:


un aggiornamento (15)

Impiego del Benazepril


nel gatto: farmacocinetica ed efficacia nel trattamento della cardiomiopatia dilatativa (30)
C. Amberger (CH) e
J.N. King (UK)

Alterazioni
muscolo-tendinee nel cane
atleta (15)
A. Piras (I) e B. Jones (IRL)

Annual General
Meeting of the IEWG

Giuseppe Visigalli (I)

18,30

21

4 C O N G R E S S O F E C AVA S C I VA C

15,00
Film Reading Seminar
Participants are encouraged to
interpret some 2 dozens elbow
cases, which then will be discussed with Dr. Alida Wind, former
Small Animal staff surgeon at the
University of California Veterinary
Medical Teaching Hospital.
Participant may also bring their
own ED cases along for discussion
(if time permits)

Gioved Pomeriggio 18 Giugno 1998

Stephen Divers (UK)

PROGRAMMASCI
S

8,30

A
R

L
E

A
G

D
S

I
T R

SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

EMATOLOGIA
Chairman: Marco Caldin

ORTOPEDIA
Chairman: Gildo Baroni

OFTALMOLOGIA
Chairman: Claudio Peruccio

Formazioni ossee
patologiche (60)
Segni clinici e radiologici,
eziologia, trattamento e prognosi
delle patologie caratterizzate da
formazioni ossee: panosteite,
osteodistrofia ipertrofia, ecc.

RELAZIONE SULLO STATO


DELLARTE
Recenti acquisizioni
nellinterpretazione della GPRA
Atrofia retinica generalizzata
progressiva (60)

9,30 Interpretazione della conta


cellulare ematica:
Prima parte
Lemogramma completo
(60)

Venerd Mattina 19 Giugno 1998

Bernard Feldman (USA)


10,30

H.A.W. Hazewinkel (NL)

EMATOLOGIA
Chairman: Marco Caldin

Simon Petersen-Jones (UK)

ORTOPEDIA
Chairman: Antonio Ferretti

Bernard Feldman (USA)

Il ruolo della nutrizione nelle


patologie ortopediche (60)
Linfluenza del contenuto
energetico, proteico, minerale e
vitaminico nella dieta sullo
sviluppo scheletrico e
sullaccrescimento

RELAZIONE SULLO STATO


DELLARTE
La cataratta nel cane:
eziologia, evoluzione
e riscontri clinici (60)

H.A.W. Hazewinkel (NL)

11,00 Interpretazione della conta cellulare ematica: Seconda parte


RELAZIONE SULLO STATO
DELLARTE
Procedure diagnostiche speciali
in ematologia (40)

OFTALMOLOGIA
Chairman: Stefano Pizzirani

Ellen Bjerkas (N)

Approccio clinico allanemia


(50)

12,00

Anemia nel cane giovane (30)

George Lubas (I)


13,00

Interpretazione clinica delle


emorragie oculari (60)

Aldo Vezzoni (I)

Bernard Feldman (USA)

Diagnosi precoce di displasia


dellanca (60)
Elementi clinici e radiografici che
permettono una diagnosi precoce
di displasia dellanca in funzione
della selezione cinofila e delle
scelte terapeutiche pi opportune

Claudio Peruccio (I)

Livello di Aggiornamento

Livello Avanzato

22

Relazione sullo Stato de

ellArte
S

Sessione Specialistica
O

23
Sessione Interattiva
M

13,00

Induzione dellestro nella gatta con


cabergolina: studi preliminari
Daniele Zambelli (I)

Displasia follicolare (60)

Safety trial in bitches with tablets containing oestriol (Incurin)


S. Hendriks (NL)

12,00

RIPRODUZIONE
Chairmen: Matteo Spallarossa (I)
e Patrizia Ponzio (I)

Medicina durgenza degli


uccelli (60)

Patologie infiammatorie dei follicoli piliferi (60)

Efficacia luteolitica ed effetti


collaterali dellalfaprostol,
un analogo sintetico della
prostaglandina F2alfa, nella cagna:
risultati preliminari
Sandra Annarella (I)

11,00

10,30

4 C O N G R E S S O F E C AVA S C I VA C

Patologie cutanee degli uccelli:


un incubo per il veterinario
pratico (60)

DERMATOLOGIA
Sessione specialistica
Chairman: Chiara Tieghi (I)

Venerd Mattina 19 Giugno 1998

Luca Mechelli (I)

?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
M0@@M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I?@4I?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I4I
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
?Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4VI?
M(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'
Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4V?
?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
?MY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'I
gh?Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4V
ghY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
fh?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
fh?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3N?
fhH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
eh?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
ehY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
h?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
h?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
h(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
g?YH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
g?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
gH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
g5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
f?H@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N
f?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3N?
fH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
f@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N
e?H5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
e?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
e?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
eH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
e5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
e@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
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g?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7
g?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
hL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7J?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
h?1)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
h?X@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
ehX)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W?
eh?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@ @@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
fhL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
fh?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7J?
@@
fh?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
ghX)6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
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gh?X?K)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&O2WW?
@@@@
X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W?
?XX6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2W?
)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
K)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&
?X6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2WO?
?K?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O2O
6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?K?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O2O
6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
K6@@K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O?@2O?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O

Peter Scott (UK)

Luis Ferrer (E)

Trattamento con finasteride in cani


affetti da patologie prostatiche
Daniele Zambelli (I)
Treatment of urinary incontinence in
the bitch: clinical trail with tablets containing oestrol (Incurin)
S. Hendriks (NL)

Lorenzo Crosta (I)

Interruzione di gravidanza nella cagna


mediante somministrazione endovaginale di PGF2 alfa
Mario Cinone (I)
Induzione dellestro nella cagna con un
analogo del GnRH
Stefano Belluzzi (I)

MEDICINA PER ANIMALI ESOTICI


Chairman: Massimo Millefanti

Peter Scott (UK)


Alimentazione e patologie
nutrizionali degli uccelli (60)

9,30

MEDICINA PER ANIMALI ESOTICI


Chairman: Lorenzo Crosta

SALA BIANCA 200

N G R
A Z I

SALA BLU 120

SALA AZZURRA 100

E S S O
O N E

8,30

IENTIFICO

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

EMATOLOGIA
Chairman:
George Lubas

ORTOPEDIA
Chairman:
Carlo Maria Mortellaro

OFTALMOLOGIA
Chairman:
Claudio Peruccio

Displasia del gomito:


eziologia, epidemiologia,
genetica, segni clinici, segni
radiologici, diagnosi e
approccio terapeutico (120)

Approccio alla cecit


improvvisa (60)

14,30 RELAZIONE SULLO STATO


DELLARTE
Coagulopatie nel cane e nel
gatto (60)

Venerd Pomeriggio 19 Giugno 1998

Marco Caldin (I)

Simon Petersen-Jones (UK)

15,30 Daccordo: una coagulopatia!


Ma non potrebbe essere
Ehrilichiosi? (60)

Guillermo Couto (USA)


16,30

Mancata unione del processo anconeo e frammentazione del processo coronoideo mediale, osteocondrosi e
incongruit articolari del gomito: fattori eziologici e metodi di controllo. Una procedura guidata per il veterinario
pratico per arrivare alla diagnosi. Indicazioni terapeutiche, vantaggi e svantaggi dei trattamenti chirurgici pi
comunemente impiegati.

H.A.W. Hazewinkel (NL)

ENDOCRINOLOGIA
Chairman:
Alessandra Fondati

Segni oculari di patologie


sistemiche nel cane (60)

Ellen Bjerkas (N)

ORTOPEDIA
Chairman:
Aldo Vezzoni

17,00 RELAZIONE SULLO STATO


DELLARTE
Approccio diagnostico e
terapeutico allipotiroidismo
(60)
A.D. Rijnberk (NL)

Nuove tecniche e nuovi materiali in


ortopedia (120)

OFTALMOLOGIA
Chairman:
Antonella Vercelli
Masse oculari pigmentate e
non pigmentate (60)

Fissatore esterno tubolare, PC-FIX, mini-placca


maxillofacciale Trattamento chirurgico alternativo
nellartrosi dellanca del cane (15) Tenotomia dellileopsoas, neurectomia della capsula articolare,
miectomia del pettineo Protesi totale danca non
cementata (20) Dagli studi sperimentali allimpiego clinico

Adolfo Guandalini (I)

*
Hills

18,00
RELAZIONE
SULLO STATO DELLARTE
Approccio diagnostico
e terapeutico
alliperadrenocorticismo (60)
A.D. Rijnberk (NL)

Descrizione di una modifica della tecnica di


Slocum per il trattamento non convenzionale della
rottura del legamento crociato anteriore nel cane
(25) Trattamento della lussazione rotulea nel
cane e nel gatto (30) Cranializzazione della tuberosit tibiale per il ripristino della biomeccanica
articolare

Pierre Montavon (CH) e


Cornelius Von Werthern (CH)

Manifestazioni oculari del


complesso eosinofilico del
gatto (60)

Stefano Pizzirani (I)

19,00 Interruzione
19,30

C E R I M O N I A
20,30

Livello di Aggiornamento

Livello Avanzato

24

S A L A
E
D A P E R T U R
Q U A
F E T

R
D

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

MEDICINA PER
ANIMALI ESOTICI
Chairman:
Peter Scott

NEUROLOGIA
Sessione interattiva
Chairmen: Massimo Baroni e
Tommaso Furlanello

MALATTIE INFETTIVE
Chairman:
Alessandra Fondati (I)

Trattamento chirurgico delle


pi comuni patologie delle
tartarughe (60)

Il grande dibattito:
vantaggi e svantaggi nelluso
dei corticosteroidi nelle
patologie spinali del cane (60)

Mielopatia degenerativa del


Pastore Tedesco: una patologia
controversa difficile da
diagnosticare e da trattare (60)

Rick LeCouteur (USA)


e Simon Wheeler (UK)

15,30

Efficacy of a high titre MLV against CDV in


puppies with maternal antibodies
J.G.H.E Bergman (NL)
Canine leptospirosis, do we use proper vaccination programmes? - D. Salgado (E)
Un caso clinico di Febbre delle Montagne
Rocciose in un cane del nord est dellItalia
Tommaso Furlanello (I)

16,30

MEDICINA PER
ANIMALI ESOTICI
Chairman:
Leonardo Brunetti

TECNICHE DIAGNOSTICHE
MINI-INVASIVE
Sessione interattiva
Chairman: Stefano Romussi

MEDICINA FELINA
Chairmen: Stefano Bo (I) e
Hans Lutz (CH)

Anestesia e chirurgia dei pesci


ornamentali (50)

Metodiche mini-invasive per


lapproccio diagnostico alle
principali patologie addominali
Una discussione interattiva basata
su casi clinici con lausilio della
valutazione citologica (120)

Attempts to cure feline leukemia virus


infection with biologic response modifier
treatment
Karin Hartmann (D)

17,00

Peter Scott (UK)

Efficacia della marbofloxacina iniettabile nel


trattamento delle infezioni delle vie urinarie
distali nel cane - Claudio Brovida (I)

Pi comuni malattie virali,


batteriche e parassitarie dei
pesci ornamentali (50)

Mario Caniatti (I)


e Roberto Santilli (I)

ellArte

Effect of recombinant human granulocyte


colony-stimulating factor on hematopoiesis
in neutropenic cats caused by different
diseases
Manuela Kuffer-Frank (D)

18,00

19,00

E U R O P A
A
E
C O N C E R T O

P O
B E

Comparative studies of the efficacy of two


leukemia virus vaccines
Hans Lutz (CH)
Serum bile acids and feline trypsin-like
immunoreactivity after exogenous pancreatic
stimulation with ceruletid in normal cats
Thomas Spillmann (D)
Adenocarcinoma of a labial minor salivary
gland in a cats
Dimitrios Tontis (GR)
Monitoraggio ecografico di morte fetale nel
gatto: caso clinico
Iacopo Vannozzi (I)

Massimo Millefanti (I)


Recenti acquisizioni nellimpiego
dei glucani come integrazione
nutrizionale nei pesci ornamentali (20)
Giuseppe Mosconi (I)

R T I C O
N V E N U

19,30

L I R I C O
20,30

Sessione Specialistica

Sessione Interattiva

25

4 C O N G R E S S O F E C AVA S C I VA C

Treatment of canine leishmaniosis with


Amphtotericin B (Fungizone): four years
later - Jacques Lamothe (F)

Venerd Pomeriggio 19 Giugno 1998

Rick LeCouteur (USA)


e Simon Wheeler (UK)

Stephen Divers (UK)

14,30

A new drug for the teatment of canine leishmaniosis: Amphotericin B lipid complex
(Abelcet) - Jacques Lamothe (F)

Leonardo Brunetti (I)

RELAZIONE SULLO STATO


DELLARTE
Trattamento demergenza e
stabilizzazione medica dei rettili (60)

Protective effect of an insecticidal spray


against Phlebotomus perniciosus , a vector
of leishmaniasis - Frederic Ascher (F)

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

ONCOLOGIA
Chairman:
Claudio Capurro

EPATOLOGIA
Chairman:
Marco Caldin

OFTALMOLOGIA
Chairman:
Alberto Crotti

Recenti applicazioni e
interpretazioni degli esami
epatici (60)

Segni oculari di patologie


sistemiche nel gatto (60)

Denny Meyer (USA)

Ellen Bjerkas (N)

8,30 RELAZIONE SULLO STATO


DELLARTE
La chemioterapia da un punto
di vista pratico (60)
Guillermo Couto (USA)

Sabato Mattina 20 Giugno 1998

9,30

Guillermo Couto (USA)


10,30

DERMATOLOGIA
Chairman:
Antonella Vercelli

Gli effetti delle patologie


extra-epatiche sul fegato
(60)

Trattamento delle ulcere


corneali nei piccoli animali
(60)

Denny Meyer (USA)

Complicazioni della
chemioterapia ed emergenze
oncologiche (60)

Simon Petersen-Jones (UK)

EPATOLOGIA
Chairman:
Ugo Lotti

Dominique Heripret (F)

OFTALMOLOGIA
Chairman:
Adolfo Guandalini

La biopsia epatica: quando e come


eseguirla alla luce di una corretta
interpretazione del referto clinico (60)
Quando il clinico e il patologo hanno
bisogno luno dellaltro

Modificazioni oculari
nellanimale anziano
(60)

Denny Meyer (USA)

11,00 Manifestazioni dermatologiche


di patologie sistemiche
(60)

Claudio Peruccio (I)


R

12,00
Patologie cutanee da
micobatteri (60)

Novit nellapproccio
terapeutico alle patologie
del fegato (60)

Denny Meyer (USA)

Luis Ferrer (E)


13,00

Lussazioni della lente (60)

Stefano Pizzirani (I)

Livello di Aggiornamento

Livello Avanzato

26

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

DERMATOLOGIA
Chairman:
Alessandra Fondati

ORTOPEDIA
Sessione specialistica
Chairman: Piermario Piga

NEUROLOGIA
Chairman: Stefano Pizzirani (I)

Discussione clinico-patologica
di casi dermatologici (120)

Progressi nel trattamento delle


pi frequenti patologie
ortopediche
Il metodo di Ilizarov in ortopedia dei piccoli animali: dallanalisi retrospettiva alle possibilit
per il futuro (60)
Antonio Ferretti (I)
e Matteo Tommasini (I)

Atypical behaviour of a nasopharyngeal


polyp causing a vestibular syndrome in a
cat - Marco Bernardini (I)

CITOLOGIA
Chairman:
Davide De Lorenzi

Tre casi di cisti aracnoidee nel


cane: valutazione a lungo termine
del protocollo terapeutico
Stefano Romussi (I)

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman: Carlo Scotti

Citologia pratica per il


veterinario.
Dalla corretta preparazione
allinterpretazione dello
striscio citologico (120)

9,30

GM 1 - Gangliosidosis in Alaskan
Huskies
Andreas Moritz (CH)

Daniele Cotto (I)


e Gianluca Rovesti (I)

A case of canine central diabetes insipida caused by a chromophobe cell adenoma of the hypophysis
J.H. Duarte Correia (P)

Problemi in chirurgia toracica


(120)
Da una discussione interattiva di
casi clinici lanalisi dei principali
problemi riscontrati dal veterinario
nellesecuzione delle tecniche di
chirurgia toracica
R

10,30

CARDIOLOGIA
Chairmen: Claudio Bussadori (I)
e Chris Lombard (CH)
Electrocardiographic features of
Deerhounds - A.R. Bodey (UK)

11,00

Valutazione dellanestesia generale con


propofol in cani normali e con
compromesse funzioni cardiorespiratorie
Antonello Bufalari (I)
Clinical trial of pimobendan: a new
inotropic/vasodilator drug: Long term
survival time study: the results
D. Bruyre (B)
Correlazione tra dilatazione atriale sinistra,
peso corporeo ed insorgenza della
fibrillazione atriale nel cane
Carlo Guglielmini (I)

12,00

Clinical efficacy of the new inodilator


pimobendan, in comparison to digoxin for
the treatment of congestive heart failure in
dogs - Rainer Kleeman (D)

ellArte

Percutaneous balloon valvuloplasty in


dogs with pulmonic stenosis
M Schneider (D)

Dan Smeak (USA)


e Richard A. White (UK)

Corinne Fournel (F)

Sessione Specialistica

Sessione Interattiva

27

13,00

4 C O N G R E S S O F E C AVA S C I VA C

Vercelli/Schiavi
Noli/Fabbrini
Mechelli/Galeotti
Noli/Scarampella
Tieghi/Abramo

Neurological findings in Cocker


Spaniels with familial vitamin E deficiency and retinal pigment Epithelial
Dystrophy - Rodolfo Cappello (I)

Sabato Mattina 20 Giugno 1998

*
Hills
Fissazione con chiodo
bloccato: un nuovo metodo di
fissazione ossea nei piccoli
animali (60)

8,30

PROGRAMMASC
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

DERMATOLOGIA
Chairman:
Chiara Noli

EMATOLOGIA
Chairman:
Marco Caldin

NEUROLOGIA
Chairman:
Marco Bernardini

Linterpretazione dello striscio


ematico

Identificazione delle lesioni


neurologiche (localizzazione,
diagnostica per immagini
e altri esami)

14,30 RELAZIONE FECAVA


Patologie ungueali nei cani e
nei gatti: diagnosi e trattamento
(60)

Alterazioni morfologiche dei


globuli rossi e dei globuli
bianchi (120)

Prima parte:
Lesioni cerebrali (40)

Sabato Pomeriggio 20 Giugno 1998

Didier Carlotti (F)

15,30

*
Hills
Approccio diagnostico
allalopecia nel cane e nel gatto
(60)

Dominique Heripret (F)


16,30

Seconda parte:
Lesioni del midollo spinale (40)
Terza parte:
Lesioni a livello
neuromuscolare (40)
Rick LeCouteur (USA)
e Simon Wheeler (UK)

Bernard Feldman (USA)

DERMATOLOGIA
Chairman:
Alessandra Fondati
17,00 Reazioni cutanee da farmaco
(60)

MEDICINA INTERNA
Chairman:
Tommaso Furlanello
Febbre di origine sconosciuta
(60)

NEUROLOGIA
Chairman:
Donatella Lotti
Diagnosi e trattamento
dellepilessia nel cane e nel
gatto (60)

Guillermo Couto (USA)


Luis Ferrer (E)
Simon Wheeler (UK)
18,00
Prurito cronico nel cane e nel
gatto e impiego di farmaci
antiprurito (60)

Dominique Heripret (F)

Trattamento clinico
e chirurgico del paziente
con trauma spinale (60)
Infezioni recidivanti nel cane
(60)

Guillermo Couto (USA)

Rick LeCouteur (USA)

19,00

Livello di Aggiornamento

Livello Avanzato

28

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

UROLOGIA E
NEFROLOGIA
Chairman:
Claudio Brovida

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman:
Carlo Maria Mortellaro

ONCOLOGIA
Chairmen: Giorgio Romanelli (I)
e Claudio Capurro (I)

Utilit dellultrasonografia nella


diagnosi delle malattie delle
vie urinarie nel cane e nel
gatto (60)

Approccio al paziente con


patologie delle prime vie
respiratorie (120)

Su un caso di pseudocisti pancreatica


associata a carcinoma acinoso, pancreatite cronica e steatite multifocale necrotizzante in un gatto.
Andrea Boari (I)

14,30

Parametri istologici di prognosi nei tumori


mammari maligni della gatta
Cinzia Benazzi (I)

Claudio Bussadori (I)

A.R. Michell (UK)

Micrometastasi linfonodali nei tumori


mammari maligni della cagna
Giuseppe Sarli (I)
Valutazione dellerogazione locale di
cisplatino in un modello di carcinoma
mammario murino
Emanuela Morello (I)

Richard A. White (UK)

UROLOGIA E
NEFROLOGIA
Chairman:
Fabio Vigan

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman:
Giorgio Romanelli

Insufficienza renale acuta:


dallemergenza alla
stabilizzazione del paziente
(60)

Claudio Brovida (I)

Chirurgia plastica ricostruttiva


(120)
I concetti pratici per una corretta
applicazione dei principi della
chirurgia plastica ricostruttiva
dallanalisi di casi clinici

Pericardiectomia toracoscopica per il


trattamento della pericardite effusiva
recidivante: prime esperienze in due
casi - Fabio Acocella (I)

A.R. Michell (UK)

ellArte

17,00

Evaluation of Valtrac biofragmentable


anastomosis ring on thoracal esophagus in the dog - T. Nmeth (H)
Systemic response of blood inflow
occlusion to the liver in dogs
Jani Pecar (SI)

Trattamento della contrattura in flessione


del carpo mediante la tecnica di Ilizarov:
4 casi - Gianluca Rovesti (I)
Bone defects in dogs treated by a new
tissue transplantation
Nenad Sesic (Croatia)

Dan Smeak (USA)

18,00

Clinicopathological features of multiple


cartilaginous exostosis in three littermate dogs - M. Novales (E)

Approccio terapeutico alle


patologie renali (60)

16,30

CHIRURGIA E ORTOPEDIA
Chairmen: Carlo Scotti (I) e
Aldo Vezzoni (I)

Medial approach for Total Hip


Replacement in Dogs: an experimental
study - Z. Diszegi (H)

15,30

Sessione Specialistica

19,00

Sessione Interattiva

29

4 C O N G R E S S O F E C AVA S C I VA C

Parametri istologici di prognosi nei tumori


mammari maligni della cagna
Marco Galeotti (I)

Tecniche diagnostiche
impiegabili per il
riconoscimento precoce delle
patologie renali (60)

Sabato Pomeriggio 20 Giugno 1998

Integrazione dei parametri clinici ed istologici nella prognosi dei tumori mammari
maligni della cagna e della gatta
Ombretta Capitani (I)

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

CHIRURGIA DEI TESSUTI MOLLI


Chairman:
Massimo Gualtieri

CARDIOLOGIA
Chairman:
Gino DAgnolo

NEUROLOGIA
Chairman:
Marco Bernardini

Tachicardia sopraventricolare
nel cane (60)

Patologie discali cervicali:


approccio diagnostico e
modalit di trattamento (60)

8,30 Concetti attuali nel trattamento


della peritonite (60)

Simon Wheeler (UK)


Dan Smeak (USA)

Domenica Mattina 21 Giugno 1998

9,30
RELAZIONE SULLO STATO
DELLARTE
Trattamento chirurgico delle
lesioni retto-anali, anali,
perianali e perineali (60)

CHIRURGIA DEI TESSUTI MOLLI


Chairman:
Carlo Maria Mortellaro

Patologie discali
toraco-lombari: diagnosi e
trattamento (60)

Stefano Pizzirani (I)

12,00

Richard A. White (UK)

CARDIOLOGIA
Chairman:
Claudio Bussadori

NEUROLOGIA
Chairman:
Massimo Baroni

Considerazioni terapeutiche
sulla cardiomiopatia dilatativa
del cane (60)

Patologie lombo-sacrali (60)

Karsten E. Schober (D)

Rick LeCouteur (USA)

Cardiomegalia nel gatto: cosa


fare dopo la diagnosi (60)

11,00 Approccio chirurgico alle patologie dellorecchio esterno e


dellorecchio medio (120)

13,00

Istruzioni per un approccio


ragionato alle extrasistoli
sullECG (60)

Cristophe Lombard (CH)

Gert Niebauer (A)


10,30

Karsten E. Schober (D)

La Sindrome di Wobbler:
considerazioni sul
trattamento (60)

Cristophe Lombard (CH)

Livello di Aggiornamento

Simon Wheeler (UK)

Livello Avanzato

30

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

ODONTOSTOMATOLOGIA
Chairman:
Dea Bonello

CITOLOGIA
Sessione specialistica
Chairman: Mario Caniatti

MEDICINA INTERNA
Chairmen: Tommaso Furlanello (I)
e A.R. Michell (UK)

Urgenze in odontostomatologia (60)

Citologia linfonodale:
quadri normali, infiammatori e
neoplastici (120)

Un caso di discinesia ciliare primaria


nel cane - Davide De Lorenzi (I)
Analysis of morbidity of dogs in the
region of the city Kosice, Slovakia
during 1995-1997 - M. Kozak (SK)

Frank Verstraete (B)

Preliminary results on the use of


cabergoline, a prolactin inhibitor, for
the control of mammary tumors in
the bitch before surgery
J. Verstegen (B)

Corinne Fournel (F)

ODONTOSTOMATOLOGIA
Chairman:
Simon Kleinjan
La radiologia come strumento
diagnostico delle patologie del
cavo orale (60)

ellArte

Incidence of atopic diseases


in dogs in Slovakia
Pavol Chandoga (SK)

10,30

Granulomatosi linfomatoide cutanea


primaria in un cane
Leonardo Della Salda (I)

Sessione Specialistica

12,00

Efficacy of terbinafine against


dermatophytosis in cats an open randomized blind study
(preliminary results)
R. Wagner (A)

Guillermo Couto (USA)

11,00

Efficacia delle permetrine CIS:


Trans 25/75 microincapsulate
nella terapia delle otoacariasi
in cani e gatti
Fabrizio Fabbrini (I)

Le leucemie (60)

Linfomi extranodali nel cane e


nel gatto (60)

Tavola rotonda su casi clinici


Etica, limiti e compromessi nel
trattamento delle malocclusioni (60)

DERMATOLOGIA
Chairmen:
Alessandra Fondati (I) e
Luca Mechelli (I)

Guillermo Couto (USA)

Dea Bonello (I), Thomas Eriksen


(DAN), Peter Fahrenkrug (D),
Frank Verstraete (B),
Aldo Vezzoni (I)

ONCOLOGIA
Sessione specialistica
Chairman:
Claudio Capurro

Frank Verstraete (B)

*
Hills

9,30

Prolactin and antiprolactinic drugs in


dogs and cats: relative efficacy and
mode of action of the veterinary available drugs - J. Verstegen (B)

Aggiornamenti in odontoiatria
felina (60)

Sessione Interattiva

31

13,00

4 C O N G R E S S O F E C AVA S C I VA C

Diagnosi di glomerulopatia nel cane:


valutazione qualitativa della proteinuria - Paola Scarpa (I)

*
Hills

Domenica Mattina 21 Giugno 1998

Comparative diagnostic imaging of


the pelvic cavity in dogs
Dieter Malleczek (A)

Frank Verstraete (B)

8,30

PROGRAMMASC
SALA ITALIA 350

SALA TOPAZIO 300

CHIRURGIA DEI TESSUTI MOLLI


Chairmen:
Carlo Maria Mortellaro
e Matteo Tommasini

Domenica Pomeriggio 21 Giugno 1998

SALA EUROPA 900

CARDIOLOGIA
Chairman:
Michele Borgarelli

NEUROLOGIA
Chairman:
Stefano Pizzirani

Meccanismi patogenetici e
trattamento delle patologie
pericardiche (60)

Neoplasie del Sistema


Nervoso Centrale (60)

14,30 RELAZIONE SULLO STATO


DELLARTE
Concetti attuali nel trattamento
della dilatazione-torsione di
stomaco nel cane (60)
Dan Smeak (USA)

Claudio Bussadori (I)


Rick LeCouteur (USA)

15,30
Polipi auricolari, otite media e
sinusite nel gatto (60)
Esperienze e metodi personali di
trattamento di queste frequenti
patologie chirurgiche del gatto

Dan Smeak (USA)


16,30

Ipertensione nel cane (60)


Una patologia difficile
da riconoscere e trattare

A. R. Michell (UK)

RELAZIONE SULLO STATO


DELLARTE
Aggiornamenti in chirurgia
spinale (60)

Simon Wheeler (UK)

S A L A
C E R I M O N I A
D I
C H I U S U R A
A R R I V E D E R C I
A
L

17,00

T E R M I N E

D E L

INCONTRA
Durante il Congresso, saranno organizzate sessioni di
approfondimento con i relatori, durante le quali i partecipanti potranno porre domande ai relatori.
Sar cos possibile approfondire un argomento o prolungare una discussione in un contesto rilassato ed informa-

Livello di Aggiornamento

Livello Avanzato

32

Relazione sullo Stato de

IENTIFICO
SALA AZZURRA 100

FARMACOTERAPIA
Chairman:
Enrico Febbo

ONCOLOGIA
Sessione interattiva
Chairmen: Claudio Capurro e
Richard A. White

ODONTOSTOMATOLOGIA
Chairmen: Dea Bonello (I) e
Frank Verstraete (USA)

Farmacoterapia pratica: dove possiamo arrivare con un uso pi ragionato dei farmaci a nostra disposizione?

Discussione interattiva da casi


clinici di oncologia
Questo un caso trattabile o
no? (120)
Da una discussione tra i relatori e
luditorio le linee guida pratiche
per un corretto approccio
terapeutico al paziente oncologico

Dalla farmacocinetica
allapplicazione clinica (40)
David Aucoin (USA)

Sialadenitis and salivary gland infarction in cats and dogs


Mahmut Sozmen (UK)

15,30

Utilizzo di una corona tipo Richmond per


la ricostruzione del canino inferiore in
un cane di razza Boxer
Paolo Squarzoni (I)
Estrazione di un canino superiore paratopico in un cane
Enrico Stefanelli (I)

Paolo Buracco (I)


e Giorgio Romanelli (I)

E U R O P A
E
C O C K T A I L
D I
L I O N E
N E L
1 9 9 9

14,30

Risultati del trattamento di 56 tumori


del cavo orale nel cane
Emanuela Morello (I)

Criteri di utilizzo dei punti di fulcro per gli


elevatori durante le estrazioni dentali nel
cane - Paolo Squarzoni (I)

Trattamento antibiotico
empirico nelle malattie infettive
del cane e del gatto (40)
David Aucoin (USA)
Recenti acquisizioni in tema di
trattamento con corticosteroidi (40)
Tommaso Furlanello (I)

Valutazione radiologica dei tumori


maligni non odontogenici del cavo
orale del cane - Dea Bonello (I)

16,30

C O M M I A T O :
! ! !
17,00

C O N G R E S S O

IL RELATORE

ellArte

le. Lelenco dei relatori e gli orari delle sessioni saranno inseriti nella cartella congressuale ed affissi presso gli stand dei main sponsor, grazie al cui sostegno la partecipazione alle sessioni gratuita anche se limitata ad un numero massimo di 15
partecipanti per sessione. Le iscrizioni avranno luogo presso la segreteria
Congressuale fino ad esaurimento dei posti disponibili.

Sessione Specialistica

Sessione Interattiva

33

4 C O N G R E S S O F E C AVA S C I VA C

SALA BLU 120

Domenica Pomeriggio 21 Giugno 1998

SALA BIANCA 200

COMMISSIONESC
COMMISSIONE SCIENTIFICA
Presidente

GIORGIO ROMANELLI
STEFANO BO
DEA BONELLO
CLAUDIO BUSSADORI
ALESSANDRA FONDATI
TOMMASO FURLANELLO
SIMON KLEINJAN
MASSIMO MILLEFANTI
CLAUDIO PERUCCIO
STEFANO PIZZIRANI
ALDO VEZZONI

Coordinatore Congressuale FULVIO STANGA


Segreteria Congressuale

Med Vet,
Med Vet
Med Vet
Med Vet,
Med Vet
Med Vet
DVM
Med Vet
Med Vet,
Med Vet,
Med Vet,

DECVS

DECVIM-CA

DECVO
DECVS
DECVS

Med Vet

LUDOVICA BELLINGERI

DIRETTIVI
Consiglio Direttivo
SCIVAC in carica

CARLO SCOTTI
GIORGIO ROMANELLI
PIERMARIO PIGA
UGO LOTTI
GILDO BARONI
MARCO CALDIN
MATTEO SPALLAROSSA

Presidente
Past President
Vice Presidente
Segretario
Tesoriere
Consigliere
Consigliere

Direttivo FECAVA
in carica

BEN ALBALAS
MARC BUCHET
RAY L. BUTCHER
SIMON KLEINJAN

Presidente
Vice Presidente
Segretario
Tesoriere

58

I componenti dei Consigli Direttivi della FECAVA


e della SCIVAC ringraziano le aziende che attraverso
la sponsorizzazione hanno sostenuto la realizzazione
del Programma Scientifico e del Programma Sociale
di questo Congresso.
Grazie al loro contributo si sono potute contenere
le quote di iscrizione congressuale.

MAIN SPONSORS

MAJOR SPONSORS

*
Hills

Animal Health

4th European FECAVA SCIVAC Congress

SPEAKERS CURRICULAE VITAE


DAVID AUCOIN
DVM, Dipl ACVCP
Dr. David Aucoin graduated in 1980 at the Michigan State
University. He then attended an Internship in Medicine and
Surgery in 1981 until 1983 at the Animal Medical Center of
New York. In 1985 he attended a Fellowship at the Cornell
University Medical College in Clinical Pharmacology. In
1984-85 he became Associate Staff Professor at the Animal
Medical Center in New York then Visiting Assistant Professor
at the North Carolina State University Raleigh from 1985 to
1990. From 1990 to 1992 he was Associate Research Professor at the same University. He is a Diplomate of the American College of Veterinary Clinical Pharmacology since 1992
and Board Qualified of the American College of Veterinary
Internal Medicine

ELLEN BJERKAS
DVM, PhD, Dipl ECVO
Graduated from the Norwegian College of Veterinary medicine in 1972. Associate Professor at the Norwegian College of
Veterinary Medicine. Head of the outpatient clinic and the
ophthalmology section.
1991: PhD degree. Thesis: Inherited eye diseases among dogs
in Norway. Founding member of the Norwegian panel for diagnosing inherited eye diseases. ECVO Diplomate.

CLAUDIO BROVIDA
Med Vet
Graduated in Veterinary Medicine at the University of Turin
in 1974. He has always been a small animal private practitioner with main interest in urology/nephrology and respiratory tract. He has spent long periods of updating in veterinary
medicine in Great Britain, Holland and USA. Author of articles on national and international scientific reviews and
speaker at veterinary conferences. He has been President of
AIVPA, President of the Organising Committee of the 7th
WSAVA Congress held in Rome in 1992. Currently he is vice
President of WSAVA.

LEONARDO BRUNETTI
Med Vet
Graduated in Veterinary Medicine at the University of Pisa in
1982. His interest has always been on Exotic Animals and he
has spent many years carrying out researches in numerous

zoos in Italy and abroad. He has attended the Italian edition


of a book on anaesthetics on wild animals and is author of scientific papers on exotic animals. For many years he has been
co-ordinator of the SCIVAC Exotic Animal Study Group.

PAOLO BURACCO
Med Vet
Graduated in Veterinary Medicine at the University of Turin
in 1981. In 1987/88 he was Visiting Professor at the School
of Veterinary Medicine of the Purdue University (Indiana,
USA) in the Comparative Oncology Group. Since November
1992 he is Associate Professor of Semiotics Surgery at the
University of Turin. He has been speaker at numerous national and international meetings on veterinary oncology and his
main interests are on early diagnosis of primitive animal tumours, of their metastasis and of the most effective treatments. He therefore studies mainly skeletal, oral, endonasal,
endothoracic and cutaneous neoplasias. He is author of 89 papers, including congress communications and papers published on national and international veterinary journals.

CLAUDIO BUSSADORI
Med Vet, Dipl ECVIM
Graduated in Veterinary Medicine at the University of Milan
in 1982. He is a private practitioner and consultant in cardiology and has carried out numerous cardiological researches for the Universities of Turin and Parma where he has also
been lecturer. His main researches are on lung and systemic
hypertension, treatment of congenital cardiopathies, experimental echocardiography and cardiac tumours. He is a Diplomate of the European College of Internal Medicine (ECVIM)
and since 1990 he is Study Director of international research programmes on the use of cardiovascular drugs in veterinary cardiology.

MARCO CALDIN
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna with a thesis on Instrumental Diagnosis in Small
Animal Cardiology. He has been the co-ordinator of SCIVAC Study Group on Imaging Diagnostics from 1988 to
1990. He has been speaker at numerous meetings, practical
courses and seminars as well as lecturer at the University of
Pisa and University of Padova. He has also been SCIVAC
Board member and co-ordinator of SCIVAC Study Group on

Internal Medicine. He is a private practitioner in Padova at the


San Marco Veterinary Clinic.

MARIO CANIATTI
Med Vet
Graduated in Veterinary Medicine at the University of Milan.
In 1990-1994 he worked at the University of Milan in the department of Veterinary Pathologic Anatomy
and Avian
Pathology. In 1994 he became researcher at the University of
Milan. From September 1988 to March 1989 he carried out a
research work at the University of California (Davis) at the
Department of Pathology on immunoistochemicals of cutaneous neoplasias in the dog with Professor Peter F. Moore. In
April/May 1989 he stayed at the University of Barcelona for
a research work on immunistochemicals of cutaneous tumours.
His current research work is on diagnostic cytology, comparative pathology of cutaneous neoplasias of linphoproliferative
diseases. He has published over 40 scientific articles on Italian and international scientific journals.

DIDIER CARLOTTI
DVM, Dipl ECVD
Dr. Didier Carlotti graduated from Toulouse University in
1977 and has been a private practitioner in Carbon Blanc, near
Bordeaux, Aquitaine, France since 1979. He has been a full
member of the AAVD since 1985 and was the President of
the French Small Animal Dermatology Study Group
(GEDAC) from 1985 to 1991. The GEDAC is a specialised
group of the French Small Animal Veterinary Association
(CNVSPA), of which he was the representative at WSAVA
since 1985 and Vice-President since April 1989 until April
1993. He is currently the General Secretary of CNVSPA. He
was also the Chairman of the Federation of European Companion Animal Veterinary Associations (FECAVA) from May
1990 to June 1995. He is a founder Member and Past President (1988-1990) of the European Society of Veterinary Dermatology (ESVD). He is a Diplomate (and currently the honorary secretary) of the European College of Veterinary Dermatology (ECVD). He has published about 50 papers and has
given numerous lectures in the field of Veterinary Dermatology.

GUILLERMO COUTO
DVM, Dipl ACVIM
Graduated from Buenos Aires University in 1976. From 1976
to 1981 he was Assistant Professor at the Department of
Pathology of the same University. He attended a Residency on
Clinical Oncology at the University of California, Davis from
1981 to 1983 and for the following 5 years he was Assistant
Professor at the Ohio State University Department of Veterinary Clinical Sciences. He then became Associate Professor
at the same University and from 1995 he is Professor at the
Department of Veterinary Clinical Sciences of the Ohio State

4th European FECAVA SCIVAC Congress

University.
Moreover he is Charter Diplomate of the American College of
Veterinary Internal Medicine, Specialty of Veterinary Medical
Oncology, co-editor of Essentials of Small Animal Internal
Medicine, Editor in Chief of the Journal of Veterinary Internal
Medicine and has over 150 scientific publications in the areas
of oncology, haematology and immunology.
He was President of the Veterinary Cancer Society from 1990
to 1992.

LORENZO CROSTA
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1989 with a thesis on avian diseases. He is member of the
Association of Avian Veterinarians and has attended various stages in avian clinics abroad.
Author of papers at international avian meetings and organiser of practical courses and seminars for SCIVAC and for the
University of Milan. His current interest is exclusively in
avian medicine with a particular interest in problems linked to
breeding in captivity. The preferred species are parrots, eagles
and ostriches. He is one of the founders of Clinica Veterinaria Fiera, a private practice in Milan.

STEPHEN J. DIVERS
BSc (Hons), BVetMed, CBiol, MIBiol, MRCVS
Dr. Stephen Divers achieved a bachelor of Veterinary Medicine degree (BVetMed) at the Royal Veterinary College, University of London in 1994 with a distinction in the exotic animal elective. He has been lecturer on MSc degree course in
Wild Animal Medicine at the London Zoo and lecturer on the
final year elective at the Royal veterinary College (small animals, reptile pharmacology, reptile therapeutics and reptile
anaesthesia). Dr. Divers has been speaker at numerous national and International Meetings and is author of over 50 articles mainly on reptile medicine.

BERNARD F. FELDMAN
DVM, PhD, Dipl ACVIM
Dr. Bernard F. Feldman is currently Professor of Veterinary
Clinical Haematology and Biochemistry at the Virginia
Maryland Regional College of Veterinary Medicine (VMRCVM). He is formerly Professor of Veterinary Clinical
Pathology at the University of California at Davis. Dr. Feldman has received numerous teaching and research awards, has
published 3 books and over 250 articles. He has been on the
faculty at the Veterinary College of the University of Utrecht,
The Netherlands, and the Royal Veterinary College in Copenhagen, Denmark. He was recently nominated as Outstanding
Alumnus (1997) of the University of California at Davis,
School of Veterinary Medicine. Currently he is Chief of Laboratory Diagnostics Services and Director of the Clinical
Pathology Laboratory at the VMRCVMs Veterinary Medical
Teaching Hospital. Dr. Feldman is President of the American

4th European FECAVA SCIVAC Congress

Society for Veterinary Clinical Pathology and on the Board of


Directors of the Veterinary laboratory Association.

LUIS FERRER
DVM, PhD, Dipl ECVD
Graduated in Veterinary Medicine in 1981 in the Veterinary
School of Zaragoza (Spain) and obtained the PhD in 1984 in
the Veterinary School of Hannover (Germany). Since 1984 he
is Professor of Pathology and Dermatology in the Veterinary
School of Barcelona (Spain). His major research lines are dermopathology, canine leishmaniosis and the role of mast cells
in canine allergic dermatitis.

ANTONIO FERRETTI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Milan
in 1979. He is a private practitioner and has always carried out
researches on small animal surgery especially Orthopaedics
and Traumatology. In 1982 he began studying the Ilizarov
Method and the year after he started its application. In 1988
and 1991 he spent time with Prof. G.A Ilizarov at the Orthopaedic and Traumatological Institute of Kurgan in Siberia
to deepen the knowledge on his method. Since 1993 he is a
Diplomate of the European College of Veterinary Surgeons
and is SCIVAC co-ordinator of the orthopaedics study group.
He is currently a veterinary surgeon in a private practice near
Milan.

speaker at numerous SCIVAC national meetings and seminars on internal medicine which represents his scientific and
professional interest. He has been instructor at SCIVAC Practical Courses on Laboratory Diagnostics and Problem Oriented Clinical Approach. He is co-author of SCIVAC Therapeutical Manual. He is author of numerous scientific papers and
has been speaker also at international meetings. He has been
lecturer in Infectious Diseases in the Dog and Cat at the University of Padova in the years 1996-1997.

ADOLFO GUANDALINI
Med Vet
Graduated in Veterinary Medicine in 1998 with honours at
the University of Perugia. In 1990/1991 he attends an Internship in Veterinary Ophthalmology at the National Veterinary
School of Lyon. In 1993 he is Visiting Assistant Professor at
the College of Veterinary Medicine, Ophthalmology Department of the University of Florida. From 1991 to 1997 he attends externships at: Animal Eye Associates (Chicago, Illinois), Animal Ophthalmology Clinic (Dallas, Texas), Ohio
State University, Sacramento Animal Medical Group (Sacramento, California), Veterinary Ophthalmology Services (Warwick, Rhode Island), University of North Carolina at Chapel
Hill. He is author and co-author of various scientific paper on
veterinary ophthalmology . Since 1993 he is Board member of
SOVI (Italian Association of Veterinary Ophthalmology). He
has been Board member for abroad of AIVPA in 1993/1996.

HERMAN A. W. HAZEWINKEL
DVM, PhD, Dipl ECVS
CORINNE FOURNEL-FLEURY
DVM, PhD
In 1978-1980 she was Resident in Internal Medicine and in
1981 to 1986 she has been Assistant Professor in Internal
Medicine and in 1991 she became Professor. 1993 she became
Chief Internal Medicine Service/Domestic carnivores at the
National School of Veterinary Medicine Lyon, France. She
has had an intense clinical laboratory activity starting in 1988
with the creation and direction of the Immunopathology - Cytology - Haematology Diagnostic and Research Laboratory
and in the same year achieved the specialised studies certificate in immunology and immunopathology. In 1989 she specialised in General Haematology and in 1990 in Cellular Biology Methods and achieved a Masters in Immunology and
haematology biological sciences. Her PhD in 1996 was on
Morphological and Phenotypical characterisation of canine
lymph node lymphoid cells. Application to the study of canine
non-Hodgkin lymphomas.

TOMMASO FURLANELLO
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna in 1991. He is a small animal private practitioner at
the Clinica Veterinaria San Marco. Since 1992 he has been

Graduated in 1976 at Utrecht University. After working in private practice he joined the Universitys Department of veterinary Sciences in Companion Animals. Responsible for education and treatment of referred orthopaedic patients, he became interested in nutritional and hormonal related skeletal
diseases. He is member of AO-Vet, Diplomate of the European College of Veterinary Surgeons, Board member of the
European Society for Veterinary Orthopaedics and Traumathology, and chaired the organisation of the annual congress of
the European Society for Veterinary and Comparative nutrition.

DOMINIQUE HERIPRET
DVM, Dipl ECVD
Dr. Heripret graduated from the Vet School of Maisons Alfort
in 1981, he then completed a PhD on Use of skin-tests in the
diagnosis of FAD: about 169 cases. From 1987 to 1994 he
worked at the referral practice Clinique Fregis in France
where he was in charge of the internal medicine service mainly of dermatology and endocrinology. In 1990 he was Member of the scientific comity of GEDAC (French Dermatology
Group) and in 1991 he was secretary of the same group. In
1992 he was Board member (Treasurer) of the ESVD and in
1996 he became Diplomate of the European College of Vet-

erinary Dermatology. He has done more than 75 presentations and his main interests include Endocrinology, Non
steroid antipruritic drugs and hypersensitivity in dermatology.

RICHARD LeCOUTEUR
BVSc, VMD, PhD, Dipl ACVIM (Neurology), Dipl
ECVN
Rick graduated from the University of Sydney in Australia
in January 1975. After a year in private small animal practice in Sydney, he completed an Internship and Residency in
Surgery at the University of Guelph in Canada in 1976-78.
He then completed a Residency in Neurology and Neurosurgery at the University of California Davis from 1978 to
1980. From July 1980 through January 1984, Rick completed a PhD in Comparative Pathology at the University of California in Davis. The area of Study was spinal Cord Injury.
From 1984 to June 1988 he was on faculty at Colorado State
University, where he was an Assistant Professor and then
Associate Professor until 1989. In September 1989 he returned to Australia to establish a Specialty Practice in Neurology and Neurosurgery in Sydney. In January 1995 he returned to the USA to assume the position of Professor in
Neurology and Neurosurgery at the University of California
at Davis.
he is Diplomate of the American College of Veterinary Internal Medicine (Neurology) and a Diplomate of the European College of Veterinary Neurology. He is currently President of the ACVIM Specialty in Neurology.

CHRISTOPHE LOMBARD
DVM, Dipl ACVIM, Dipl ECVIM
Dr. Christophe Lombard graduated in 1971 at the University of Zurich Switzerland. From 1972 to 1974 he attended a
Residency in Physiology at the University of Zurich - College of Veterinary Medicine - from 1975 to 1977 a Residency in cardiology at the University of Pennsylvania, Philadelphia followed by a Residency of another two years in Internal Medicine at the same University. He then started in 1978
his career as Assistant and Associate Professor of Medicine
and Cardiology at the College of Veterinary Medicine of the
University of Florida Gainesville until 1991. Since 1991 and
presently he is Professor of Medicine at the College of Veterinary Medicine at the University of Bern/Switzerland. His
special interests cover clinical cardiovascular medicine especially echocardiography. The Specialty Boards he is currently in are ACVIM and ECVIM-CA. He has currently 67
scientific publications and bookchapters in various professional journals.

GEORGE LUBAS
Med Vet
Graduated in Veterinary Medicine at the University of Pisa
in 1975 where he also specialised in Small Animal Diseases
in 1977.

4th European FECAVA SCIVAC Congress

In 1979 he became Assistant Professor and since 1983 he is


Associate Professor of Comparative Haematology at the
University of Pisa. Since 1985 he is also Professor of Genetics in the Specialisation Section of the University of Pisa.
He is author and co-author of about 150 papers on immunohaematology and clinical haematology in the dog, cat ,
horse and cattle. He has been speaker at numerous veterinary
conferences, meetings, seminars and practical courses on the
above topics.

LUCA MECHELLI
Med Vet
Graduated in Veterinary Medicine at the University of Pisa
in 1981. In 1982-83 he was Resident at the Institute of Veterinary Medicine, University of Perugia and in 1984-85 Veterinary Pathologist at the Ministry of Health in Rome. In the
years 1986-90 he was an instructor pathologist at the Institute of Veterinary Medicine of the University of Perugia and
since 1991 he is teaching general pathology at the Institute
of Veterinary Medicine, University of Perugia. Author of
over 65 scientific papers and reviews on many aspects of
companion animal dermopathology and oncology.

DENNY MEYER
DVM, Dipl ACVP, Dipl ACVIM
Dr. Denny Meyer received a BS and DVM from the University of Minnesota in 1970 and 1972, respectively, followed
by an Internship and Residency in Small Animal Medicine
at the University California-Davis. While at the University
of Florida (1976-1989), he was granted tenure as an Associate Professor , served as Service Chief for both Small Animal Medicine and Clinical Pathology, achieved Diplomate
status in both the American College of Veterinary Internal
Medicine and the American College of Veterinary Pathologists. This was followed by a career in industry; Associate
Director of Veterinary Affairs-Hills Pet Products and Director of Clinical Pathology and safety Pharmacology-Smith
Kline Beecham Pharmaceuticals (appointments in both the
US and UK). Upon return to academia at the Colorado State
University as Professor of Pathology, he served as Service
Chief-Clinical Pathology and was awarded the Carl J. Norden Distinguished Teaching Award which complemented six
prior teaching awards at the University of Florida. Currently he is a Senior Clinical Pathologist at IDEXX Veterinary
Services/California Veterinary Diagnostics. In addition to
more than 70 scientific papers and book chapters, he is an
author of Veterinary Laboratory Medicine-Interpretation and
Diagnosis and is a co-author on Strombecks Small Animal
Gastroenterology, 3rd edition. He has given more than 100
invited lectures. He has served as President of the Comparative Gastroenterology Society and established the Veterinary Liver Study Group. He recently completed terms as Associate Editor of the Journal of Veterinary Internal Medicine
and member of the editorial Board-Veterinary pathology
Journal. His clinical and investigative interests are haematology, cytopathology, hepatic histopathology, and the

4th European FECAVA SCIVAC Congress

pathophysiology of hepatic disease.

nicians (C.E.F.A., IRECOOP, ITTIOCONSULT, AIVPA,


SCIVAC etc.).

A R MICHELL
DSc, MRCVS

GERT NIEBAUER
Med Vet, PhD, MS, Dipl ECVS

Professor Michell has recently joined the AHT from the Royal Veterinary College (University of London) where he was
Professor of Applied Physiology & Comparative Medicine.
He is a former President of the Association of Veterinary
Teachers & Research workers and a current member of the
Council of the British Veterinary Association and the Royal
College of Veterinary Surgeons. He received the Blaine
Award from the BSAVA in 1991 and shared the George Fleming Prize in 1992. His main interests are the physiology and
clinical disturbances of fluids, electrolytes and acid-base balance and the links between renal disease, salt intake and hypertension.

Gert Niebauer has been professor of Surgery at the Small Aninmal Department of the Pennsylvania University at Philadelphia. He is author of numerous scientific publications and
various chapters of Surgery texts including the latest edition
of the Slatter. He is Diplomate of the European College of
Veterinary Surgeons of which he is also Chairman of the Credentials Committee.

MASSIMO MILLEFANTI
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1982. He is a private practitioner near Milan. His main interests have always been on Exotic Animals especially on rodents, reptiles and fishes. In 1987 he helped with the birth of
SCIVAC Study Group of Medicine and Surgery of Exotic
Animals of which he is currently the co-ordinator since 1995.
He has been speaker at meetings, seminars and practical
courses and has written articles for journals, a book on iguanas and one on diseases of ornamental fishes. He has also
been invited to TV shows and radio broadcasts.

PIERRE MONTAVON
DVM
Prof. Pierre Montavon graduated at the University of Zurich
and then attended a Residency from 1979 to 1985 at the Ohio
State University Department of Clinical Sciences were he
then became Assistant Professor. In 1985 he entered The University of Zurich as Assistant and then as Lecturer and since
1994 he is Professor at the Surgery Clinic of the University of
Zurich. Since 1980 he has been instructor at the AO Vet
Courses in Davos, Waldenburg, Courcheval , Cremona,
Columbus and Zurich. He is currently author of over 30 original articles published in National and International Journals.

GIUSEPPE MOSCONI
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna in 1978 and in 1979 started working as fish pathologist at the EUROAQUARIUM of Bologna where he is currently brand manager. He attended two intensive courses
(1981-1983) at the University of Hobenheim of Stuttgart on
ornamental fish pathology. He has been speaker at numerous
post-degree courses for veterinarians, biologists and fish tech-

CLAUDIO PERUCCIO
Med Vet, Dipl ECVO
Graduated in Veterinary Medicine at the University of Turin
in 1970 with honours. Specialised in small animal diseases in
1974 at the University of Milan with the highest marks discussing a thesis on surgery of cataract in the dog. Since 1974
he is employed at the University of Turin at first as Researcher
then as Associate Professor. His main interest is small animal
veterinary and comparative ophthalmology. Since 1987 is Adjunct Associate Professor at the Department of Clinical Medicine, College of Veterinary Medicine, University of Illinois,
USA. Since 1993 he is a Diplomate of the European College
of Veterinary Ophthalmologists of which currently he is Vice
President. Speaker at numerous national and international
meetings and author of 130 papers and numerous text books.
Secretary, Vice-President and President of AIVPA in the years
1978-1984; Secretary, Vice-President, President and PastPresident of ISVO (International Society of Veterinary Ophthalmology) from 1980 to 1994; President of SOVI (Italian
Society of Veterinary Ophthalmology affiliated to SCIVAC)
since 1989; he has been Vice-President of SINVET. He has
been in SCIVAC Board and has been director of numerous
national and international veterinary journals.

SIMON M. PETERSEN - JONES


DVetMed, DVO, Dipl ECVO, MRCVS
He completed his undergraduate and ophthalmology residency training at the Royal Veterinary College, London and was
awarded a Doctorate of Veterinary Medicine in 1990. He
holds Ophthalmology specialist qualifications from the Royal
College of Veterinary Ophthalmologists. From 1998 to 1994
he was a lecturer in Veterinary Ophthalmology at the Royal
(Dick) School of Veterinary Studies, Edinburgh. Currently he
is conducting a research into the molecular genetics of generalised progressive retinal atrophy at the Veterinary University
of Cambridge. Additionally he is the current Chief Panellist of
the British Veterinary Association/Kennel Club Eye Scheme
and also runs a private ophthalmology referral service.
In 1994 he was awarded the BSAVA Simon Award for outstanding contributions in the field of veterinary surgery and
also a Pfizer Academic Award for young British research scientists. He is a co-editor of the successful BSAVA Manual of

Small Animal Ophthalmology.

STEFANO PIZZIRANI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Pisa
in 1979. In July 1993 he became a Diplomate of the European College of Veterinary Surgeons. Founder in 1984 of
SCIVAC where he has been Board Member (1985-86),
Vice-President ( 86-87), President (87-89), President senior
(89-91). He has spent various periods of updating in neurology at the Veterinary Teaching Hospital of the Colorado
State University; in ophthalmology at the Cornell University of the State of New York and in small animal surgery at
the North Carolina State University. His main interests are
in ophthalmology, neurology and small animal surgery. He
has been speaker in more that 50 occasions at national and
international meetings and seminars on ophthalmology, neurology, orthopaedic surgery and leishmaniosis. he is author
and co-author of articles, manuals and is co-translator of the
Handbook of Small Animal Orthopaedics and fracture
treatment.

ADAM RIJNBERK
DVM, PhD
Ad Rijnberk graduated from the Faculty of Veterinary Medicine of Utrecht University in 1962. In 1971 he completed a
thesis entitled Iodine metabolism and thyroid disease in the
dog. In 1973 he became reader and in 1976 professor of
companion animal medicine at Utrecht University. Over the
years his research interests have concentrated on endocrine
diseases in dogs and cats, with currently some emphasis on
the pathophysiology of the pituitary-adreno-cortical axis and
of growth hormone release at pituitary and extra-pituitary
sites.
Ad Rijnberk is Diplomate of the European College of Veterinary Internal Medicine-Companion Animals. In 1986 he was
awarded the Walter Frei Preis of the University of Zurich and
in 1993 he received the Scientific Achievement Award at the
18th World Congress of the World Small Animal Veterinary
Association.

4th European FECAVA SCIVAC Congress

has spent various periods at the University of Cambridge


(UK), North Carolina (USA) and Purdue-Indiana (USA).

GIANLUCA ROVESTI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Parma
in 1982. Since 1983 he has been working in a private practice
for dogs and cats where he is mainly involved in surgery, with
a particular interest in orthopaedics, neurology and ophthalmology. In 1992 he spent time at the Colorado State University in the Small Animal Surgery Department, in 1993 at the
University of Zurich - Surgery Session of the Kantonales Tierspital and in 1997 at the North Carolina State University
Small Animal Surgery, Veterinary Teaching Hospital. He has
been speaker and instructor at SCIVAC AO/ASIF Courses,
at the SCIVAC Course on Total Hip Replacement in the Dog
with Prof. Bardet and Prof. Matis held in January 1997, speaker at SCIVAC Course on Surgery of Limb Distal Extremities
with Prof. Jon Dee. He is a Diplomate of the European College of Veterinary Surgeons since June 1997.

ROBERTO SANTILLI
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1990. In 1991 he attended a specialisation course on small
animal cardiology at the University of Turin and then started his updating periods in small animal cardiology at the
North Carolina State University, Ohio State University, University of California (Davis) and Cornell University. He is a
private practitioner in a small animal veterinary clinic near
Milan. he is an instructor at SCIVAC practical courses on
small animal cardiology and abdominal ultrasonography. Author of articles on ultrasonography and echocardiography.
His main research is on feline cardiomiopathies and has presented at an annual congress of the European Society of Veterinary Internal Medicine the results of a study on the diastolic
functions in feline cardiomiopathies through the doppler
method.

KARSTEN E. SCHOBER
DVM
GIORGIO ROMANELLI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Milan
in 1981. Immediately after the graduation he carries out a
research on experimental surgery on the transplantation of
the heart and of the pancreas. He is a small animal private
practitioner in Milan and his main interests are on general
and orthopaedic surgery and surgical and medical oncology.
He is a Diplomate of the European College of Veterinary
Surgeons since 1993 and has been SCIVAC President in
1993-1995 and is currently Chairman of the SCIVAC Scientific Committee.
Speaker at about 40 national and international meetings. He

Graduated at the Leipzig University in 1990 with a degree


thesis on Acid-base disorders in venous blood and erythrocytic hemolysate in dogs. From 1990 to 1991 he was scientific
assistant (Intern) at the small animal clinic of the University
of Leipzig and from 1991 to 1994 he was research student
(Resident) at the same University. He then won a grant Award
from the above mentioned university and went to attend a
clinical work at the Virginia Tech, Virginia Maryland Regional College of Veterinary Medicine, Small Animal Clinic,
Blacksburg USA. He then won another grant award of 12
months from the German Academic Exchange Service in
Bonn for postdoctoral scientific and clinical work on cardiology at the University of Edinburgh. From 1995 he is assistant

4th European FECAVA SCIVAC Congress

at the Small Animal Clinic, Faculty of Veterinary Medicine,


University of Leipzig.
He is author of several scientific publications and has been
speaker in numerous veterinary congresses.
His non professional interests are ornithology, music and art.

PETER W. SCOTT
MSc, BVSc, FRCVS
Peter W. Scott is a veterinarian with a special interest in
birds, fish, reptiles and amphibians. He is recognised by the
Royal College of Veterinary Surgeons as a Specialist in both
Zoo & Wildlife Medicine and Fish Health & Production
and in 1997 became Fellow of the RCVS in Psittacine Medicine.
Since doing field work in Kenya for his MSc, he has worked
with exotic species for 20 years. Since 1984 this has been
full time and now as the principal of the Zoo and Aquatic
Veterinary Group he works with many professional and keen
amateur aviculturists, plus many fish keepers and fish farms.
He is a member of the Association of Avian Veterinarians,
an ex-President of the British Veterinary Zoological Society
and Veterinary Adviser to several companies. He is the author of four books (on Axolotls, dogs, livebearing fishes, and
the latest The Complete Aquarium), an editor of three conference proceedings and a contributor to many other books
including four BSAVA Manuals related to exotic pets, Genus
Amazona, and Lories and Lorikeets. He established VETARK PROFESSIONAL, an animal health company dealing especially with exotic species, and also VETGEN EUROPE to provide diagnostic DNA probe technology to veterinarians.

DANIEL D. SMEAK,
DVM, Dipl ACVS
Graduated with Honours at the Michigan State University,
College of Veterinary Medicine in 1979. He then attended a
Small Animal Rotating Internship at the Colorado State University in 1980 and a Residency in Small Animal Surgery at
the Ohio State University College of Veterinary Medicine in
1983. He became Assistant Professor in Surgery at the Ohio
State University in 1984 and Professor in 1989. Since 1995
he is Professor of Surgery at the Ohio State University and
Chief of the Small Animal Surgery Section until 1997.
As far as publications are concerned he has 61 Peer reviewed articles authored, he is Co-editor of the book Disease Mechanisms in Small Animal Surgery, he is section editor of the Manual of Small Animal Practice and has 18
Book Chapters Authored.

FRANK J.M. VERSTRAETE


DrMedVet, BVSc, MMedVet, FAVD, Dipl AVDC, Dipl
ECVS
Frank Verstraete graduated as a veterinarian at the University of Gent (Belgium) in 1980. He pursued his graduate stud-

ies at the University of Pretoria (South Africa) where he


completed a residency in small animal surgery and became
board- certified in surgery in 1985. At Pretoria University
he started a Dental Clinic in 1982, which proved to be most
successful, and in 1988 he was appointed Associate Professor of Surgery and Head of the Small Animal Surgery Section.
Since the end of 1994, he is Chief of the Dentistry Service
at the School of Veterinary medicine of the University of
California at Davis. His main research interests are comparative dentistry and oral pathology.
He is charter fellow of the Academy for Veterinary Dentistry, a Diplomate of the American Veterinary Dental College (and current Secretary) and a Diplomate of the European College of Veterinary Surgeons. He is also a member of
the Organising Committee of the European Veterinary Dental College.

ALDO VEZZONI
Med Vet, SCMPA, Dipl. ECVS
Born in 1947 in the province of Cremona, North Italy, married with Franca in 1972, two sons, Dario 21 years old and
Luca 18 yeras old.
Degree in Veterinary Medicine in 1975, Veterinary School of
the University of Milan, with maximum score cum laude.
Specialisation degree in Small Animal Medicine in 1978,
Veterinary School of the University of Milan, with maximum score cum laude.
In 1976 starts his veterinary practice in Cremona where he is
still working with other two colleagues.
President of the Italian Small Animal Veterinary Association
(SCIVAC) in 1989-1991, member of its Board from 1984 to
1993, its national representative in FECAVA from 1989 to
1994, Chairman of its Scientific Committee from 1987 to
1993, Chairman of its Publication Committee from 1993.
Secretary of the European Society of Veterinary Orthopaedics and Traumatology (ESVOT) from 1993.
Board Certified by the European College of Veterinary Surgeon in 1993 in Cambridge, and Chairman of its PR Committee from 1994 to 1996.
Chairman of the Scientific Committe of the two Italian Scientific Meetings on Canine Heartworm Disease in 1988 and
in 1993.
Member of the Board of the Italian Federation of Veterinary
Orders (FNOVI) from 1994 to 1997 and its Secretary from
1997.
President of the Veterinary Order of the Province of Cremona since 1997.
Speaker in several national and international meetings on
parasitology (heartworm), orthopaedics, surgery and dentistry.
Editor and co-Author in 1987 of a book on canine heartworm disease La filariosi cardiopolmonare; co-Author in
1991 of Small Animal Drug Formulary, 2nd edition in
1995; italian editor of the following american books: 1990
Brinker, Piermattei and Flo Handbook of Small Animal
Orthopedics and Fracture Treatment , 1995 S.J.Plunkett
Emergency procedures for the small animal veterinarian,

10

1996 W.R.Fenner Quick reference to Veterinary Medicine,


1996 G.T.Wilkinson &R.C.Harvey Color atlas of small animal dermatology, 1998 S.I.Bistner & R.B.Ford Kirk and
Bistners Handbook of veterinary procedures & emergency
treatment.
Author of several papers on scientific journals on heartworm
disease and on small animal surgery and orthopaedics.

SIMON WHEELER,
BVSc, PhD, CertVR, Dipl ECVN, MRCVS
Graduated from the University of Bristol in 1981, Simon J.
Wheeler was appointed House Surgeon at the Glasgow University Veterinary School. Following a year in general practice in Wales, he was appointed Clinical/Research Assistant
in neurology at the Veterinary Royal College. He received a
Veterinary Research Training Scholarship from the Horserace
Betting Levy Board and a Grant from the BSAVA Clinical
Studies Trust Fund to pursue his interest in neurological disorders, particularly peripheral nerve and spinal conditions.
He was awarded PhD by the University of London in 1988.
From 1988-1992 he was assistant Professor of Neurology at
the College of Veterinary Medicine, North Carolina State
University. Currently he is Senior Lecturer in Neurology and
Director of Clinical Training at the Department of Small Animal Medicine and Surgery, The Royal Veterinary College. He
is President of the European Society of Veterinary Neurology
. He is editor of the BSAVA s Manual of Small Animal Neurology, co-author of Small Animal Spinal Disorders: Diagnosis and Surgery and of Self Assessment Colour Review of
Small Animal Neurology. He has published research and continuing education articles and textbook chapters in the USA
and Great Britain.

RICHARD A.S. WHITE


BVetMed, PhD, DVR, Dipl ACVS, Dipl ECVS, FRCVS
Dr. Dick White is a Lecturer in Small Animal Soft Tissue
Surgery at the University of Cambridge. He is a graduate of
the Royal Veterinary College in London, gaining his doctorate
in small animal oncology from the University of Cambridge.
His areas of expertise covers all aspects of soft tissue surgery
but his particular interests and publications include oncology
surgery, wound management and reconstructive surgery,
surgery of the upper airways and surgery of the head and
neck.
He is a Diplomate of the American College of Veterinary Surgeons and the European College of Veterinary Surgeons and
an RCVS recognised Specialist in Small Animal Surgery.
Dick White was a member of the founding committee and
Past President of the European College of Veterinary Surgeons.

4th European FECAVA SCIVAC Congress

13

SCIVAC EXOTIC ANIMALS STUDY GROUP

Anaesthesia and surgical conditions of reptiles


Stephen John Divers
BSc (Hons) - C Biol. MI Biol - B Vet Med - MRCVS
The Exotic Animal Centre - Essex - United Kingdom

Summary
Veterinarians are increasingly been asked to perform
surgery on non-domesticated animals. The surgical procedures themselves are often not complicated but successful
anaesthesia remains the greatest concern. This paper introduces the clinician to reptile anaesthesia and surgery, highlighting the importance of pre-anaesthetic stabilisation and
fluid therapy, suitable environment, monitoring and safe
drug regimes. Reptile surgery is discussed using common reproductive disease (dystocia) as examples in snakes, lizards
and chelonia.

Starvation. Putrefaction of undigested foods is a hazard


of ectothermic anaesthesia and therefore fasting for 24-96
hours is recommended. Larger species, particularly the boas
and pythons should be starved for 7-14 days to enable full
digestion of their large meals.
Pre-existing disease. Metabolic disturbances, cachexia,
chronic infections etc must be considered prior to any anaesthetic induction.
Handling. Reptiles should be handled as little as possible
to prevent bruising and trauma. During induction, skilled
staff and correct handling techniques are essential to minimise stress.

Introduction

INDUCTION AND INJECTION SITES

Anaesthesia and sedation permit surgery, but sedation


and chemical restraint are equally important to facilitate
handling, clinical examination and investigation (e.g. blood
sampling, endoscopy, radiography etc) of animals that may
be dangerous. The requirements of anaesthesia are restraint,
muscle relaxation, analgesia, and uncomplicated recovery.

Induction can be achieved using an injectable agent or an


inhalational agent via a mask or induction chamber. Intravenous injection sites for reptiles vary from those commonly
employed in mammals. Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral body withdraw slightly and redirect. Avoid the
hemipenes of males.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25 g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapins-

ANAESTHETIC CONSIDERATIONS1,2,3
Body weight. It is vital that an accurate body weight is
recorded for drug calculation and assessment of hydration
and fluid deficits.
Premedication. Atropine is considered unnecessary as
salivary secretions are insignificant during surgery, however
low-dose ketamine can be used as pre-anaesthetic sedative.
Temperature. Reptiles are ectothermic and it is important
that they are maintained at their species-specific preferred
body temperature at all times i.e. pre-induction, at induction,
during maintenance and recovery.
Fluid therapy. Dehydration (reduced skin elasticity,
sunken eyes, elevated packed cell volume) must be corrected prior to induction and monitored after surgery, especially
when recovery is prolonged. Bathing tortoises in warm water for several hours may be sufficient, but intracoelomic fluids (e.g. Hartmanns, lactated Ringers) at a rate of 15-35
ml/kg/24 hours can be easily administered to most species,
even chelonia. In cases of moderate to severe dehydration,
intravenous or intraosseous fluid therapy is to be recommended.

PRE-CONGRESS DAY MEETINGS

4th European FECAVA SCIVAC Congress

14

Dorsal tail vein; A 5/8 21-25 g needle is angled at 45-90


and placed, as cranial as possible, in the dorsal mid line of
the tail. The needle is advanced while maintaining a slight
negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species.
Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with neostigmine), and it may be necessary to use large spinal needles (3-8) to reach the vein.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90o in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Larger crocodilians (over 1.5 m)
may require chemical restaint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with
neostigmine).
Intramuscular injections can be given into the epaxial
muscles of snakes and proximal forelimb muscles of chelonia, lizards and crocodilians.

INHALATIONAL ANAESTHESIA
Inhalational anaesthesia can be induced via a face mask
(e.g. iguanas and other large lizards) or by conscious intubation (e.g. snakes). Endotracheal intubation is recommended
in all species. Open, semi-closed and closed circuits (Ayres
T-piece, Bain Co-axil) can be used giving considerations to
circuit resistance and animal size. Assisted ventilation (IPPV)
is often required and therefore artificial ventilation, either
manual or mechanical should be available. Anaesthetic
chambers can be used for the induction of small or venomous
species, but beware that prolonged breath holding can occur.
Intubation using a standard uncuffed endotracheal tube is
preferable but often not possible. A dog urinary catheter cut
down to size makes a suitable ET tube for many species, and
even the smallest specimen can be intubated using an intravenous catheter.

4th European FECAVA SCIVAC Congress

MONITORING ANAESTHESIA
ECG machines can be utilised in reptiles to monitor cardiac function. The heartbeat of snakes is visible ventrally
about a third of the way caudal to the head while the heart
beat of many lizards can be seen within the axillae.
Reflexes and muscle tone diminish as the depth of anaesthesia increases. Muscle relaxation progresses in an anterior
to posterior direction. The righting reflex is lost during the later stages of anaesthesia but this may not represent a surgical
plane. Loss of the corneal reflex is a good indicator of deep
anaesthesia, except in the snake and certain gecko lizards
which possess a spectacle covering the cornea. In snakes the
tongue withdrawal reflex and the ventral muscle reflex can be
used to good effect, while the deep pain withdrawal reflex of
the tail or foot can be used in lizards and chelonia. The authors preferred method of monitoring is pulse oximetry which
provides information on peripheral pulse and pulse strength,
and possibly an indication of blood oxygen saturation.

POST-OPERATIVE CARE
Post-operative recovery requires maintenance at the animals preferred body temperature. Respiration must be
monitored during recovery, especially following the use of
ketamine, halothane or methoxyflurane. Respiratory stimulants can be used to reduce post-operative observation, e.g.
doxapram (Dopram, Willows Francis) at 0.25 ml/kg i/v, i/o.
Recovery is considered to have occurred when the righting
and pedal reflexes have returned.
Hydration status should be assessed and it is good practice to give i/c, i/v, i/o or oral fluids up to 35 ml/kg/24 hours.
Antibiotics may also be indicated but until the culture
and sensitivity results are obtained, broad spectrum antibiotic cover can be provided using enrofloxacin (Baytril 2.5%,
Bayer) at 10 mg/kg i/m, i/o, po q 24 hrs or ceftazidime (Fortum 500 mg, Glaxo) at 40 mg/kg i/m i/v, i/o q 72 hrs.

SURGICAL PROCEDURES5,6,7,8
A wide range of surgical and medical procedures are now
commonly performed thanks to the safer, modern anaesthetics;
jugular cut-down and catheter placement in snakes, cardiac catheterisation in snakes, pharyngostomy tube placement, lung catheterisation and pulmonary lavage, joint
lavage/aspiration, abscess removal, tumour removal, wound
debridement, fracture repair, limb/tail amputation, enucleation, hemilaminectomy in large lizards, exploratory coeliotomy, cystotomy, enterectomy, enterotomy, pneumotomy,
biopsy, endoscopy (diagnostic, biopsy and sexing), rib removal in snakes, bone marrow aspiration in lizards and chelonia, prolapse repair, penis amputation, etc etc.
In general, the surgical techniques are similar to those established for mammals, however certain anatomical differences peculiar to reptiles must be considered by the surgeon
prior to operating. As an example reproductive disease (dystocia) and their surgical treatments will be described.7,8

15

Injectable anaesthetic and immobilisation regimes for reptiles


DRUG

DOSAGE

COMMENTS
CHELONIANS

Ketamine HCl

20-60mg/kg s/c, i/m

Useful and safe. Doses less than 50mg/kg produce tranquillisation, while doses
above 50mg/kg produce anaesthesia. Recovery time proportional to dose, often
several hours. Ketamine (50mg/kg) and xylazine (10mg/kg) combination has
been recommended. C/I - debilitated or dehydrated reptiles, hepatic or renal
dysfunction.

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Rapid, predictable response if given i/v with intubation possible within three
mins. I/m route less predictable, induction is slower at 25-40 mins. Anaesthesia
lasts 15-35 mins, recovery 1.5-4 hours.

Propofol

14-15mg/kg i/v

Rapid, smooth induction, minimal accumulation, 20 mins anaesthesia, rapid recovery. AUTHORS AGENT OF CHOICE

Succinylcholine*

0.25-1.5mg/kg i/m

Very effective at facilitating E/T intubation and diagnostic procedures. Paralysis lasts 20 mins, recovery takes 45 mins.

Tiletamine HCl and Zolazepam HCl 10-20mg/kg i/m

Most suitable for sedation to facilitate E/T intubation. Zolazepam incorporated


to reduce convulsions and improve muscle relaxation. Not yet available in UK.

Etorphine

0.3-2.75mg/kg i/m

Used in terrapins up to 5mg/kg.

Ketamine HCl

20-100mg/kg s/c, i/m

Same as for chelonians

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Same as for chelonians

Propofol

10-15mg/kg i/v

LIZARDS

Same as for chelonians. AUTHORS AGENT OF CHOICE

Tiletamine HCl and Zolazepam HCl 30mg/kg i/m

Produces mild to moderate plane of surgical anaesthesia with rapid induction


time, recovery may be prolonged. Particularly suited to iguanas. Not readily
available in UK.
SNAKES

Metomidate*

10-20mg/kg i/m

Very useful sedative to facilitate blood sampling, radiography, intravenous injections. Rapid onset with heavy sedation after 15 mins. Safely used on a daily
basis for cleaning, debriding wounds.

Propofol

10-12mg/kg i/v

Same as chelonians. AUTHORS AGENT OF CHOICE

Ketamine HCl

20-130mg/kg s/c, i/m

Rapid induction, prolonged recovery. May need to IPPV at higher doses, lower
dose for pre-anaesthetic sedation.

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Same as chelonians

Tiletamine HCl and Zolazepam HCl 10-20mg/kg i/m

Same as chelonians. Fatalities at 55mg/kg

Methohexital sodium

Induction and recovery times rapid, concentration should not exceed 0.5%.

5-15mg/kg i/m, s/c

CROCODILIANS
Propofol

10-15mg/kg i/v

Same as for chelonians. AUTHORS AGENT OF CHOICE FOR SMALL


SPECIMENS

Succinylcholine*

0.4-1mg/kg i/m

Rapid onset of paralysis in American alligators, recovery in 45-90 mins.

Gallamine triethiodide*

0.6-4mg/kg i/m

Good in Nile crocodiles, unsafe in American alligators at 1mg/kg. Reverse with


0.05mg/kg neostigmine i/m and 0.02mg/kg atropine i/m. AUTHORS AGENT
OF CHOICE FOR LARGE SPECIMENS

Ketamine HCl and Xylazine HCl

20mg/kg i/m 1mg/kg i/m

Good in Nile crocodiles, ketamine given 30 min after xylazine, anaesthesia lasts
50 mins, recovery in 4 hours.

Etorphine

0.3-2.75mg/kg i/m

10-30 mins induction, 45-100 mins of analgesia hence combine with muscle
relaxant.

*Provides no analgesia - must be combines with local or general analgesia for painful procedures. It may be necessary to assist respiration, especially at higher doses
or in debilitated patients.

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4th European FECAVA SCIVAC Congress

16

4th European FECAVA SCIVAC Congress

Inhalational anaesthetic agents used in reptiles


AGENT
Methoxyflurane

INDUCTION/
MAINTENANCE

COMMENTS

3-4%/1.5-2% in oxygen

All species. Excellent relaxation and analgesia, prolonged induction and recovery times,
myocardial depressant and nephrotoxic.

Halothane

3-5%/1-3% in oxygen

All species. Rapid induction and recovery times, respiration and myocardium depressed with
respiratory and cardiac arrest occurring simultaneously, hepatotoxic, lizards more sensitive.

Isoflurane

3-5%/1-3% in oxygen

All species. Rapid induction and recovery, minimal organ toxicity, ideal for debilitated reptiles. AUTHORS AGENT OF CHOICE

Nitrous oxide

1:1 to 1:3 with oxygen

All species. May be used with volatile anaesthetics to reduce induction time and improve
muscle relaxation and analgesia.

PRE-OVULATORY OVA STASIS (POOS)


In cases where the ova enlarge but do not ovulate and remain within the ovary the term pre-ovulatory ova stasis
(POOS) is applicable. In such circumstances the presence of
the greatly enlarged ovaries severely reduces the coelomic
space available to the gastrointestinal tract resulting in prolonged anorexia particularly in saurians. In most untreated
cases affected females usually die from the secondary
changes associated with dehydration and anorexia. A diagnosis of POOS can be made by ultrasonography, laparoscopy or more commonly radiography. It is possible for
the ova to be spontaneously reabsorbed over a period of 412 weeks. However, if affected animals are completely
anorexic and becoming debilitated then further deterioration
and death can ensue before the problem resolves naturally. If
medical therapy is contemplated then intensive
nutritional/fluid support will be required for many weeks
and ova reabsorption should be monitored using radiography
or ultrasonography. In the authors experience medical management is seldom successful in lizards presented late in the
course of the disease and does not prevent recurrence the
following year. Greater success has been seen with short
term patient stabilisation using fluid therapy for 1-3 days
followed by surgery (ovariosalpingectomy). A case of follicular aspiration as a treatment for POOS has been reported.

POST-OVULATORY EGG STASIS (POES)


In cases of post-ovulatory egg stasis (POES), the eggs
(usually shelled) or foetuses are located within the shell
glands or oviducts but normal laying or birth at term fails to
occur because of the lack of a suitable nesting site (temperature, humidity, nest material, seclusion), excessive disturbance by the owner, competition for nesting sites (overcrowding), stress of transportation, metabolic disturbances
(particularly involving calcium), systemic or localised infections of the shell glands, oviducts or cloaca and obstructions
due to abnormal eggs, foetuses or cloacal prolapse. The
space occupied by the eggs/foetuses again compresses the
gastrointestinal tract and leads to secondary hypophagia or
anorexia.

If there is no indication of infection, metabolic disease or


obstruction as determined by radiography, digital palpation
and direct visualisation of the cloaca and a limited haematological and biochemical assessment, then conservative treatment should be attempted. Complications including abnormal eggs, abnormal foetuses, cloacal prolapse, suspected infection of the cloaca, shell glands or oviducts will prevent
normal laying or birth and in these, and refractory medical
cases, surgery is indicated.

SURGICAL TECHNIQUE
Once the patients hydration status has been returned to
normal (as determined by serial packed cell volume, total
protein and albumin) surgery can proceed. Preoperative antibiotics, for example 40 mg/kg ceftazidime (Fortum, 500
mg, Glaxo), IM is advisable. The rate of fluid administration
can be increased to 5 ml/kg/hour during anaesthesia, surgery
and the immediate postoperative period.
Anaesthesia is induced with 10-14 mg/kg propofol
(Rapinovet, 10 mg/ml, Mallinckrodt Veterinary), IV or IO
followed by intubation and maintenance on oxygen and 24% isoflurane. It is vital than the preferred body temperature
of the patient is maintained before, during and after surgery.
The use of a low wattage heat mat or water bed to maintain
a core preferred body temperature is recommended. The
subject is connected to an ecg or pulse oximeter (cloacal/oesophageal) and prepared for aseptic surgery. The use of plastic adhesive drapes enables better monitoring and are to be
preferred over cotton drapes. Post operative analgesics
should always be considered and the author prefers 2-4
mg/kg carprofen IM (Zenecarp, 50 mg/ml, C-Vet).

LIZARDS
A standard paramedian or mid-line coeliotomy is performed, avoiding the large, ventral, mid line venous sinus
and, often voluminous, saurian bladder. The incision may
have to extend from the xiphoid process to just cranial to the
pelvis to provide sufficient exposure. The bladder must be

identified to prevent accidental incision, and emptied by cystocentesis if necessary. In cases of POOS, the enlarged
ovaries will be immediately obvious, often resembling clusters of yellow-orange grapes. Each ovary, supplied by 4-8
ovarian vessels that branch off the aorta and renal veins, is
lifted to expose these vessels which can be clamped using hemoclips, or ligated using vicryl (3/0-5/0). Once clamped the
ovaries can be carefully dissected free and removed. The
oviducts are usually small and involuted. Theoretically it
may be possible to leave the oviducts in place but subsequent
infection is always a possibility and therefore removal is recommended. The small blood vessels can usually be sealed using radiosurgery, hemoclips or ligatures as necessary. The
oviducts should be double ligated using 3/0-5/0 vicryl as far
distally as possible, close to their insertion to the cloaca.
In cases of POES, it is the thin shell glands full of eggs
that are immediately obvious. Multiple salpingotomy incisions can be made to remove the eggs in an effort to maintain
future breeding capacity, however, surgery time is greatly extended. In most cases complete salpingectomy is recommended. The large, numerous blood vessels that supply each
oviduct must be ligated or hemoclipped. Hemoclips greatly
reduce surgery time and several vessels can often be clamped
with a single medium clip. The oviducts must be ligated close
to the cloaca and removed as described above. In these cases, the ovaries are often small lying on top of the renal veins.
Their removal is considered by some to be unnecessary as it
has been suggested that folliculogenesis requires feedback
from the shell glands. The author prefers complete ovariosalpingectomy due to the possible danger of ectopic ova in the
future. When removing inactive ovaries the ovarian vessels
are smaller and shorter and it is generally easier to clamp
these vessels with hemoclips than to ligate them. Special care
is also required not to damage the closely associated adrenal
glands. The coelomic membrane and muscle layers are
closed in a routine manner using 3/0-5/0 vicryl. The skin is
sutured using 3/0 -5/0 nylon in an everting horizontal mattress pattern. This will prevent the natural inverting tendency
of reptilian skin and prevent dysecdysis in the future. The patient is returned to a vivarium at 30-35C to recover. Postoperative antibiotics are not routinely required unless infection
was confirmed at surgery but parenteral fluid therapy remains
essential for the next 24 hours. Discharge typically occurs the
next day with a return to normal feeding within a week. Skin
sutures are removed in 6-8 weeks.

SNAKES
The procedure is similar in snakes. In general a long incision is made between the ventral and lateral scales over the
area of greatest coelomic distension. POOS is rarer in snakes
and in most cases the eggs (or foetuses) will be within the
shell glands. Dissection is continued through the muscle layer and a standard salpingotomy incision is made in the thinly walled shell gland. The eggs or foetuses can then be removed, and it may be possible to milk eggs or foetuses from
further up or further down the shell gland into the surgical
site so preventing the need for additional salpingotomies.
The shell gland incision is closed using 5/0 vicryl in a single

17

or double inverting suture pattern. Suturing may be made


easier by the administration of oxytocin or vasotocin which
causes contraction and thickening of the shell gland wall.
Skin closure is routine.
A less invasive surgical option is the aspiration of the infertile egg contents through a needle (14-20 g) which is introduced through the coelomic and shell gland walls into the
retained egg. The skin surface must be aseptically prepared
prior to this technique but there is a danger that egg contents
may leak from the egg and into the shell gland or coelomic
cavity causing an intense coelomitis. In general, the collapsed egg is voided within 12-96 hours, but this may be facilitated by the use of oxytocin, vasotocin or prostaglandins.
Ovariosalpingectomy is more difficult to perform in
snakes but is certainly possible and with practice will produce a satisfactory and permanent cure to reproductive problems in these species.

CHELONIA
Access to the reproductive tract of chelonians presents
an obvious challenge to the surgeon, notably the shell. In
those species with large inguinal fossae including the large
land tortoises and many species of terrapin and turtle, an inguinal soft tissue approach will provide sufficient access for
egg removal and prevent the need for plastronotomy. In
species with small inguinal fossae, or in those cases where
there are large numbers of retained eggs, or extensive disease that warrants complete ovariosalpingectomy, then a
transplastron approach is often indicated.
Using an oscillating sector cutter or small diameter circular saw, a plastronotomy with a bevelled edge is performed,
making sure that any functional plastron hinges are avoided.
It is important that the clinician makes the plastronotomy incision large enough to operate through as it is difficult to subsequently enlarge the incision. The bone segment is carefully lifted and dissected free from the underlying soft tissues
and placed in sterile normal saline. In chelonia there are
paired ventral abdominal veins, and the coeliotomy incision
is made between these vessels to gain access to the coelomic
cavity. Ovariosalpingectomy and salpingotomy procedures
are carried out in much the same way as previously described
for squamates, but the chelonian shell gland is often thicker
than that of lizards and snakes. The coelomic membrane is
closed in a simple continuous or interrupted pattern. The
bone segment is replaced and secured in place using autoclaved fibreglass patches and epoxy resin.

Key words
Anaesthesia, surgery, reptile, propofol, isoflurane, dystocia.

References
1.

2.

Bennett, R.A. (1996). Anaesthesia. In: Reptile Medicine and Surgery.


First edition (Ed. D. R. Mader). W.B. Saunders, Philadelphia. Pages
241-247.
Lawton, M.P.C. (1992). Anaesthesia. In: Manual of Reptiles (Eds.

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18

3.
4.
5.

4th European FECAVA SCIVAC Congress


P.H. Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham.
Pages 170-183.
Mader, D.L. (1996) Reptile Medicine and Surgery. WB Saunders,
Philadelphia.
Malley, A.D. (1997) Reptile anaesthesia and the practising veterinarian. In Practice 19(7):351-368.
Lawton, M.P.C. (1992). Surgery. In: Manual of Reptiles (Eds. P.H.
Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham. Pages
184-193.

6.

7.

8.

Bennett, A.R. and Mader, D.R. (1996). Soft tissue surgery. In: Reptile Medicine and Surgery. First edition (Ed. D. R. Mader). W.B.
Saunders, Philadelphia. Pages 287-298.
DeNardo, D. (1996). Dystocias. In: Reptile Medicine and Surgery.
First edition (Ed. D. R. Mader). W.B. Saunders, Philadelphia. Pages
370-374.
Divers, S.J. (1996). Medical and surgical treatment of pre-ovulatory
ova stasis and post-ovulatory egg stasis in oviparous lizards. ARAV
1996 Proceedings, Pages 119-123.

19

SCIVAC EXOTIC ANIMALS STUDY GROUP

Diagnostic techniques for reptiles


Stephen John Divers
BSc (Hons) - C Biol. MI Biol - B Vet Med - MRCVS
The Exotic Animal Centre - Essex - United Kingdom

Summary
Making a definitive diagnosis is the end point of a clinical journey. This may start with history taking and the clinical examination may provide a list of possible differential diagnoses. However, it is often necessary to take clinical samples, perform laboratory techniques and utilise diagnostic
imaging before a definitive answer can be found. This paper
attempts to clarify the major aspects of reptile diagnostics
from taking a history from the owner to sending a liver biopsy for histopathological confirmation of fungal hepatitis!

Introduction
The art of veterinary medicine and making that previously elusive reptile diagnosis rests upon our abilities as
clinicians to untangle the complex clinical web and piece together the pathology to determine the underlying aetiology
and clinical picture. A logical approach to reptiles will provide the veterinarian with most of the information required
to successfully diagnose and treat the majority of ailments.
When discussing diagnostic techniques it is vital that we
do not forget that a thorough history and full clinical examination are important diagnostic aids in their own right and
should be performed ahead of any other diagnostic tests.
Further investigations include haematology, serum biochemistry, parasitology, microscopy, cytology, microbiology, radiography, endoscopy, ultrasonography, MRI and CT, and
exploratory surgery.

History Taking1
Reptiles should be transported to the practice in linen or
cloth bags within styrofoam boxes, and their owners encouraged to keep and bring along their own husbandry
records. The identity of an unfamiliar species should be ascertained before arrival to permit the clinician to become familiar with the species specific husbandry requirements.
The vast majority of reptile diseases are due either directly
or indirectly to substandard husbandry and therefore a thorough review of husbandry practices, hygiene and nutrition is
essential. It is often useful when dealing with an unfamiliar
species to have a sample history which can be followed during the consultation. Exotic animals invariably require an

extended consultation period but the extra time taken to obtain a detailed history will be clinically valuable and will often provide a tentative diagnosis. Qualitative and, where
possible, quantitative changes in husbandry, food and water
consumption, faeces, urine/urates, and behaviour should be
identified. Specific changes associated with breeding and hibernation are frequently associated with disease problems
and therefore careful questioning is required. Recent additions to the reptile collection are also significant, especially
as few owners operate the recommended 3-6 month quarantine period.
Sample history form
1).reptiles name or identification.
2) species, subspecies, native locality, colour morphology.
3) date of birth, age.
4) sex.
5) duration in owners care/captivity.
6) origin (captive bred, wild caught, when imported).
7) details of source (breeder, retailer, importer).
8) enclosure/vivarium specifications:
type (arboreal, terrestrial, aquatic).
size (length x depth x height).
construction (materials, paints, sealant, internal fittings,
or purchased ready-made).
furnishings (bark, plants, floor material).
provision for vivarium ventilation (mesh, air holes).
frequency of cleaning.
detergents, disinfectants used.
9) environment: vivarium (temperate, tropical).
outdoor enclosure (grassland, wooded, overgrown).
10) heating equipment (spot lights, ceramics, heating cables, heat mats).
11) temperature control (thermostat, rheostat) and method
of recording (type and position of thermometer).
12) temperatures (daytime air, daytime basking, night
time air).
13) lighting equipment (spot lights/fluorescent strip lights).
14) lighting control (photoperiod, manual/timer).
15) humidity level (day, night and seasonal changes, method
of provision - spray, sprinkler).
16) diet (varieties and quantities).
17) feeding: amount of food normally offered/actually eaten.
frequency of feeding.
time food offered (morning, overnight etc).
changes in appetite.

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18) method of water provision (bowl, spray).


how often is water changed.
how often is the water container cleaned.
what disinfectant/detergent is used.
changes in drinking behaviour.
18) food and water vitamin/mineral supplements.
19) breeding details (recent breeding attempts including
changes of temperature, humidity, feeding and animals
groupings).
20) other specimens in same vivarium or have shared the
same vivarium within the last 6 months.
21) other specimens in same room or that have been in the
same room in the last 6 months.
22) disease history of animal in question or any in-contact
animals.
23) quarantine protocol for all new additions (length of
quarantine period, position of quarantine vivarium in relation to established collection).
24) other details of relevance.

Clinical Examination1,2
Reptiles as a group are relatively easy to evaluate and
the standard examination techniques used for domestic pets
apply equally to reptiles. Calm specimens should be observed from a distance without handling to observe demeanour, locomotion and any obvious neurological disorders. Nervous or aggressive species are best restrained using appropriate techniques, including towels and gloves, at
all times. Observation of reptiles within their vivarium or
enclosure is particularly valuable and should be performed
whenever possible.
Reptiles present no more of a zoonotic danger than domestic animals, however the risks of Salmonella sp,
Pseudomonas sp, Rickettsia sp and pentastomids (arachnid
lung parasites) does necessitate adequate hygienic precautions at all times.
All reptiles should be accurately weighed. It is also
worth taking the cloacal temperature of any reptile weighing
more than 1 kg which has not been out of the vivarium environment for more than an hour. This temperature will give
an accurate indication of a large reptiles core temperature
and consequently an indication of that of its environment.
For example, a 5 kg iguana with a cloacal temperature of
15C is unlikely to have been removed from a 30C environment within the last hour. Length is also an important measurement that should be routinely recorded. The snout-vent
length of lizards and snakes is usually recorded, while the
horizontal carapace length of chelonians is more useful, especially when combined with weight to give a weight-length
(Jacksons) ratio.
Useful equipment for the reptile consulting room
Electronic scales, 0-2000 g accurate to 1 g, 0-100 kg accurate to 0.2 kg.
Handkerchiefs, tea-towels and bath towels.
Rubber gloves, thin leather gloves, gauntlets.
Snake hooks.
Transparent plastic boxes to observe small reptiles unre-

4th European FECAVA SCIVAC Congress

strained.
Plastic or wooden spatulas.
Sexing probes.
Dedicated auroscope attachment for cloacal examination.
Assortment of plastic gags.
Focused light source, preferably flexible for transillumination.
Digital thermometer with remote probe and a range of 0-50C.
Stethoscope with swab attached to diaphragm.
A systematic examination from rostrum to tail tip is always indicated, including a thorough palpation of all accessible areas for any abnormalities. It not uncommon for a reptile to void faeces and urates during the clinical examination,
and this material should be collected for immediate laboratory investigation.
Transillumination using a powerful light source is particularly useful for visualising the internal structures of small
lizards and snakes, although care must be exercised due to
the heat produced by these appliances. A flexible endoscope
is ideal but a far cheaper alternative is the flexible light
source recently introduced by Medical Diagnostic Services.
The light source can be held against the body of small reptiles or lubricated and inserted into the oesophagus or cloaca and rectum. Transillumination enables coelomic masses
to be identified and the cardiac shadow can be located for
cardiocentesis in small specimens.
Auscultation is possible and useful in reptiles but does
require a silent consulting room. The adventitious sounds
produced between the shell or scales and the stethoscope diaphragm can be reduced by placing a dampened swab or
towel between the stethoscope and the surface of the reptile.
Intractable animals are best sedated to facilitate a safer
more thorough examination. Ketamine HCl (Vetalar, ParkeDavis; Ketaset, Willows-Francis) at 20-50 mg/kg IM can be
employed but greater care must be exercised when using this
drug in debilitated reptiles.
Snakes
Aggressive snakes should be restrained before they are
removed from their transportation bag. The head is held behind the occiput using the thumb and middle finger, while
the index finger is placed on top of the head. The larger
pythons and anacondas can exceed 6 metres and 150 kg and
are powerful and potentially dangerous. In such circumstances, a second or even third handler will be required to
support the body during the examination. It is usually safer
and more convenient to sedate a large pugnacious snake than
to struggle on and risk injury to the snake, client or staff.
Non-venomous species should be removed from their
cloth bag when an assessment of demeanour and muscle
tone will quickly become obvious. Sick snakes will usually
remain limp while healthy specimens will grip or move over
the clinicians hands and arms giving a sense of strength. A
healthy snake that is permitted to wrap a coil around the handlers wrist while the head is allowed to hang down should
be able to raise its head to the level of the tail. Head position,
body posture, cloacal tone and righting reflexes can be used
to assess neurological function.
The integument, particularly the ventral scales, should be
carefully examined for any evidence of dysecdysis (poor
shedding) and trauma. Skin tenting and ridges may indicate

cachexia or dehydration while ticks and the snake mite


(Ophionyssus natricis) may congregate in skin folds, infraorbital pits and corneal rims. The infraorbital pits (where
present) and the nostrils should be free from any discharge
or retained skin. The eyes should be clear, unless ecdysis is
imminent when a bluish haze may be present. The spectacles
covering the eyes should be smooth as any wrinkles may indicate the presence of a retained spectacle. Ocular swellings
are often due to a build up of lachrymal secretions within the
sub-spectacular space because of a blockage within the nasolachrymal duct. Such swellings may become infected resulting in abscessation.
The body should be thoroughly palpated for any abnormal masses, and their position related to that of the major organs to identify their likely significance. Depending upon
the musculature of the snake the heart and faecal masses are
often palpated and erroneously considered pathological. The
cloaca should be free from faecal staining and discharge. Examination of the cloaca can be carried out using an auroscope and digital palpation. In the large constrictors it is possible to insert a lubricated gloved hand to perform an internal cloacal and even rectal examination. The sex of the
snake can be ascertained by examination of the tail length
and probing of the hemipenes. The tail length (and the number of sub-caudal scales) is always smaller in females than
males but this method requires access to published information on tail length and scale counts unless both sexes are
available for examination. The hemipenes are entered by
placing a caudally pointing probe, either side of mid line,
just inside the caudal cloacal rim. In males the probe passes
to a depth of 6-12 subcaudal scales whereas in females the
probe enters a musk sac to a depth of only 2-4 subcaudal
scales.
Examination of the oral cavity is best left until last as
most snakes object to such manipulation. However, even before the mouth is opened the tongue should have been seen
frequently flicking in and out of the labial notch. The mouth
can be gently opened using a plastic or wooden spatula to
permit an assessment of mucous membrane colour and examination for signs of mucosal oedema, hypersalivation,
haemorrhage, necrosis and the presence of caseous exudates.
The presence of white deposits may indicate uric acid deposition due to visceral gout. The pharynx and glottis should be
examined for haemorrhage, foreign bodies and discharge. It
is important to observe the glottis during respiration in an attempt to differentiate between discharges originating from
the respiratory and gastro-intestinal tracts.
Body organ position in boas and pythons
Organ

Percentage position from snout

Heart
Lung
Air sac
Liver
Stomach
Small intestine
Cranial pole of right kidney
Caudal pole of left kidney

22-33
33-45
45-65
38-56
46-67
68-81
69-77
74-82

21

Colon

81-100

Figures relate to the percentage distance of each organ from


the snout. The total length being that from the snout to the
cloaca. The organ positions of other species of snake are
broadly similar although differences in anatomy certainly
exist between the major serpentine groups.
Lizards
Lizards vary greatly in size and temperament and therefore a variety of handling techniques are required to cover all
situations. The tegus and monitor lizards are renowned for
their powerful bites while other species, particularly the
green iguana, are much more likely to use their claws and tail
to painful effect. The main problem of handling small lizards
is restraining them before they flee from the cloth bag. In all
cases, the lizard should be transported in a securely tied cloth
bag so that the position of the lizards head can be identified
and restrained before the bag is even opened.
The large lizards are best restrained with the forelimbs
held laterally against their thorax and the limbs held laterally against the tail base. Smaller lizards can be restrained
around the pectoral girdle holding the forelimbs against the
thorax, although care is required not to impair respiratory
movements. Never grasp a lizard by the tail because many
species can perform autotomy and shed their tails in an attempt to evade a predator (or in this case clinician!). Restricting the vision of these animals is often the simplest way
to facilitate handling and a towel placed over the head will
enable the clinician to thoroughly examine the rest of the
body and limbs. A useful restraint technique for iguanid
lizards utilises the vaso-vagal response: gentle digital pressure is applied to both orbits and in many cases the lizard
will enter a state of stupor for up to 45 minutes or until a
painful stimulus is applied. This technique can be employed
to calm nervous iguanids and monitors but, more importantly, enables the mouth to be gently opened without the need
for excessive force.
The integument should be examined for parasites and evidence of trauma due to fighting, mating and burns. Lizards
tend to shed their skin in a piecemeal fashion and therefore
retained skin (often dry and brown) must be differentiated
from normal ecdysis (flexible and transparent). Classically,
dysecdysis and skin retention occurs around the digits and
tail causing ischaemic necrosis. Extensive skin folding and
tenting are indicators of cachexia and possible dehydration.
The nostrils, eyes, and tympanic scales should be clean
and free from discharges, although some iguanids excrete
salt through specialised nasal glands which is then expelled
through the nostrils. The rostrum should be examined for
trauma due to repeated escape attempts from a poorly designed vivarium. The head and limbs must be palpated for
masses which may be abscesses or fibrous periosteal reactions associated with metabolic bone disease. Lizards suffering from severe hypocalcaemia due to metabolic bone disease may exhibit periodic tremors and muscle fasiculations.
The cloaca should be free from faecal staining, while visual
and digital examination should be considered routine. The
mouth can be opened using a spatula to examine the oral
cavity as described previously. In addition, the internal ex-

PRE-CONGRESS DAY MEETINGS

4th European FECAVA SCIVAC Congress

22

tent of any rostral abrasions can be evaluated.


Many species of lizards are sexually dimorphic, although
sexing juveniles can be very difficult. Adult males tend to be
larger, more colourful, exhibit more courting (head bobbing)
and aggressive behaviours, possess paired hemipenal bulges
at the tail base and more developed femoral or pre-anal pores.
Tortoises, turtles and terrapins
The commonly presented tortoises such as the spurthighed and Hermanns (Testudo spp) are not difficult to
handle, although a persistently withdrawn head can hinder
the examination. A little patience while holding the tortoise
upside down will usually persuade a shy individual to protrude the head from the shell when the thumb and middle
finger can be placed behind the occipital condyles. The
mouth can then be opened by applying steady distractive
pressure to the maxilla and mandible, and once open the index finger can be inserted into the corner of the mouth to
prevent closure. This method enables the handler to keep the
mouth open using one hand, leaving the other free to examine the buccal cavity, remove foreign bodies, and take samples for laboratory investigation. The limbs can also be withdrawn by applying steady traction. The coelomic space within the shell is restricted and therefore, gently forcing the
hindlimbs into the shell, leads to protrusion of the forelimbs
and head, and vice versa. The more aggressive species, especially the terrapins and turtles should be held at the rear of
the carapace. Some larger species (snapping turtle, Chelydra
serpentina; soft shelled turtles, Trionyx spp) can deliver an
extremely powerful bite and so great care is required at all
times. Certain species also possess functional hinges at the
front and back of the plastron. The box tortoises are becoming increasingly common since the importation ban on
Mediterranean tortoises, and care should be exercised not to
trap a finger when the hinge closes.
The chelonian shell presents an obvious barrier to a thorough clinical examination, however much can still be
achieved in the consulting room before resorting to imaging
techniques. The head must be extended and the mouth
opened to permit a thorough buccal examination including
an assessment of the mucous membranes and tongue for
signs of stomatitis. The glottis should be examined for signs
of discharge suggestive of pneumonia. The eustachian tubes
enter the lateral walls of the pharynx and any solid deposits
in this area may indicate otitis or urate deposition. The nostrils should be clear and free from any discharge. The eyelids should be open and not obviously distended while the
eyes should be clear and bright. The tympanic scales should
be examined for any swellings indicative of ear abscessation.
The neck and limbs should be palpated for masses and
signs of skin damage, parasites and dysecdysis. The inguinal
fossae should be palpated with the chelonian held upright.
Gently rocking the animal may then enable the clinician to
palpate eggs, uroliths or other coelomic masses. The shell
should be examined for poor conformation, trauma and infection. Pyramiding or softening of the shell is often caused
by inappropriate nutrition while shell infection may present
as loosening and softening of the scutes, erythema and haemorrhages within the shell, and discharges from shell lesions.

4th European FECAVA SCIVAC Congress

Prolapses through the cloaca are obvious but it is necessary to differentiate between prolapses of the cloaca and
those of the male penis. Internal examination using digital
palpation and an auroscope or endoscope is recommended.
Male chelonians can be differentiated from females by their
longer tails and the position of their cloaca caudal to the
edge of the carapace.
A detailed history and clinical examination will usually
indicate which further investigations may be necessary to
make a definitive diagnosis. Radiography, ultrasonography,
MRI and CT, endoscopy, haematology, blood biochemistry,
microbiology, cytology and parasitology are all proven techniques that are used extensively in reptile medicine.

Haematology and biochemistry


There is now a great deal more clinicopathological data
available for many of the common pet reptile species and so
blood sampling offers a great wealth of information. Unfortunately, venepuncture is often blind in reptiles but with
practice it can be efficiently and consistently performed.
Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Avoid the hemipenes of
males. Preferred site for larger specimens.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
Preferred site for smaller specimens.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining
slight negative pressure. If the needle hits a vertebral body
withdraw slightly and redirect. Preferred site for all lizards.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapinsDorsal tail vein; A 5/8 21-25 g needle is angled at 45-90
and placed, as cranial as possible, in the dorsal mid line of
the tail. The needle is advanced while maintaining a slight
negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species. Preferred
site for those aggressive chelonians that possess a well de-

veloped dorsal tail vein.


Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation. Preferred site
for most chelonians.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation. Preferred site for very small
specimens.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversed with neostigmine), and it may be necessary
to use large spinal needles (3-8) to reach the vein. Preferred
site for smaller specimens.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90o in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Preferred site for larger crocodilians (over 1.5 m) but chemical restraint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversed
with neostigmine) must be considered for both animal and
operator safety.

Haematology3
Some species are sensitive to EDTA as an anticoagulant
and so lithium heparin is the anticoagulant of choice. Reptiles
possess nucleated red and white blood cells and so differential cell counts must usually be performed manually using either the Eosinophil Unopipette or Toluidine blue technique.
Erythrocytes
 nucleated
 blood parasites common but not usually significant
Thrombocytes
 smaller than erythrocytes
 dense basophilic nucleus
 often found in clusters
Lymphocytes
 most common leucocyte
 variable in size and colour
 eccentric nucleus
 reactive lymphocytes are called plasma cells
Monocytes
 large in size but rare in number

23

 bluish-grey fine granular cytoplasm with vacuoles


 indented or U-shaped nucleus
Azurophils
 non-segmented nucleus
 basophilic cytoplasm with azurophilic area but without granules
 reactive azurophils may contain vacuoles, granules,
phagocytosed material
 often considered an acute inflammatory cell
Heterophils
 variable nucleus
 spiculate eosinophilic granules
 reptilian equivalent of the mammalian neutrophil
 elevated during bacterial infections and tissue necrosis
Eosinophils
 may be difficult to distinguish from heterophils
 eosinophilic granules are usually more rounded
Basophils
 small but common leucocyte
 intensely basophilic granules
 fragile cells that may disintegrate during slide processing.
Interpretation may be difficult and requires experience
so try to locate an experienced, preferably avian and exotic
haematologist. When developing an in-house haematology
service there are various normal ranges scattered throughout
the literature that can be employed, but nothing is superior
to developing your own series of normal ranges. In cases of
emergency, haematocrit (PCV) estimations and qualitative
evaluations of the buffy coat and stained blood smear may
be very useful until a full haematology can be obtained.

Biochemistry3
Various biochemical parameters and electrolytes can be
routinely used to assess organ damage and metabolic disturbance. Heparinised plasma or serum can be should be used
for most estimations. The author uses two main biochemistry profiles for reptile;
Mini-profile: Calcium, phosphorus, uric acid, AST, total
protein, albumin and globulin.
Extended profile: Calcium, phosphorus, uric acid, AST,
ALT, GGT, bile acids, cholesterol, triglycerides, CPK, glucose, total protein, albumin, globulin, sodium, chloride,
potassium.
Normal blood ranges for green iguanas (Iguana iguana).4
Biochemical parameter
Total protein g/l
Albumin g/l
Globulin g/l
Uric acid mmol/l
Alkaline phosphatase u/l
Alanine aminotransferase u/l
Aspartate aminotransferase u/l
g-Glutamyl transferase u/l
Cholesterol mmol/l
Triglycerides mmol/l
Glucose mmol/l

Normal range
50-78
21-28
25-43
70-140
50-290
5-68
5-52
0-3
2.7-8.6
0.6-7.8
9.4-16.0

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4th European FECAVA SCIVAC Congress

24

4th European FECAVA SCIVAC Congress

Calcium mmol/l
Phosphorus mmol/l

2.2-3.5
1.5-3.0

Haematological parameter

Normal range

Total red blood cell count x10^12/l


Packed cell volume l/l
Haemoglobin g/dl
MCV fl
MCH pg
MCHC g/dl
Total white blood cell count x10^9/l
Heterophils x10^9/l
Azurophils x10^9/l
Lymphocytes x10^9/l
Eosinophils x10^9/l
Monocytes x10^9/l
Basophils x10^9/l

1.0-1.9
0.25-0.38
6.0-10.0
165-305
48-78
20-38
3-10
0.35-5.2
0.0-1.7
0.5-5.5
0.0-0.3
0.0-0.1
0.0-0.5

mogenous predominant bacterial


population
Faecal floatation
- use a concentrated floatation medium and examine for helminth ova
Faecal culture
- Mixed bacterial/fungal growths are
less clinically important (even if
Gram-negative) than a heavy pure
growth of a single bacteria or fungus
Beware of pseudo parasites e.g. pollen, prey parasites etc
Urine tests;
Direct wet mount
Dip-stick tests
Specific gravity
Cytology
Microbiology

Faecal and urine examination6,7


Reptiles will often void faeces and urates during the consultation, usually all over the veterinarian who should be
grateful for this gift of clinical material. When dealing with
an anorexic reptile that may not be voiding faeces it is a simple process to perform a cloacal wash;
 insert a lubricated catheter (attached to a syringe containing warm normal saline) into the cloaca and advance into the colon
 Instil up to 1% body weight of normal saline and repeatedly flush and aspirate until a sample is obtained
Faecal tests;
Direct wet mount

- examine under x400 for flagellate


protozoa, helminth larvae and ova
Mix with eosin
- examine under x400 for encysted
amoeba
Acid-fast (ZN) stain - examine for acid fast Cryptosporidia spp
Gram-stain
- examine Gram-positive and Gramnegative bacteria. Most reptiles
possess G- bacteria, look for ho-

- examine under x400 for protozoa


(e.g. Hexamita sp)
- blood, leucocytes (glucose, protein)
- not very useful as reptile urine is
isosthenuric
- active inflammation, renal casts
- bladder urine is not sterile but
heavy pure growth may be clinically significant.

Radiography8,9
Radiography is an important tool in reptile diagnostics that
should be utilised more often. It is important to remember that
lower kV values will be required for smaller exotic species.
Adequate restraint is vital to facilitate proper positioning;
 place conscious lizard in radiolucent cloth bag or box
 place conscious snake into restraint tube
 place chelonian on a raised column to keep limbs clear
of table
 use the vaso-vagal response in larger lizards
 consider chemical restraint and anaesthesia
 use tape to secure animals in position
Standard views for various species are as follows;
Snakes: dorsoventral views of straight body (not coiled)
horizontal beam laterals of straight body
remember to use markers along body length
Lizards: dorsoventral views of whole body or particular part
horizontal beam lateral
Chelonia: dorsoventral view of whole body

Observed normal haematological and biochemical ranges used to assess dehydration and biochemical
imbalances in selected reptiles
(adapted from references 4 and 5, and the authors unpublished observations)

Green iguana

Gila monster

PCV (l/l)
TP (g/l)
Urea (mmol/l)
Creatinine (mmol/l)
Uric acid (umol/l)

25-38
50-78
0-0.7
42-80
70-140

Glucose (mmol/l)
Sodium (mmol/l)
Chloride (mmol/l)
Potassium (mmol/l)

9.4-16.0
140-183
102-125
1.3-5.2

25-30
60-85
na
na
100-1000
0
2.5-6.0
150-190
114-130
4.1

Tortoise
(Testudo sp)

Box tortoise

Boa constrictor

Rat snake

Caiman

19-40
50-75
0.25-6.70
20-150
75-200

20-38
40-50
na
na
100-200

20-32
46-80
0-1.67
0-26.5
75-250

20-30
40-70
na
na
75-250

26
50-65
na
na
175

2.6-5.2
120-158
98-128
4.0-7.0

2.0
130-149
104-108
4.6-4.7

0.6-4.0
130-152
104-124
3.0-5.7

na
130-160
125-147
4.1-5.2

4.1-6.3
139-150
109-132
3.8-7.9

horizontal beam lateral


horizontal beam anterior-posterior view

Ultrasonography8,9
Ultrasound permits the visualisation of soft tissues and
may be most useful in the chelonia. 7.5 and 10 MHz transducers with stand-off are usually better at providing good
resolution in small reptile patients. 5 and 3.5 MHz transducers can be used for larger reptiles. Copious contact gel must
be applied to the reptilian scaly skin, especially in heavily
keeled species.
In some cases a water bath may be more appropriate. Organ position will change with rotation of the reptile and
therefore (as with radiography) try and maintain the animal
in a normal body posture.
Chelonia: sector scanners can be used in the soft tissue
spaces between the carapace, plastron and limbs. The reproductive tract, heart and liver can all be assessed for major abnormalities, but identifying subtle differences in tissue structure may be more difficult.
Lizards and snakes: the ribs of snakes almost extend
along the whole body-length and will be a hindrance to ultrasound. Nevertheless, gonads, ova, eggs can be assessed
and masses can be differentiated.

25

veterinary use.

Cytology and microbiology


Cytology2
The submission of clinical material (e.g. impression
smears, skin scrapes, fine needle aspirates, lung washes,
stomach washes, faeces, urine, spinal fluid, tissue biopsies
or post mortem tissues) for microscopy, histopathology and
microbiology is often the best means of obtaining a definitive diagnosis. However, the often unique tissue structure of
reptiles does necessitate the services of a pathologist with
experience in reptile pathology. This is especially true when
submitting small biopsies obtained from endoscopy.
When time permits full histopathology is to be preferred,
but in cases of emergency cytology offers the clinician a good
second best. Cytology will usually not provide a complete diagnosis and therefore cannot replace histopathology, however
it can provide a working diagnosis while histology is pending.
Impression smears from skin lesions, fine needle aspirates,
lung wash smears, stomach wash smears etc can be stained
using Diff Quik stains and examined under a microscope.

Microbiology11
10

Endoscopy

Fibre-optic endoscopy is the diagnostic imaging and


sampling technique of choice in the authors experience. The
use of small flexible and rigid endoscopes (1-2 mm) enable
the clinician to get inside the animal and depending on the
reptiles size, permits;
visualisation of the gastro-intestinal tract via the mouth and
cloaca
visualisation of the respiratory tract via the glottis
laparoscopy
 visualisation and biopsy of kidneys
 visualisation and biopsy of liver
 visualisation and biopsy of pancreas
 visualisation and biopsy of spleen
 visualisation of the heart
 visualisation of the lungs
 visualisation of the reproductive tract
 visualisation of the bladder (where present)
 visualisation of the gastro-intestinal tract
 visualisation and biopsy of any masses, neoplasia etc
With new endoscopic operating equipment such as the
Storz endoscopic scissors, forceps and injection needle it is
also possible to debride, cut, retrieve foreign bodies, aspirate
and execute remote local injections.

MRI and ct8,9


These sophisticated imaging techniques are unlikely to
be easily accessible to most clinicians or financially unacceptable to most clients. However, the quality of the images
are excellent and some hospitals may be prepared to tolerate

Gram-negative bacteria are common (often commensal)


organisms in reptiles, but heavy pure growths of a single
predominant bacteria is often significant. Anaerobic bacteria
are often important pathogens that are simply overlooked on
routine microbiological culture. Mycotic infections also appear to be more common in reptiles than domesticated mammals. In summary request aerobic, anaerobic and fungal culture with appropriate sensitivity testing.
Viruses are becoming more clinically apparent. Aspirates
used be sent on dry swab while tissues are best transported
fresh on ice. Scanning electronmicrscopy may reveal virus
particles while virus culture and isolation is now possible in
many labs using reptile and avian cell lines.

Post mortem examination12,13,14


No clinician can save every animal. Death, however unfortunate to the animal and owner, does provide the clinician
with a huge resource for not only making an elusive diagnosis but also for learning the pathogenesis of reptile disease.
Every reptile clinician needs to familiarise themselves with
normal reptile anatomy and post mortem examination is invaluable. A systemic approach is vital and useful histopathological and microbiological information will only be obtained if the submitted tissues are fresh at sampling and
stored correctly.

Key words
Reptile, diagnostics, history, clinical examination,

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4th European FECAVA SCIVAC Congress

26

4th European FECAVA SCIVAC Congress

haematology, biochemistry, faecal examination, radiography,


ultrasonography, endoscopy, cytology, microbiology, post
mortem.

References
1.
2.

3.

4.

5.

6.

7.

8.

9.

Divers, S.J. (1996). Basic reptile husbandry, history taking and clinical
examination. In Practice 18(2): 51-65.
Jackson, O.F. and Lawton, M.P.C. (1992). Examination and diagnostic
techniques. In: Manual of Reptiles (Eds. P.H. Beynon, M.P.C. Lawton,
J.E. Cooper). BSAVA, Cheltenham. Pages 32-39.
Campbell, T.W. (1996). Clinical pathology. In: Reptile Medicine and
Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 248257.
Divers, S.J., Redmayne, G. and Aves, E.K. (1996). Haematological and
biochemical values of 10 green iguanas (Iguana iguana). Veterinary
Record 138:203-205.
Stein, G. (1996). Hematologic and blood chemistry values in reptiles.
In: Reptile Medicine and Surgery, p473-483 (Ed. D. R. Mader). WB
Saunders, Philadelphia.
Lane, T.J. and Mader, D.R. (1996). Parasitology. In: Reptile Medicine
and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages
185-202.
Frye, F.L. (1991). Applied clinical nonhemic parasitology of reptiles.
In: Biomedical and Surgical Aspects of Captive Reptile Husbandry
(Ed. F.L. Frye, second edition). Pages 281-325.
Silverman and Janssen, D.L. (1996). Diagnostic imaging. In: Reptile
Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia.
Pages 258-264.
Rubel, A., Kuoni, W. and Frye, F.L. (1991). Radiology and imaging.
In: Biomedical and Surgical Aspects of Captive Reptile Husbandry
(Ed. F.L. Frye, second edition). Pages 185-208.

10.

11.

12.

13.
14.

Jenkins, J.R. (1996). Diagnostic and clinical techniques. In: Reptile


Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 264-276.
Rosenthal, K. and Mader, D.R. (1996). Microbiology. In: Reptile
Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 117-125.
Cooper, J. E. (1992). Post mortem examination. In: Manual of Reptiles (Eds. P.H. Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham. Pages 40-49.
Mader, D.R. (1996). Euthanasia and necropsy. In: Reptile Medicine
and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages
277-281.
Frye, F.L. (1991). Euthanasia and necropsy. In: Biomedical and Surgical Aspects of Captive Reptile Husbandry (Ed. F.L. Frye, second
edition). Pages 513-528

27

EUROPEAN SOCIETY OF FELINE MEDICINE-ESFM

Diagnostic and therapeutic approaches to neutropenia


and neutrophil dysfunction
The neutropenic and pyrexic cat

Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

OVERVIEW
Neutropenia
Neutropenia may indicate excessive tissue demand for
neutrophils, decreased production, or immune-mediated destruction. Neutropenia is as great a concern as neutrophilia
and is possibly a more serious a problem because neutrophils are the bodys first line of defense against invading
microorganisms. Neutropenia is any decrease in neutrophil
numbers below the reference interval. However, clinical
signs associated with neutropenia are seldom observed unless the neutrophil count is below 1000 per microliter and,
perhaps, less than 500 per microliter. Neutropenia is associated with infection, drugs, immune dysfunction, acquired
immunodeficiency, neoplasia, and may be idiopathic.

Fever
Temperature, like so many biologicial functions, normally displays circadian rhythmicity. In the cat, temperatures
are often lowest in the morning and highest in the afternoon.
Temperature is regulated by homeostatic mechanisms that
strike a balance between heat production and heat dissipation. Abnormal elevation in body temperature, or pyrexia,
can occur due to hyperthermia or fever. Hyperthermia is
treated with physical cooling methods whereas fever is often
treated with drugs. Fever is often a positive response and, in
most instances, is simply noted. Interleukin-1 is produced by
mononuclear phagocytes and directly acts upon the hypothalamic control center causing fever.

Fever of undetermined origin


Fever of undetermined origin (FUO) is an unusual presentation of a usual problem. FUO is caused by infection,
immune dysfunction, or neoplasia

CLINICAL AND THERAPEUTIC APPROACH


Diagnostic Evaluation of Granulocytopenia (less than
5000 cells per microliter in the dog and less than 3300 cells
per microliter in the cat).

Diagnostic evaluation should include an extensive history of current and recent (including the past 6 weeks) drug
therapy and physical examination to evaluate or estimate
splenic size.
1. Hematologic evaluation - the total white blood cell count
and differential in absolute terms with or without relative
lymphocytosis.
2. Bone marrow aspiration (and/or biopsy) is necessary
when the white cell count is persistently below 3000 cells
per microliter. This is especially needed when another cell
line is also abnormal to determine marrow cellularity or
arrest in cell maturation.
3. Screening tests for antinuclear antibodies in both systemic
lupus erythematosus or rheumatoid arthritis. Again, this is
especially required when rheumatoid arthritis is suspected
of being associated with hypersplenism.
4. Radiographic, ultrasound or cytologic examination of the
spleen to evaluate size, and potential for cellular sequestration since hypersplenism may be associated with leucopenia as well.

Neutropenia
Leucopenia is most often caused by neutropenia. Neutropenia may be the result of overwhelming inflammatory
processes which shorten circulating neutrophil survival especially when myelopoiesis -specifically neutrophil production - is ineffective, or when there is bone marrow myelosuppression. Neutropenia and toxic morphologic alterations
of neutrophils may be anticipated in Gram-negative sepsis or
endotoxemia. If mature neutrophils are fewer than immature
cell forms, this is regarded as a degenerative left shift. Degenerative left shifts may appear with both neutrophilia or
neutropenia and indicate inappropriate - deficient - bone
marrow response. Increased neutrophil margination, adherence of neutrophils to microvascular endothelium pseudoneutropenia - may result from endotoxemia or from
anaphylactic reactions. Viral infections, a wide variety of
disparate drugs and environmental toxins, and neoplasia (especially during chemotherapy) may induce severe neutropenia as well as affecting other cell lines in a similar manner.
Feline immunodeficiency virus (FIV) infection is characterized by moderate to severe leucopenia, neutropenia,
and often, lymphopenia and eosinopenia. Appropriate
myeloid activity or mild bone marrow myeloid hyperplasia

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28

with a left shift to progranulocytes often accompanies the


neutropenia. Chronic infection is characterized by intermittent neutropenia and lymphopenia. Viral infection of bone
marrow myeloid precursors may be involved with the cytopenias. Feline immunodeficiency virus induces progressive immunodeficiency, opportunistic infections, nutritional
deficiencies, as well as some forms of neoplasia. The cytopenias that develop during the symptomatic disease induced by FIV may play a significant role in these processes.
Experimental inoculation of canine parvovirus in the cat induces a decrease in total numbers of both myeloid and erythroid cells in the bone marrow.
Feline leukemia virus infection (FeLV) is a retrovirus
(oncovirus subfamily) that causes immunodeficiency and
neoplastic disease in domestic cats. The physiologic systems
affected are the hematopoietic, lymphatic, and immune systems possibly by neuroendocrine dysfunction, resulting in
immunosuppression with secondary infections and/or development of neoplastic disease. Anemia is often severe. Lymphopenia and neutropenia may be present; however neutrophils can be elevated in response to secondary infections.
Serology and bone marrow examination are indicated
among diagnostics.
Feline panleucopenia is an acute, enteric, viral infection
of cats characterized by sudden onset, depression, vomiting
and diarrhea, severe dehydration, and a high mortality caused
by feline parvovirus. The systems affected are the
hematopoietic, lymphatic, and immune systems with loss of
all white blood cells and atrophy of the thymus. Panleucopenia is the most consistent finding with total leucocyte counts
between 500 and 3000 cells per microliter. Immunoassays
and serology are the only useful diagnostics. Supportive
treatment is indicated as specific therapy is not usually successful.
Bacterial-induced myelonecrosis occurs in dogs and cats.
Reduced survival neutropenia can be caused by bacteremia (pneumonia, peritonitis, pyothorax), immune-mediated destruction, drug-induced destruction, hypersplenism
(sequestration), and paraneoplastic syndrome (the precise
mechanism is unknown).
Drug/Chemical-induced Neutropenia is often caused by
chloramphenicol or benzene ring compounds in cats - eucalyptus oil, menthol, camphor.
Mitoxanthrone is a chemotherapeutic agent which induces myelosuppression. The myelosuppression has been
successfully treated with recombinant canine granulocytecolony stimulating factor (rcG-CSF).
Administration of zidovudine (> 30 mg/kg) in cats resulted in dose dependent progressive neutropenia and anemia.
Griseofulvin administration has been associated with the
development of absolute neutropenia in cats. This is especially apparent in cats infected with FIV.
Cephalosporin administration may induce bone marrow
suppression in both dogs and cats as the result of ineffective
marrow erythropoiesis and myelopoiesis.
Other potential drugs include gold salts, thiacetarsamide, meclofenamic acid, quinidine gluconate, captopril, and penicillamine.
Recombinant canine G-CSF (2.5 ug/kg q 12 h) administration had been observed to be effective in stimulating

4th European FECAVA SCIVAC Congress

myelopoiesis in dogs.

Cyclic neutropenia
Cyclic neutropenia is an inherited disease in Grey Collies
(Grey Collie Syndrome; Cyclic Hematopoiesis) and is suspected in other canine breeds. It is characterized by recurrent
episodes of neutropenia lasting 12 to 14 days. Thrombocytopenia and anemia may accompany cyclic neutropenia. Neutrophil functions are also impaired and frequent infections are
therefore anticipated. Affected dogs given low dose rcG-CSF
continued to have neutropenic cycles but the degree of neutropenia and the clinical signs were ameliorated. Cyclic
hematopoiesis has been described in the cat as an acquired disease possibly related to feline leukemia viral infection (FeLV).

Chronic idiopathic neutropenia syndrome


Persistent neutropenia has been described in the cat that
resembles chronic idiopathic neutropenia syndrome of man.
Decreased numbers of mature granulocytic cells and colony
forming units-granulocyte macrophage (CFU-GM) have
been observed in bone marrow and in bone marrow culture
respectively.

Diagnostic evaluation of functional


granulocytic defects
Neutrophils function as phagocytes by a complex interaction of immunoglobulins, complement, and neutrophil enzymes. Total evaluation involves evaluation of patients who
exhibit an inability to handle infections.
1. Chemotaxis may be tested in agar media or in a three part
Boyden chamber.
2. Quality and quantity of immunoglobulins and complement must be determined. Quantity is determined my immunoelectrophoresis and determination of the presence of
various complement components. Quality of immunoglobulins may be tested similarly to chemotaxis in
agar media. A screening test of complement function is
the total lytic complement test.
3. The nitroblue tetrazolium dye test (NBT) is a test of nonimmune phagocytosis and measures the contribution of
peroxidase qualitatively.
4. The myeloperoxidase stain which measures the presence
of the enzyme in neutrophil cytoplasm also provides qualitative measures.

Functional defects of granulocytes


Neutrophil function involves chemotaxis, phagocytosis,
and bacterial killing. Problems with neutrophil function can
involve one or all of these functions. Chemotaxis and phagocytosis are dependent on external factors involving immune
(antibody) globulin and complement opsonins C3a, C5a, and
C567. Bacterial killing involves production of hydrogen per-

oxide intracellularly by anaerobic glycolysis and the hexose


monophosphate shunt and utilizes myeloperoxidase of granulocytic primary granules.
Diseases associated with functional defects of granulocytes are characterized by repeated bacterial or fungal infection beginning early in life or infections with otherwise lowvirulence organisms in patients with appropriate granulocyte
counts. Most involve inherited disorders of immunoglobulins, complement, or the hexose monophosphate shunt. Acquired transient deficiencies secondary to drugs are poorly
understood.
Leucocyte dysfunctions in small animals include the
Chediak-Higashi Syndrome, canine granulocytopathy, and
defective neutrophil function of the Doberman Pinscher.
Neutrophil dysfunctions may also be associated with complement or immunoglobulin deficiencies. Defective humoral
immune components include specific IgA deficiency of German Shepherds, Beagles, Shar Peis, and other breeds, IgM
deficiency of the Doberman Pinscher, C3 deficiency of the
Brittany Spaniel and possible IgG deficiency of the
Weimaraner.
The Pelger-Huet Anomaly is in inherited defect observed
in dogs and cats as well as numerous other species. Mature
neutrophils of affected individuals have nuclear hyposegmentation and, possibly, moderate dysfunction associated
with diminished migratory capabilities.
Myeloproliferative disorders - leukemias - often have associated neutrophil dysfunction and/or neutropenia. Decr-

29

reased production of neutrophils (or other hematopoietic


cells can occur from infiltrative bone marrow diseases leukemia, nonhematopoietic neoplasia metastatic to the marrow cavity, myelofibrosis or ostesclerosis, disseminated
granulomatous disease, or myelodysplasia.

Suggested reading
Gabbert NH: Cyclic neutropenia in a feline leukemia-positive cat: a case report. J Amer Animal Hosp Assoc 20:343, 1984.
Helton KA, Nesbitt GH, Caciolo PL: Griseofulvin toxicity in cats: literature
review and report of seven cases. J Amer Animal Hosp Assoc 22:453,
1986.
Latimer KS, Rowland GN, Mahaffey MB: Homozygous Pelger-Huet anomaly and chondrodysplasia in a stillborn kitten. Vet Pathol 25: 325, 1988.
Obradovitch Je, Ogilvie GK, Stadler-Morris S et al: Effect of recolmbinant
canine granuloctye colony-stimulating factor on peripheral blood
neutrophil counts in normal cats. J Vet Intern Med 7: 65, 1993.
Breitschwerdt EB, Brown TT, de Buysscher E et al: Rhinitis, pneumonia,
and defective neutrophil function in the Doberman Pinscher. Am J
Vet Res 48:1054-1062, 1987.
Withbread TJ, Batt RM, Garthwaite G: Relative deficiency of serum IgA in
the German Shepherd dog: a breed abnormality. Res Vet Sci 37:350352, 1984.
Hansen P, Clercx C, Henroteaux M et al: Neutrophil phagocyte dysfunction
in a Weimaraner with recurrent infections. J Small Animal Practice
36:128-131, 1995.
Mandell CP, Jain NC, Farver TB et al: The significance of normoblastemia
and leucoerythroblastic reaction in the dog. J Amer Animal Hosp Assoc 25, 665-672, 1989.

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4th European FECAVA SCIVAC Congress

31

EUROPEAN SOCIETY OF FELINE MEDICINE-ESFM

Feline anemia: practical investigation and management


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Summary
Red blood cell production and its control are intrinsic to
understanding anemia. Anemia is a sign of underlying disease. Complete physical examinations are complemented by
complete hemograms. Responsive anemias are caused by hemorrhage and hemolysis. Nonresponsive anemias are more
common in the cat than are responsive anemias. The prior use
of drugs must be considered. Retroviral diseases are another
consideration. Bone marrow examination may be beneficial.
Treatment of anemia is directed against the underlying cause.

The erythroid cell system comprises the population of


circulating red blood cells (RBCs) and their nucleated precursors located in the bone marrow of normal feline adults.
A complex and not yet fully understood homeostatic mechanism (involving in part the hormone erythropoietin) operates upon marrow precursors to maintain a circulating RBC
population at a size and hemoglobin content adequate to preserve normal tissue oxygen tensions. The critical factor in
the homeostatic mechanism that regulates the production of
erythropoietin is tissue oxygen tension, not RBC number or
blood hemoglobin concentration.1-3
RBCs traditionally have been considered to be solely
oxygen-carrying and oxygen-delivering cells, functions certainly of critical importance. These cells are now being reexamined in terms of their role in physiologic defense. The surface area of RBCs is enormous - and is known to be adsorptive. The redefinition of RBC function has to do with this adsorptive capacity and the intrinsic ability of RBCs to remove
or cleanse the plasma component of blood. RBCs adsorb
many microscopic materials, which are removed by the
phagocytes of the mononuclear-phagocyte system (MPS) located primarily in the liver and spleen. The RBC membrane
is thus cleansed, and for the most part the cleansed cell is returned to the circulation. This phagocytic processing also has
an impact on the RBC in terms of its longevity (or senescence). Repeated phagocytic incursions does affect the
shape, viability, and longevity of the RBC.1,2,4,5

ANEMIA IN PERSPECTIVE
Anemia, defined as a lower than normal blood hemoglobin
(Hb) concentration or packed cell volume (PCV; hematocrit

[HCT]), occurs if RBC production is acutely or chronically insufficient to replace RBC losses, which may be caused by normal RBC senescence, accelerated RBC destruction (hemolysis), or extracorporeal blood loss (bleeding). Some examples
of anemia result from relatively uncomplicated alterations in
single factors, for example, transient anemia following an
acute hemorrhagic event in an otherwise healthy individual. In
most cases, however, the pathophysiology of anemia involves
the interplay of several disturbances in RBC homeostasis, including limitations of production as well as abnormal red cell
survival. Our first obligation is to examine these factors in a
general sense and to evaluate the significance and limitations
of the techniques for distinguishing and quantitating them.1-3

RED BLOOD CELL PRODUCTION


Basic knowledge about feline RBC production is intrinsic to understanding how the cat responds to a lowered red
cell mass (i.e., anemia). In the normal adult, RBC production is confined to the axial skeleton. When erythropoiesis
is required, the volume of active marrow may expand into
the distal long and flat bones, that is, into the fatty marrow
and at the expense of bony matrix. Under extreme and prolonged stress or when marrow is replaced by pathologic tissues, extramedullary sites such as spleen, liver, and lymph
nodes may develop foci of erythropoiesis. All of these tissues including the marrow are capable of a six- to eightfold
increase in RBC production in response to the stimulus of
anemia. Thus even under conditions of accelerated red cell
destruction, blood Hb concentration may remain nearly normal as long as the rate of destruction does not exceed the
capacity for compensatory expansion of the RBC precursor
population.6

ERYTHROPOIETIN
Erythropoietin (EPO) has a number of effects. High concentrations of EPO, in concert with granulocyte macrophage
colony-stimulating factor (GM-CSF), stimulate the erythroid progenitor to become an erythroid burst forming unit
(BFU-E), an explosive erythroid productive cell. In low concentrations EPO together with GM-CSF and interleukin 3
(IL-3) convert the BFU-E to an erythroid colony-forming
unit (CFU-E), a cell capable of producing colonies of red

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32

cell precursors. Low concentrations of EPO also convert the


CFU-E into the first recognizable RBC precursor in the bone
marrow. In addition, EPO accelerates RBC production and
maturation, internal cell Hb production, and finally modulates the movement of marrow reticulocytes into peripheral
blood reticulocytes. To summarize, EPO activates erythropoiesis, accelerates erythropoiesis, and is intrinsic to the successful delivery of RBCs to peripheral blood.2

4th European FECAVA SCIVAC Congress

aggregate reticulocytes greater than 50,000/l is evidence of


regeneration.7 Basophilic stippling, a dark bluish stippling of
some immature RBCs, is commonly found in some RBCs
released into peripheral blood in response to anemia. This
finding has no special significance insofar as the etiology of
anemia in the cat is concerned.6

FELINE HEMOGLOBIN
MORPHOLOGY OF ERYTHROPOIESIS
The process of red cell production from blast to adult RBC
takes from 4 days to 1 week. The first morphologically identifiable bone marrow erythroid precursor is the rubriblast. In
this cell is the initiation of characteristic RBC protein production (Hb and enzymes), as well as surface antigens and metabolic machinery. One of these cells can have as many as 16 to
32 progeny erythrocytes. When this cell divides giving rise to
the prorubricyte (which in turn leads to the formation of the
basophilic rubricyte) loss of replicative function and loss of
the nucleus itself begins. The basophilic rubricyte gives rise to
the polychromatophilic rubricyte, a cell in which morphologic recognition of cytoplasmic hemoglobin production is first
possible. Whether the polychromatophilic rubricyte is the last
of the dividing RBC precursors is arguable, but from it arises
the metarubricyte, in essence the nucleated RBC (nRBC) often observed in peripheral blood smears of anemic patients.
The nucleus of this cell is almost nonfunctional, and when extruded the metarubricyte becomes the earliest bone marrow
reticulocyte. Under normal circumstances bone marrow reticulocytes mature in the marrow for approximately 3 days and
then move from the extravascular hematopoietic space to the
intravascular space via the bone marrow venous sinus. Here
the cell is simply called a reticulocyte. After approximately 24
hours the reticulocyte loses its intracellular materials (which
stain with new methylene blue). The cell is now an adult RBC
destined to live approximately 80 days in a normal blood volume of about 70 ml/kg (a number different than in other common domestic animals).6
Nucleated RBCs may appear in peripheral blood of adult
cats without evidence of intensified erythropoiesis and may
be a sign of systemic stress of disease or splenic inactivity.
This finding is unique to the cat. Nucleated RBCs do acutely accompany increased reticulocyte numbers in early, active erythropoiesis. The presence of increased nRBCs without reticulocytes or in nonanemic states also suggests bone
marrow disease or cardiopulmonary dysfunction. These
cells are often observed in myeloproliferative disease.6

FELINE RETICULOCYTES
Feline RBCs retain stainable reticulum for several
weeks. Type I forms have a punctate reticulum staining and
are not counted in traditional peripheral blood reticulocyte
counts. Types II and III with dense aggregates of reticulum
and conforming to the morphologic appearance of reticulocytes of other species are counted in peripheral blood as a
gauge of erythroid response.6 A reticulocyte concentration of

Two hemoglobins, designated major and minor, in the


cat differ from other mammalian hemoglobins in that they
have the largest number (eight) of reactive sulfhydryl
groups. The physiologic occurrence of small eccentric refractile bodies (erythrocyte refractile bodies; Heinz bodies;
Schmauch bodies) indicates the unusual propensity for hemoglobin denaturation in cats. This is most probably related
to the unique structure of feline hemoglobins.6 This may also be related to the fact that cats have a unique nonsinusoidal
spleen, which does not readily remove atypical RBCs.8

ADULT FELINE RED BLOOD CELL


ANALYTES
With respect to PCV, Hb, and RBC number as well as
RBC indices, cats generally attain adult values by 4 or 5
months of age. There are significant differences between kitten and adult values, as discussed in more definitive texts on
the subject.6,9

PHYSICAL EXAMINATION
A thorough physical examination is essential in the diagnosis of feline anemia. For example, icterus can be caused
by hemolysis, cats with lymphatic diseases often have concurrent or associated anemia, and cats with petechiae and/or
ecchymoses most probably have thrombocytopenia and/or
thrombocytopathia or vasculitis.

ANEMIA AS A DIAGNOSTIC SIGN


Anemia is the result of only a few processes and when
these processes are considered, a series of diagnostic steps
may be set in motion, often revealing the underlying cause.
Iron- deficiency anemia in kittens may result from portosystemic shunts (microcytosis without evidence of RBC regeneration), all milk diets, or from external or internal parasitism: in adults parasitism would be lower on a differential
list and blood loss through ulceration or neoplasia would be
more common causes. Decreases in total protein (TP) and
the RBC indices along with decreases in serum iron (SI) and
increases in total iron-binding capacity (TIBC) would be anticipated. Anemia of inflammatory disease (AID; anemia of
chronic disease) is mild if detectable and is associated with
decreases in both SI and TIBC. Anemia associated with hemorrhage is not difficult to diagnose and is usually associated with a history of trauma.

Hemorrhagic anemia and hemolytic anemia are unique


in terms of increasing reticulocyte percentage once the bone
marrow reaches increased productive status 3 to 4 days after
the insult. Often in intravascular hemolysis or hemolysis induced by Heinz bodies, the mean corpuscular hemoglobin
concentration (MCHC) is above the reference interval.
Whenever this analyte is increased, the preceding causes
should be considered.
Hypohormone anemia, which is anemia associated with
renal disease, hypothyroidism, and hypoadrenocorticism, requires specific and incisive testing. Anemia associated with
bone marrow disease is usually accompanied by cytoses or
cytopenias in at least one other cell line.

EVALUATING LABORATORY TESTS


A complete hemogram complete with all three RBC indices (mean cell volume [MCV], hemoglobin concentration
by percentage [MCHC] and hemoglobin by weight [MCH]),
HCT, Hb, RBC number, reticulocyte and nRBC numbers,
TP, examination of RBC, white blood cell (WBC) and
platelet morphology, and a differential in absolute numbers
is the first step in solving the mystery of anemia. Regenerative anemias are those with elevated reticulocyte counts (see
above) and are indicative of hemolysis or hemorrhage. Only
when they are accompanied by large numbers of reticulocytes can nRBCs be associated with RBC regeneration.
All other forms of anemia are considered nonregenerative or hypoproliferative. When these anemias are severe,
transfusion is indicated.

33

dogs because the occurrence of natural isoantibodies is common. Approximately 70% of all type B cats have anti-A antibody in a high enough titer to cause decreased RBC survival
and acute hemolysis. As little as 5 ml of incompatible blood
is enough to cause a fatal reaction. In 35% of all type A cats
anti-B is present but usually in low titer; reaction in these animals is less frequent. Although the incidence of type B cats
in the United States is low, many purebred cats (excepting the
Siamese) such as the Cornish and Devon Rex, British shorthair, Abyssinian, and Himalayan cats have a high frequency
of B blood types. Crossmatching is strongly recommended
for all cats about to receive blood or blood products. The
presence of natural isoantibody always result in decreased
RBC survival posttransfusion. Mean RBC survival is approximately 30 days in cats of the same blood type and less
than 10 to 14 days in cats with differing blood types.10
Donor cats should be screened for red cell parasites,
heartworms and feline leukemia virus (FeLV), feline infectious peritonitis (FIP), and feline immunodeficiency virus
(FIV). At 2 week intervals 10 ml/kg can be collected. The use
of citrate-phosphate-dextrose-adenine (CPD-A1) is the recommended anticoagulant. Heparin is contraindicated as it activates platelets and antithrombin III and can result in many
unwarranted and disparate reactions including hemorrhage.
When delivering feline whole blood taken in a citrate anticoagulant care must be taken not to cause hypocalcemia,
which may be severe and even lethal. Citrate is a strong calcium chelator. Caution must also be used not to induce volume overload. Generally if less than 20% of blood volume is
delivered to a normovolemic but anemic feline patient during
an 8 hour period, volume overload does not occur. As mentioned, cats have a normal blood volume of approximately 70
ml/kg.6

BONE MARROW BIOPSY


Bone marrow aspiration or core biopsy is reserved for
any unexplained cytopenia or when neoplasia is staged.
When bone marrow examination is used to help explain cytopenia, it is imperative that the bone marrow preparations
be accompanied by a concurrent hemogram (i.e., blood
drawn at the same time as the marrow sampling). Because
normal diurnal and day-to-day variation is quite significant
and the hematologists diagnostics are always referable to
peripheral blood numbers, it is incorrect and poor science to
draw information from a bone marrow aspirate without reference to a concurrent hemogram. A core biopsy is indicated when attempts at aspiration do not yield bone marrow
particles or sufficient cells.
Bone marrow aspirate or core biopsy are helpful in the
diagnosis of myelofibrosis, myelophthisis, and myeloproliferative diseases in general. These samples may also aid in
the diagnosis of pure red cell aplasia or aplastic pancytopenia, which are often drug induced.

FELINE BLOOD GROUPS AND FELINE


TRANSFUSION MEDICINE
Three feline blood groups have been described: A, B, and
AB. The feline blood group system is different than that in

CONSIDERATIONS11
Acepromazine, Chloramphenicol, Trimethoprim Sulfa, Griseofulvin
These are drugs that can cause hemolytic anemia in the
cat or cytopenias due to bone marrow suppression. Pancytopenia commonly occurs in cats when griseofulvin is used
in the treatment of dermatomycosis.
Oxidative RBC Injury
Denaturation of feline hemoglobin and Heinz body anemia results from excessive doses of Vitamin K. In dosages
in excess of 5 mg/kg/day vitamin K results in severe Heinz
body hemolysis. Other drugs that can cause oxidative injury
are benzocaine, acetaminophen, methylene blue, and acepromazine. Onions can also cause Heinz bodies.
Severe Heinz body hemolysis can result when tiny
amounts of lidocaine are sprayed into the oral cavity before
intubation or when urinary antiseptics containing methylene
blue are used. MPS removal of these cells leads to dramatic
and severe anemia.11
Propylene Glycol in Semi-Moist Cat Foods
These materials cause Heinz bodies in cats. In cats receiving these foods red cell masses are generally lower than

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in other cats.

Retroviruses
FeLV and FIV induce a variety of bone marrow diseases
including anemia. These viruses also cause erythroid dysplasia. The peripheral blood manifestations of these viral incursions are macrocytic RBCs that are not reticulocytes and
nucleated cells that are unclassifiable. These anemias are not
regenerative, but often the MCV is elevated significantly
above the reference interval.

4th European FECAVA SCIVAC Congress

but not observed, the examiner should place the ethylene diamine tetracetate (EDTA) anticoagulated blood in the refrigerator for 8 to 10 hours and look for autoagglutination on the
test tube walls or hemolysis in plasma.
Doxycycline is the drug of choice in treating hemobartonellosis in cats and it has the advantage of once a day dos-

Table 1. Effects of erythropoietin


Direct activation of stem cells and erythroid precursors

Immune-Mediated Hemolysis
Positive direct antiglobulin test (DAT; direct Coombs
test), albeit useful in detecting immune-mediated hemolysis,
is positive when there is a detectable concentration of immunoglobulin on the red cell surface for any reason.4,5 For
example, hemobartonellosis can cause a positive DAT, which
will remain so until this organism is cleared from the body.10
In treating immune-mediated hemolytic anemia (IHA) in
the cat, prednisone at 2 to 4 mg/lb (in contrast to the dog in
which low dosage glucocorticoid is successful), is administered every 12 hours. In confirmed cases of IHA in the cat,
chlorambucil, which is not expensive and has few side reactions, has also been reported to be successful as a second
drug. Chlorambucil comes in 2 mg tablets; typically, cats receive 2 to 3 tablets of chlorambucil once every other week.
It is an excellent immunosuppressive agent. Azathioprine is
not recommended as an immunosuppressive agent in the cat.

Increased erythroid precursor hemoglobin production


Decreased bone marrow erythroid maturation time
Increased (earlier) release of bone marrow reticulocytes

Table 2. Classification of anemia


Nonregenerative, hypoproliferative anemia
Iron deficiency
Anemia of inflammatory disease
Early stages of hemolysis and hemorrhage
Hypoendocrine diseases
Bone marrow disease

RBC Morphologic Changes


There are numerous morphologic changes in RBCs that
are diagnostically helpful. Unfortunately, spherocytes are
difficult to recognize in feline blood smears. Schistocytes,
(fragmented RBCs) are recognized in disseminated intravascular coagulation (DIC). Leptocytes and acanthocytes,
which are suggestive of hepatic diseases in other domestic
species are rare in the cat. Basophilic stippling, although
rare, may be associated with lead toxicity.
Howell-Jolly bodies (remnants of nuclear materials), are
observed when erythropoiesis is active and suggest bone
marrow activity in the erythroid cell line. Often Howell-Jolly bodies are associated with increased reticulocyte numbers
in a new methylene blue stain or with polychromasia in a
Wrights stained smear. Heinz bodies (sometimes described
as signet ring cells) are evidence of hemoglobin denaturation and may involve certain drugs as has been described.
They may also be seen in anorectic cats that are not receiving vitamin B complex in their diets.
Although not common, autoagglutination is indicative of
immune-mediated hemolytic processes, most probably involving immunuoglobulin M or some forms of immunoglobulin G.
Hemobartonellosis
The DAT is often positive in cats with hemobartonellosis. This disease is always secondary to another physiologically stressing event, and an infectious etiology must be
considered. Most commonly these are viral- or bacterial-induced primary processes. If hemobartonellosis is suspected

Regenerative, hyperproliferative anemia


Hemolytic disease: after 3-4 days
Acute hemorrhage: after 3-4 days

Table 3. Feline hematologic reference intervals


Analyte

Interval

Hemoglobin
Hematocrit
Red blood cells
MCV
MCHC
MCH
Reticulocytes
White blood cells
Neutrophils
Band neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Platelets
Total protein
Fibrinogen

6.9 - 9.6 nmol Hb(Fe)/L


33 - 46 L/L
7.55 - 10.87 (1012/L)
38.2 - 48.0 fL
19.7 - 22.5 nmol/L
0.81 - 1.02 fmol
0.2% - 1.6%
5.7 - 16.3% 109/L
2,500 - 12,500/l
0 - 300/l
1,500 - 7,000/l
0 - 800/l
0 - 1,500/l
Rare
140 - 500 x 109/L
6.0 - 8.0 g/dL
0.1 - 0.3 mg/dL

*Modified from deBruijne JJ, Feldman BF: Referentiewaarden van laboratoriumonderzoek bij hond en kat. Analyse 38:11, 248 - 252, 1983.

ing. Tetracycline generally suppresses the feline appetite and


sometimes induced fever. Hypersalivation and vomiting are
other feline tetracycline reactions.
Total Protein, Total Bilirubin, Urine Bilirubin
In cats hemorrhaging is associated with decreases in total plasma or serum proteins accompanying the decreases
observed in red cell mass whereas hemolysis is characterized by normal to increased total proteins. Increases are often artifactual and are caused by the amount of hemolysis or
red cell membrane debris in the plasma or serum. Cats with
hemolysis often have increases in both total bilirubin and
urine bilirubin. Cats that are hemorrhaging would not have
increases in these analytes.

35

ic renal disease. Dosage is 100 to 150 units/kg subcutaneously every 2 to 3 days. As it is a human recombinant
product, about one fourth to one third of cats receiving this
hormone will produce antibodies against it in 6 to 8 weeks.
Care must be taken against overzealous use of this product,
which can lead to as polycythemia with severe to fatal results. As the Hct reaches the reference level, the interval
dosage of erythropoietin is reduced to every fourth of fifth
day. The underlying renal disease is unaffected, but the quality of life is markedly improved.12

References
1.

Zinc
The ingestion of zinc containing pennies and the resultant intravascular hemolysis is seen more often in dogs than
cats. Nevertheless, many of the cat carriers have zinc containing materials in the carrier locks or clamps. Stressed or
angry cats that chew on these could be subject to severe intravascular hemolysis.
Insulin
Cats that are being aggressively treated with insulin for
diabetes mellitus have reduced serum phosphate content, often to a concentration incompatible with RBC integrity.
When intracellular phosphorus is reduced, the adenosine
triphosphate ion and water exchanges are also reduced,
causing spherocytosis and intravascular hemolysis.

2.
3.
4.

5.

6.
7.
8.
9.

Erythropoietin as a Therapeutic Agent


Erythropoietin (Epogen[TM] - Amgen) is used almost
exclusively in treating anemia associated with feline chron-

10.

Rifkind RA, Bank A, Marks PA, Nossel HL: Fundamentals of Hematology, Chicago, Year Book Medical Publishers, 1976, pp 7 - 24.
Schrier S: Hemopoiesis and red blood cell function. Scientific Am
Med 5(1): 1-8, 1988.
Hillman RS, Finch CA: Red Cell Manual, ed 5, Philadelphia, FA
Davis Company, 1985, pp 33 - 55.
Jones DRE, Gruffyd-Jones TJ, Stokes CR, et al: Investigation into
factors influencing the performance of the canine antiglobulin test.
Res Vet Sci 48:53 - 58, 1990.
Jones DRE, Stokes CR, Gruffyd-Jones TJ, et al: An enzyme-linked
antiglobulin test for the detection of erythrocyte-bound antibodies in
canine autoimmune haemolytic anemia. Vet Immunol Immunopathol,
16:11-21, 1987.
Jain NC: Schalms Veterinary Hematology, ed 4 Philadelphia, Lea &
Febiger, 1986, pp 126 - 139.
Kociba GJ: Feline anemia, in Kirk RW (ed): Current Veterinary Therapy X, Philadelphia, WB Saunders Co, 1989, pp 425 - 429.
Weiss L, Blue J: Anatomy of the spleen, in Lichtman MA (ed): Hematology and Oncology. New York, Grune & Stratton, 1980, pp 49 - 53.
Mackey L: Haematology of the cat, in Archer RK, Jeffcott LB (eds):
Comparative Clinical Haematology. Oxford, Blackwell Scientific
Publications, 1977, pp 441 - 482.
Giger U: Feline blood groups and incompatibility reactions. Proceedings of the 8th ACVIM Forum, Washington, DC, 1990, pp 319 - 321

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ITALIAN SOCIETY OF VETERINARY DERMATOLOGY - SIDEV

.D.

Diagnostic approach to canine and feline autoimmune


skin diseases
Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Auto-immune skin diseases are rare dermatoses (less


than 1% of canine dermatoses). Even if the clinical presentation of these dermatoses is often suggestive, the suspicion
must be established only after a good differential diagnosis,
elimination of frequent other dermatoses by routine diagnostic procedures (mainly pyoderma, dermatophytosis, demodicosis), and the final diagnosis must be established
based on compatible history, clinical aspect and histolopathological findings. Direct immunofluorescence or
immuno-histochemical testing may also be helpful but these
procedures have relatively poor diagnostic sensitivity and
specificity

A - Classification (Suter M - Olivry T)


1) Autoimmune diseases with cutaneous
target
Autoimmune disease with keratinocyte surface molecules
as targets:
- Pemphigus foliaceus (PF): far most frequent autoimmune
skin disease in the dog. It is a crusting and scaling dermatitis starting bilaterally symmetrical at the face and/or
paws, sometimes spreading as a general disease. Antigen:
Desmoglein 1
- Pemphigus erythematosus: it is a variation of PF. A linear
deposition of immunoglobulins at the basement membrane (in addition to the keratinocyte membrane fluorescence) as seen on immunopathological staining is the difference with PF.
- Pemphigus vulgaris (PV): it is the most severe form but is
very rare. Oral and mucocutaneous junctions lesions (with
ulcerations) are seen.
Antigen: Desmoglein 3 (in man).
- Panepidermal Pustular Pemphigus: it has been recently described based on the location of the lesions within the stratified squamous epithelium.
- Paraneoplastic Pemphigus: frequently described in human
medecine
Pathogenesis of Pemphigus (Suter MM): binding of autoantibody to desmosomal cadherin adhesion molecules
(Desmoglein 1 or 3) - Activation of keratinocytes - Disruption of intercellular adhesion.
Autoimmune diseases with basement membrane targets:
- Bullous Pemphigoid (BP): it resembles PV with blisters

and ulceration in the oral cavity and at the mucocutaneous


junctions. Histopathology: subepidermal cleft formation
within the lamina lucida.
Antigen: BPAG II (collagen XVII)
Pathogenesis: autoantibody binding to collagen XVII Cytokine production by keratinocytes - Attraction of
eosinophils and neutrophils - Cytokine and protease secretion - Lesion formation.
- Acquired Epidermolysis bullosa: a case of suspected collagen type VII subepidermal bullous dermatosis as been described (Olivry)
- Linear IgA dermatosis of Dachshund
Miscellaneous:
- Alopecia areata: in man, hair keratines are antibodies target, but in the dog, it seems that trichohyalin may be the
target.
- Vitiligo and uveo-dermatologic syndrome (VKH-like syndrome) are autoimmune diseases of pigmentation. Antimelanocytes antibodies have been described in vitiligo.

2) Autoimmune diseases with circulating


auto-antibodies non specific of cutaneous
antigens
- Systemic Lupus Erythematosus: it is an autoimmune disease with cutaneous immuncomplex deposition. It is a systemic disease.
- Chronic Discoid Lupus Erythematosus: in classical cases,
depigmentation and ulceration of the nose and planum
nasale. There is no circulating auto-antibodies.
- Vasculitis: they may be related to various antigens (infectious, neoplastic, drug induced, vaccination, chemical).
Pathogenesis of vasculitis involves type III hypersensitivity.
- Cold Agglutinin disease

B - Biopsy site selection (Gross TL)


Pustular autoimmune dermatitis: because of the fragile and
transient nature of primary lesions (pustules, vesicopustules),
early lesions should be obtained. If no pustules are available,
crusted lesions or sites directly adjacent to early pustules
should be sampled. Crusted lesions should be procured carefully and the veterinary pathology service should be instruct-

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ed to include any dissociated crusts in the slide preparation.


If a low number of pustules or vesicles or bullae are present, they should be removed carefully, preferably by excisional biopsy.
Non bullous autoimmune skin diseases:
- Discoid Lupus: recent sites of depigmentation, with partial
lost of pigment, are optimal sites for skin biopsy. Traumatized lesions or lesions with severe crusting, ulceration or
scarring should be avoided. Lips, dorsal muzzle and
planum nasale are the best sites for skin biopsy.
- Systemic Lupus: erythematous areas adjacent to ulcers are
the best sites since an intact epidermis is necessary to yield
diagnostic results.
- VKH-like syndrome: areas of depigmentation, erythema
and scaling are beneficial sites. Lips and dorsal muzzle are
preferred sites. Secondary infected or self-traumatized lesions should be avoided.
General considerations:
- multiple biopsies should be taken
- samples should be selected from the most representative
lesions of the suspected disease
- excision biopsy should be prefered in bullous diseases
- if possible, biopsy specimens should be taken when the animal is not under the effects of glucocorticoid or immunosuppressive therapy
- dermatopathologic examination should be performed by a
veterinary pathologist.

C - Direct immunofluorescence (DIF)


and Immunohistochemical testing (IHT)
DIF and IHT are methods used to detect the presence of
abnormal antibody or immune complex deposition on tissue

4th European FECAVA SCIVAC Congress

specimens. In human medecine, these procedures are considered highly valuable for many of the immune-mediated
dermatoses. however, their value in veterinary medecine is
considerably less. There are many false negative (glucocorticoid treatment, low quality of biopsy site selection, small
biopsy, technical problems) and many false positive (intercellular and basement membrane zone deposition of immunoglobulins or complement can be detected in a wide variety of chronical inflammatory dermatoses, and are physiologicaly found in footpads and planum nasale). For exemple,
DIF is positive in 100% of cases of sarcoptic mange, 73% of
superficial chronical pyoderma, 67% of dermatophytosis,
50% of Demodicosis.
Results of immunopathologic testing can never be appropriately interpreted in the absence of histopathologic
findings.
For DIF, biopsy site selection is the same as for
histopathological examination but biopsy specimens should
be snap-frozen or placed in Michels fixative. IHT is performed on formalin-fixed, routinely processed tissues (immunoperoxidase methods) or on frozen sections. Generally,
biopsy specimens should be selected from areas not secondarily infected and representing the earliest lesion typical for
that disease. Planum nasale (dogs and cats) or footpads
(dogs) should not be sampled or should be interpreted with
great caution.
Intercellular intraepidermic autoantibody deposits: Pemphigus (95% IgG in Pemphigus foliaceus).
Linear dermo-epidermal autoantibody deposit: Bullous
Pemphigoid, Discoid and Systemic Lupus, Linear IgA dermatosis of Dachshund
Because of the high incidence of false positive, DIF or
IHT are of low interest, except in the differential diagnosis
between Bullous Pemphigoid and Epidermolysis bullosa,
and in the differential diagnosis of interface dermatitis.

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.D.

Discoid and systemic lupus erythematosus


Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Systemic and Discoid Lupus Erythematosus are dermatosis associated with circulating auto-antibodies, non specific of cutaneous antigens.

A - SYSTEMIC LUPUS ERYTHEMATOSUS


SLE is a circulating immune complex disease characterized by multisystemic involvment and the presence of a
wide variety of autoantibodies.

1) Etiology
Although the etiology of Lupus is unknown, most reports
emphasize the interaction of various factors:
- a genetic predisposition
- hormonal factors
- viral factors
- inducing drugs
- UV light
Genetic predisposition: it has been proven in man (familial
studies, relationship with MHC, ...), in mice (NZB et NZW,
SWAN, ...) and in dogs (Manathos family, German shepherd, Lyon Vet School, France). When crossing infected
dogs, 70% of second generation dogs are ill, 15% are ANA
positive but healthy and 15% are ANA negative and healthy.
This crossings have been able to demonstrate a positive
relationship between Ag DLA-A7 (Dog Leukocyte Antigen
= DLA) and SLE, and a negative relationship between Ag
DLA-A1, DLA-B5 and SLE.
Actual research in human and in dogs are looking for the
gene involved in SLE transmission. A close relationship between SLE and TcR gene (Lymphocyte T - antigen receptor)
seems to exist in human.
Hormonal factors: in human, there is a strong predilection of
young women before 40 years old (90%); in dogs results show
no sexual predisposition or male predisposition (50-68%).
Androgens may increase suppressive T lymphocytes activity (and be protective) and oestrogens may induce abnormalities of antigen presentation.
Hormonal treatments (androgens or anti-oestrogens) in
human have given various (desappointing) results
Viral factors: C-type viruses have been involved. The SP
104 virus (retrovirus) has been found to contain an antigen
that cross-reacts with an antigen present on the surfaces of

circulating lymphocytes of humans and dogs with SLE. But


the mere presence of such a virus is not sufficient to provoke
the expression of clinical disease.
A study has shown a higher incidence of SLE in owners
of dogs with SLE; this result has not been confirmed by other studies.
Inducing drugs: drug-induced SLE is a well recognized
syndrome in human (hydralazine, procainamide, methyldopa, penicillins, tetracycline, griseofulvin, sulfonamides,
...). Experimental dogs treated with hydralazine developed a
similar syndrome to SLE. In a dog, SLE appears after a routine vaccination, and in hyperthyroid cats, SLE has been described after giving propylthiouracil.
For the moment, in animals, it is better to name it SLE
like drug reaction than drug induced SLE.
UV light: in dogs, cutaneous lesions are mostly localized
on the face, suggesting an action of UV light, which may
change cutaneous nuclear antigens.
Actually, SLE occurs in the presence of a disturbed immune system in a genetically susceptible host, and with various favourable environmental factors (viral, UV).

2) Pathogenesis
In human and animals, most lesions are due to type III
hypersensitivity reactions. Antibodies (IgG) are formed secondarily to increased circulating antigens (mainly nuclear
antigens). Circulating soluble Ag-Ac immune complexes are
set down along epithelial and vascular basement membrane
zones inducing complement activation which induces neutrophiles chemotactism. Lysosomial enzymes and free radicals create local lesions.
In SLE, deposition of immune complexes in joints, muscles, renal glomerules, CNS, ... is responsible of problem in
the affected organ.

3) Immunological abnormalities
Various and numerous auto-antibodies are produced in
SLE.
antinuclear antibodies (ANA).
- Total ANA: they are present in 97-100% of SLE , but their
presence is not specific for SLE. For exemple, dogs with
Leishmaniasis would present frequent positive ANA.

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There is a wide variety of ANA depending on the target


(nuclear antigen): anti native DNA, anti-histones, antiENA, ...
- Anti native DNA antibodies: Antibodies against DNA
(double chain) are quite characteristic of the human disease
(80%), but in dogs their presence is very rare (< 5%). This
is the main difference between canine and human SLE.
- Anti-histones antibodies: in human, anti-histones antibodies are frequently reported(30-70%) but mainly in drug induced SLE; anti-H1, anti-H2B, anti-H3 are frequent. In
dogs, they are frequently reported too (55-65%) but have
been found in non lupoid dogs; moreover, antiH3, anti-H4
et anti-H2A are frequent.
- anti-ENA antibody (ENA = Extractable Nuclear Antigens):
these antigens come mainly from nucleoplasmic constituants and for a small part of them from chromatin molecules. Positive anti-ENA is an other difference between
dogs and human; in dogs anti-type I (20%) and anti-type II
(9%) are found but not in human, anti-Sm is found occasionaly in dogs (16%) but frequently in human (70%).
Moreover, other known anti-ENA in human (anti-SSA and
anti-SSB) are not found in dogs.
- other nuclear antibodies: non histone proteins like HGM
(High Mobility Group) type I and II have been seen in canine SLE.
Important facts in canine SLE:
- high frequency and elevated titer of ANA
- rarely or no anti-nDNA
- anti-type I and anti-Sm highly diagnostic
other auto-antibodies
Auto-immune response in SLE is not exclusively directed
against nuclear antigens. Other antibodies have been found:
- seric auto-antibodies
* rhumatoid factors: low title in canine SLE
* anti erythrocyte antibodies, detected by Coombs test,
but hemolytic anemia is only a criteria of SLE (2030%) and each AIHA with positive Coombs test is not
linked to SLE.
- fixed antibodies
* on skin biopsies, detected by direct immunfluorescence (IFD)
* on renal biopsies (in case of glomerulonephritis), detected by IFD
other abnormalities
- lymphocytic abnormalities: in dogs, some recent works
show
* lymphopenia
* decrease of peripherical population of CD8+ T cells
and increase in CD4+
* decrease suppressive activity of T cells
* increase in CD5+ when there is no activity of the disease
- NK cells, Ag presentating cells, cytokines: no study in canine SLE

4th European FECAVA SCIVAC Congress

* localized CLE
* generalized CLE
* oral LE
* lupus panniculitis
- LE-non specific skin disease
* vasculitis
* vesicobullous lesions
Systemic LE (SLE)
- SLE without CLE
- SLE with CLE

5) Epidemiology and history


Male dogs seem overrepresented (different from human
condition) in some studies (70%) but equallly in others (51%).
Medium class of age is 5 years old (6 months to 14 years
old) but we have to consider the moment when symptoms began or when diagnostic was made because SLE is a slow evoluting disease (episodic evolution), worsening with time. SLE
begins in young adults and may be very severe at 5 years.
Breed predilection: German shepherd, Belgium shepherd, Shetland sheepdogs, collies, beagles, ...

6) Clinical presentation
SLE is evoluting subacutely or more often chronically
with episodic attacks and remission periods. Symptoms are
numerous but non erosive polyarthritis (76-90%), proteinuria (50-65%) and cutaneous lesions (54-65%) are the principles figures. All these symptoms are not present at the
same time but more often successively.
lameness: non erosive polyarthritis (no radiologic signs),
beginning intervertebraly with difficulties to stand up and
jump, amyotrophy of lombo-dorsal muscles. Then carpus
and tarsus are involved with turning lameness. At the
end of evolution, temporo-mandibular joint is sytematicaly
involved.
skin lesions: they are often erythematosus and seborrheic
in nature and commonly involve the face, ears and limbs.
Erythema is also frequent in less hairy areas. Mucocutaneous ulceration or erosion and nasal depigmentation are
also seen. The butterfly pattern often referred to in human medecine, is common to many canine dermatosis.
Chronic ulcerative stomatitis may be the only cutaneous manifestation.
others: glomerulonephritis with proteinuria (50-65%), hemolytic anemia (10-20%), thrombocytopenia (< 5%) and
purpura, spleen and lymp nodes enlargment, central neurologic symptoms, pleural and pericardic inflammation
(10%).

7) Diagnosis
4) New classification (T Olivry)
LE related skin disease:
- LE specific skin disease (Cutaneous LE = CLE): acute or
chronic

Diagnosis is based upon ARA (American Academy of


Rhumatology) criterions:
1) facial erythema (butterfly appearance)
2) disoid lupus

3)
4)
5)
6)
7)
8)
9)

UV sensitivity
oral ulcerations
polyarthritis
pleural or pericardic inflammation
renal troubles (proteinuria)
neurologic disturbances
haematological disturbances: hemolytic anemia, leucopenia, lymphopenia, thrombocytopenia
10) immunological abnormalities: LE cells, anti-nDNA
Ab, anti-Sm Ab
11) ANA positive
Suspect SLE: 2 positive criterions.
Possible SLE: 3 positive criterions or polyarthritis +
ANA positive.
SLE: 4 positive criterions.
This list of criterions is a human one and not perfectly
adapted to canine SLE:
- criterion 11 is an obligation because there is no SLE without positive ANA (97-100%);
- anti-nDNA create many false ANA positive in human, but
these Antibodies do not exist in dogs;
- transposition from human to dogs of criterion 1 (butterfly
appearence), 3 and 8 , is difficult;
- episodic hyperthermia is very frequent in dogs and is a
missing criterion;
- anti-type I is very specific of canine SLE;
- Leishmaniasis should be excluded before just thinking of
SLE (be careful, there are many cases of canine Leishmaniasis with positive ANA).
It seems better to interpret ARA criterions in this way:
- positive ANA is mandatory (with exclusion of Leishmaniasis) with high titer
+ 3 criterions: diagnostic
+ 2 criterions: possible SLE; perform analysis of ANA (anti-type I or anti-Sm highly suggestive of canine SLE)
An other classification of criterions has been proposed by
Halliwell (1989) with major and minor symptoms . Definitive diagnosis is made with: positive ANA + 3 majors
symptoms or positive ANA + 2 major symptoms + 2 minor
symptoms:
- major symptoms
* non infectious polyarthritis
* compatible skin lesions with characteristic histopathology
* hemolytic anemia
* severe thrombocytopenia
* glomerulonephritis and proteinuria
* neutropenia
* polymyositis
- minor symptoms
* hyperthermia with unknown origin
* CNS symptoms
* pleural inflammation
Cutaneous histopathology: avoid ulcers and erosions for
biopsy site selection; intact erythematous epidermis adjacent to ulcers may yield diagnostic results.
Histopathology reveals:
* patchy, mild to moderate vacuolar degeneration of the
basal cell layer
* colloid (Civatte) body formation is a consistent finding
but may be rare

41

* lichenoid mixed inflammatory dermal infiltrate


* pigmentary incontinence
Indirect immunofluorescence of skin biopsies (Michels
medium) reveals: deposition of granular and irregular deposits of immunoglobulin (usually IgG) and complement
at the dermal-epidermal junction. One must be aware that
similar but normal IgM deposits are found in normal canine and feline nose and footpath.
ANA: high title is required (> 1/256), but ANA are not
specific of SLE because they are found in other diseases
(Leishmaniasis).

8) Treatment: (see therapeutic protocols)


Prednisolone 2 mg/kg/day tapered slowly after clinical
remission + levamisole 2-5 mg/kg each other day (max 150
mg/day) 4 months. Heamatological control after 10 days
(neutropenia).
Results: 57% in remission for months or year(s) (no
longer than 3 years) without treatment.
Other treatments (mainly if severe side effects of glucocorticoids): azathioprine 2 mg/kg/day, cyclophosphamide 50
mg/m2 four days a week, vincristine if severe thrombocytopenia (0,7 mg/m2 once a week).
Prognosis is always guarded, especially when renal lesions are severe.

B - DISCOID LUPUS ERYTHEMATOSUS


DLE is a cutaneous form of SLE without involvment of
internal organ. It has been described in human, dogs, cats,
horses, seals.
epidemiology: there is no real age predilection but must
animals presenting this dermatoses are young adults.
Breed predilection: Collie, German shepherd, Siberian
Husky, Shetland Collie.
clinical signs are mostly localized on the face, the nose,
and periocular areas. Oral and pinnae lesions are very rare.
Podal lesions are seen.
Lesions: hypopigmentation, erythema, scales, erosion, ulceration, crusts.
diagnosis
- histopathology: best sites for skin biopsy are areas of early
depigmentation with partial loss of pigment; traumatized
lesions or lesions with severe crusting or ulceration should
be avoided. Histopathology reveals:same lesions as SLE
with less severe basal cell vacuolisation.
- immunofluorescence: see SLE
- ANA are negative and there is no haematological or biochemical abnormalities
treatment
- mild cases: sun screen, vitamin E, avoid sun exposure, topical glucocorticoid
- more severe cases: glucocorticoids until remission (1-2
mg/kg/day), then nicotinamide-tetracycline
- very severe cases or refractory cases (large ulcerations,
spontaneous bleeding, pain): glucocorticoids and immunosuppressive drugs

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ITALIAN SOCIETY OF VETERINARY DERMATOLOGY - SIDEV

.D.

Clinical differential diagnosis of autoimmune


skin diseases
Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Clinical aspects and localizations of auto-immune skin


diseases (AISD) are common with a great number of other
dermatosis.
Because of the low incidence of this diseases, we must
always rule out other more common dermatosis before
thinking to AISD.
Clinical differential diagnosis depends on the lesions
(crust, ulcerations, erosions, depigmentation, pustules) and
on their localizations (facial, podal, generalized).

FACIAL DERMATOSIS
Virtually any skin disease may affect the face, but AISD
are often symmetrical, involving periocular areas, lips, nose
and pinnae. Pruritus is generally mild but secondary pyoderma or Malassezia dermatitis may be pruritic.
* If pruritus is present:
- atopic dermatitis: erythema, lesions of self trauma, often
secondary pyoderma and crusts
- food allergy: erythema, secondary pyoderma, erosions or
ulcerations in cats
- contact allergy or irritation: erythema, macules, papules,
rarely erosions (plastic dish contact allergy)
- eosinophilic furonculosis of the face: papules, pustules
- eosinophilic granuloma complex (cats)
- sarcoptic mange (dogs)
- pyoderma
- mucocutaneous pyoderma
- demodicosis with secondary pyoderma
- dermatophytosis: some dermatophytes may creat an autoimmune like dermatosis (M persicolor)
- Malassezia dermatitis
- Mucocutaneous Candidiasis
- Juvenile cellulitis of the adult dog
- Zinc responsive dermatitis
- Drug reaction
* If pruritus is absent or mild:
- Leishmaniasis
- Nasal hyperkeratosis
- Superficial necrolytic dermatitis
- Neoplasia (cutaneous lymphoma, mycosis fungoides)
- Vitiligo

- Demodicosis
- Dermatophytosis
- Dermatomyositis
- VKH-like syndrome
* Facial dermatosis which may affect the planum nasale
- Vitiligo
- VKH-like dermatosis
- Nasal hyperkeratosis
- Dermatophytosis
- Drug eruption
- Leishmaniasis
- Neoplasia

PODODERMATITIS
- Pyoderma
- Demodicosis
- Dermatophytosis
- Malassezia dermatitis, Candida dermatitis
- Peladora and hookworm infestations
- Leishmaniasis
- Hypersensitivities (atopic dermatitis, food allergy, contact
allergy)
- Superficial necrolytic dermatitis
- Irritant contact dermatitis
- Trauma
- Zinc responsive dermatitis
- Digital hyperkeratosis
- Sterile pyogranuloma
- Neoplasia (squamous cell carcinoma, metastasis of pulmonary adenocarcinoma in cats)
- Plasma cell pododermatitis (cats)

LESIONS OF THE NAILS AND NAILBED


- Dermatophytosis
- Candidiasis
- Leishmaniasis
- Superficial necrolytic dermatitis
- Lupoid onychodystrophy
- Drug eruption

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PUSTULES AND CRUSTING PAPULES


- Primary or secondary pyoderma
- Sarcoptic mange and other ectoparasitic infections
- Hypersensitivity

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- Drug eruption
- Contact irritant dermatitis
- Sub corneal pustular dermatosis
- Sterile eosinophilic pustular dermatitis
- AISD

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Therapeutic protocols of autoimmune skin diseases


Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Management of autoimmune skin diseases requires


changing, varying or adjusting the immune response by
pharmacological therapy. Suppressing the immune response
is often easy to do, however, controlling the degree of immunosuppression can be difficult.
Prior to use an immunosuppressive drug, there are important pretreatment considerations:
- ensure that the diagnosis is correct
- ensure that there is no contraindication to immunosuppressive treatment
- control secondary pyoderma, Malassezia dermatitis
- precribe the less toxic drug as possible
- avoid predisposing factors (UV, some drugs, ...)
Selection of an immunosuppressive treatment and then
control of the disease on a long term basis is individual and
the main rule is: dont do worse with the treatment that the
disease would do alone.
The goals of immunosuppressive treatment are:
- decrease production of autoantibody
- decrease or suppress activation of cytotoxic lymphocytes
- suppress the migration or activation of inflammatory cells

tolone) are indicated when lesions are small or well circumscribed (Discoid lupus erythematosus). Owners have
to wear glothes. Unsing topicals q12h the first week, q24h
the second week and q48h the third week is recommended
to avoid systemic side effects or localized reactions (atrophy).
dosages: induction with prednisolone/prednisone 2-4
mg/kg/day for dogs, 4-6 mg/kg/day for cats; if there is no
change in 10 days, increase the dosage by 30%. Use maintenance therapy when the lesions regress: decrease frequency of administration to every other day (same dosage)
and the step down doses 20-30% every two to four weeks
(depending on the speed of regression speed of lesions). If
regression of lesions is complete and quick, it is possible to
try to stop treatment after a few months (4-6 months); otherwise, look for the lower efficious dosage to control lesions with minimum side effects (0,5-1 mg/kg AD).
side effects: iatrogenic Cushings disease, polyuria polydipsia, steroid hepatopathy, feline skin fragility syndrome,
gastric ulceration, secondary infections (ITU, pyoderma),
diabetes mellitus.

A - DRUGS

2) Alkylating drugs: cyclophosphamide


and chlorambucil

1) Glucocorticoids:
Glucocorticoids (GC) represent the first choice treatment
of most autoimmune skin diseases.
mechanism of action: paralyze Fc receptors on
macrophages, suppress immunoglobulin production (high
doses), suppress leukocyte accumulation at inflammatory
site, decrease lymphoblastogenesis, decrease abnormal auto-antibodies production, decrease neutrophils function.
compounds:
- prednisolone and prednisone, methyl-prednisolone (1,6
mg/kg/day for dogs): may be used on alternate day basis
- methyl-prednisolone succinate: used for pulse therapy
(10-30 mg/kg IV 3 consecutive days)
- dexamethasone (0,25-0,75 mg/kg/day), triamcinolone
(0,2-0,7 mg/kg/day): may be more effective in cats but
cannot be used on an alternate day basis
- injectable methyl-prednisolone acetate: is only indicated in
cats unwilling to accept oral medications
- topical therapy: the potency of topical GC can be geared to
the severity of lesions. High power GC (clobetasol, flucor-

mechanism of action: interaction with DNA of cells under


divison: they replace an hydrogene by an alkyl group which
create a wrong lecture or DNA breaking. They affect induction and effector phases of immune response, suppress antibody formation and production, affect neutrophil and
macrophage function. They act slower than GC (10 days).
drugs:
- cyclophosphamide 50 mg/m2/day, po, 4 consecutive days
each week; during maintenance therapy with GC, every
other day cyclophosphamide may be used. Treatment of
more than 2 months must be prescribed with great caution
(sterile hemorrhagic cystitis).
- chlorambucil (0,1-0,2 mg/kg/day po for cats, 2-6
mg/m2/day initially then q 48h for dogs). Chlorambucils
action is slower (4 weeks) than cyclophosphamides one
(10 days).
indications: Cyclophosphamide is indicated mostly in
dogs, in severe or non-responsive AID. Chlorambucil is
excellent for cats requiring cytotoxic drugs in combination
with glucocorticoid.

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4th European FECAVA SCIVAC Congress

46

side effects: bone marrow suppression with neutropenia,


sterile hemorrhagic cystitis (cyclophosphamide but not
chlorambucil), gastroenteritis, anorexia, alopecia.

3) Thiopurines: azathioprine
and 6-mercaptopurine
Azathioprine is metabolized in the liver to 6-mercaptopurine.
mechanism of action: these drugs are antimetabolites
which inhibit enzymes contribuating to the synthesis of
puric basis and so interfering with DNA and RNA synthesis. They are active on rapidly developping cells, affecting
mainly the effector phase of immune response and are
more effective in modifying T lymphocyte responses.
dosage: 50 mg/m2 or 2 mg/kg/day in association with GC
during the induction phase (4 weeks minimum) and then
on an alternate day basis with GC. After a few months,
some dogs would only require azathioprine.
side effects: azathioprine is CONTRAINDICATED IN
CATS. There is a very strong bone morrow suppression,
leading to death in a few weeks. In dogs, azathioprine is
very well tolerated. Platelet count must be checked every 2
or 3 months.

4) Gold salts: chrysotherapy


mechanism of action: inhibition of chemotaxis, suppression of autoantibody formation, inhibition of complement
activation, inhibition of phagocytosis.
Drugs:
- aurothioglucose: 1 mg/kg IM q7days for induction then
q30days as maintenance therapy. Test doses of 0,25 and
then 0,5 mg/kg are recommended on weeks 1 and 2 respectively.
- auranofin: 0,05-0,2 mg/kg q12h for induction
Side effects: cutaneous drug eruption, thrombocytopenia

5) Cyclosporin
This is a very potent immune suppressor.
mechanism of action: inhibition of IL2 and gamma-interferon production, inhibition of cytotoxic T cells, decreased
production of sensitized cytotoxic T cells.
dosage: 5-10 mg/kg/day po
side effects: gastroenteritis, gingival hyperplasia, surinfections, ...
This drug is very expensive and has been reported to be
rather unsuccessful for autoimmune skin diseases treatment
(Rosenkrantz 1989).

6) Others
Tetracycline/niacinamide: this treatment seems to be interesting in Discoid Lupus Erythematosus (25-64% positive
results).

4th European FECAVA SCIVAC Congress

Dosages for dogs less than 10 kg: 250 mg tetracycline


and 250 mg niacinamide po, tid for induction. For dogs
greater than 10 kg: 500 mg tetracycline and 500 mg niacinamide po, tid for induction. For maintenance therapy, doses are decresed incrementally. Side effects are minimal (occasional vomiting).
Methotrexate: it is a competitive enzyme inhibitor of folic
acid reductase. Used in SLE in human medecine (0,5-0,8
mg/kg IV q7-14 days or 2,5 mg/m2 po q 48h). Side effects
include leukopenia, vomiting, renal tubular necrosis with
high doses.
Heparin: it has been used in one case of Pemphigus vulgaire
(Olivry, Hripret) with GC at a dose of 100 UI/kg/day SC.
Heparin seems to inhibit proteases involved in acantholysis.
Vitamin E: mechanism of action is unknown but its efficacy may be related to anti-oxydant properties (stabilization
of lysozomial membrans against effects of free radicals
and superoxides ions). Used in DLE and PE with GC (200400 mg/kg/j or 400-800 UI bid po).
Vitamin E is a relatively benign drug that may reduce the
need for other therapy. Some authors have found vitamin
E to be rarely effective by itself.
Levamisole: it seems to have immunostimulating properties (not in normal dogs but in immunodepressed dogs) by
increasing production of T Helper lymphocytes. Used in
SLE in conjonction with GC: 2-3 mg/kg every other day.
Sulphones (dapsone): mechanism of action: inhibition of
lysosomial enzymes and prostaglandines synthesis. It has
been used in Pemphigus cases (1 mg/kg bid or tid) with
some good results (less than 50%) and in immune complexing vasculitis. Side effects include: anemia, neutropenia, thrombocytopenia, hepatotoxicity, gastrointestinale
disorders.
Antimalarial drugs: quinacrine, chloroquine, hydroxychloroquine have been use in the treatment of DLE in humans but they have not been evaluated in dogs.
Sun avoidance: sun screen or dog kept indoor between 10
am and 5 pm.

B - TREATMENT OF AUTO-IMMUNE
DERMATOSIS
1) Superficial Pemphigus (PF and PE)
Treatment should be individualized depending on severity and extension of lesions.
Secondary pyoderma should be treated (empirical selection of agents effective against coagulase positive Staphylococcus).
Crusts have to be removed, lesions have to be cleaned
(often under general anesthesia).
Systemic glucocorticoids is the treatment of choice
(prednisone 2 mg/kg/day in dogs, 4-5 mg/kg/day in cats). If
the response to GC is good, the dose is tappered on an alternate day basis as previously described.
If the response is poor (recheck after 10-15 days of treatment), a cytotoxic drug may be added for at least one month
(delay of activity of these drugs): azathioprine (dogs only),
chlorambucil (cats). When lesions regress, GC are slowly

stopped and azathioprine or chlorambucil given 3 then 2


then 1 time a week.
If the response is still weak or if undesirable side effects
develop (polyuria polydipsia), alternate GC (dexamethasone, triamcinolone) may be tried.
Some individuals may be cured after more than 4 months
of treatment, others should be treated all their life long.
In PE, sun avoidance is indicated; nicotinamide-tetracycline may be used too.
If drugs were given previously to diagnosis (antibiotics,
antifungal therapy, ...), they have to be stopped in case of
drug induced Pemphigus like reaction.
NB - The benefit of association between GC and cytotoxic drugs is not realy proven in auto-immune skin diseases.

47

quires long term therapy. Ocular examination is recommended every 4 months even though the cutaneous component is controlled.

7) Disoid lupus erythematosus


This is a cutaneous disease with a rather good prognosis.
GC must be used carefuly.
In mild cases, when lesions are localized and superficial,
topical therapy (high power GC at the beginning, then low
power GC) + sun avoidance or sunscreen are prescribed.
When ulcrations or spontaneous bleedings are present, GC
are prescribed until remission, then niacinamide + tetracycline are indicated. Vitamin E may be added.
Spontaneous total remission have been described.

2) Deep Pemphigus (PV)


Treatment must be very potent because PV is a life
threatening condition. GC have to be associated to cytotoxic drug at the beginning of treatment (cyclophosphamide).
Antibiotic treatment is important because lesions are deep
and sepsis is always possible. Pronostic is guarded and total
remission very rare. If GC and cyclophosphamide fail, heparin may be tried.

8) Systemic lupus erythematosus


Treatment should be individualized but initial treatment
of choice is large doses of systemic GC. Some cases respond
to the only GC therapy but most dogs need a combined therapy with levamisole and cytotoxic drugs.
Prognosis is poor: Over 40% of the dogs are dead within 1 year after the diagnosis is made.

3) Bullous Pemphigoide (BP)


9) Vasculitis
In human medecine, relationship between internal diseases (neoplasia) and PB has been proven in a majority of
cases. Complete work up is indicated (haematological, biochemical, radiographs, ...). Previous drugs should be stopped
(PB like drug reactions). Otherwise the treatment is the same
as in PV.

Prognosis and treatment depend on the underlying problem, affected organs and disease severity. All previous treatments should be stopped at the time of diagnosis.

Conclusion
4) Alopecia aerata
No treatment; lesions may regress in a few months.

Therapy of auto-immune skin diseases have to follow


two rules:
- treatment should not been worse than the disease
- treatment should be individualized, depending on the precise diagnosis of the disease, the animal and the owner

5) Vitiligo
No treatment; lesions are only cosmetic ones.

6) VKH-like syndrome
(uveo-dermatologic syndrome)
Treatment should be aggressive because of the possibility of blindess; moreover, cutaneous lesions may be reversible if therapy is started early in the disease progress:
GC + cyclophosphamide, topical ocular treatment (ocular
topical dexamethasone 0,1% or prednisolone 1% qid + mydriatic/cycloplegic like 1% atropine quid at the beginning).
Prognosis is guarded. Control of the disease usually re-

Readings
HALLIWELL (REW), GORMAN (NT) - Anti-inflammatory drugs, immunosuppressive agents, and immunomodulators. In Veterinary Clinical Immunology, Halliwell and Gorman, WB Saunders Co, Philadelphia, 1989, 493-507.
KUMMEL (BA) - Medical treatment of canine Pemphigus-Pemphigoid. In
Kirks Current Vet Therapy XII, Bonagura and Kirk, WB Saunders
Co, Philadelphia, 1995, 636-638.
SCOTT (DW), MILLER (WH), GRIFFIN (CE) - Immunologic skin diseases. In Muller & Kirks Small Animal Dermatology V, WB Saunders Co, Philadelphia, 1995, 484-626.
ROSENKRANTZ (WS) - Management of immune mdeiated disorders. In
Manual of Small Animal Dermatology, Harvey Locke P Ed, BSAVA,
1993, 270-275.

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SCIVAC EXOTIC ANIMALS STUDY GROUP

Survey of the resident flora of the upper respiratory


tract in psittacine birds and its antimicrobial sensitivity
S.O.T.S. Jesus
DVM, MSc
Dept. of Pathology and Infectious Diseases, Royal Veterinary College, University of London

To try to clarify the hypothesis that the resident flora of


the upper respiratory tract of psittacine birds can behave as
opportunstic pathogens, this project was set out to study, by
means of a survey, its resident flora and compare it with that
of birds with upper respiratory infections.
Swabs were taken from the choanal slit of nineteen
healthy psittacines and four birds with upper respiratory disease - three with sinusitis and one with an unspecified upper
respiratory pathology. The isolation and identification of
bacteria and fungi was accomplished by standard microbiological methods and the use of commercial identification
systems.
A total of 44 isolates were recovered from the choanae of
the 23 psittacines sampled. Twenty six precent of the isolates
recovered from the choanal slits of healthy birds were grampositive bacteria, 62% gram-negative and 12% fungi. From
sick birds, 60% of the isolates were bacterial and 40% fungal. Fifty eight percent of the healthy birds yielded more
than one isolate, whereas in sick birds 75% had more than
one isolate.

Among other organisms, Streptococcus spp., Staphylococcus spp., Alcaligenes sp., Klebsiella pneumoniae pneumoniae, K. oxytoca, Pasteurella spp., Pseudomonas alcaligenes, P. stutzeri and Xanthomonas maltophila, all considered to be potential pathogens to the respiratory tract, were
isolated from the choanal slits of healthy birds, suggesting
that these animals can harbour in their upper respiratory tract
microorganisms which can behave as opportunistic
pathogens.
From the choanal slits of sick animals the following potential organisms were isolated: Streptococcus sp., Staphylococcus sp., Escherichia coli, Klebsiella pneumoniae pneumoniae, K. oxytoca, Proteus mirabilis, Candida albicans
and Aspergillus flavus. All of them have been reported to be
associated with upper respiratory disease under certain circumstances.
The sensitivity testing showed the drugs of choice, for
gram-positive and gram-negative organisms, to be, in decreasing order: gentamicin, amikacin, enrofloxacin, tetracycline, ticarcillin, kanamycin and sulfamethoxazole+trimethoprim.

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EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline vestibular disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
Vestibular disorders produce varying degrees of loss of
equilibrium, causing imbalance and ataxia. Strength is not
lost and therefore paresis is not observed. Most commonly
the disturbance is unilateral and the clinical signs are those
of asymmetrical ataxia without the loss of strength. Unilateral vestibular signs may result from either central (brain
stem) or peripheral (labyrinth) disease. It is important to
differentiate central from peripheral disease, because of the
difference in treatment and prognosis. Signs of vestibular
disease include falling, rolling, head tilt, circling, nystagmus, positional strabismus, and asymmetrical ataxia. Hearing disorders are often associated with vestibular dysfunction (and vice versa) as the auditory and vestibular systems
are closely associated anatomically.

tympanic cavity of cats and dogs. In dogs the tympanic cavity is composed of a small dorsal epitympanic recess and a
large ventral tympanic bulla. The auditory ossicles are located in the middle portion of the tympanic cavity of dogs. The
feline tympanic cavity is divided into two compartments by
a thin, bony septum that arises along the cranial aspect of the
bulla and curves to attach to the mid-point of the lateral wall.
The majority of the lateral wall of the smaller craniolateral
compartment is formed by the tympanic membrane. These
compartments communicate through a narrow fissure on the
caudomedial aspect of the bony septum. Near this fissure the
sympathetic nerves form a plexus on a structure called the
promontory. Because of their location, these sympathetic
nerves are easily traumatized during surgical curettage of the
feline middle ear, resulting in a Horners syndrome.

Receptors - General information


INTRODUCTION
The vestibular system has 2 main functions: (1) to maintain the visual image by stabilizing the eyes in space during
head movements; the stabilization is performed utilizing
phasic or tonic vestibulo-ocular reflexes; and (2) to stabilize
the position of the head in space - thus ensuring that the position of the body is stable. The stabilization is performed
utilizing phasic or tonic vestibulospinal reflexes.

ANATOMICAL CONSIDERATIONS

Two sets of mechanoreceptors are involved in vestibular


function: (1) a set responsive to angular (rotational) acceleration (or deceleration); these receptors are located in the
membranous semicircular canals; and (2) a set responsive to
linear acceleration (or deceleration) and gravity. These receptors are found at 2 locations, one in the utriculus and one
in the sacculus. The mechanoreceptor generates a receptor
potential that results in the development of a generator potential in the primary afferent fibre. The cell bodies of the
primary afferent fibers are bipolar cells located in the
vestibular ganglion. The primary afferent fibers comprise
the vestibular part of the vestibulocochlear (VIIIth) nerve.

Gross anatomy
The ear is composed of three parts: (1) the inner ear,
which consists of a membranous and bony labyrinth, and
which functions for hearing and balance, (2) the middle ear,
which comprises the tympanic cavity, and communicates
with the nasopharynx by means of the auditory tube (eustachian tube), and (3) the external ear, formed by the auditory meatus and a short canal.
The middle and external ears are separated by the tympanic membrane, and the opening of the horiziontal canal into the middle ear is called the external acoustic meatus. The
theree auditory ossicles (stapes, malleus, and incus) connect
the tympanic membrane to the inner ear.
There are important diferences between the air-filled

Receptors for angular acceleration


These receptors are located in the petrous portion of the
temporal bone. The vestibular organ consists of interconnecting canals in the bone called bony (or osseous)
labyrinths, and a single large cavity within the bone to which
all canals connect, called the vestibule. Within the bony
labyrinths are fluid-filled membranous tubes called the
membranous labyrinths. These membranous labyrinths contain a fluid called endolymph. Surrounding the membranous
labyrinths, filling the osseous labyrinths, is a fluid called
perilymph. Three membranous semicircular canals form the
mechanism for detection of angular (or rotational) accelera-

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tion. These 3 canals join the utriculus located in the osseous


vestibule. On each membranous semicircular canal is an enlargement called the ampulla. Running transversely across
each ampulla is a connective tissue crest with receptor cells
(hair cells) on its surface - called the crista ampullaris. The
receptor cells have cilia protruding from them in stepwise
gradations of length. The largest cilium is called the kinocilium and the rest are called stereocilia. The cilia project into
a gelatinous substance called the cupula. The cupula extends
across the entire ampulla. Endolymph does not flow past the
cupula. The hair cells produce receptor potentials, that give
rise to generator potentials, that produce action potentials in
the vestibular portion of the vestibulocochlear nerve. The
vestibular fibers show a tonic discharge even at rest.
When the head is rotated, the inertia of the endolymph
places a shear force on the cupula. This bends the cilia. If the
shear on the cupula bends the stereocilia towards the kinocilium, the tonic nerve impulse rate from all of the nerve fibers
supplying that crista is changed from a tonic to a phasic response. If the rotation is slight, the resting tonic rate is
quickly resumed. If the rotation is a sustained movement, the
friction of the endolymph on the walls of the membranous
labyrinth results in acceleration of the movement of the endolymph until the velocity of the endolymph equals the rotational velocity of the head; thus the shear exerted on the
cupula is removed. The tonic firing rate is then resumed as
though the head were not rotating. If the head rotation is
stopped, the momentum of the endolymph places a shearing
force on the cupula in the opposite direction. This bends the
kinocilium towards the stereocilia and this inhibits the generation of nerve impulses. As soon as the friction of the endolymph on the walls slows down the movement of the endolymph, the cupula returns to the non-rotational position
and the tonic rate of discharge is resumed. If the rotation of
the head is in the opposite direction so that the kinocilium is
first displaced towards the stereocilia, the tonic rate of discharge will be first inhibited and then accelerated at the end
of head rotation.
There are 3 semicircular canals on each side of the head
- a rostral, a caudal and a lateral. Each pair of semicircular
canals works in a push-pull arrangement. When the rate of
discharge from the crista on one side is increased, the rate of
discharge from the opposite crista is decreased. Note that the
hair cells are excited only when acceleration (velocity is increasing) or deceleration (velocity is decreasing) of the endolymph is occurring.

Receptors for linear acceleration and


gravity
These receptors are located in raised areas called the
macula utriculus in the utriculus, and the macula sacculus in
the saccule. The cilia of hair cells project into a gelatinous
mass in which small granules, called otoliths (or otoconia)
are embedded. The mass and its contents are together called
the otolithic membrane. The macula in the utricle is horizontal, and the macula in the saccule is vertically orientated,
when the head is upright.
If the head is tilted to one side or the other, the force of

4th European FECAVA SCIVAC Congress

gravity slightly displaces the otolithic membrane towards


the tilted side. This places shearing forces on the cilia. If the
head tilt is such that the movement of the otolithic membrane forces the stereocilia toward the kinocilium, then an
increase in the tonic rate of discharge results. If it is in the
opposite direction, a decrease in the tonic rate of discharge
results. These discharges continue for as long as the pull of
gravity displaces the otolithic membrane. For this reason,
these receptors are often referred to as statolithic organs.
The maculae respond to linear acceleration because the
otolithic membrane has an inertia during acceleration of the
linear movement of the head. If acceleration does not continue (i.e. velocity remains constant), the otolithic membrane returns to its resting position, and the frequency returns to the resting rate. During deceleration of the head, the
otolithic membrane has momentum; thus, a shearing force is
exerted on the hair cells until the momentum ceases.
In linear acceleration, acceleration (or deceleration) is
necessary to alter activity in the vestibular fibers. Velocity
(movement of the head at a constant speed) will not stimulate the maculae. There is no push-pull effect from left and
right maculae as occurs relative to the semicircular canals.

Central vestibular connections


Primary afferent fibers from the crista of the semicircular canals and the maculae directly terminate in 2 central
nervous system (CNS) sites: (1) cerebellar cortex of the flocculonodular lobe of the cerebellum; (2) 4 vestibular nuclei
(rostral, medial, lateral, caudal). Primary afferent fibers from
the crista ampullaris of the semicircular canals (angular acceleration) terminate in rostral, medial, and caudal nuclei.
Primary afferent fibers from the macula (linear acceleration
and gravity) terminate mostly in the lateral vestibular nuclei.

Central pathways and reflex connections


of the vestibular nuclei
These connections descend via the lateral vestibulospinal
tract to lower motor neurons of neck muscles, and muscles
of thoracic and pelvic limbs; they descend via the medial
vestibulospinal tract to the neck muscles and ascend to motor nuclei of the eye muscles via the medial longitudinal fasciculus. Other pathways include connections to the cerebellum via the caudal cerebellar peduncle, to the reticular formation, to the ventrobasilar nucleus of the thalamus, to the
post-sigmoid gyrus of the cerebral cortex, for conscious processing of vestibular inputs (vestibulothalamic pathway) and
to the hypothalamus via the medial longitudinal fasciculus.

Lateral vestibulospinal tract


This is an important tract for posture and locomotion.
Cells of origin of this pathway are located in the lateral
vestibular nucleus (Dieters nucleus). The cells in this nucleus are organized topographically. Afferents to the lateral
vestibular nucleus include: (1) macula (gravity and linear ac-

celeration - tonic input); (2) crista cells of rostral semicircular canal (tonic input); (3) cerebellar nuclei (tonic input); and
(4) collaterals from ascending pathways, particularly muscle
spindles and Golgi tendon organs.
All fibers of the lateral vestibulospinal tract produce EPSPs at their synapses. This tract establishes monosynaptic
connections with lower motor neurons innervating neck,
back, thoracic and pelvic limb antigravity muscles (mostly
extensors). It is the largest (and thus the fastest) of all the descending pathways. It also has facilitatory polysynaptic connections with other extensors and inhibitory polysynaptic
connections with flexors. It modulates segmental reflexes
and it is an ipsilateral tract.

Medial vestibulospinal tract


This pathway originates from the medial and caudal
vestibular nuclei, with some fibers coming from the lateral
vestibular nucleus. It descends in the medial longitudinal
fasciculus. Afferent inputs to this pathway mainly come
from the semicircular canals (angular acceleration), cerebellar nuclei (tonic input) and the cerebellar cortex (tonic input
- inhibitory).
Terminations of the medial vestibulospinal tract include
monosynaptic inhibition of ipsilateral and contralateral lower motor neurons (LMNs) to extensor muscles of the neck
and to some back muscles, and monosynaptic excitation of
contralateral LMNs supplying extensors of the neck.

Ascending vestibular fibers


Fibers from all vestibular nuclei synapse with LMNs of
the III, IV, and VI cranial nerves. Some are crossed and some
uncrossed. They all ascend via the medial longitudinal fasciculus. These fibers are involved in the vestibulo-ocular reflexes, such as compensatory rolling of the eyes when the
head is moved. Vestibular fibers also go to the flocculonodular lobe of the cerebellum.

Reticular formation
There are numerous projections from vestibular nuclei
into the ascending and descending reticular formation. Some
of these descending reticular projections are involved in the
vomiting and cardiovascular reactions that may occur in
vestibular disturbances.

CLINICAL SIGNS OF VESTIBULAR


DISEASE
Vestibular disease produces varying degrees of loss of
equilibrium causing imbalance and ataxia. Strength is not interfered with, and therefore paresis is not observed. As a
rule, the disturbance is unilateral or asymmetrical, and the
signs are those of an asymmetrical ataxia with preservation
of strength.

53

Unilateral vestibular signs may result from either central (brain stem) or peripheral (labyrinth) disease. It is important to differentiate central from peripheral disease because of the differences in treatment and prognosis. Signs
of vestibular disease include: falling, rolling, tilting of the
head, circling, nystagmus, positional strabismus (deviation
of one eye in some head positions), and an asymmetrical
ataxia.

Nystagmus
The sign of disturbed vestibular input to the neurons that
innervate extra-ocular eye muscles is abnormal nystagmus.
Nystagmus probably occurs at some time during all types of
vestibular disease. Nystagmus is an involuntary rhythmic
oscillation of the eyeball, that nearly always affects both
eyes equally. Typically, nystagmus consists of a slow phase
in one direction and a fast phase in the other.
n cats, oscillations of the head that are synchronous with
the nystagmus will frequently be seen. It is customary to describe nystagmus clinically in terms of the fast phase, despite the fact that in most cases the slow phase will be directed towards the affected side. Nystagmus tends to occur
early in the course of peripheral vestibular disease, and to
disappear later, which means that nystagmus may not be obvious at the time of clinical examination in all acts with
vestibular disease.
Nystagmus may be induced in normal animals, where it
may be termed physiological nystagmus. For example, it occurs with normal turning of the head from side to side, or up
and down (vestibular in origin), or when watching the passing scenery from a railway carriage (visual in origin). Also,
it occurs normally after rotation, and is then called post-rotational nystagmus. If nystagmus occurs when the head is
still, and there is no rotation or movement of the surroundings, it is called spontaneous nystagmus. Spontaneous nystagmus is usually pathological in origin. Spontaneous nystagmus may be horizontal, rotatory, or vertical in direction.
If nystagmus occurs only when the head is placed in an unusual position (e.g. laterally or dorsally), it is known as positional nystagmus.
Nystagmus that consists of eye movements of the same
velocity in each direction is termed pendulous nystagmus,
and is not of vestibular origin. Pendulous nystagmus is usually associated with visual deficits.
Caloric testing consists of irrigation of the external ear
canals with warm or cold water. This sets up currents in the
endolymph, stimulating nystagmus and head tilt. It is difficult to interpret the results of this test in an animal already
showing clinical signs of vestibular disease. The test may
have some value in demonstrating whether or not the
labyrinth or VIIIth nerve is functional, since a complete absence of response to caloric stimulation usually indicates total loss of receptor function or nerve function. Nystagmus in
an inappropriate direction, and dissociated (disconjugate)
nystagmus, are abnormal responses to caloric testing, and
suggest a lesion of the vestibular nuclei or of the medial longitudinal fasciculus.

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4th European FECAVA SCIVAC Congress

Abnormal posture and ataxia

Central vestibular disease

Loss of co-ordination between head, trunk, and limbs, results in loss of balance. This is reflected in a head tilt, with
the more ventral ear directed towards the side of the vestibular disturbance. The trunk may fall, or even roll, towards the
side of the lesion. The trunk may be flexed laterally, with the
concavity directed towards the side of the lesion. The animal
may tend to circle towards the side of the lesion. These are
usually circles with a small radius. It may be possible to elicit mild hypertonia and hyperreflexia in the limbs on the side
of the body opposite to a vestibular system lesion.
An animal will often fall when attempting to shake its
head. Vision will assist an animal to compensate for a
vestibular system deficit. Blindfolding an animal with a
vestibular lesion will accentuate the clinical signs.

Any signs of brainstem disease in association with


vestibular signs indicate that central involvement is present.
The most frequent differentiating feature is a deficit in postural reactions, as central vestibular lesions most often result
in paresis or loss of conscious proprioception. Alterations in
mental status, or deficits in Vth or VIth cranial nerves, are
also indicative of central disease. Nystagmus may be a key
to differentiating central from peripheral disease. Nystagmus occurs in most central syndromes, and appears to be a
permanent deficit. It is a positional nystagmus; therefore it
may be present in some head positions (with respect to gravity), but not in others. Also the nystagmus may vary in direction with change in head position. Vertical nystagmus in
any head position is most consistent with central vestibular
disease.

Postural reactions - Strabismus


When the head is extended in a tonic neck reaction, the
eyeballs should remain in the center of the palpebral fissure
in dogs and cats. This often fails to occur on the side of a
unilateral vestibular disturbance, and results in a ventrally
deviated eyeball. Occasionally, in vestibular disease, an eyeball is noticed to deviate ventrally or ventrolaterally without
extension of the head and neck. This appears as a LMN strabismus, and can be corrected by moving the head into a different position or by inducing the patient to move its eyeballs to gaze in different directions. This is referred to as
vestibular strabismus. The ventrally deviated eyeball is on
the side of the vestibular lesion. Occasionally, the opposite
eyeball will appear to be deviated dorsally.

Peripheral vestibular disease


Peripheral lesions involve the middle and inner ear. Middle ear (bulla ossea) lesions usually produce head tilt (ipsilateral to the lesion) only, in the absence of other signs. Horizontal or rotatory nystagmus may be seen occasionally. Inner ear disease, which actually involves the receptors and
vestibular nerve within the petrosal bone, usually produces
other signs in addition to the ipsilateral head tilt - falling,
rolling, circling, nystagmus, positional strabismus, asymmetrical ataxia.
Horners syndrome (miosis, ptosis, enophthalmos) of the
ipsilateral eye may be present with either middle or inner ear
disease in dogs and cats, because the sympathetic trunk
passes through the middle ear in close proximity to the petrosal bone. The facial nerve may be affected in inner ear disease, as it courses through the petrosal bone in contact with
the vestibulocochlear nerve.
The primary characteristics of unilateral peripheral
vestibular disease are: asymmetrical ataxia without deficits
in postural reactions, and a horizontal or rotatory nystagmus
that does not change in direction with different head positions. The fast phase of the nystagmus is directed away from
the affected side.

Paradoxical central vestibular syndrome


Unilateral lesions of the peripheral vestibular system
produce a head tilt towards the side of the lesion. With few
exceptions, the same occurs with lesions of the central components of the vestibular system. Exceptions to this rule are
therefore termed paradoxical. Some unilateral lesions of
the central vestibular pathways, especially unilateral involvement of the flocculonodular lobe of the cerebellum or
the supramedullary part of the caudal cerebellar peduncle,
produce a head tilt and ataxia directed toward the side opposite to the lesion, and a nystagmus with the fast component
towards the side of the lesion. Such lesions are usually
space-occupying lesions. Usually these lesions will produce
postural reaction deficits or additional cranial nerve abnormalities on the affected side, which aid in determining on
which side a lesion is located.

Bilateral vestibular disease


Bilateral peripheral vestibular disease with complete loss
of function is characterized by symmetrical ataxia and loss
of balance of either side, with strength preserved. There is
no postural asymmetry. A characteristic side-toside head
movement often accompanies these signs. Abnormal nystagmus is not observed, and with bilateral destruction of the receptor organs, normal vestibular nystagmus cannot be elicited by head movement or caloric testing.

DISEASES OF THE VESTIBULAR SYSTEM


PERIPHERAL VESTIBULAR DISEASES
Otitis Media-Interna (or Labyrinthitis)
Etiology & Pathogenesis. Labyrinthitis refers to inflammation of the inner ear that results in dysfunction of the membranous labyrinths. This disorder is almost always an extension of otitis externa. Retrograde infection may occur via the
auditory tubes. Another source of infection of middle ear
structures is hematogenous spread. Medial extension of mid-

dle ear infection to involve meninges is not uncommon in


cats.
The majority of infections are caused by bacteria, including Staphylococcus spp., Streptococcus spp., Proteus
spp., Pseudomonas spp., Enterococcus spp. and Escherichia
coli. Occasionally, yeast infection (e.g. Pityrosporon spp.
and Candida spp.) is observed. Rarely, fungal infection may
be confined to the middle ear (e.g.. Cryptococcus sp.). Foreign bodies such as grass awns may initiate inflammation
and predispose to secondary bacterial infection.
Cinical Findings. Varying degrees of vestibular dysfunction accompany otitis media-interna or labyrinthitis. Ipsilateral head tilt, nystagmus (usually rotatory), and ataxia are almost always present. Circling, falling, and rolling, may be
seen in more severely affected animals. Ipsilateral facial
paresis/paralysis and Horners syndrome may occur. Because the facial nerve contains the parasympathetic preganglionic neurons that modulate lacrimal gland secretion, animals with labyrinthitis may have decreased tear production
and develop ipsilateral keratoconjunctivitis sicca. Ipsilateral
hemifacial spasms, resulting from irritation of the facial
nerve, have been reported in dogs in association with otitis
media. Deafness, resulting from involvement of the cochlear
nerve, may accompany otitis interna.
Diagnosis. The diagnosis may be confirmed by otoscopic examination and skull radiography. Otoscopy may reveal
otitis externa, and evidence of erosion or rupture of the tympanic membrane. Fluid in the middle ear may produce discoloration or bulging of the tympanic membrane. Inflammatory exudate or fluid should be submitted for culture and sensitivity testing. Fluid may be obtained by either aspiration or
myringotomy. Radiographic examination of the temporal
bones may reveal fluid within the tympanic cavity, or osteitis,
sclerosis, or erosion of the tympanic bulla. Computed tomography (CT) images are more sensitive in outlining these
alterations. Magnetic resonance imaging (MRI) is useful
when central extension of otitis media/interna is suspected.
Myringotomy procedure: Myringotomy is a surgical
puncture of the tympanic membrane to relieve pressure or to
obtain samples for analysis. The procedure should be completed under general anesthesia. Positioning - lateral recumbency, with affected ear uppermost, or if fluid is difficult to
obtain, there may be an advantage in having the affected ear
on the down (lowermost) side. The tympanic membrane consists of a loose dorsal section (pars flaccida) and a larger more
rigid ventral portion (pars tensa). Whereas the pars flaccida is
pink or white and contains small branching blood vessels, the
pars tensa is tough, glistening, pearly gray, and often striated.
The ear canal should be gently flushed with dilute (1:10)
aqueous povidone-iodine solution several times until the ear
canal is clear of debris. A myringotomy is then done using a
20-gauge or 22-gauge spinal needle. The use of a needle permits both collection of fluid for cytology and culture, and introduction of a small volume of sterile saline (0.2-0.4 ml) for
lavage of the middle ear cavity when a fluid sample is not abtained following aspiration through the needle. The needle
should penetrate the tympanic membrane in the ventral and
caudal aspect of the pars tensa, in order to avoid the bony ossicles. Some authors recommend the routine flushing of the
middle ear cavity with dilute povidoneiodine after fluid for

55

cytologic examination and culture has been withdrawn, followed by a saline flushing and introduction of a broad spectrum antibiotic. This author recommends a gentle flushing
with saline only after a myringotomy procedure, followed by
the use of systemic broad spectrum antibiotic therapy.
Treatment. The prognosis is usually favorable with prolonged oral antibiotic therapy, where selection is based on
culture and sensitivity studies. Some authors recommend the
use of repeated ear cleanings and irrigation, and topical antibiotic therapy, in cases of otitis media/interna. This author
recommends these procedures for otitis externa associated
with otitis media/interna only when the tympanic membrane
is intact. In addition, the use of topical therapies should be
avoided for four or five days following myringotomy. Cats
with concurrent mite infestation should be treated with a
topical miticide. In more chronic cases, surgical drainage of
the middle ear cavity may be required by means of lateral or
ventral bulla osteotomy.

Idiopathic peripheral vestibular disease


Etiology & Pathogenesis. This is an acute vestibular syndrome of unknown etiology of cats of all ages. A similar
condition occurs in older dogs. There is no evidence of inflammatory disease in affected animals. Some affected cats
have had a concomitant or recent upper respiratory tract infection, suggesting that previous viral infection may directly (due to seeding of virus in the inner ear) or indirectly (because of altered antigenicity) cause inflammation of the
vestibular sensing apparatus. Pathological or immunological
confirmation of this hypothesis is lacking, however. In one
study of 75 affected cats, 80% were diagnosed in the months
of July and August, suggesting an environmental factor may
be involved, however none was identified.
The syndrome in cats has been compared to Mnires
disease of humans, a disorder characterized by recurrent
bouts of vertigo, nystagmus and tinnitus. Abnormal flow of
endolymph within the membranous labyrinth apparently
contributes to the pathogenesis of Mnires disease in humans, and an increased concentration of potassium ions
within the perilymph (separating the bony and membranous
labyrinths) may also have a role. Considering that, unlike
Mnires disease of humans, the feline syndrome spontaneously resolves and generally does not reoccur, it is not
clear whether these factors have a role in the development of
the problem in cats.
Clinical Findings. A breed or sex predilection does not
exist for feline idiopathic peripheral vestibular disease. The
median age of affected cats is approximately four years.
Both cats and dogs exhibit signs of peripheral vestibular involvement. The signs of vestibular dysfunction usually are
unilateral, however occasionally bilateral signs may be seen
in affected cats. In addition to neurological deficits of peripheral vestibular disease, some affected cats may have
vomiting or anorexia. The signs appear suddenly, and often
result in severe dysfunction and inability to stand and walk.
In a few days the affected animals tend to stabilize and improvement continues for 4-6 weeks. Residual deficits such
as mild head tilt may persist, and blindfolding or darkness

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4th European FECAVA SCIVAC Congress

will cause a re-occurrence of signs well after apparent recovery has occurred.
Diagnosis. A diagnosis of idiopathic feline peripheral
vestibular disease is made by excluding other causes. There
is not a definitive antemortem or postmortem finding. It is
important to distinguish this idiopathic benign disorder,
which resolves spontaneously without therapy, from otitis
media-interna, which requires vigorous therapy, and may
produce recurrent or persistent signs. The idiopathic disease
is characterized by a peracute onset of head tilt, asymmetrical ataxia, and horizontal or rotatory nystagmus, in the absence of facial paresis, Horners syndrome, or signs of CNS
involvement. An absence of otitis externa, normal tympanic
membranes, and normal radiographs of the temporal bones,
further support this diagnosis.
Treatment. While the cause of this idiopathic disorder remains undetermined, prognosis for spontaneous recovery is
good, however, recovery may require 4-6 weeks. Re-occurrence may be seen, especially in dogs, either on the same
side or the opposite side. There is no evidence that treatment
of any type alters the course of the disease. Cats with concurrent otitis externa or otitis media/interna should be treated for these problems as previously described. Antiemetics
may be considered in cats that vomit.

following retraction of the soft palate.


Diagnosis. Polyps should be suspected in cats with appropriate clinical signs, particularly in young cats. Most
polyps can be visualized with a thorough otoscopic or pharyngeal examination. Opacitiy of the tympanic cavity, associated with sclerosis of the tympanic bulla, may be seen on
plain skull radiographs. Computed tomography provides
precise information regarding location and extent of polyps.
Bony lysis is rarely seen in association with nasopharyngeal
polyps. Cerebrospinal fluid analysis may be abnormal in
cats with extension of inflammation to brain or meninges.
Excised polyps are variable in size, red in color, and of
smooth appearance. Many have a stalk or pedicle of attachment. Microspcopically, there is a central core of well-vascularized fibrous tissue that is covered by epithelium (varying from stratified squamous to pseudostratified columnar
cells). Glands composed of goblet cells may be seen within
the fibrous tissue. There may also be an infiltration of a
mixed population of inflammatory cells within the polyp.
Treatment. Many polyps in the external ear, or in a nasopharyngeal location, may be removed by means of gentle
traction, thus avulsing the stalk from its attachment. Bulla
osteotomy with curettage has been advocated to remove
residual polyps from within the tympanic cavity.

Nasopharyngeal polyps

Neoplasia

Etiology & Pathogensis. Inflammatory or nasopharyngeal polyps are benign masses that may be located in the nasophaarynx, auditory tube, and/or the tympanic cavity.
Rarely the polyp may rupture the tympanic membrane and
protrude into the external ear canal. Polyps consist of wellvascularized fibrous tissue lined by epithelium. The site of
origin of the polyps has not been determined. It has been
speculated that some polyps may arise subsequently to otitis
externa or otitis media, however otitis media appears to frequently be a complication of auditory tube obstruction by
the polyp, rather than an initiating factor. Vestibular dysfunction follows extension of otitis media into the labyrinth
(otitis interna). Occasionally there may be further extension
of infection into the brain, resulting in central vestibular
signs and brainstem dysfunction. In one published report,
calici virus was isolated from one of three young cats affected in a household. Another report suggested a congenital
origin, as two young cats affected with polyps were siblings.
Clinical Findings. The majority of cats affected with
polyps are less than two years of age at the time of initial
clinical signs (age range 2 months to 15 years). There is no
apparent breed or sex predilection. Clinical signs in affected
cats vary widely, depending on the location of the polyp or
polyps. Polyps originating within the auditory tube or middle ear cavity may interfere with drainage of middle ear secretions, resulting in signs of otitis externa and/or middle ear
involvement and subsequent otitis interna and signs of peripheral vetsibular disease. Polyps may be seen by means of
otoscopic examination. Cats with a polyp or polyps in a nasopharyngeal location have signs of upper respiratory compromise (coughing, dyspnea, sneezing, stertorous respiration). Polyps in a nasopharyngeal location usually are seen

Neoplasms that involve the temporal bone may produce


peripheral vestibular disease, often in association with facial
paralysis or paresis. Fibrosarcoma, osteosarcoma, chondrosarcoma, and squamous cell carcinoma have been reported. Squamous cell carcinoma and ceruminous gland adenocarcinoma may involve adjacent soft tissues. It has been reported that squamous cell carcinoma is the most frequently
occurring tumor affecting the middle ear of cats, whereas
papillary adenomas and extension of adnexal or ceruminous
gland tumors appear to be more common in dogs in this location. Rarely, middle ear tumors may extend directly into
brainstem. Neurofibroma or lymphoma of the vestibulocochlear nerve usually cause signs of unilateral vestibular
disturbance prior to signs associated with compression of
brainstem.

Congenital vestibular syndromes


Signs of peripheral vestibular disease, usually in the absence of deafness, have been observed in several breeds of
dog (including English cocker spaniels, German shepherd
dogs, and Tibetan terriers), and in cats (Siamese and
Burmese kittens). Severe head tilt, circling, and falling or
rolling, may be noted from birth to 4 months of age. Nystagmus is rarely present. The cause is undetermined. Pathological lesions have not been demonstrated. Prognosis is
guarded, as clinical signs may regress completely, re-occur,
or remain static. There is no effective treatment.
Congenital pendular nystagmus has been recognized in
Siamese cats. The head may oscillate synchronously with
the nystagmus. Signs of vestibular dysfunction are not ap-

parent, and lesions of the visual pathways are responsible for


this syndrome.

Toxicity
Prolonged therapy with aminoglycoside antibiotics may
result in degeneration of the labyrinth receptors of the
vestibular or auditory systems, or both. Vestibular dysfunction may be fully or partially reversible, however hearing
may be permantly affected. In the southeastern U.S.A., acute
peripheral vestibular signs may follow ingestion by cats of
the tail of the blue-tail lizard.

Trauma
Cranial trauma may result in signs of peripheral vestibular disease secondary to fractures of the temporal bone or
tympanic bulla. Facial paralysis may accompany petrosal
bone injury.

CENTRAL VESTIBULAR DISEASES


Any cause of meningo-encephalitis may result in involvement of central vestibular structures. The vestibular
deficits may occur alone, or with signs indicating involvement of other areas, such as spinal cord, cerebellum, or cerebrum. Reported causes in cats include feline infectious peritonitis, toxoplasmosis, and cryptococcosis. Aberrant parasitic migration may produce severe signs of vestibular disturbance. Neoplasms of the cerebellomedullary angle affect
the vestibular system. Neoplasms may be located at the surface of the parenchyma (e.g. meningioma, neurofibroma,
choroid plexus papilloma or malignant lymphoma), or may
be located within the parenchyma (e.g. astrocytoma or lymphoma). Neoplasms at these locations occur in cats of all
ages. Thiamine deficiency may produce a mild vestibular
ataxia as the earliest sign of degeneration.

57

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59

EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline spinal cord disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
The spinal cord may be divided into four major longitudinal divisions. These divisions are : 1) cervical (C1 to C5);
2) cervical enlargement ( C6 to T2); 3) thoracolumbar ( T3
to L3); 4) lumbar enlargement (L4 to Cd5). Diseases of each
of these regions results in a combination of neurological
signs that is specific for the region involved. Recognition of a
characteristic group of clinical signs is essential in the accurate localization of the spinal cord lesion. This lecture will
review the clinical signs in cats associated with spinal cord
disease and localization of the lesion to a particular level of
the spinal cord. The lecture will also review the congenital,
degenerative, metabolic, infectious, parasitic, traumatic,
vascular, and idiopathic causes of feline spinal cord disorders.

INTRODUCTION
Motor, sensory, reflex and sphincter abnormalities may
be used to determine the location of a lesion within one of
four major longitudinal divisions of the spinal cord. The divisions are cervical (C1 to C5 spinal cord segments), cervical enlargement (C6 to T2), thoracolumbar (T3 to L3), and
lumbar enlargement (L4 to Cd5). It is essential to remember
that these divisions refer to spinal cord segments, not vertebrae, and that spinal cord segments do not correspond exactly with vertebrae of the same number. Some variations
may be encountered due to slight differences between animals in segments that form cervical or lumbar enlargements.
A disorder of each of the four regions of the spinal cord
results in a combination of neurologic signs that is specific
for the region involved. Recognition of a characteristic
group of clinical signs therefore allows accurate localization
of a spinal cord lesion. The presence of neurological deficits
indicative of involvement of more than one region of the
spinal cord is highly suggestive of multifocal or disseminated spinal cord disease.
The functional differences between upper motor neurons (UMNs) and lower motor neurons (LMNs) may be
used to localize lesions to one of the functional regions of
the spinal cord.
Cell bodies of spinal cord LMNs are located in the spinal
cord gray matter. Their axons leave the spinal cord via the
ventral nerve roots to become part of a peripheral nerve, and

to terminate on a muscle. The LMNs of the thoracic limb


have their cell bodies in C6 to T2 spinal cord segments that
form the cervical enlargement, while LMNs of the pelvic
limb arise from the L4 through S1 spinal cord segments of
the lumbar enlargement. Anal and urethral sphincter LMNs
originate from S1 through S3 spinal cord segments. Signs of
LMN dysfunction, which in diseases affecting the spinal
cord reflect damage to the spinal cord segment(s) from
which LMNs originate, are: depression or loss of voluntary
motor activity, normal or depressed segmental spinal reflexes, depression or loss of muscle tone, and rapid, severe atrophy of an affected muscle due to denervation.
Upper motor neurons arise from cell bodies located in
the brain. Their axons form descending pathways of the
spinal cord, and terminate on interneurons that in turn
synapse with LMNs. Lesions affecting UMNs result in
UMN signs. These UMN signs result from an increase in the
excitatory state of LMNs. Upper motor neuron signs include: depression or loss of voluntary motor activity, normal
or exaggerated segmental spinal reflexes, appearance of abnormal spinal reflexes (e.g., crossed extensor reflex), increased muscle tone, and muscle atrophy due to disuse.
Unilateral signs resulting from spinal cord disease are
unusual, however signs frequently are asymmetrical. In the
majority of cases, a lesion resulting in asymmetrical signs
will be located on the side of greater motor and sensory
deficit.

CERVICAL (C1 to C5)


Fatal respiratory paralysis resulting from interruption of
descending respiratory motor pathways or damage to motor
neurons of the phrenic nerve (C5 to C7 spinal cord segments) occurs in a complete transverse myelopathy. Lesions
that are less than complete may not affect respiration, and in
such cases other signs may be detectable.
Ataxia and paresis of all four limbs usually are seen.
Tetraplegia rarely is seen, as lesions of sufficient severity to
cause tetraplegia also produce respiratory paralysis. Hemiparesis occasionally may be present in association with a
cervical lesion. Lesions of the cervical spinal cord may result in paraparesis with minimal neurologic deficits in thoracic limbs. The reasons for this are poorly understood.
Spinal reflexes and muscle tone are intact in all limbs,
and may be normal or exaggerated. Muscle atrophy general-

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60

ly is not present, however disuse atrophy may develop in


cases that have a chronic course. Anal reflexes are intact and
anal tone usually is normal.
Bladder dysfunction may occur with normal or increased
urinary sphincter tone, and loss of voluntary control of micturition. Reflex dyssynergia may also be seen. Although voluntary control of defecation may be lost, reflex defecation
will occur when faeces are present in the rectum.
Horners syndrome (ptosis, miosis, and enophthalmos)
rarely may be present in an animal with a severe destructive,
cervical lesion.
Conscious proprioception and other postural reactions
usually are depressed or absent in all limbs. It should be remembered that complete loss of conscious proprioception
may be present without detectable loss of pain perception.
Cervical hyperesthesia (spasms, apparent pain on palpation, cervical rigidity, and abnormal neck posture) may be
seen in some animals with cervical myelopathy. Occasionally an animal may hold a thoracic limb in a partially flexed
position, a posture that may be consistent with C1 to C5
nerve root or spinal nerve entrapment (root signature), although this posture is seen more commonly with a disorder
of the cervical enlargement.
Disorders that affect the cervical region of the spinal
cord must be differentiated from brain lesions that result in
tetraparesis. This may be accomplished by doing a complete
neurological examination, however occasionally this distinction may be difficult. In most circumstances a cervical
lesion does not result in neurological deficits attributable to
involvement of the medulla oblongata, however, there are
several notable exceptions to this rule. Positional strabismus
resulting from loss of the vertebral joint proprioceptive input
to the attitudinal reflexes, may be seen in association with a
cranial cervical lesion (C1 to C3 spinal cord segments). A
cranial cervical lesion may also cause facial hypesthesia as a
result of involvement of the spinal nucleus and tract of the
trigeminal nerve. Cranial cervical trauma often results in
clinical signs referable to injury of the caudal brain stem
(head tilt, pharyngeal paresis, facial paresis) or cerebellum.
The Schiff-Sherrington sign (syndrome or phenomenon)
consists of hypertonicity of thoracic limb muscles and hyperextension of the neck, and is seen in association with
spinal cord lesions caudal to the cervical enlargement. It is
essential to differentiate this sign from thoracic limb hypertonicity caused by a cervical lesion, or an injury rostral to the
foramen magnum.

CERVICAL ENLARGEMENT (C6 to T2)


Ataxia and paresis of all four limbs usually are present.
Occasionally paresis of thoracic limbs and paralysis of
pelvic limbs may be seen. Spinal reflexes and muscle tone
may be normal or depressed in thoracic limbs, and normal
or exaggerated in pelvic limbs. The nature of thoracic limb
reflex alterations depends on the exact craniocaudal location of a lesion within this region. Muscle atrophy often is
severe in thoracic limbs. Panniculus reflex may be depressed or absent unilaterally or bilaterally due to interruption of the LMNs involved in this reflex (C8 and T1 spinal

4th European FECAVA SCIVAC Congress

cord segments).
Should bladder dysfunction occur it is similar to that observed with a lesion in the cervical region, with loss of voluntary control of urination. Anal reflexes and anal tone most
often are normal although voluntary control of defecation
may be absent.
Unilateral Horners syndrome commonly is observed
with a spinal cord lesion of the cervical enlargement, particularly a lesion involving T1 to T3 spinal cord segments or
nerve roots.
Conscious proprioception and other postural reactions
usually are depressed in all four limbs. Alterations in these
functions may be more pronounced in the pelvic limbs than
in thoracic limbs. Occasionally conscious proprioception
will be absent only in a thoracic and pelvic limb on the
same side.
Severe depression or loss of pain perception rarely are
seen in association with a lesion of the cervical enlargement,
except in intrinsic myelopathies (e.g., ischemic myelopathy). Hyperesthesia at the level of a lesion of the cervical enlargement, thoracic limb lameness, or apparent neck pain
may be present.

THORACOLUMBAR (T3 to L3)


The majority of spinal cord lesions of dogs or cats occurs
in this region. Typically thoracic limb gait is normal, and
paresis and ataxia, or paralysis, are seen in pelvic limbs.
Thoracic limb spinal reflexes are normal. Pelvic limb spinal
reflexes and muscle tone are normal to exaggerated, depending on the severity of the lesion. Muscle atrophy is not
seen in thoracic limbs. Pelvic limb muscle atrophy, if present, is the result of disuse and is seen in animals with a severe, chronic lesion.
Anal reflexes and anal tone usually are normal or exaggerated. Voluntary control of defecation may be lost. Reflex
defecation will occur when the rectum is filled with faeces,
however may not be at an appropriate time or place. Degree
of bladder dysfunction varies depending on the severity of a
spinal cord lesion. There may be loss of voluntary control of
urination, detrusor muscle areflexia with normal or increased urinary sphincter tone, or reflex dyssynergia where
initiation of voiding occurs and is stopped by involuntary
contraction of the urethral sphincter. The bladder may be
manually expressed in some animals, and not in others, due
to increased tone of the urinary bladder sphincter. This is often referred to as an UMN bladder. Although overflow
incontinence may occur with lesions of the spinal cord in
this region secondary to overfilling of the bladder, detrusor
muscle tone and urinary sphincter tone are present, distinguishing this type of incontinence from that due to lesions of
the lumbar enlargement and cauda equina (LMN bladder).
Conscious proprioception and other postural reactions
are normal in the thoracic limbs, and depressed or absent in
the pelvic limbs.
Pain perception is normal in the thoracic limbs and may
be normal, depressed or absent in the pelvic limbs. Panniculus reflex may be reduced or absent caudal to a lesion. In the
lumbar region the panniculus reflex may be present in le-

sions caudal to L3 due to the pattern of cutaneous innervation of lumbar spinal nerves. There may be an area of hyperesthesia at the level of a lesion.
The Schiff-Sherrington sign may be seen with a lesion in
this region. Usually it is an indication of an acute and severe
spinal cord lesion, although such a lesion may be reversible.

LUMBAR ENLARGEMENT (L4 to Cd5)


and CAUDA EQUINA
Involvement of this region by a pathological process results in varying degrees of pelvic limb paresis and ataxia, or
paralysis, and is often accompanied by dysfunction of bladder, and paresis or paralysis of anal sphincter and tail. Thoracic limb function is normal.
Pelvic limb reflexes and muscle tone are reduced or absent. Muscle atrophy often is present in pelvic limbs. Conscious proprioception and other postural reactions are reduced or absent in pelvic limbs.
Anal tone and anal reflexes are reduced or absent. The
rectum and colon may become distended with feces, and fecal incontinence, with continual leakage of feces, often is
seen. Constipation may result from the inability to void feces. Paresis or paralysis of the urethral sphincters and detrusor muscle result in overfilling of the bladder and overflow incontinence. Affected animals have a large residual
volume of urine in the bladder, and the bladder is easily expressed manually.
The Schiff-Sherrington sign occasionally may be seen
with an acute lesion affecting this region of the spinal cord.
The term cauda equina is used to describe the lumbar,
sacral, and caudal nerve roots and spinal nerves as they extend caudally from the caudal tip (conus medullaris) of the
spinal cord within the vertebral canal. Lesions that affect
cauda equina result in clinical signs that are indistinguishable from lesions that affect the spinal cord segments from
which the nerves of the cauda equina arise (L6 to Cd5).

ALPHABETICAL LISTING OF FELINE


SPINAL CORD DISORDERS
Bacterial or Fungal meningomyelitis
Etiology and Pathogenesis. Bacterial or fungal meningitis and/or myelitis occur infrequently in cats. Several routes
of infection exist. Direct implantation of organisms may occur following a bite wound, spinal puncture, or surgery, or
may accompany migration of a foreign body such as a grass
awn. Extension may occur from a focus of infection such as
a paravertebral infection or diskospondylitis. Infection may
also result from hematogenous spread of systemic infection
such as endocarditis. As clinical signs produced by bacterial
or fungal agents depend more on the neural structures affected than on the agent responsible, these agents are discussed together.
Meningitis may be accompanied by infection of the underlying parenchyma of the spinal cord (myelitis). Meningitis and/or myelitis may be focal, multifocal, or disseminated

61

in distribution and are frequently accompanied by meningoencephalitis. Pathologically, meningitis is characterized


by infiltration of inflammatory cells into the leptomeninges.
Inflammation may occur throughout the entire subarachnoid
space of the brain and spinal cord. Myelitis is characterized
by necrosis and infiltration of inflammatory cells within
spinal cord parenchyma.
Bacteria that have been isolated from cats with meningitis and myelitis include Pasteurella multocida, Actinomyces
viscosus, Fusobacterium sp, Eubacterium sp and Bacteroides sp.
The most common fungi that infect the CNS of cats are
Cryptococcus neoformans, Blastomyces dermatitidis, and
Cladosporium bantianum. Cryptococcus neoformans is
found ubiquitously and frequently causes infection in immunosuppressed animals. Cryptococcosis is more common
in cats than dogs and infection may result from extension of
nasal infection through the cribriform plate. Blastomyces infections are found in certain geographic areas in the United
States and in such cases the CNS is infected by hematogenous spread.
Focal epidural infections have been reported to occur,
generally as a result of migrating grass awns or penetrating
wounds. Proliferation of inflammatory tissue may result in
an extradural space-occupying lesion causing spinal cord
compression and clinical signs of a transverse myelopathy.
Abscessation may occur within the spinal cord and may
have the radiographic appearance of an intramedullary mass.
Clinical Findings. Clinical signs of meningitis include
apparent spinal pain, hyperesthesia, and cervical or thoracolumbar rigidity, occasionally manifest as a sawhorse
posture. Irritation of the numerous nerve endings in the
meninges results in reflex muscle spasms when affected animals are stimulated. Fever is intermittent and is more likely to occur in association with concurrent bacteremia or disseminated fungal infection. Fever may occur in association
with primary CNS infections due to presence of leukocytic
pyrogens in the CSF or in the hypothalamic circulation.
Neurologic deficits are indicative of associated myelitis
or radiculitis, and abnormalities depend on the location and
extent of infection. Focal myelitis may result in signs of
transverse
myelopathy.
Disseminated
bacterial
meningomyelitis often is associated with meningoencephalitis, and clinical signs usually are acute and rapidly progressive. Focal bacterial meningitis and/or myelitis and fungal
meningomyelitis may be associated with development of
more slowly progressive clinical signs.
Paraparesis and pelvic limb ataxia are common presenting signs in cats with cryptococcal meningitis and/or
myelitis. Progressive paralysis of a single pelvic limb has
been reported in two cats with cryptococcal infection of the
lumbar spinal cord. Cats with CNS cryptococcal infections
may show an acute onset of clinical signs despite chronic destruction of nervous tissue.
Clinical signs of bacterial or fungal meningitis and
myelitis are indistinguishable from other causes of meningitis and myelitis in cats. Causes include CNS toxoplasmosis,
FIP meningomyelitis, intervertebral disk protrusion (especially in the cervical spine), spinal fracture, diskospondylitis, polymyositis, and polyarthritis.

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Diagnosis. A diagnosis of bacterial or fungal meningitis


and/or myelitis is made on the basis of results of CSF analysis, and isolation of a causative organism by culture of CSF.
Clinical signs may reflect meningeal irritation or myelopathy that may be indistinguishable from signs caused by other noninfectious myelopathies such as intervertebral disk
disease. Presence of fever or abnormal hemogram cannot be
relied upon for diagnosis of meningitis/myelitis, as neither
may be present in affected animals.
Bacterial or fungal meningitis has been reported to result
in moderate to severe CSF pleocytosis. More than 5000
white blood cells/ill may be present in some cases. Polymorphonuclear (PMN) cells predominate. Mixed mononuclear and PMN pleocytosis occurs with fungal meningitis,
and eosinophils may be present, especially in cases of cryptococcal meningitis. The CSF appears turbid if the cell count
is greater than 500 white blood cells/ill. In our experience,
disseminated bacterial meningomyelitis is rarely recognized
antemortem in dogs or cats. Focal bacterial epidural,
meningeal, or parenchymal infections more commonly occur. Cerebrospinal fluid findings in affected animals reflect
the degree of leptomeningeal or ependymal involvement,
and the CSF white blood cell count may be normal or only
slightly elevated (less than 50 white blood cells/u1).
Cerebrospinal fluid protein is usually moderately to
markedly elevated due to increased capillary permeability
and leakage of serum proteins into the CSF, and probably also due to local production of immunoglobulins. If CSF protein content is high, fibrin clots may develop. Cerebrospinal
fluid pressure is usually normal but occasionally is elevated,
especially in animals with cryptococcal meningitis. Hemorrhage into the CSF may occur; a red or pink supernatant is
indicative of recent hemorrhage. Xanthochromia develops if
more than 48 hours have elapsed following hemorrhage.
Cerebrospinal fluid glucose content may be decreased (CSF
glucose is normally 60 to 80 per cent of a simultaneously determined plasma glucose concentration) as a result of glucose utilization by microorganisms and possibly by PMN
leukocytes. However, low CSF glucose concentration is not
a consistent finding in animals with bacterial meningitis.
Bacteria or fungal organisms may be identified by
Grams stain or acridine orange stain of sedimented or centrifuged CSF. Cryptococcal organisms often are observed in
cell preparations of CSF and can be identified by staining
with Wrights stain or Grams stain, or using a wet mount
preparation with India ink.
Cerebrospinal fluid from all animals with CSF abnormalities consistent with meningitis should be submitted for
both aerobic and anaerobic bacterial culture, and antibiotic
sensitivity testing of any cultured bacterial isolates. Because
of the prevalence of anaerobic bacteria in CNS infections of
cats, anaerobic culturesare essential when bacterial meningitis is suspected. Cerebrospinal fluid fungal culture may also
be done. Negative CSF cultures are common, even in those
animals in which bacteria or fungal organisms can be identified in CSF. Culturing the sediment of centrifuged CSF, or
filtering CSF and culturing the filter, may increase the likelihood of obtaining a positive CSF culture. Causative organisms may be isolated from blood cultures of animals that are
bacteremic or have systemic fungal infection. It is recom-

4th European FECAVA SCIVAC Congress

mended that a large volume of CSF, preferably 2 or 3 ml, be


collected for bacterial and/or fungal culture. If a delay in
processing of a CSF sample is anticipated, CSF can be aseptically inoculated into a blood culture bottle for submission
to a diagnostic laboratory.
Serology may also be useful in diagnosis of CNS fungal
infections. The titer of antibody-coated latex agglutination
to cryptococcal (capsular) antigen may be useful in the diagnosis of cryptococcal meningitis and in assessing the response to therapy. The latex cryptococcal agglutination titer
(LCAT) is more sensitive than the indirect fluorescent antibody test and can be used on CSF. However, animals with
localized CNS infection may have a negative titer.
Focal epidural inflammatory lesions may appear as an
extradural mass on myelography. Chronic focal meningitis
may result in obstruction of CSF flow and blockage of contrast material on myelography due to arachnoid adhesions.
Treatment.
Bacterial Infections. In treating bacterial meningitis and/or
myelitis it is desirable to use an antimicrobial that is specific
for the causative organism, and that crosses the blood-brain
barrier (or blood-spinal cord barrier) in therapeutic concentrations, in order that drug concentrations may be maintained after the acute phase of inflammation has subsided. The bloodbrain, blood-spinal cord, and blood-CSF barriers are most permeable to antimicrobials with high lipid solubility, low ionization potential, and low protein binding affinity.
Antibiotics may be administered to animals with suspected bacterial meningitis prior to obtaining results of culture and sensitivity testing. Selection should be based on
tentative organism identification (by Grams stain or acridine orange stain) from CSF, the suspected source of infection, and the ability of an antibiotic to reach effective tissue
concentrations in CNS.
High-dose intravenous therapy with a bactericidal drug
should be used when possible, although many bactericidal
drugs penetrate poorly into the CSF. Penicillin and penicillin derivatives in high doses have been recommended for
the treatment of CNS infections caused by gram-positive
cocci (e.g., penicillin G 5000-10,000 units IV every 6 hours
for at least 7 days). Oxacillin may be used for the treatment
of meningitis caused by penicillin-resistant strains of
Staphylococcus.
Most cephalosporins penetrate poorly into the CNS. Several third-generation cephalosporins (e.g., cefotaxime) reach
effective CNS concentrations and are considered the drugs
best suited for treatment of gramnegative meningitis. Firstand second-generation cephalosporins do not reach effective
CSF concentrations, and should not be used in treatment of
CNS infections. The cephalosporins largely have replaced
the aminoglycosides, which penetrate poorly into the CNS.
Metronidazole is useful for treatment of most anaerobic
infections, is bactericidal, and diffuses well into all tissues
including the CNS. Metronidazole has had an increasing
role in the therapy of brain abscesses of humans. Metronidazole is used in combination with high doses of penicillin
when aerobes are present. Toxicity (central vestibular signs
and cerebellar dysfunction) has been reported in dogs treated with metronidazole.
Chloramphenicol reaches higher CSF concentrations

than most other antibiotics; however, it is bacteriostatic, and


many strains of Staphylococcus have been shown to be resistant to this drug. Chloramphenicol may be given at a
dosage of 20 mg/lb IV four times a day or 25 mg/lb orally
three times a day in dogs, and 5 to 10 mg/lb/day divided
twice a day in cats. Adverse effects of chloramphenicol include gastroenteritis in dogs and cats, and bone marrow depression in cats. Because of the high frequency of adverse
effects, and as bactericidal drugs are preferred for treatment
of CNS infections, use of chloramphenicol is restricted to infections caused by susceptible organisms that are resistant to
other agents.
Most sulfonamides penetrate effectively into the CSF.
Sulfadiazine (which is less protein-bound than other sulfonamides) penetrates into the CSF and nervous tissue better
than sulfamethoxazole and is effective if given orally. Data
are not available regarding the concentration of trimethoprim in CSF of dogs; however, CSF concentrations may be
as high as 35 per cent of serum concentrations in other
species. Trimethoprim-sulfadiazine combinations usually
are bactericidal in action, and are effective for treatment of
some bacterial CNS infections.
In general, tetracycline, a broad-spectrum bacteriostatic
drug, only reaches effective CNS concentrations when
meninges are inflamed. However, newer tetracyclines
(minocycline, doxycycline) penetrate the CNS better than
tetracycline and have better activity against anaerobes and
some aerobic organisms.
Intrathecal administration of antibiotics has been used in
humans. Although possible for use in dogs, multiple CSF
punctures, each requiring anesthesia, are needed. Some drugs
are toxic when directly introduced into the CNS (e.g., penicillin may cause seizures), and drugs may not diffuse freely
through CSF especially if there is a blockage of CSF flow.
Treatment with antibiotics should be started as soon as
possible after submission of CSF for culture. After results of
culture and sensitivity are known, therapy may be altered.
Treatment is continued for 2 to 4 weeks; however, treatment
for longer periods is often necessary and relapses are possible. It is also important to identify possible sources of infection outside the CNS (endocarditis, diskospondylitis, paravertebral abscess). Localized spinal cord or meningeal infections that are well encapsulated may be resistant to antibiotic therapy. Surgical exploration is indicated if focal
meningeal or epidural infection refractory to medical therapy is suspected.
Use of corticosteroids in cases of bacterial meningitis
and myelitis is controversial. Corticosteroids may decrease
inflammation and thereby decrease the resulting spinal cord
and nerve root damage; however, such treatment may also
decrease host defense mechanisms, and in turn may result
in worsening of clinical signs and in a higher incidence of
relapse.
Prognosis in cases of bacterial meningitis and myelitis
depends both on the ability to eliminate the causative organism, and on the extent of neurologic deficits. Neurologic
deficits occurring as a result of spinal cord or nerve root inflammation may be permanent.
Fungal Infections. Fungal infection of the CNS of cats is
extremely difficult to eliminate. The disease is often multi-

63

systemic, and is seldom recognized in the early stages of


CNS involvement.
Amphotericin B is frequently used to treat systemic fungal infections, although it is poorly absorbed into the CSF
and nervous tissue. Intrathecal administration of amphotericin B has been recommended, especially in animals with
Coccidioides immitis meningitis, but may result in arachnoiditis and cranial nerve toxicity.
Combinations of drugs have been recommended. Amphotericin B, ketoconazole (poor CNS penetration), and
flucytosine (good CNS penetration) are the main agents
used. Rifampin has been used to enhance amphotericin B activity. Combined treatment with amphotericin B and 5- fluorocytosine (SFU) has been recommended for use in cases
of cryptococcosis. Long-term, high-dose ketoconazole therapy is reported to be effective for treatment of cryptococcosis in cats.
Because of the difficulty in obtaining therapeutic concentrations of antifungal agents within nervous tissue, the
prognosis for CNS mycotic infections is poor. In the future,
newer generation imidazoles (e.g., fluconazole, itraconazole) that are currently under investigation may be efficacious for treatment of fungal infections of the CNS.

Congenital vertebral anomalies


Etiology and Pathogenesis. Congenital anomalies frequently occur in the vertebral column of cats; however, the
majority of such anomalies are not clinically significant. If a
vertebral anomaly causes instability or deformity of the vertebral canal, spinal cord compression and associated clinical
signs may result.
Clinical Findings. Clinical signs related to anomalous
vertebrae are not present in the majority of affected animals.
In most animals in which clinical signs develop, trauma to
the spinal cord has occurred secondary to vertebral instability or progressive deformity with growth. Block vertebrae
and butterfly vertebrae most often are stable and rarely are
associated with clinical signs of spinal cord dysfunction.
Hemivertebrae are more often associated with neurologic dysfunction than are other vertebral anomalies. Hemivertebrae may result in vertebral instability and/or narrowing of
the spinal canal, especially in the dorsoventral plane, owing
to moderate to severe angulation of the spine, which can result in spinal cord compression or intermittent trauma to the
spinal cord. Clinical signs produced depend on the location
of the anomaly and usually reflect a progressive or intermittent transverse myelopathy.
Diagnosis. Diagnosis of a vertebral anomaly is made by
means of radiographs of the vertebral column. Radiographically, hemivertebrae and adjacent vertebrae appear to be
formed of normal bone, and disk spaces are usually well
formed or widened. Vertebral bodies appear to have a portion absent and do not appear to be compressed. Adjacent
vertebrae frequently have an altered shape that conforms to
the defect found in the congenitally affected segment. Vertebral end- plates are smooth and of normal thickness. In most
cases, myelography is necessary to determine the presence
of spinal cord compression resulting from a congenital

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anomaly.
Treatment. Vertebral anomalies resulting in spinal cord
compression and instability of the vertebral column may be
treated by means of surgical decompression and stabilization.
It is important to determine that a congenital anomaly is the
cause of an animals myelopathy by ensuring that the clinical
signs are consistent with the observed abnormality. Caution
must be exercised in completing surgery on an animal with a
vertebral anomaly, and prognosis must be guarded. Animals
may have more than one spinal abnormality, and vertebral
anomalies may be associated with congenital spinal cord
anomalies that are not amenable to surgical treatment.

Degenerative myelopathy
Etiology and Pathogenesis. Degenerative myelopathy
has been described in a 6-year-old cat. Histologic examination of spinal cord confirmed diffuse demyelination and
marked astrocytosis in white matter. The etiology of the
myelopathy was not determined; however, the cat was FeLV
positive, and the possibility of virus-induced myelopathy
was considered. Retroviruses have been associated with the
development of chronic progressive myelopathy in humans.
In light of this information, all cats with progressive
myelopathy should be tested for both FeLV and FIV.

Diskospondylitis (spondylitis, vertebral


osteomyelitis)
Etiology and Pathogenesis. Diskospondylitis has been
reported to occur in cats. Bacterial or fungal infection of the
intervertebral disks and adjacent vertebral bodies
(diskospondylitis), or of only the vertebral bodies (spondylitis), may result in extradural spinal cord or cauda equina
compression due to extension of granulation tissue and bony
proliferation within the vertebral canal, or due to pathologic
fracture or luxation of an infected vertebra or vertebrae.
Hematogenous spread of bacteria or fungi is probably the
most common cause of diskospondylitis. Sources of infection include bacterial endocarditis and sites of dental extraction. Urinary tract infections have been implicated as a primary focus of infection. Retrograde flow in the vertebral
veins has been suggested as a possible route of infection to
the vertebral column.
Affected intervertebral disks may have evidence of degeneration (collapsed disk space, spondylosis deformans) or
trauma (traumatic disk protrusion, vertebral luxation). Prior
disease or injury to the disk has been suggested as a factor in
the pathogenesis of diskospondylitis.
Clinical Findings. Diskospondylitis may occur at any
level of the vertebral column, and multiple lesions may be
seen. Diskospondylitis occurs more commonly in thoracic
and lumbar spine than in cervical spine. The lumbosacral
disk space frequently is involved. Clinical findings depend
on the location of the affected vertebra or vertebrae. The
most common clinical signs are weight loss, anorexia, depression, fever, reluctance to run or jump, and apparent
spinal pain (which may be severe). Hyperesthesia may be

4th European FECAVA SCIVAC Congress

present only over the site of the lesion or may be poorly localized, especially with involvement of multiple sites.
Diagnosis. Diagnosis may be difficult, as clinical signs
often are nonspecific. Diskospondylitis should always be
considered in an animal with fever of unknown origin. Clinical signs commonly are present for several weeks or months
before a diagnosis of diskospondylitis is made.
Neurologic deficits associated with spinal cord or cauda
equina compression may be present, and may reflect either a
transverse or a multifocal myelopathy. Neurologic deficits
associated with a transverse myelopathy (T3-L3) occur most
commonly and include paraparesis, decreased conscious
proprioception, exaggerated spinal reflexes, and much less
commonly, paraplegia. Cervical lesions most commonly
cause only apparent cervical pain, and lumbosacral lesions
may cause neurologic deficits due to compression of nerves
of the cauda equine.
Affected animals may have a normal or elevated peripheral white blood cell count. Typical radiographic findings are
destruction of the bony end-plates adjacent to an infected
disk, collapse of the intervertebral disk, and varying degrees
of new bone production. Early lesions may consist only of
lytic areas in affected vertebral endplates. More advanced lesions show a mixture of bone Iysis and extensive new bone
production, with osteophytes bridging adjacent vertebrae
containing a central destructive focus. Affected vertebral
bodies may be shortened, and bony proliferation may result
in fusion of one or more vertebrae. Dogs with paravertebral
grass seed migration may have radiographic abnormalities
suggestive of paravertebral abscess formation and periosteal
bone formation on the ventral aspect of vertebral bodies. This
occurs most frequently in the cranial lumbar region.
Collection of CSF is indicated in animals with neurologic deficits. Cerebrospinal fluid may be normal, or may have
an increased protein content in cases in which
diskospondylitis lesions cause extradural compression of
spinal cord or result in meningitis and/or myelitis. The CSF
white blood cell count may be normal, or may be elevated,
with an increase in PMN neutrophils in CSF from animals
with meningitis or myelltls.
Myelography is indicated in animals with neurologic
deficits indicative of spinal cord compression and is mandatory in cases in which decompressive surgery is considered.
Myelographic findings usually indicate extradural compression, which results from extension of granulation tissue and
bony proliferation within the spinal canal. Clinical signs do
not always correlate well with the degree of compression
seen on myelography, and depend on factors such as rate and
duration of compression as well as degree of compression.
Aerobic, anaerobic, and fungal cultures of blood and
urine should be done prior to treatment in an attempt to isolate causative organisms.
Surgical biopsy may be indicated in affected dogs in
which a causative organism is not isolated from blood or
urine, and/or animals that are unresponsive to treatment with
broadspectrum antibiotics.
Treatment. Treatment consists of long-term use of an antimicrobial that is effective against the causative organism(s)
determined by results of blood and/or urine cultures. If an
organism is not cultured, cats without severe neurologic

deficits may be treated empirically, assuming infection with


the most common organism isolated from animals with
diskospondylitis (coagulase-positive Staphylococcus sp).
Antibiotics that are most effective for this purpose are
cephalosporins, or (beta- lactamase resistant penicillins such
as oxacillin and cloxacillin. A trimethoprim/sulfonamide
combination or chloramphenicol is less effective but is less
expensive, and may be effective in some cases.
Clinical signs may recur if the infection is not completely eliminated prior to cessation of antibiotic therapy, and repeated cultures of blood and urine and ongoing treatment
with an appropriate antibiotic may be necessary. Treatment
is continued for at least 6 weeks, and vertebral radiographs
are done every 2 to 3 weeks to monitor progression/ regression of a lesion. Antibiotic administration may be necessary
for up to 6 months before radiographic evidence of resolution of lesions is seen. Obtaining radiographs to monitor response to therapy is important also to monitor for development of new lesions.
Clinical improvement in animals with diskospondylitis
(resolution of fever, improved appetite, reduction of apparent spinal pain) should be seen within 2 weeks of starting antibiotic therapy. If clinical improvement is not seen, treatment should be reevaluated. Antibiotic therapy should be reviewed, and surgical biopsy of a lesion may be considered.
Use of analgesics and restriction of exercise during the first
weeks of treatment may be helpful.
Prognosis for animals with diskospondylitis depends on
the ability to eliminate the causative organism(s) and on the
degree of neurologic dysfunction. Animals with severe neurologic deficits have a guarded to poor prognosis.

Feline infectious peritonitis (meningitis


and myelitis)
Etiology and Pathogenesis. Pyogranulomatous meningitis and myelitis may occur in cats with FIP. Feline infectious
peritonitis results from a coronavirus infection and is most
commonly seen in younger cats between 6 months and 5
years of age. Infected cats may also have concurrent FeLV
infection. Meningeal and spinal cord lesions are probably
the result of immune complex-mediated vasculitis. Involvement of the CNS is more frequently observed in the noneffusive (dry) form than in the effusive (wet) form of FIP.
Multifocal and diffuse involvement of the CNS is common,
and a consistent clinical course is not associated with FIP.
Clinical Findings. Feline infectious peritonitis may result
in focal, multifocal, or diffuse involvement of the spinal cord,
brain, and meninges, and clinical signs reflect the location of
these lesions. Leptomeningitis with infiltration of spinal
nerve roots has also been reported. The most commonly recognized neurologic signs are pelvic limb ataxia, hyperesthesia (especially over the back), and generalized ataxia.
Affected animals usually manifest other clinical signs indicative of disseminated disease such as persistent fever
(frequently greater than 105 F), weight loss, enlarged kidneys, chorioretinitis, panophthalmitis, or anterior uveitis.
Diagnosis. Diagnosis is made on the basis of clinical
signs, clinical pathology (blood, CSF), and serology. Hema-

65

tologic changes include neutrophilia, Iymphopenia, and elevated serum fibrinogen and gamma globulins. Cerebrospinal
fluid usually is abnormal with an elevated white blood cell
count and protein level. The differential CSF white blood
cell count is variable but PMN cells, Iymphocytes, and
monocytes usually are present. Polymorphonuclear cells
may be the predominant cell type in CSF. Protein concentration may be very high (greater than 2000 mg/dl), and CSF
may be viscous and may clot. This should be taken into consideration when a CSF puncture is performed, as fluid may
flow into the needle very slowly.
Results of cytologic examination of CSF depend on the
degree of meningeal involvement. Meningeal inflammation
may be extensive, and CSF in these cases is generally highly abnormal. In the presence of focal or parenchymal inflammation, CSF may be normal.
Cats with FIP generally have a high antibody titer. Presence of a positive antibody titer is not diagnostic of FIP, but
in the presence of clinical signs, hypergammaglobulinemia
and abnormal CSF findings consistent with FIP, a positive
antibody titer is highly suggestive of FIP infection. Similarly, a low antibody titer does not rule out FIP. The differential
diagnosis list for CNS FIP includes toxoplasmosis, cryptococcosis, and lymphosarcoma.
Treatment. Prognosis for cats with FIP of the CNS is
poor. The FeLV status of cats suspected to have FIP should
be determined prior to commencing treatment, as the prognosis for cats with both viruses is hopeless. The most effective treatment protocols combine high levels of corticosteroids (prednisolone, I to 2 mg/lb orally once daily in the
evening), cytotoxic drugs (either cyclophosphamide, 1 mg/lb
orally once daily for 4 consecutive days of each week, or
melphalan, 1 mg orally every third day) and broad-spectrum
antibiotics (ampicillin, 10 mg/lb orally q8h), together with
maintenance of nutrient intake and electrolyte balance. Cats
receiving cytotoxic drugs should be routinely monitored for
evidence of kidney dysfunction or bone marrow suppression.
If a positive response to therapy is seen, treatment should be
continued for at least 3 months. Cats with neurologic disease
associated with FIP usually respond poorly to treatment.

Feline polioencephalomyelitis (feline


non-suppurative meningencephalomyelitis)
Etiology and Pathogenesis. Feline polioencephalomyelitis is a chronic, slowly progressive encephalomyelitis of unknown etiology described in immature
and mature cats. Histopathologically, the disease is characterized by neuronal degeneration and perivascular cuffing by
mononuclear cells. Demyelination and axonal loss are most
conspicuous in the ventral and lateral columns of the spinal
cord and most severe in the thoracic spinal cord segments.
Lymphocytic meningitis, neuronophagia, and glial nodules
also have been described, and lesions may be found in the
cerebral cortex, diencephalon, midbrain, and medullary nuclei.
The pathogenesis of the disease is unknown. A viral etiology is suspected on the basis of the histopathologic changes,
although a specific viral agent has not been isolated The

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chronic clinical course, distribution of lesions, and lack of inclusions distinguish this disease from rabies, pseudorabies,
and FIP. Feline panleukopenia virus, FeLV, and arboviruses
have been suggested as possible agents in the pathogenesis of
lesions. Further virologic and serologic tests are needed to determine the role of viral infection in the pathogenesis of this
disorder. It has been proposed in a recent study that a tickborne virus may be the causative agent in Sweden.
Clinical Findings. Clinical signs include ataxia, paraparesis, tetraparesis, hypermetria, head tremors, and localized hyperesthesia. Spinal reflexes, pupillary light reflexes,
and postural reactions may be normal or depressed. Two animals have been described as having episodes of hallucinations, clawing, hissing, and biting at imaginary objects during sleep. These seizures preceded other clinical signs by
more than 2 years in one cat. Clinical signs usually are indicative of multifocal CNS disease but may be suggestive of
focal transverse myelopathy in the thoracolumbar region or
lumbar enlargement. Clinical signs are slowly progressive
over several months.
Diagnosis. Antemortem diagnosis is difficult and is
made by ruling out other multifocal CNS diseases. Two affected cats have been reported to be leukopenic, and one affected cat had an elevated CSF protein concentration (40
Treatment. Treatment of affected cats has not been reported.

Hypervitaminosis A of cats
Etiology and Pathogenesis. Hypervitaminosis A in cats
is characterized by extensive confluent exostosis that is most
prominent in the cervical and thoracic spine. It is caused by
a chronic excess of dietary vitamin A and is usually a result
of feeding a diet consisting largely of liver. Exostosis may
extend to involve the entire spine, ribs, and pelvic and thoracic limbs with complete fusion of the spine and joints.
Compression of spinal nerve roots or nerves may occur if
new bone formation extends into intervertebral foramina.
Clinical Findings. Clinical signs in affected cats include
apparent cervical pain and rigidity, thoracic limb lameness,
ataxia, reluctance to move, paralysis, and hyperesthesia or
anesthesia of the skin of the neck and forelimbs. The three
most proximal diarthrodial joints of the cervical spine are
almost always first affected. Osseous lesions develop insidiously, and clinical disease usually is advanced in cats older
than 2 years of age before significant clinical features are
recognized.
Diagnosis. Radiographic evidence of extensive exostosis
of the cervical vertebral column and a history of excessive dietary intake of vitamin A or liver are necessary for diagnosis.
Treatment. Reduction of dietary intake of vitamin A prevents the development of further exostosis, however it may
be difficult to persuade affected cats to eat anything other
than liver.

Intervertebral disk disease


Etiology and Pathogenesis. Degenerative disk disease

occurs in cats, although the incidence of clinical signs associated with disk protrusion is low compared to that in dogs.
Degenerative changes and distribution of disk protrusions
are similar to type II disk protrusions in nonchondrodystrophoid dogs. Clinical signs seen usually are indicative of a
slowly progressive transverse cervical or thoracolumbar
myelopathy. Type I disk extrusion associated with calcification of intervertebral disks and an acute onset of neurologic
deficits have been reported in cats. Diagnosis and treatment
are similar to that described for dogs.
Clinical Findings. Clinical signs seen with intervertebral
disk disease vary, depending on whether type I or type II
disk herniation is present, the location of the lesion, and
severity of the spinal cord lesion. Clinical signs seen in association with type I disk extrusion include apparent pain
and/or motor and/or sensory deficits.
Clinical signs associated with type II disk protrusion
generally are slowly progressive over a period of months,
but may develop acutely over days in some animals. Neurologic deficits usually are indicative of a cervical or thoracolumbar myelopathy. Paraparesis or tetraparesis, depending on the site of the lesion, is the most common clinical
finding, and deficits may be asymmetric. In the cervical
spine, type II protrusions most commonly occur in caudal
cervical disks. In some cases, caudal cervical type II disk
protrusion may be part of the spectrum of abnormalities associated with cervical spondylomyelopathy. Apparent neck
or back pain may or may not be a feature of type II disk protrusion.
Diagnosis. The differential diagnosis in animals with
type II disk protrusion includes other causes of progressive
transverse myelopathy, the most likely being neoplasia or
degenerative myelopathy. Spinal radiographs and, in almost
all cases, CSF analysis and myelography are necessary to
confirm a diagnosis of disk extrusion or protrusion. General
anesthesia is required to achieve the precise positioning
needed to obtain radiographs of diagnostic value. Foam
wedges or sandbags are usually needed to align the vertebral
column parallel to the table top for lateral projections. Care
must be taken, however, in anesthetizing and positioning animals that have acute type I disk extrusions, as further extrusion of disk material and further spinal cord compression
may occur with manipulation and movement of the spine.
Type II disk protrusion may be associated with narrowing of the disk space, osteophyte production, and end-plate
sclerosis. Calcification of disk material rarely is seen in association with type II disk protrusion. In some animals with
type I or type II disk herniation obvious abnormalities are
not seen on noncontrast vertebral radiographs.
Myelography is almost always necessary to confirm that
disk material has herniated into the spinal canal resulting in
spinal cord compression. Myelography is most important in
determining the site (or sites) of disk herniation and in lateralization of disk material within the spinal canal prior to surgical decompression. Myelography is necessary for diagnosis in most cases of type II disk protrusion in order to distinguish disk protrusion from other causes of slowly progressive transverse myelopathy, such as spinal neoplasia and degenerative myelopathy.
Cerebrospinal fluid should be collected and analyzed pri-

or to myelography to rule out inflammatory or infectious


disease of the spinal cord and/or meninges. Clinical signs in
animals with GME, distemper myelitis, FIP, spinal lymphoma, and other disorders may mimic those of cervical or
thoracolumbar disk disease. The characteristic myelographic findings in both type I and type II disk herniation into the
spinal canal are extradural compression of the spinal cord
with displacement of the spinal cord and narrowing of the
subarachnoid space on lateral and/or ventrodorsal views, depending on the location of the compressive mass. Type II,
and most type I, disk herniations result in a ventral or ventrolateral epidural mass that causes dorsal displacement of
the spinal cord.
Treatment. Type I Disk- Extrusion. The appropriate treatment for animals with type I disk extrusion depends on the
animals neurologic status. Each animal should be evaluated
individually. Medical treatment directed at decreasing spinal
cord edema may be appropriate for animals with apparent
pain only or animals that have mild neurologic deficits but
are ambulatory and have not had previous clinical signs associated with disk disease. These animals should be strictly
confined to a small area such as a hospital cage or a quiet
place away from other pets for at least 2 weeks. Very cautious use of analgesics or anti-inflammatory agents occasionally may be indicated; however, strict confinement followed by a period of restricted exercise is imperative.
Surgical decompression of the spinal cord and removal
of disk material from the spinal canal should be considered
in animals with neurologic deficits such as paresis or paralysis with deep pain perception intact. Surgical decompression should be done as soon as possible to prevent further
spinal cord damage incurred as a result of sustained compression or further extrusion of disk material. In addition, if
surgery is delayed 2 to 3 weeks, disk material hardens and
becomes adherent to dura mater, and becomes difficult or
impossible to remove from the spinal canal.
Regardless of whether medical or surgical treatment is
instituted, animals that are paretic or paralyzed require intensive nursing care. Neurologic improvement may take
weeks or months and this requires owner cooperation and
enthusiasm regarding care and physical therapy. Manual expression, intermittent catheterization, and /or indwelling
catheterization of the bladder are often required to ensure
emptying of the bladder. Weekly urinalysis, especially in animals that do not have voluntary control of micturition, is
important in monitoring for urinary tract infection. It is also
important to keep animals well padded, clean, and dry to
prevent formation of pressure sores, and to ensure that
caloric and water intake is adequate.
Type 11 Disk Protrusion. Treatment with corticosteroids
may result in neurologic improvement for variable periods
of time in animals with type II disk protrusion. However,
corticosteroid therapy is not curative. The reason for this improvement is not clear as intramedullary hemorrhage and
edema seen in cases of acute spinal cord injury are not a feature of chronic spinal cord compression.

Ischemic myelopathy due


to fibrocartilaginous embolism

67

Etiology and Pathogenesis. Fibrocartilaginous embolism


and ischemic myelopathy have been reported in a cat Ischemic myelopathy results from ischemic necrosis of spinal
cord gray and white matter associated with fibrocartilaginous emboli that occlude arteries and/or veins of the leptomeninges and spinal cord parenchyma. This disease is
characterized by an acute onset of neurologic deficits and is
generally nonprogressive after several hours.
The substance occluding spinal cord arteries and veins
has histologic and histochemical properties similar to fibrocartilage of intervertebral disks and is presumed to originate
from the nucleus pulposus of an intervertebral disk. Pathogenesis of the fibrocartilaginous embolism is not known.
Clinical Findings. Ischemic myelopathy is characterized by an acute onset of neurologic deficits that may be
severe. Clinical signs may progress over several hours but
are generally not progressive after 12 hours. Affected animals usually do not have a history or evidence of trauma
but may have a history of exercise prior to the onset of clinical signs. Apparent pain usually is not present at the time
of examination or during the course of the disease, although dogs are often reported to cry out at the onset of
clinical signs.
Diagnosis. Ischemic myelopathy should be suspected in
any cat with an acute onset of nonprogressive neurologic
deficits that are not associated with apparent spinal pain, especially if deficits are asymmetric or indicate that at least
several spinal cord segments are involved. A diagnosis is
made by ruling out other causes of myelopathy. Spinal radiographs are normal. Cerebrospinal fluid may be normal or
may have an elevated protein concentration as a result of
leakage of protein through damaged vascular endothelium.
The white blood cell count of CSF may be normal or may be
mildly increased in the early stages, probably as a result of
an inflammatory response triggered by spinal cord ischemia.
Xanthochromia may be present 48 hours or more after a subarachnoid hemorrhage. Appearance on a myelogram usually
is normal, although mild intramedullary swelling as a result
of spinal cord edema may be seen for as long as 24 hours after the onset of clinical signs .
Treatment. Corticosteroids (as recommended for spinal
trauma) may be given initially to reduce any secondary
spinal cord edema; however, after several days, edema usually is resolved. Good nursing care is essential in recumbent
animals to prevent pressure sores, urinary tract infections,
and contracture of denervated muscles. Prognosis depends
on the severity of an animals neurologic deficits. Animals
that retain pain perception in affected limbs and tail usually
regain neurologic function, although recovery may take several weeks to months and LMN signs may persist (muscle
atrophy and/or paresis). Animals with absent pain perception
for 24 hours are likely to have irreversible spinal cord damage and have a poor prognosis for return of function in affected limb or limbs. Many animals show improvement
within 2 weeks of onset of signs, unless extensive gray matter destruction has occurred.
Clinical improvement seen in the first 2 weeks may be
accounted for by resolution of edema and hemorrhage, and
establishment of collateral circulation to areas that were is-

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chemic but not necrotic. Later clinical improvement is


proably due to compensation by remaining spinal cord neurons.

Mucopolysaccharidosis
Etiology and Pathogenesis. The mucopolysaccharidoses
are a group of genetic diseases that result from defects in the
metabolism of glycosaminoglycans. Two subclasses have
been recognized in cats, and paraparesis associated with
spinal cord compression has been reported in Siamese cats
with mucopolysaccharidosis VI (MPS VI). Mucopolysaccharidosis VI is the result of a deficiency of the lysosomal
enzyme arylsulfatase B and, in addition to causing characteristic physical deformities, can result in skeletal changes,
including fusion of the cervical vertebrae, variable fusion of
thoracic and lumbar vertebrae, bony proliferation and bony
protrusion into the vertebral canal in the thoracic and lumbar
spine causing compression of the spinal cord, and bony proliferation in the intervertebral foramina causing nerve root
compression. Bony proliferative changes and associated
spinal cord compression occur prior to, or at the time of, epiphyseal closure (about 9 months of age) and are probably
nonprogressive after this time. Mucopolysaccharidosis VI is
an inherited abnormality and has an autosomal recessive
mode of inheritance.
Mucopolysaccharidosis I due to a deficiency in alpha-Liduronidase has been reported in a domestic shorthaired cat.
The clinical features were similar to MPS VI, but bony proliferative changes and associated spinal cord compression
were not found. Although vacuolar changes were observed
in neurons of brain and cervical spinal cord, presumably as
a result of storage of glycosaminoglycans, neurologic
deficits were not found clinically. Mucopolysaccharidosis I
probably has an autosomal recessive mode of inheritance.
Clinical Findings. The characteristic physical findings in
cases of MPS VI are small head, flat broad face, widely
spaced eyes, corneal clouding, small ears, depressed bridge
of the nose, large forepaws, and concave deformity of the
sternum. Affected kittens are smaller than normal littermates, and physical deformities are noticeable by 8 weeks of
age. Neurologic deficits due to skeletal changes and spinal
cord compression are seen between 4 and 7 months of age
and progress over 2 to 4 weeks. Neurologic findings are indicative of a transverse myelopathy between T3 and L3, and
include absent conscious proprioception, normal to exaggerated pelvic limb reflexes, and decreased pain perception in
the pelvic limbs. The thoracic limb gait may be normal or affected cats may have a crouching posture. Spinal reflexes in
the thoracic limbs are normal.
Diagnosis. Radiographs of the spine show vertebral fusion and bony protrusions into the spinal canal and intervertebral foramina of the thoracolumbar spine. However, bony
proliferation is not an indication of neurologic dysfunction.
Myelography is necessary to demonstrate spinal cord compression. Subarachnoid CSF puncture may be difficult due
to proliferative changes around the vertebrae. MPS VI can
be confirmed by measurement of arylsulfatase B activity in
leukocytes.

Treatment. As skeletal changes are nonprogressive after


about 9 months of age, decompressive surgery may result in
improvement in neurologic signs. However, spinal cord
compression may be present at more than one site. The underlying lysosomal enzyme deficit is not amenable to treatment at present. Bone marrow transplantation is being investigated as a possible therapy for MPS VI.

Neoplasia
Etiology and Pathogenesis. The spinal cord may be a site
of primary or metastatic neoplasia, or may be compressed or
invaded by primary or metastatic tumors arising from the
vertebrae and surrounding tissues. Primary neural tumors include astrocytoma, glioma, ependymoma, neuroepithelioma,
malignant nerve sheath neoplasm (schwannoma, neurofibroma, neurofibrosarcoma), meningioma, meningeal sarcoma,
and reticulum cell sarcoma.Tumors of spinal nerves that extend into the spinal canal or spinal nerve roots may cause extradural or intradural compression of the spinal cord. These
tumors may also invade the spinal cord parenchyma. Lymphosarcoma may also involve peripheral nerves and extend
along spinal nerves and nerve roots into the spinal canal, resulting in clinical signs of spinal cord disease.
Meningeal sarcomatosis is a rare condition characterized
by diffuse infiltration of the leptomeninges by neoplastic
mesenchymal cells. In one reported case in a dog, clinical
signs were lameness, reluctance to sit, apparent spinal pain,
seizures, and urinary incontinence.
The spinal cord may also be compressed by tumors originating from surrounding structures. Most commonly these
tumors arise from bone, cartilage, fibrous tissue, and blood
vessels of vertebrae, and less commonly from the hemopoietic elements of bone and tissue outside the vertebral column
including muscle, fat, and paraganglia. Secondary tumors
result from hematogenous or Iymphatic spread of tumor emboli and include hemangiosarcoma, lymphosarcoma, mammary adenocarcinoma, pulmonary carcinoma, prostatic carcinoma, and malignant melanoma.
Epidural Iymphosarcoma is the most commonly occurring spinal tumor in cats. Primary intramedullary tumors
rarely occur in cats. Etiology of vertebral and spinal cord tumors is unknown. Lymphosarcoma in cats may be associated with FeLV or FIV infection; however, not all cats with
spinal Iymphosarcoma test positive for FeLV or FIV.
Clinical Findings. Clinical signs depend on the location
of the tumor. Tumors may involve more than one spinal cord
segment and more than one spinal tumor may be present, resulting in multifocal signs. However, most animals present
with clinical signs referable to a transverse myelopathy. Tumors may occur anywhere within the spinal cord or spinal
canal and usually result in progressive neurologic deficits.
The duration of clinical signs may vary considerably (from
one week to one year in one study). Animals may present
with the following signs: an acute onset of severe neurologic deficits associated with pathologic fracture of a vertebra,
resulting in spinal cord compression; epidural, subarachnoid, or intramedullary hemorrhage; or spinal cord ischemia
associated with tumor expansion. Neurologic deficits are

usually bilateral but may be asymmetric.


Tumors of nerves of the brachial plexus initially cause
progressive LMN signs in the ipsilateral thoracic limb, including muscle atrophy and paresis. The affected limb is often painful on palpation or movement; cutaneous sensation
generally remains intact. If the tumor extends into the spinal
canal, UMN signs to the pelvic limbs may become apparent.
Tumors of the nerves of the cauda equine or lumbosacral
plexus, with extension into the spinal canal, may cause unilateral or bilateral LMN signs in the pelvic limbs, tail, perineum, urinary bladder, and anal sphincter.
Apparent pain is a common finding associated with extradural and intradural tumors. Apparent pain may be intractable, especially in animals with a tumor affecting spinal
nerve roots. This may be due to stretching or inflammation
of the meninges surrounding the expanding tumor. In general, however, extradural, intraduralextramedullary, and intramedullary tumors cannot be distinguished on the basis of
clinical findings.
Diagnosis. A tentative diagnosis of spinal tumor can be
made on the basis of radiographic, CSF, and myelographic
findings. Definitive diagnosis can only be made after biopsy
of a suspected lesion.
Radiography. Bone lysis with a cortical break is the most
common radiographic finding in animals with vertebral tumors. Other radiographic findings include destruction of
vertebral end-plates, collapse of an adjacent disk space, collapse and shortening of a vertebral body, pathologic fracture,
bone sclerosis and bony production, cystlike expansile lesions, or adjacent soft tissue masses.
Vertebral lesions may also occur with spread of tumors
from surrounding soft tissues into the vertebrae. Bone tumors are not always easily detected by means of radiography, owing to inconsistent vertebral shape, overlying rib and
soft tissue shadows, and improper patient positioning. Other
diseases, such as bacterial or fungal diskospondylitis,
spondylitis, or vertebral osteomyelitis, must be considered in
the differential diagnosis of vertebral tumors.
Expanding tumors within the spinal canal may result in
widening of the vertebral canal and loss of bone density due
to ischemia and necrosis of overlying bone. Similarly, tumors of spinal nerves extending into the spinal canal may
cause widening of intervertebral foramina.
Cerebrospinal fluid analysis. Cerebrospinal fluid may be
normal or may have an increased protein concentration
and/or white blood cell count. A mild to moderate increase
in CSF white blood cell count may occur in animals with tumors arising from or invading the leptomeninges. Polymorphonuclear cells may predominate, probably as a result of
meningeal inflammation and necrosis. Tumor cells rarely are
found in CSF, except in CSF from animals with lymphosarcoma, in which abnormal lymphocytes are often present in
association with meningeal infiltration. Collection of CSF
from the lumbar subarachnoid space may yield more cells
than cisternal collection, owing to probable caudal flow of
CSF in animals. Inability to demonstrate tumor cells in CSF
may be the result of the methods used to analyze CSF. The
use of cell concentrating techniques that yield a greater percentage of cells present in CSF may result in the preservation of more neoplastic cells. Xanthochromia, suggesting

69

previous subarachnoid hemorrhage, occasionally is present.


Cerebrospinal fluid protein concentration may be increased
due to abnormal permeability of blood-spinal cord or bloodmeningeal barrier, as a result of extradural compression or
meningeal or parenchymal tumor infiltration.
Myelography. Myelography may be helpful in differentiating intramedullary, intradural-extramedullary, and extradural tumors. Cisternal and lumbar injection of contrast
material may be necessary to outline both the cranial and
caudal extent of a tumor. It is important to obtain survey radiographs of the entire vertebral column prior to and after injection of contrast, as more than one tumor may be present
and the neurologic deficits of one tumor may mask those
produced by another. Several radiographic views (at least
lateral and ventrodorsal) are necessary to determine whether
a tumor is intramedullary, intradural-extramedullary, or extradural. Tumors may have a mixed myelographic appearance, with extradural, intradural, and/or intramedullary components (e.g., nerve root tumors, meningioma, and spinal
cord blastoma).
Other Diagnostic Tests. As many spinal tumors are secondary tumors and primary vertebral tumors commonly
metastasize, careful attention should be directed toward
eliminating the presence of other tumors by performing a
thorough physical examination, survey thoracic and abdominal radiographic examinations, rectal examination, complete blood count, and other diagnostic tests as necessary.
For example, animals with Iymphosarcoma may show abnormal circulating lymphocytes and/or hypercalcemia, and
animals with plasma cell myeloma may show aplastic anemia, myelophthisis, hypercalcemia, elevated serum protein,
monoclonal gammopathy on serum electrophoresis, and/or
Bence Jones proteinuria.
Both CT and MRI aid in exact determination of location
and extent of spinal tumors. Use of these advanced imaging
modalities aids in precise surgical planning and radiation
therapy planning.
Biopsy. Biopsy of suspected lesions is necessary to differentiate neoplasms from other vertebral and spinal cord
abnormalities and to determine histologic type. An open
surgical technique is most often used to obtain an adequate
specimen of most spinal tumors; however, in the future, fluoroscopy- or CT-guided needle biopsy techniques will become available for use in dogs and cats.
Treatment. The majority of vertebral tumors are not surgically resectable, owing to the malignant characteristics of
the tumor and the decreased stability of the vertebral column
that may result from extensive surgery. Surgical decompression of the spinal cord and debulking of tumor mass may be
palliative in some cases. Some tumors within the spinal
canal are surgically resectable, including some tumors that
appear intramedullary on myelography, such as spinal cord
blastoma.
There is not a direct relationship between tumor size and
rate of progression or severity of clinical signs. The spinal
cord is able to compensate for pressure applied gradually,
and animals with spinal tumors may remain ambulatory despite having little normal spinal cord tissue remaining. Compression applied to the spinal cord rapidly, such as may occur with a pathologic fracture, may cause severe and irre-

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versible spinal cord damage.


Corticosteroids may decrease spinal cord edema associated with spinal cord tumors and result in clinical improvement for a variable period of time. Radiation therapy and
chemotherapy may be helpful in animals with spinal lymphosarcoma. Most chemotherapeutic agents do not cross the
blood-spinal cord or blood-CSF barrier in concentrations to
eliminate tumor cells in the meninges or spinal cord. Several chemotherapeutic agents, including methotrexate and cytosine arabinoside, may be given intrathecally and have been
used in the treatment of meningeal lymphosarcoma and
leukemic meningitis. Complications of intrathecal use of
chemotherapeutic agents include arachnoiditis and seizures.
Chemotherapy may be helpful in the treatment of plasma
cell myeloma.
Chemotherapy and radiotherapy have not been used in
the treatment of a sufficient number of primary spinal cord,
nerve root, and meningeal tumors to assess results; however, initial experience suggests that further use of radiation
therapy is warranted. Various chemotherapeutic regimens
have been used in the treatment of various bone tumors and
tumors that metastasize to bone, generally with poor results.
Chemotherapy regimens in the future may offer more hope
in the treatment of vertebral tumors. In general, the prognosis for animals with nonresectable spinal tumors is poor.

Osteochondromatosis
(multiple cartilaginous exostoses)
Etiology and Pathogenesis. A skeletal osteochondroma
is a cartilage-capped exostosis arising from the surface of a
bone formed by endochondral ossification. An animal with a
monostotic lesion has a solitary osteochondroma. Polystotic
skeletal involvement is called osteochondromatosis (synonyms: multiple cartilaginous exostoses, hereditary multiple
exostoses , multiple osteochondromatosis , diaphyseal aclasis, dyschondroplasia, and hereditary deforming chondrodysplasia). There are consistent differences between cats
and dogs regarding age of onset of lesions, patterns of skeletal involvement, and pathogenesis.
The incidence of feline osteochondromatosis is unknown. Feline osteochondromatosis is characterized by an
initial appearance of lesions in the skeleton of mature cats (2
to 4 years of age). Growth of the lesions is progressive. The
disease has no apparent sex or breed predilection in cats, and
a hereditary pattern has not been demonstrated in cats. Malignant transformation to osteosarcoma has been reported to
occur in an osteochondroma of a cervical vertebra in a cat.
The incidence of osteochondromatosis in dogs remains
undetermined. The disease is frequently demonstrated in the
skeleton of dogs radiographed for unrelated reasons. Onset
of clinical disease is usually in dogs less than 18 months of
age. Onset in mature dogs is infrequently recognized. A
hereditary basis has been indicated in dogs, although a sex
or breed predilection is not apparent. Continued growth or
reactivation of growth of exostoses in dogs is suggestive of
neoplastic transformation.
The etiology of canine osteochondromatosis is unknown.
The current view regarding pathogenesis of feline osteo-

4th European FECAVA SCIVAC Congress

chondromatosis is that the disease is virus-related, and probably virus-induced. The random distribution of lesions is
compatible with a hematogenous distribution of a virus. The
virus may be FeLV, feline fibrosarcoma virus acting in an
atypical manner, or another member of the feline retrovirus
family.
Clinical Findings. Osteochondromatosis may occur anywhere in the vertebral column but most commonly is found
in the thoracic and lumbar spine. The disease may result in
spinal cord compression and clinical signs indicative of a
progressive transverse myelopathy between T3 and L3.
Neurologic deficits are often asymmetric.
Diagnosis. Radiographically, vertebral lesions tend to be
circular and smooth, with sclerotic borders. Lesions are usually multiple and may be cystic or proliferative, with an increased radiodensity. Myelography is necessary to demonstrate associated spinal cord compression. Extension of exostoses into the spinal canal results in extradural compression of the spinal cord. Surgical biopsy is necessary to differentiate osteochondromatosis from benign bone tumors
(osteomas), neoplastic lesions, or infectious processes.
Treatment. Treatment of canine osteochondromatosis affecting the vertebral column is unnecessary unless a lesion
results in clinical sequelae. An osteochondroma should be
removed if it impinges on spinal cord, or if malignant transformation is suspected. Surgical excision of cartilaginous
exostoses and spinal cord decompression are the recommended treatments for lesions causing spinal cord compression and neurologic deficits. Intraoperative spinal stabilization may be indicated following lesion removal. The prognosis for dogs that have stopped growing is good; however,
the prognosis for animals that are still growing is guarded, as
lesions may continue to expand and subsequently result in
spinal cord compression.
Treatment of feline osteochondromatosis is complicated
by the association with FeLV and the progressive nature of
lesions in cats. It seems that at best the surgical removal of a
lesion may provide only temporary relief to a cat, because of
the tendency for excised lesions to recur and for new lesions
to develop.

Protozoal myelitis
Etiology and Pathogenesis. Toxoplasma gondii infection
may cause a focal or disseminated myelopathy in cats. Animals are infected after ingesting meat containing toxoplasma
bradyzoites and/or tachyzoites, after ingesting cat feces containing sporulated oocysts, or by transplacental or congenital infection. The infective organism is spread hematogenously to most organs of the body, including the CNS. The
incidence of disease associated with Toxoplasma gondii is
thought to be low; however, opportunistic infection in immunosuppressed animals may be more widespread than previously reported. Immaturity and concurrent CD virus infection may result in an increased susceptibility of dogs to toxoplasmosis. In dogs with systemic toxoplasmosis, the incidence of CNS involvement is high. In cats, concurrent infection with FeLV or FIV or administration of corticosteroids may predispose to the development of clinical signs

of toxoplasmosis through immunosuppression and reactivation of latent infection.


Pathologically, CNS toxoplasmosis lesions are characterized by diffuse perivascular cuffing, infiltration of tissues
by inflammatory cells (predominantly mononuclear cells),
hemorrhage, necrosis, edema, and neuronal degeneration.
Granulomatous reactions may be seen. Encysted or free
forms of Toxoplasma gondii may be present. Observed tissue reactions may occur as a result of cell rupture, immune
complex deposition, delayed hypersensitivity reaction, or
degeneration of toxoplasma cysts.
Clinical Findings. Affected animals usually have clinical
signs of progressive multifocal or disseminated CNS disease. Clinical signs indicating a focal transverse or diffuse
myelopathy only may be seen initially. Neurologic deficits
depend on site of involvement and may be UMN or LMN. If
lower motor neurons are involved, denervation may result in
severe muscle atrophy.
Animals with CNS toxoplasmosis may or may not have
other clinical signs indicative of systemic infection (fever,
Iymphadenopathy, pneumonia, apparent muscle pain, gastrointestinal tract disease, iritis, or chorioretinitis).
Diagnosis. Antemortem confirmation of CNS toxoplasmosis in dogs or cats is extremely difficult. Results of routine hematologic and biochemical tests may be abnormal in
cats or dogs with acute systemic toxoplasmosis; however,
such results reflect only the organ systems involved and are
not specific for toxoplasmosis. Cerebrospinal fluid may be
normal, or may have an elevated white blood cell count with
a mixed mononuclear pleocytosis, and an elevated protein
concentration. Xanthochromia may be present if subarachnoid hemorrhage has occurred. Radiography of the thorax or
abdomen of animals with acute disease may demonstrate effusion, pneumonia, or abdominal masses.
Toxoplasma organisms may be identified in cytologic
preparations of thoracic or peritoneal effusions, or in biopsies of Iymph node or muscle examined by conventional
histopathologic techniques, or by other methods such as immunoperoxidase staining. It is difficult, however, to be certain of the association between clinical disease and demonstration of organisms.
Numerous serologic tests have been used in the diagnosis of toxoplasmosis. Serologic testing for antibody (immunoglobulin G or IgG) is of limited use for determining active infection, unless paired titers done 2 to 3 weeks apart
demonstrate a fourfold increase. Certainly, a negative titer
does not rule out a diagnosis of toxoplasmosis. Currently it
is recommended that for serologic diagnosis of toxoplasmosis in dogs or cats a single serum sample should be submitted for immunoglobulins G and M (IgG and IgM) determinations, and for calculation of levels of circulating antigen to
Toxoplasma gondii. Further, in cats suspected of having toxoplasmosis, both FeLV and FIV titers should be determined.
Fecal examination for oocysts is the most practical
method for determining the public health risk of a cat suspected to have toxoplasmosis. Oocysts are shed in feces of infected cats for only a short time (5 days to 2 weeks postinfection).
Treatment. Several antibacterial agents have been recommended for treatment of toxoplasmosis and neosporosis in

71

dogs and cats. Available drugs are effective in CNS tissues


only against actively proliferating forms of the organism, and
are not active against encysted forms, which are dependent
on host humoral and cell-mediated immune responses for
eradication. Clindamycin is currently recommended for treatment of systemic infection of dogs or cats. Oral therapy at a
total daily dosage of 12 mg/lb (25 mg/kg) divided ql2h appears effective in cats, whereas a daily dose of 5 to 18 mg/lb
(10 to 40 mg/kg) divided q6h or q8h should be effective in
dogs. Therapy should be continued for 2 to 4 weeks. The effectiveness of clindamycin in penetrating CNS tissues of
dogs or cats has not been determined, and it is therefore recommended that sulfadiazine or triple-sulfas be given orally at
a daily dosage of 50 mg/lb divided ql2h for CNS toxoplasmosis. Addition of pyrimethamine at a daily dosage of 0.25
to 0.5 mg/lb permits reduction of the sulfadiazine dosage by
half. Hematologic monitoring for bone marrow suppression
is essential for cats placed on this therapeutic regimen.
The public health risk posed by a cat with active Toxoplasma gondii infection must be considered prior to and during treatment for toxoplasmosis.

Sacrocaudal dysgenesis in manx cats


Etiology and Pathogenesis. Manx cats have varying degrees of taillessness associated with sacral and/or caudal
vertebral deformities. Some tailless cats have a normal
sacrum, spinal cord, and cauda equina. Others show varying
dysgenesis or agenesis of the sacral and/or caudal vertebrae
that may be associated with spine bifida and/or malformations of the terminal spinal cord and/or cauda equina. Spinal
cord malformations include absence or partial development
of sacral and caudal spinal cord segments or cauda equina,
myelodysplasia, meningocele, meningomyelocele, diastematomyelia of sacral segments (duplication), myeloschisis
(cleft within the spinal cord), syringomyelia in the lumbar
and sacral spinal cord segments, shortening of the spinal
cord, and subcutaneous cyst formation. These spinal cord
and cauda equina malformations are associated with variable
neurologic deficits.
Sacrocaudal dysgenesis is inherited as an autosomal
dominant trait and may be lethal in some homozygote cats.
Sacrocaudal dysgenesis and associated malformations have
been recognized in most breeds of cats, many not of true
Manx breeding. Sacrocaudal agenesis in a Maltese kitten has
been reported.
Clinical Findings. Clinical signs are variable depending
on the degree of spinal cord and cauda equina malformation
and include paraparesis, paraplegia, megacolon, atonic bladder, absent anal and urinary bladder sphincter tone, absent
anal reflex, urinary and fecal incontinence, and perineal
analgesia. Affected cats often walk plantigrade in the pelvic
limbs with a bunny-hopping gait. Vertebral abnormalities
may be palpable in the lumbosacral region, and in some cats
a meningocele, congenital or the result of necrosis of the
overlying skin, may exit through the skin and drain CSF.
Clinical signs usually are evident soon after birth and
may remain static or may be progressive. Worsening of neurologic deficits may be due to progressive syringomyelia in

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the lumbar and sacral spinal cord.


Diagnosis. Diagnosis is made on the basis of clinical
findings and radiographic findings indicative of dysgenesis
or agenesis of the sacral and caudal vertebrae. Myelography
may demonstrate meningocele or attachment of spinal cord
to subcutaneous tissues in the lumbosacral region. The degree of spinal deformity does not always correspond with the
degree of neurologic impairment. Clinical findings are the
most important factors to consider in determining prognosis.
Treatment. Prognosis for severely affected cats is hopeless and treatment is not available. Cats with urinary and fecal incontinence may be managed with manual bladder expression and fecal softening agents; however, recurrent urinary tract infection, megacolon, and chronic constipation are
common problems. Meningocele in cats with minimal neurologic deficits may be surgically correctable. Many tailless
cats do not have neurologic deficits, and sacral and caudal
deformities often are an incidental radiographic finding.

Spina bifida
Etiology and Pathgogenesis. Spina bifida is a term used
to describe a group of developmental defects characterized
by failure of fusion of the vertebral arches with or without
protrusion or dysplasia of the spinal cord, meninges, or
both. It has been described in cats. Malformations have
been variously named spine bifida occulta, cystica, manifesta and operta, depending on whether vertebral arch only,
vertebral arch and spinal cord, and/or meningeal abnormalities are present.
Anomalies of the vertebral arch and spinal cord are influenced by the development of the neural tube. Normally an
area of embryonic ectoderm thickens along the dorsal midline to form the neural plate. The neural plate subsequently
folds (forming the neural groove and then the neural tube
that separates from the ectoderm and develops into the
spinal cord) and is surrounded by the sclerotomic masses
that form the vertebrae.
Spina bifida is a midline cleft in one or more vertebral
arches. The cleft may consist of only nonfusion of the dorsal
spinous processes, or most of the vertebral arch of one or
several adjacent vertebrae may be absent. The spinal cord
and meninges may be normal (spine bifida occulta) or may
be abnormal and there may be protrusion of the meninges
and/or spinal cord through the vertebral defect. Spina bifida
may be caused by nonfusion of the two halves of the primordial vertebral arch due to failure of the neural tube to
close as the result of overgrowth of the cells of the neural
tube, or may be due to cleft formation in the neural tube after closure. It has been suggested that after formation of the
neural tube, clefts split its dorsal wall and a neuroschistic
bleb encroaches on the somites and prevents fusion of the
vertebral arches. If the neuroschistic bleb is retained, defects
of the spinal cord occur. Healing of the bleb may also occur
and result in spine bifida occulta (vertebral arch defect without concomitant spinal cord abnormalities).
Myelodysplasia consisting of hydromyelia, syringomyelia, anomalies of the dorsal septum, anomalies of
the central gray matter, abnormal position of the central gray

4th European FECAVA SCIVAC Congress

matter, anomalies of the dorsal and ventral horns, and


myeloschisis (cleft in the dorsal part of the spinal cord) may
occur in association with spine bifida. The most severe defects involve myelorachischisis, with superficial location of
the neuroectoderm that is continuous with the skin. Myelorachischisis may be due to failure of the formation of the
neural tube or rupture of the neuroschistic bleb after neural
tube closure. Spina bifida with myelorachischisis has been
reported to occur in dogs and cats.
Etiology of spine bifida is unknown and probably multifactorial with genetic and environmental components. Nutritional factors may have a role in the neural tube defects.
Spina bifida can be induced in the offspring of laboratory
animals by exposing pregnant females to a variety of chemical or environmental toxins.
Clinical Findings. Spina bifida is usually an incidental
radiographic finding; however, if associated with spinal cord
malformations, it may result in clinical signs of spinal cord
or cauda equina dysfunction. Large dorsal arch defects are
most often associated with spinal cord abnormalities. There
is a high incidence of spine bifida in English bulldogs. Spina
bifida may occur anywhere in the spinal column but occurs
most commonly in the caudal lumbar spine where clinical
signs are indicative of a transverse myelopathy from L4 to
S3 spinal cord segments (pelvic limb ataxia or paresis, complete paraplegia, fecal and urinary incontinence, decreased
or absent anal and urinary bladder sphincter tone, perineal
analgesia, and decreased spinal reflexes in the pelvic limbs).
Clinical signs usually become evident when affected animals start to walk.
Spina bifida also has been reported in the thoracic spine
of a dog and may be associated with other spinal deformities
such as scoliosis. Other associated anomalies include dimpling of the skin or streaming (abnormal direction) of the
haircoat over the affected region or a palpable abnormality
in the spinal column. Meningoceles may cause necrosis of
the overlying skin and drainage of CSF. Meningoceles may
be present in the absence of clinical signs associated with
spinal cord malformation.
Diagnosis. Absence of the vertebral arch or failure of fusion of the dorsal spinous processes in one or more vertebrae
may be evident on plain radiographs. Myelography may
demonstrate meningocele.
Treatment. Treatment is not effective for affected animals with clinical signs of spinal cord malformation.
Meningocele may be amenable to surgery if neurologic abnormalities are not evident. Treatment is not necessary for
animals with vertebral defects in the absence of spinal cord
dysfunction (spine bifida occulta).

Spinal cord trauma


Etiology and Pathogenesis. Acute spinal cord injuries of
dogs or cats result most commonly from direct physical trauma such as missile injury or vertebral fracture or luxation.
Also, spinal cord trauma is the underlying cause of neurologic signs in numerous myelopathies (e.g., intervertebral
disk protrusion or extrusion). Chronic spinal cord compression usually is seen in association with chronic progressive

diseases such as neoplasia or type II disk protrusion.


Following injury, the spinal cord may undergo sustained
compression, distraction, or both. The severity of a spinal
cord injury, as determined by the eventual degree and quality of recovery, is related to three factors: the velocity with
which the compressive force is applied, the degree of compression (transverse deformation), and the duration of the
compression. The relative roles of these factors in determining the severity of a spinal cord injury have yet to be determined.
An understanding of differences between acute and
chronic spinal cord injury is essential for effective management and determination of prognosis in cats or dogs with
spinal trauma. Extensive experimental work has been done
in order to elucidate the mechanisms involved in the production of lesions following spinal cord trauma, and results
of such research provide information that is essential for effective therapy of spinal injuries.
Acute Spinal Cord Injury. It has long been recognized
that blunt traumatic injury to the spinal cord causes neurologic deficits through both direct and indirect mechanisms.
The direct effects are due to immediate disruption of neural
pathways in spinal gray or white matter produced by the
trauma. These effects have also been termed immediate
effects and have been considered by most investigators not
to be amenable to therapy. Indirect effects develop during
the first few hours following injury, and result in delayed
secondary injury to the spinal cord. The mechanisms of this
secondary process remain largely undetermined, however, it
is likely that they result in part from release of endogenous
pathophysiologic factors in response to the initial trauma. It
has been hypothesized that such factors produce injury by
reducing spinal cord blood flow or by altering the local
metabolic environment within injured spinal cord tissue.
The secondary damage has been considered potentially reversible through the use of either physical (e.g., hypothermia) or pharmacologic interventions.
Trauma to the spinal cord triggers a progressive series of
autodestructive events that lead to varying degrees of tissue
necrosis, depending on the severity of the injury. Pathologic
changes that occur in traumatized spinal cord tissue include
petechial hemorrhages that progress to hemorrhagic necrosis, lipid peroxidation, lipid hydroxylation with subsequent
prostaglandin and leukotriene (eicosanoid) formation, loss
of calcium ions from the extracellular space and loss of
potassium ions from the intracellular space, ischemia with
consequent decline in tissue oxygen tension and energy
metabolites and development of lactic acidosis, and inflammation and neuronophagia by PMN leukocytes.
In spite of extensive investigation, the mechanisms responsible for the initiation and propagation of these pathophysiologic and biochemical events remain undetected. Recent evidence suggests, however, that the overall initiator of
this autodestructive cascade of events is mechanical deformation of any type (i.e., impact or compression injury), and
that the primary sites of injury are the cellular and subcellular membranes of glia, neurons, and vascular endothelial
cells. Lipid peroxidation and activation of membrane lipases, with release of fatty acids leading to production of
eicosanoids, are the earliest mechanically stimulated bio-

73

chemical events described at the present time.


The sequence of pathologic alterations that occurs following spinal cord injury has been reviewed by several authors.
Within 5 minutes of injury postcapillary venules become congested. This is followed by opening of endothelial gap junctions here and at the capillary level, resulting in diapedesis of
red blood cells and extravasation of fluid proteins and electrolytes through the leaky vasculature. Within 30 minutes
of injury, microscopic hemorrhages appear in the central gray
matter, and coalesce over the following several hours (central
hemorrhagic necrosis). Vacuolization develops within endothelial cells, indicating a profound ischemic or hypoxic insult, which subsequently leads to coagulative necrosis of the
neuronal population. Adjacent white matter is relatively less
severely affected; however, periaxonal swelling and retraction balls may be observed. These events may lead to autodissolution of the spinal cord within 24 hours, even in the
absence of ongoing mechanical compression.
A special feature of spinal cord injury is progressive hemorrhagic myelomalacia. This condition occurs following
spinal cord trauma and appears to be a progression of central
hemorrhagic necrosis and edema to areas of the spinal cord
not directly involved in the initiating injury.
Chronic Spinal Cord Compression. It has been shown
experimentally that when slow compression of the spinal
cord is compared to dynamic (or rapid) compression of an
equal amount, the extent of spinal cord dysfunction is determined by the contact velocity of compression. The major
pathologic substrate for neural dysfunction after slow balloon compression is thought to be physical injury to the
neural membranes, irrespective of blood flow changes, and
the ability of that membrane to recover appears to be related
to rapidity and duration of compression. Clinical observations support the conclusion that spinal cord conduction is
resistant to slow compression. Further, it has been demonstrated that levels of compression that do not have an effect
when applied slowly cause an immediate loss of conduction
through the injured site when applied rapidly.
Chronic spinal cord compression results either from a
slowly developing lesion (e.g., neoplasia), or from an acute
compression that is sustained. In contrast to acute spinal
cord injury, chronic compression affects white matter more
severely than it affects gray matter. Hemorrhage and edema,
the major findings of acute trauma, are not significant in
chronic compression. Characteristic lesions are degeneration
of myelin, focal areas of malacia, vacuolization, and loss of
white matter axons. Mechanical deformation is likely to be
the major factor in pathogenesis of these lesions; however,
ischemia and venous obstruction also may be important considerations.
Clinical Findings. Acute Spinal Cord Injury. Dogs or
cats with a spinal injury frequently have serious injuries to
other organ systems. A primary concern is to balance the relative urgency of non-neurologic injuries (hemorrhage,
shock, airway obstruction, or limb fractures) and the need
for early treatment of spinal cord injury.
A complete neurologic examination is done to localize
the site(s) of injury and to determine severity. Careful palpation of the vertebral column may aid in identification of a
vertebral fracture or luxation. Administration of tranquiliz-

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ers or analgesic drugs should be delayed until completion of


the neurologic examination, as such medications may alter
an animals responses. A neurologic examination should be
done with care to prevent further injury resulting from excessive movement of a vertebral instability.
Several aspects of the neurologic examination are of special importance in assessment of a dog or cat with a spinal
cord injury. Recognition of the Schiff-Sherrington sign is
important. Following trauma, this sign must be differentiated from other postures associated with cranial injury (e.g.
decerebrate rigidity or decerebellate posture). Both deep and
cutaneous pain perception should be assessed, as results of
these tests are important in determining prognosis. It should
be remembered that vertebral column injuries may be multiple, and that a neurologic examination may not indicate
presence of a second lesion.
Chronic Spinal Cord Compression. Clinical signs of
chronic spinal cord compression may progress over weeks
or months, or may be seen to occur acutely. Acute onset of
neurologic signs with chronic spinal cord compression frequently is seen in association with such disorders as spinal
neoplasia or type II disk protrusion. Sudden onset of signs
may accompany pathologic fracture of a vertebra, and
spinal cord hemorrhage or infarction. In some cases sudden
decompensation of chronically compressed spinal cord may
occur in the absence of pathologic changes. In these cases it
is assumed that compensatory mechanisms within the spinal
cord are exhausted, and that sudden decompensation has
occurred.
Diagnosis. Acute Spinal Cord Injury. Results of a neurologic examination are used to determine the site and severity of a spinal injury. Radiographs of the entire spinal column should be done. Two radiographic views are essential.
Ventrodorsal views may be accomplished by means of a horizontal beam. Evoked spinal cord potential testing may be of
use in determining location and severity of a spinal cord lesion in animals following trauma.
The objectives of radiographic examination of an animal
following acute spinal trauma are the following: precise determination of location and extent of a lesion, demonstration
of multiple lesions that may not be apparent on the basis of
a neurologic examination, and assessment of the need for
surgical therapy and determination of the most appropriate
surgical procedure to be used. Accurate interpretation of radiographs depends on a knowledge of results of a neurologic examination.
We recommend that a myelogram be completed in animals that have sustained spinal trauma. Results of a myelogram may determine the extent of spinal cord swelling resulting from concussion in animals without evidence of a
spinal fracture or luxation, and may confirm that surgical decompression by means of laminectomy is not necessary in
animals with a fracture that is evident on plain radiographs.
In the diagnosis of intervertebral disk disease a myelogram
is considered essential prior to surgery.
Chronic Spinal Cord Compression. Methods for diagnosis of chronic spinal cord compression are the same as for
acute spinal cord injury. A myelogram is considered essential in all such cases.
Treatment. Management of an animal with spinal trauma

4th European FECAVA SCIVAC Congress

follows a list of priorities, with the focus of treatment being


prevention of secondary spinal cord damage that occurs after the initial injury. Immediate treatment of nonneural injuries is limited to those problems that are life-threatening,
such as shock or hemorrhage.
Acute Spinal Cord Injury. Treatment of acute spinal
cord trauma should always be instituted as soon as possible
following injury. The specific objectives of therapy are the
following: relief of edema, control of intra- or extramedullary hemorrhage, relief of spinal cord compression,
and, in cases of vertebral fracture/luxation, removal of bone
fragments from the spinal canal and stabilization of the vertebral column. Treatment of acute spinal cord trauma may be
medical, surgical, or a combination of both.
Based on experimental findings in a large number of experimental models in animals, a variety of medical treatments have been advocated for the treatment of acute spinal
cord injury. Recently, interest has focused on the use of antioxidants and free radical scavengers. Unfortunately, the
role of these numerous therapies in the management of a dog
or cat with a spinal injury remains to be determined. The
large number of suggested therapies underlines the fact that
the mechanisms responsible for delayed secondary effects in
the injured spinal cord are incompletely understood.
Corticosteroids are routinely and widely used in the
treatment of acute spinal cord injury. Despite a positive clinical impression that corticosteroids have beneficial effects,
their use is controversial. Some studies have failed to
demonstrate significant improvement of neurologic recovery in association with corticosteroid administration. The
use of low or high doses of corticosteroids in the treatment
of spinal trauma also has yielded conflicting results.
Use of high doses of corticosteroids may result in complications leading to increased morbidity and mortality (e.g.,
gastrointestinal bleeding, pancreatitis, colonic perforation);
therefore, low-dose regimens are recommended. Dexamethasone sodium phosphate should be given at an initial
dosage of 0.25 to I mg/lb IV, and may be repeated at a dose
of 0.1 mg/lb q6h or q8h. Immediate post-trauma administration of methylprednisolone sodium succinate (60 mg/lb divided q8h) has been demonstrated to be effective in preserving feline spinal cord tissue following injury.
A decision regarding surgical therapy must be made as
soon as non-neural injuries have been treated and medical
management has been instituted. Ideally, this is within 2
hours of injury. Indications for surgery following spinal cord
injury are the following: moderate to severe paresis, or
paralysis, associated with myelographic evidence of spinal
cord compression; progressive worsening of neurologic
signs despite adequate medical therapy; and luxation or fracture of the vertebral column, in association with distraction,
malalignment, instability, or myelographic evidence of
spinal cord compression. Any animal with sustained compression of the spinal cord following injury, regardless of the
cause, must be considered a candidate for surgical decompression of the spinal cord. In general, it is best to initiate
surgical therapy in any animal in which there is uncertainty
regarding the indications for surgical versus medical therapy. Neurosurgical procedures require specialized knowledge
and equipment, and prompt referral to a qualified surgeon

may be indicated.
The major objectives of surgical management of spinal
trauma are decompression of sustained spinal cord compression and realignment and stabilization of vertebrae if necessary. Surgical decompression by means of laminectomy is
beneficial when there is myelographic evidence of extradural spinal cord compression. Laminectomy alone is not sufficient for decompression in most cases, and the compressing
mass (e.g., disk material, hematoma, bone fragments) should
be removed when possible. In cases in which spinal cord
swelling is the major source of compression, or in which
there is discoloration of the spinal cord, durotomy or myelotomy may be combined with laminectomy.
The most effective methods for alignment and stabilization of the vertebral column require surgical exposure and
can therefore be done at the time of decompression. Satisfactory methods of external fixation of spinal fractures do
not exist. Methods of surgical fixation have been reviewed
by several authors. Use of polymethyl methacrylate and
Steinmann pin fixation for the majority of spinal fractures or
luxations is favored by these authors. Surgical management
of spinal cord injury of animals provides the best opportunity for rapid and complete recovery in animals with sustained
compression or instability, and facilitates postinjury care, as
the risk of further injury resulting from movement of an unstable vertebral column is minimized. However, conservative management, including strict confinement for 4 to 6
weeks, may be efficacious in animals with minimal neurologic deficits and without myelographic evidence of sustained spinal cord compression or vertebral displacement or
instability.
Regardless of the type of stabilization used, strict confinement is recommended for 2 weeks after surgery. Potential complications encountered in dogs or cats with a spinal
injury include development of a urinary tract infection or
pressure sores. Careful attention to nursing care is essential
regardless of the type of therapy.
Prognosis for an animal with an acute spinal cord injury
depends on numerous factors; however, results of a neurologic examination should be the main determinant. Assessment of pain perception is essential for accurate prognosis.
Perception of a painful stimulus must be differentiated from
reflex activity that is mediated at the level of the spinal cord.
Owners of affected animals should be made aware at the
outset of therapy of factors such as prognosis, expense involved, expected time from treatment to recovery, and the
need for prolonged physical therapy in most cases. Following a severe spinal injury, an animal may require many
months to recover, and residual neurologic deficits may persist.
Chronic Spinal Cord Compression. The approach to
treatment of chronic spinal cord compression is different
from that for acute spinal cord injury. As previously stated,
hemorrhage and edema usually are not prominent factors in
chronic compression. Therefore medical management by
means of corticosteroids would not be expected to be efficacious; however, many animals with chronic spinal cord compression improve clinically following corticosteroid administration. The reason for such a response is undetermined;
however, it may be due to effects of corticosteroids at the

75

membrane level resulting in improved conduction in remaining axons. Occasionally, animals may be maintained
for months or years by means of corticosteroid therapy
alone.
Surgical decompression of the spinal cord should be approached with caution in animals with chronic spinal cord
compression. Pathologic alterations within the spinal cord
may be irreversible, in which case the most that may be
achieved is to arrest progression of neurologic deficits. In
some cases compensation for the irreplaceable loss of neural tissue may occur. Neurologic status may be worsened by
surgical decompression, even with meticulous surgical technique. Such deterioration may be the result of reactive hyperemia that follows decompression, which in turn results in
vascular protein leakage in the affected spinal cord segment.
However, surgical decompression should be considered in
most animals that have neurologic deficits associated with
chronic spinal cord compression.

Syryngomyelia and hydromyelia


Etiology and Pathogenesis. A distinction cannot be
made clinically between syringomyelia (cavitation of the
spinal cord) and hydromyelia (dilation of the central
canal). Syringomyelia may occur secondary to hydromyelia (communicating syringomyelia) or may not
communicate with the central canal (noncommunicating
syringomyelia). Syringomyelia may be associated with
spinal cord tumors, myelitis, meningitis, and spinal cord
trauma. The cause of syringomyelia is not known, but the
condition may result from venous obstruction or distention,
or may be due to mechanical disruption or shearing of
spinal cord tissue planes.
Hydromyelia with or without syringomyelia may be associated with congenital malformations such as myelodysplasia; meningomyelocele or hydrocephalus; or lesions resulting in obstruction of CSF flow into the spinal subarachnoid space at the foremen magnum such as chronic arachnoiditis, trauma, congenital malformations, and vascular
malformations; or it may be idiopathic. Hydromyelia and syringomyelia in these animals probably results from intracranial and spinal cord venous or arterial pressure changes and
associated CSF pressure changes.
Syringomyelia in Weimaraner dogs with myelodysplasia may be the result of progressive hydromyelia, abnormalities in the central canal, or abnormal vascular patterns
in local areas of the spinal cord leading to low-grade ischemia, degeneration, rarefaction, and cavitation in the
spinal cord.
Regardless of the cause, cavitation can be progressive,
probably along planes of structural weakness such as the
gray matter of the dorsal horns, and subsequent necrosis and
edema of spinal cord parenchyma around such a cavitation
(or dilated central canal) can result in the onset and progression of clinical signs.
Clinical Findings. Clinical signs depend on the location
of the lesion and whether or not other spinal cord lesions are
present. Clinical findings include progressive spinal deformity (scoliosis, torticollis), LMN or UMN signs, depending

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on location, and apparent spinal pain. Clinical signs may be


acute or may be progressive over weeks to several years. In
Weimaraner dogs with myelodysplasia, clinical signs do not
appear to be progressive.
Diagnosis. Myelography may show obstruction of the
flow of CSF at the foremen magnum if hydromyelia or syringomyelia is due to chronic arachnoiditis or arachnoid adhesions. Cisternal puncture for the collection of CSF is contraindicated in these animals owing to likely inadvertent
puncture of the spinal cord. Lumbar CSF may show evidence
of chronic inflammation. Myelography in other cases may be
normal or may show intramedullary swelling of the spinal
cord. Computed tomography of the spinal cord may be useful in the diagnosis of cavitary lesions of the spinal cord.
Treatment. Treatment in dogs has not been reported. Surgical drainage of cavitary lesions in humans has resulted in
improvement in some cases.

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77

EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline neuromuscular disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
Neuromuscular diseases are generally classified according to the disease location, that is disease involving 1) peripheral nerves, 2) neuromuscular junctions, or 3) muscle.
Feline neuromuscular diseases produce signs of lower motor neuron disease, however significant variation in clinical
signs may occur depending on the location of the lesion. Hyporeflexia, hypotonia, ataxia, and proprioceptive positioning deficits are most characteristic of feline peripheral nerve
disease. Some primary muscle diseases may be characterized by muscle hypertrophy rather than atrophy, and neuromuscular junction disorders result in a variety of clinical
signs, that range from flaccid paralysis to exercise-induced
weakness. Diagnosis of feline neuromuscular diseases requires a complete neurological examination, minimum data
base, electrophysiological evaluation, and muscle/nerve
biopsies.

INTRODUCTION
Feline neuromuscular diseases may be classified according to their location as (1) those involving peripheral nerves
and/or nerve roots, (2) those involving the neuromuscular
junction, and (3) those that involve muscle. Each of these
neuromuscular diseases will produce lower motor neuron
(LMN) disease, however significant variation in clinical
signs may occur. Peripheral nerve and muscle diseases result
in varying degrees of paresis, muscle atrophy, hyporeflexia,
and hypotonia. Hyporeflexia, hypotonia, ataxia and proprioceptive positioning deficits are most characteristic of peripheral nerve disease. Some primary muscle disorders may
be characterised by muscle hypertrophy rather than atrophy.
Neuromuscular junction disorders (junctionopathies) result in a variety of clinical signs, that range from flaccid
paralysis to exercise-induced weakness.
Cervical ventroflexion is a dramatic sign of generalised
neuromuscular weakness in cats.The chin usually rests near
the thoracic inlet, with the eyes positioned dorsally to maintain a straight-ahead gaze. Other common physical examination findings are a slight protrusion of the dorsal aspects
of the scapulae when weight is placed on thoracic limbs, and
a stiff thoracic limb gait. A crouched, wide-based stance is
often seen in pelvic limbs. Possible causes to consider for
this posture are: subacute or chronic organophosphate toxic-

ity, potassium-depletion myopathy, thiamine-responsive


neuromuscular weakness, hyperthyroidism, immune-mediated (idiopathic) polymyositis, myasthenia gravis, polyneuropathy, hypernatraemic polymyopathy, ammonium chloride toxicity, hereditary myopathies (Burmese, Devon rex),
hypocalcaemia, and portosystemic encephalopathy.
Megaoesophagus has rarely been reported in cats, although a predisposition has been noted in Siamese and
Siamese-related breeds. In most cats the cause of acquired
megaoesophagus is unknown; however, the condition has
been associated with several systemic neuromuscular disorders, such as myasthenia gravis, botulism, polymyositis,
polyradiculoneuritis, tick paralysis, lead toxicosis, feline
muscular
dystrophy-like
conditions,
laryngeal
paralysis/polyneuropathy complex, and glycogen storage
diseases.
Diagnosis of feline neuromuscular diseases requires a
complete neurological examination, minimum data base
(full blood count, serum biochemistry panel, urinalysis, thoracic radiographs), electrophysiological evaluation, and
muscle/nerve biopsies.

NEURONOPATHIES
Feline Dysautonomia
Feline dysautonomia (Key-Gaskell syndrome) is a generalised disorder of autonomic ganglia recognised in cats in
the United Kingdom in 1981, and more recently in other
countries. There is no age or breed predilection for this disease. The disorder is a neuronal disorder; however, clinical
signs relate more to autonomic dysfunction, and are largely
gastrointestinal in nature. The most common signs are depression, anorexia, constipation, dry external nares and oral
mucosa, reduced tear production, regurgitation, protrusion
of the membrana nictitans, mydriasis, and bradycardia.
These signs usually occur acutely, but may progress insidiously over a week or more.

Tetanus
Although cats are supposedly resistant to the effects of
the Clostridium tetani exotoxin, several cases of tetanus have
been reported in this species. The toxin interferes with re-

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lease of neurotransmitters from inhibitory interneurons in the


spinal cord. Local tetanus has been reported in cats, where
the disease is characterised by tonic rigidity of a single limb.

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first noted in cats at 8-10 weeks of age. Affected cats fell frequently and had a tendency to stand and walk on their hocks,
which they held in an adducted position. The gait was characterised by a slight hypermetria in all limbs and there was
progressive pelvic limb ataxia.

INHERITED POLYNEUROPATHIES
Sphingomyelinase-deficiency polyneuropathy

ACQUIRED POLYNEUROPATHIES

Niemann-Pick disease (NPD) is an autosomal-recessive


lysosomal-storage disease characterised by a deficiency of
sphingomyelinase. A NPD-associated primary polyneuropathy has been described in 3 Siamese cats (25 months of
age). Neurological signs included a progressive tetraparesis
and ataxia, a plantigrade/palmigrade stance, fine generalised tremors, and hypo- or areflexia. Hepatosplenomegaly
was also present in affected cats. This disease is progressive
and fatal.

Diabetic polyneuropathy
A distal polyneuropathy has been reported in cats with uncontrolled or poorly controlled diabetes mellitus. Neurological abnormalities include a plantigrade stance, progressive
paraparesis, muscle atrophy, and patellar hyporeflexia. The
cause of this polyneuropathy is incompletely understood.

Ischemic neuromyopathy
Hyperchylomicronemia-associated
neuropathy
Inherited primary hyperchylomicronemia is a suspected
autosomal-recessive disease characterised by fasting hyperlipemia, lipemia retinalis, and peripheral neuropathy. Clinical signs are usually not seen prior to 8 months of age. Compression by lipid granulomas of peripheral, cranial, and sympathetic nerves, especially at the level of the intervertebral
foramina, results in neurological signs. Resolution of neurological signs and decrease in blood-lipid levels occurs following 2-3 months of dietary management.

Hyperoxaluric peripheral neuropathy


Primary hyperoxaluria is a suspected autosomal-recessive disease of domestic short-hair cats in Great Britain.
Acute renal failure, in cats between 5 and 9 months of age,
results from renal tubular deposition of oxalate crystals. Severe generalised LMN weakness accompanies the renal failure. Weakness is attributed to accumulation of neurofilaments in ventral nerve roots, proximal axons, and intramuscular nerves. All reported cats died before 12 months of age.
The pathogenesis of peripheral nerve lesions is unknown.

Hypertrophic polyneuropathy
Hypertrophic polyneuropathy has been described in 2
unrelated 12-month-old cats. Affected cats had intention
tremors, decreased postural reactions, hyporeflexia, and
mild sensory loss.

Birman cat distal polyneuropathy


A degenerative polyneuropathy has been reported in several litters of Birman cats bred from the same parents. A recessive mode of inheritance is suspected. Clinical signs were

Ischemic neuromyopathy occurs in cats with cardiomyopathy, subsequent to thrombosis of the caudal aorta or its
principal branches. The ischemic injury to both muscle and
peripheral nerve is produced by collateralcirculation vasoconstriction induced by substances such as serotonin and
thromboxane A2 released by platelets trapped in the
thrombus.

Trauma
Brachial plexus avulsion produced by severe thoracic
limb abduction with secondary stretching or tearing of nerve
roots is a commonly occurring peripheral nerve injury of
cats. Sacroiliac fracture/dislocation, sacral fracture, or caudal vertebral fracture/luxation may result in damage to the
sixth and seventh lumbar and first 2 sacral nerve roots.
Mononeuropathies of radial nerve and sciatic nerve occur in
cats following mechanical blows, gunshot wounds, fractures, pressure and stretching.

Neoplasia
Feline malignant lymphoma, often associated with
FeLV-infection, may involve nerve roots or peripheral
nerves. Other primary peripheral nerve neoplasms are rarely
seen in cats.

Toxic neuropathies
Drug-induced neuropathies are not well defined in dogs
and cats. It is likely that as chemotherapeutic treatment of
neoplasia becomes more aggressive, more drug-induced neuropathies will be recognised (e.g. vincristine). A delayed neurotoxicity may occur in cats days or weeks after minimal exposure to organophosphates. Lesions are associated with distal degeneration of motor nerves that begins in the periphery
(dying-back axonopathy). Peripheral neuropathy may occur

sporadically with spontaneous lead-poisoning. Megaesophagus and partial laryngeal paralysis, believed to be due to leadassociated neuropathy, have been reported in a cat.

79

The association of acquired myasthenia gravis and thymoma


in cats is a good example of a paraneoplastic junctionopathy.

INHERITED MYOPATHIES
Laryngeal paralysis
Muscular dystrophy
Acute laryngeal paralysis was diagnosed in 3 cats with
signs of upper airway obstruction, including dysphonia, absence of purring, and progressive inspiratory dyspnea. Varying degrees of paralysis of vocal folds and arytenoid cartilages were noted. One cat was positive for FeLV. Underlying responsible mechanisms were not defined.

Miscellaneous peripheral polyneuropathies


Single case reports exist of a variety of peripheral neuropathies in cats. These include: 2 cats with histologicallyconfirmed inflammatory polyneuropathy (a chronic relapsing polyradiculoneuritis) and an acute polyneuritis, an idiopathic chronic relapsing polyneuropathy responsive to immunosuppressive glucocorticoid therapy and an acute
brachial plexus neuropathy with a suspected relationship to
a previous vaccination. It is reasonable to expect that there
will be future reports regarding FeLV and FIV infections and
their association with neuromuscular diseases of cats, particularly polyneuropathies. Paraneoplastic neuropathies and
radiation-induced neuropathies of cats are likely to be reported in the future.

JUNCTIONOPATHIES
Myasthenia gravis
Myasthenia gravis is a condition that results from either
a congenital or an acquired reduction of acetylcholine receptors of neuromuscular junctions. Both forms have been
reported to occur in cats. Two of the acquired cases were associated with thymoma, and another with a cystic thymus.
Acquired myasthenia gravis has been reported frequently in
Abyssinians and Somalis (closely related to Abyssinians),
which may suggest a possible association with the major histocompatibility complex, as in humans. The most consistent
signs in cats include tremors, initial stiffness with progression to generalised weakness on exercise, cervical ventroflexion, dysphagia, dysphonia, ptyalism, facial weakness,
and dyspnea. Overt megaesophagus or esophageal hypomotility is common.

Miscellaneous Junctionopathies
Abnormalities in neuromuscular junction function may
also result from tick paralysis, administration of certain
drugs, selected toxins, or from envenomation. Botulism has
not been reported as a clinical entity in cats, however, it may
be produced experimentally in cats. Paraneoplastic junctionopathies are likely to be reported in cats in the future.

Muscular dystrophy-like disorders of cats have been reported in the Netherlands and the U.S.A. To date all affected cats have been males, which suggests an X-linked inheritance. Clinical signs may first be seen in cats at 5-6 months
of age, and include generalised skeletal muscle hypertrophy,
excessive salivation, reduced exercise tolerance, stiff gait
and bunny-hopping when running, difficulty in jumping,
adducted hocks, cervical rigidity, vomiting/regurgitation,
and partial protrusion of the tongue.

Hereditary myopathy of devon rex cats


This is a congenital myopathy of Devon rex cats. Characteristic clinical signs, including ventroflexion of the head
and neck, protrusion of the scapulae, and esophageal weakness, all reflect dysfunction of striated muscle, while skeletal muscle pathology is suggestive of a muscular dystrophy.

Nemaline myopathy
A suspected inherited myopathy has been described in 5
related cats between 6-18 months of age, with an onset of reluctance to walk and a forced, rapid, abrupt, hypermetric
gait. Other signs included muscle tremors, hyporeflexia, and
muscle atrophy which was more pronounced in proximal
limb musculature. This myopathy is characterised by large
but variable numbers of nemaline rods within myofibres.

Myositis ossificans
Generalised ossifying myositis, a non-neoplastic form of
heterotopic ossification affecting skeletal muscle and fibrous
connective tissue, has been described in 2 young cats with a
history of progressive weakness, stiffness, difficulty in
jumping, decreased range of limb motion, and pain on
forced movement.

Miscellaneous inherited myopathies


Glycogen storage diseases (or glycogenoses) are rare
disorders of cats. Deficient activity of one of the enzymes involved in glycogen degradation or synthesis results in inadequate glycogen utilisation, and in glycogen accumulation
within various tissues, including muscle. There are several
reports of glycogenoses in cats. Glycogen storage disease
Type IV has been reported in 3 young related Norwegian
forest cats.

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ACQUIRED MYOPATHIES

Potassium-depletion polymyopathy

Infectious polymyositis

This acute feline polymyopathy, resulting from a severe


total body potassium depletion, is usually secondary to a reduced potassium intake and increases in the fractional excretion of potassium in urine (due to renal dysfunction).
Clinical signs include muscle weakness, cervical ventroflexion, stiff and stilted gait, and muscle pain. A similar syndrome with a suspected hereditary basis has been reported to
occur in Burmese cats.

Infectious myositis may occur in association with bacterial infection, migrating parasites, or protozoan disease.
Whilst cats are the only definitive hosts for Toxoplasma
gondii (and a majority of cats may have serum antibodies to
this organism) muscle involvement is not an outstanding
feature of Toxoplasma infection of cats.
Experimental inoculation of cats with the protozoan
Neospora caninum may produce fatal, necrotising encephalomyelitis, polymyositis, pneumonia and hepatitis.
Naturally-occurring feline neosporosis has not been reported to date.

Immune-mediated (or Idiopathic)


polymyositis
Polymyositis occurs sporadically in cats, occasionally in
association with thymoma. Inflammatory infiltrates are predominantly mononuclear with small lymphocytes and
macrophages. Neutrophils are seen infrequently. Eosinophils
are rarely seen.
Clinical signs are characterised by a persistent cervical
ventroflexion, appendicular weakness, painful muscles, and
exercise intolerance.
Serum levels of creatine kinase and aldolase are elevated.
A report of polymyositis in a cat in association with myasthenia gravis and thymoma further supports an immune-mediated aetiology.

Miscellaneous myopathies
There are a number of case reports of muscle-related diseases of cats. Descriptions include: nutritional myopathy
secondary to vitamin E deficiency myositis secondary to
Clostridium chauvoei and Clostridium septicum infections
fibrotic myopathy of the semitendinosus muscle and quadriceps contracture secondary to trauma. Episodic weakness
and signs of depression have been noted in young domestic
short-hair cats (less than 1 year of age) with hypernatraemia
secondary to hypodypsia. The most common clinical sign of
hypernatraemic myopathy is ventral flexion of the neck.
Causes of hypodypsia include lesions of the hypothalamus,
and mechanical inability to swallow - a potentially serious
complication of hypertrophic feline muscular dystrophy.
The association between myositis and malignant neoplasia
(paraneoplastic myopathy) is likely to be reported in the future. Myopathies in cats may occur in association with FeLV
or FIV infections (e.g. FeLV-associated immunosuppression
may enable encystment of Sarcocystis spp. in muscle).

81

EUROPEAN SOCIETY OF COMPARATIVE GASTROENTEROLOGY

The pathophysiology of retained bile acids


Denny Meyer
DVM, Dipl ACVIM, Dipl ACVP
NeXstar Pharmaceuticals, Boulder, Colorado - USA

Summary
Bile acids of mammals and birds are amphipathic
steroids (hydroxy cholanoic acids) containing monoanionic
side chain and hydroxyl groups in various numbers and positions resulting in a variety of individual bile acids in different species. They are planar molecules with hydrophilic
groups on one side and the hydrophobic steroidal part of the
molecule projecting on the opposite. This arrangement facilitates micellar formation and permits them to act as biological detergents for the solubilization of lipids in bile and
aid in the digestion and absorption of fats in the intestine;
physiologically good news. These same physiochemical
properties also enable bile acids to solubilize biological
membranes when left in prolonged contact resulting in cytotoxicity; pathologically bad news.

Cytotoxicity of retained bile acids


Prolonged retention of bile has been shown to be associated with a variety of deleterious subcellular events within
the hepatocyte (damage to mitochondria, endoplasmic reticulum, Golgi apparatus) which exacerbate intrahepatic injury.
Recently, this ultrastructural toxicity has been attributed to
selected bile acids. The more hydrophobic ones, defined by
their HPLC migration, have the greatest potential to cause
injury. The dihydroxy bile acids, chenodeoxycholic acid and
deoxycholic acid can attain high serum and intrahepatic concentration secondary to cholestasis. In vivo and in vitro studies have shown that these bile acids can cause hepatocelluar
dysfunction and necrosis at concentrations attained in prolonged cholestasis. Hepatocytes are at greatest risk of bile
acid-induced injury due to their function of concentrating
the bile acids prior to secretion through the canalicular membrane. By analogy, the liver can be considered to treat bile
acids as sticks of dynamite with burning fuses of varied
length. There is no harm if they are efficiently eliminated.
However, the longer they are retained within hepatic tissue
the greater the risk of injury.
One bile acid, ursodeoxycholic acid, has been shown not
only to be devoid of cytotoxicity but actually protected hepatocytes from the toxic effects of the other bile acids. It is
being used in numerous clinical studies for the management
of chronic liver disease in human beings. There are a variety
of proposed mechanisms its beneficial effects. The contem-

porary areas of investigation are: (1) hypercholeresis, (2) direct cellular protection against the more hydrophobic bile
acids or their displacement from the enterohepatic circulation, (3) antioxidant effect, and (4) immunomodulation. As
mentioned previously, bile acids provide the predominant
driving force for bile flow (choleresis). Unconjugated ursodeoxycholic acid has been shown to actually cause hypercholeresis, amplified bile flow compared to the physiologic
effects of other bile acids. This is thought to be related to its
ability to enhance biliary [HCO3] and excretion via a hypothetical mechanism referred to as cholehepatic recycling.
The displacement of cytotoxic bile acids from the enterohepatic circulation would theoretically decrease the prolonged exposure of hepatocytes to their high concentrations.
The high concentration of orally administered ursodeoxycholic acid has been shown to effectively compete with chenodeoxycholic acid and deoxycholic acid for ileal absorption,
thereby displacing them from the enterohepatic circulation.
In the canine patient treated with ursodeoxycholic acid, serial determinations of the serum bile acid profiles with HPLC
demonstrated a remarkable increase in the ursodeoxycholic
acid concentration and a decrease in the chenodeoxycholic
acid and deoxycholic acid concentrations. Ursodeoxycholic
acid may afford direct hepatocellular protection by partitioning into the lipid-rich membrane and excluding the cytotoxic hydrophobic bile acids. In vitro studies with ursodeoxycholic acid in rats have found a moderate to marked
reduction of substances produced as a consequence of oxidative injury suggesting a potent antioxidant effect.
The beneficial effects associated with ursodeoxycholic
acid in certain chronic liver diseases may be related to immunomodulation. Cytokines appear to be involved in the initiation, modulation and/or perpetuation of the immune responses in the liver. Ursodeoxycholic acid has been shown to
reduce the aberrant major histocompatibility complex class I
expression on hepatocytes in human beings with primary biliary cirrhosis and other studies have shown suppression of interleukin-2, interleukin-4 and interferon-g using test systems
which employed mononuclear cells from the peripheral
blood of human beings with primary biliary cirrhosis.
In summary, the determination of the total serum bile
acid concentration provides an index of hepatobiliary function and assesses the integrity of the portal circulation. Beyond their use as a diagnostic test, recent research has
demonstrated that there are good and bad bile acids.
Prolonged retention of certain endogenous bile acids appears

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to amplify intrahepatic pathology while others, notably ursodeoxycholic acid, appear to offer a novel alternative in the
management of chronic liver disease without adverse sideeffects. Ursodeoxycholic acid clearly generates excitement
with its potential multifaceted beneficial modes of action in
the management of the complex pathophysiologic alterations associated with the diseased hepatobiliary microenvironment known as chronic liver disease.

Table 1. The enterohepatic circulation of bile acids


The primary bile acids (cholic acid and chenodeoxycholic acid) are
synthesized and conjugated by the hepatocyte > excreted by the
canalicular membrane into the biliary system > carried to the intestinal tract > participate in the emulsification of lipids for absorption > move to the ileum during which time bacteria dehydroxylate a portion of the primary bile acids forming secondary
bile acids (cholic acid to deoxycholic acid and chenodeoxycholic
acid to lithocholic acid) > reabsorbed into the portal circulation
> carried to the liver and removed by the hepatocyte for recycling. Hepatocellular excretion of bile acids into the biliary system
is the primary driving force for bile flow; termed bile acid-dependent flow.

Supplemental reading
Hoffman AF: Pharmacology of ursodeoxycholic acid, an enterohepatic
drug. Scand J Gastroenterol 1994;29:S1-S15.
Meyer DJ, Thompson MB, Senior DF: Use of ursodeoxycholic acid in a
dog with chronic hepatitis: Effects on serum hepatic tests and endogenous bile acid composition. J Vet Intern Med 1997;11:195-197.

83

SCIVAC EXOTIC ANIMALS STUDY GROUP

Anaesthesia of pet birds


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary
Anaesthesia of birds with isoflurane has become a safe
and routine procedure in practices whether or not they consider themselves avian practices. It is important to gain an
understanding of the unique anatomy and physiology of the
avian respiratory tract to appreciate the value of particular
circuits, or to contemplate the use of intubation or air sac
tubes. As with any species the aims of anaesthesia should be
to provide a smooth, reliable induction with adequate restraint, muscle relaxation, and analgesia, followed by a fast,
complete and uneventful recovery (Lawton 1996 a&b). This
paper will discuss the options available for the more conventional companion species.

Introduction
Anaesthesia of birds with isoflurane has become a safe
and routine procedure in practices whether or not they consider themselves avian practices. It is important to gain an
understanding of the unique anatomy and physiology of the
avian respiratory tract to appreciate the value of particular
circuits, or to contemplate the use of intubation or air sac
tubes. As with any species the aims of anaesthesia should be
to provide a smooth, reliable induction with adequate restraint, muscle relaxation, and analgesia, followed by a fast,
complete and uneventful recovery (Lawton 1996 a&b). This
paper will concentrate on the more conventional companion
species, Heard (1997a) provides a wider review introducing
the literature covering other species.

Anatomy & physiology


Birds do not have a functional diaphragm, they draw air
into the lungs by a cranio-ventral movement of the ribs to
expand the lungs and air sacs. Because of the importance of
the ribs in this process it is vital not to restrict their movement during handling (or by wrapping tightly for recovery.
The trachea is made up of complete interlocking cartilaginous rings (ossified in some species). Because of this
when using endotracheal tubes, plain tubes are generally
preferred to avoid damaging the trachea.
Most birds have nine air sacs associated with the lungs,
paired cervical, single clavicular, and paired cranial thoracic,

caudal thoracic and abdominals, depending on species some


of these pneumatise bones. Total volume of the respiratory
tract is of the order of 100-200 ml/kg body weight (as compared to 45 ml/kg in the dog), with only approximately 12%
of this being lung. The air sacs are functionally grouped, the
anterior group (cervical, clavicular and anterior thoracic),
and the posterior group (caudal thoracic and abdominal).
The avian lung is fixed in place and does not move appreciably during breathing, air is cycled through the system
of air sacs and lung by active inspiration and expiration. The
lung is divided in the vast majority of birds into paleopulmo
and neopulmo, the relative proportions varying between
species (penguins and emu have no neopulmo). There are no
alveoli, they are replaced with a system of parabronchi, leading to infundibulae and air capillaries. Gaseous exchange primarily occurs in the air capillaries of the paleopulmonic area.
The air flow appears to be unidirectional in the paleopulmo
and bi-directional in the neopulmo. Details of air flow
through the avian lung and air sacs has been the subject of
debate and may vary with activity and between species. The
existence of anatomic valves is in doubt, there do however
seem to be aerodynamic flow controls dependent on the
anatomy. There is a very efficient exchange system operating
in birds, due to a high gas exchange surface-to-volume ratio
and the use of a countercurrent system of opposing air flow
through air capillaries and blood flow. This makes induction
and recovery when using gaseous agents very rapid. James et
al (1976) suggest that avian lungs can be considered 10X
more effective than mammalian lungs. Birds are extremely
sensitive to CO2 levels, to the extent that they will become
apnoeic if the blood becomes depleted of CO2. The CO2 is
carried in blood as plasma HCO2, and in the lungs carbonic
anhydrase in the red cells splits the HCO2, into H+ and CO2.
The CO2 has no direct effect on oxygen/haemoglobin binding
although the released H+ exerts and influence through the
Bohr effect ( a rise in H+ leads to reduction in O2 affinity). A
rise in tissue temperature also decreases the O2 affinity of the
haemoglobin. The net effect of both effects is that active tissue, respiring and producing CO2, warmer than the lungs encourages the release of oxygen from the haemoglobin.
It is suggested that a deeply anaesthetised bird may not
generate sufficient muscular movement to pump air around
this circuit. This may be particularly acute in species with a
large pectoral muscle mass. Sinn (1994) advises the routine
use of gentle positive pressure ventilation (20-40/minute at
15 mmHg) to overcome any potential hypocapnoea and

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maintain adequate oxygenation. Air is drawn in during inspiration and is divided between the paleopulmo and the
caudal air sacs via the neopulmo. Air leaving the paleopulmo enters the anterior air sacs. During expiration the caudal
air sacs empty via the neopulmo into the paleopulmo. Air
leaves the paleopulmo mixing with spent air from the anterior air sacs, this air is expired. Duncker,H.R. (1971).

lection, radiography, fluid administration, endoscopy or


bandaging. The type of assessment used for these short procedures is normally limited to the taking of a history and a
physical examination.
Prior to a prolonged anaesthetic it may be advisable to
consider any or all of the following: PCV, WBC & differential, TP, AST, LDH, UA, bile acids, grams stains of faeces
and choana, platelets, clotting time and bile acids. Other
tests may be indicated in particular cases. Liver dysfunction
is not uncommon, and its presence would make the use of
most injectable agents, plus halothane and methoxyflurane
contraindicated. Patients which are toxic due to egg retention may require stabilisation for a day or two prior to
surgery. Obese pet birds are serious anaesthetic risks and prior to elective procedures a diet is indicated. Suspect Aspergillus cases can be pre-oxygenated before induction.

Fluid therapy
There are good grounds in assuming birds suffering from
trauma or disease are dehydrated, often in the region of 10%,
maintenance requires 50 ml/kg/day ie. 5% body weight.
Lactated ringers i/v or i/osseous are recommended. 5% dextrose is regarded as inappropriate by Phalen et al (1997) who
suggests that it may cause serious electrolyte imbalances.
Sinn (1994) suggests that subcutaneous or oral fluids are not
as effective at restoring circulating volume.

Duncker, H.R. (1971)

Pre-anaesthetic

Fasting

Mammalian-type pre-anaesthetic drugs are not normally


used in birds, atropine is contra-indicated in avian patients
because it thickens respiratory mucus and increases the heart
rate. In general a pre-anaesthetic evaluation is important to
assess whether supportive treatment is indicated prior to embarking on an intervention. Isoflurane anaesthesia is however often used simply as an aid to restraint to minimise the
stress associated with minor procedures such as blood col-

In general terms it is usually advisable to fast the bird


long enough to empty the gastrointestinal tract, in small
birds this may be 3-6 hours and in large birds overnight. Always check the crop before inducing anaesthesia, passive regurgitation may block the larynx. Special care is needed if
the crop contains food, anaesthetise with the patient upright,
block the choana with a swab while the crop is emptied,
clean the area and intubate.

Volatile anaesthetics
BLOOD GAS
PARTITION
COEFF AT 37OC

PHYSIOLOGICAL
ASPECTS

Halothane

2.3

15-20% metabolised

Poor muscle relaxation and analgesia. Causes bradycardia,


sensitises the heart to catecholamines. Respiratory and cardiac
arrest tend to happen together.

Isoflurane

1.4
low solubility makes
induction & recovery
very rapid

0.3% metabolised
MAC (1.5-2%)

Good muscle relaxation and analgesia. Less respiratory and


cardiac depression than halothane, if problems then respiratory
arrest usually precedes cardiac arrest.
Rapid induction and recovery.

0.68
quick induction etc

MAC (2-3%)

Potentially expensive, similar to isoflurane, good control over


planes of anaesthesia.

12.0

50% metabolised,
hang-over

Sevoflurane
Methoxyflurane

Lawton 1997, Heard 1997b, Greenacre 1997.

GENERAL COMMENTS

Organ toxicity, highly blood soluble so long induction


and recovery.

85

Commonly used agents


Isoflurane has achieved pre-eminence as the anaesthetic
of choice for birds, it has revolutionised avian medicine,
making much more possible. It is much safer than halothane
and the data is now so good that it would be difficult to defend the continued use of halothane in birds.
A relatively high flow rate needs to be maintained, it
should be a minimum of three times the normal minute volume. ie. approximately 3 ml/g bodyweight. (an African grey
weighing 350 g needs 1.1 litres/ minute. As a rule of thumb

2 lpm is sufficient for birds of up to amazon parrot size,


macaws need 3-4 lpm.
The normal system used for all but the shortest procedures is to intubate and use a Mini-Ayres or Bethune T-piece
system, this then allows scavenging of waste gas or ventilation should a problem occur. Cooks Veterinary Products
manufacture specialist endotracheal tubes.
Nitrous oxude is still used by some veterinarians for its
analgesic properties, it reputedly accumulates within the air
sacs and should only be used during induction, usually at
50/50 with oxygen and never more than 80%.

Injectable anaesthetics
DOSE RATE

COMMENTS

Alphaxalone/alphadalone

5-10 mg/kg i/v


36 mg/kg i/m, i/p

Alphaxalone/alphadalone is a relatively good


anaesthetic agent but with a transient apnoea following intravenous administration, the preferred route due to the large
volumes required. This can be alarming and, when compared
to other anaesthetic agents, is a major disadvantage. Despite
this, there is a wide safety margin but only a short chain of
action (Mandelker, 1987).

Ketamine

20-50 mg/kg s/c, i/m, i/p

Used in birds since 1972 (Mandelker, 1972). It is a good sedative but a poor anaesthetic, with poor muscle relaxation and
little analgesia. The dose rate of ketamine is inversely
proportional to the body size (Boever and Wright, 1975).
Ketamine is eliminated by the kidneys in birds, as it is in
mammals.

Ketamine with diazepam


or midazolam

25mg/kg ketamine + 1-2 mg/kg


diazepam or 0.2mg/kg
midozolam s/c, i/m

The addition of diazepam/midazolam produce better


relaxation than ketamine alone.

Ketamine with medetomidine

1.5-2mg/kg ketamine +
60-85 mg/kg medetomidine
(reversed with atipamazole Antisedan,
250-380 g/kg i/m)

Medetomidine has sedative and analgesic properties, but


it also has hypotensive, bradycardic, and hypothermic
effects. Medetomidine and ketamine combination
provides deep sedation and good muscle relaxation with no
arrhythmias or respiratory depression (Jalanka, 1989).
This combination is particularly good in waterfowl.

Ketamine with xylazine

Various combinations;
30-40mg/kg K+ 0.5-1.0mg/kg X
or 4.4/kg K + 2.2mg/kg X
(xylazine is reversed with yohimbine
HCl, 0.1-0.2mg/kg i/v, or atipamezole
250-380 g/kg i/m)

Once reversal agents became available the use of higher


doses of xylazine and correspondingly lower doses of
ketamine were possible. Ketamine/medetomidine is
considered a better combination, although xylazine is
cheaper. Unreversed there is prolonged recovery and post
operative depression that can result in birds being unable to
feed or drink.

Propofol

1.33mg/kg i/v

Dose dependent cardio-vascular and respiratory depression,


low therapeutic index in pigeons and chickens. Metabolised
and eliminated too quickly to be of any major use in birds.
Potential use only in larger birds in good health, when
respiratory support is available but mask induction is
considered inappropriate.

Xylazine

1-20 mg/kg i/m, i/v


(Reversed with yohimbine HCl,
0.1-0.2mg/kg i/v, or atipamezole
250-380 g/kg i/m)

Xylazine by itself is unreliable, causes bradycardia and A/V


block, and can cause serious respiratory depression
(Mandelker, 1987).

Refs: Lawton 1997, Heard 1997b

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Injectable agents still have a place, especially in the


field. For use where isoflurane is not available this author
would use ketamine/xylazine or ketamine/medetomidine in
preference to inducing with halothane and oxygen.

Analgesics
Work on pigeons suggests both kappa and mu receptors
are active in pain perception, but that they are kappa dominated (76%).
Analgesics have not yet been thoroughly studied in avian
species but butorphanol certainly appears useful.

mask first. In an respiratory-emergency situation oxygen can


be given by mask whilst the tube is placed under restraint
rather than anaesthesia. A large gauge tube (French gauge
14) is used, Cook Veterinary Products actually make a tube
specifically for the purpose. Positive pressure ventilation is
usually required because the CO2 falls below the level which
stimulates breathing, and apnoea results. Birds begin breathing spontaneously one the CO2 levels rise after the oxygen
flow ceases. It is possible if necessary to leave the air sac
tube in situ in cases where a respiratory obstruction is still a
potential problem.

Monitoring
Injectable anaesthetics
DOSE RATE

COMMENTS

buprenorphine

0.02mg/kg i/m

Opiate analgesic which can cause


some respiratory depression, not
very effective in birds even at
higher doses
Butorphanol
1-2mg/kg i/m
Appeared effective in African
greys and cockatoos but not amazons.
Has been used in parakeets
Carprofen
5-10mg/kg s/c Very effective analgesic which
can be used in conjunction with
buprenorphine to have a synergistic effect in cases of severe pain
Flunixin meglumine 1-10 mg/kg i/m Has been used but carprofen is
considered more effective
Ketoprofen
5-10 mg/kg i/m Better than flunixin but not as
good as carprofen
Meloxicam
200g/kg p.o
Effective and useful for long term
use
Lawton 1997, Paul-Murphy 1997, Bauck 1990, Malley (pers comm).

Maintenance
Birds are less efficient than mammals at retaining body
heat, during anaesthesia they cool rapidly so special care is
needed. Phalen et al (1997) showed the importance of heat
supplementation during surgery. Hypothermic birds become
acidotic. A warm room >23oC is advisable, the anaesthetic
gases themselves are cold and also have a cooling effect on
the patient. Sparing use of skin disinfection minimises the
cooling effect on the skin. Heater water circulating pads are
useful or my preference is the Vetbed type materials on a
reptile heater pad in a warm room > 25oC.

A safe anaesthetic is one which is appropriately monitored, even isoflurane which is considered extremely safe
should be treated with respect.
Suitable reflexes for monitoring are the palpebral,
corneal, cere, toe pinch and wing twitch. As is expected,
these slow and eventually are abolished. The toe, cere and
wing reflexes disappear at a medium plane of anaesthesia,
while the corneal reflex remains into deep anaesthesia. Jaw
tone and leg withdrawal can also be assessed, they are reduced in a medium plane of anaesthesia, jaw tone is also
rather difficult/dangerous to assess in a parrot being masked.
Electronic respiratory monitors are available but only
when using intubation. My own experience suggests that
the probes are not sufficiently sensitive to use via a mask.
I suggest anyone contemplating purchase of monitoring
equipment should arrange to test it in the way they wish to
use it before they buy it. Changes in pattern (becoming
more rapid) are indicative of recovery, or that the bird is
feeling pain. Normal respiratory rates have been reported
as budgerigars 55-75/min, larger parrots 10-20, and 2-20
for ostrich.
Doppler probes can be a relatively simple means of at
least ensuring that there is still a pulse.
Heart rate monitors can be useful to assess changes in
rate or especially when xylazine is used to detect possible
A/V block. Monitors need to have a wide range of sensitivities, budgerigars may have an average of 600 bpm, and ostriches 60 bpm Lawton (1996a) cites painful interventions in
a cockatiel resulting in a rise from 300 to 700 bpm.
Pulse oximetry is becoming an extremely valuable tool
with probes on the wing web or tongue, cloacal probes are
also being developed. Validation of the equipment is not yet
complete, although there is a lot of interest. Readings below
80% are considered life threatening, most birds will maintain 80-85% when self ventilating hence the advice to use
gentle positive pressure ventilation (Sinn 1994).

Air sac intubation


Emergency respiratory arrest
This route has proved useful if surgery on the head and
neck is contemplated, or if the patient is suffering from an
obstructive problem of the airway. The normal site is just behind the ribs on the left side, in the same position used for
endoscopic sexing. Routinely a bird would be induced by

Disconnect the bird from the anaesthetic.


Press the chest 40-50 x per minute, ensuring that the legs
are free to move.
Intubate or fit an air sac tube and IPPV through tube.

References
BAUCK, L. (1990) Analgesics in avian medicine. In: Proceedings of the
Association of Avian Veterinarians Annual Conference, 1990. AAV,
Lake Worth.
BOEVER, W.J. and WRIGHT, W. (1975). Use of ketamine for restraint and
anesthesia of birds. Veterinary Medicine/Small Animal Clinician 70,
86.
DUNCKER, H.R. (1971) The lung air sac system of birds. A contribution
to the functional anatomy of the respiratory apparatus. Ergeb. Anat.
Entwicklungsgesch 45 (6) 1.
JAMES, A.E., HUTCHINGS, G., BUSH, M., NATARANJAN, T.K., and
BURNS, B. 91976). How birds breathe: correlation of radiographic
with anatomical and pathological studies. Journal of American Radiological Society 17, 77.
GREENACRE,C.B. (1997) Comparison of sevoflurane to isoflurane in
Psittaciformes. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
HEARD, D.J. (1997a) Anesthesia and analgesia In: Avian Medicine and
Surgery. (Eds R.B.Altman, S.L.Clubb, G.M.Dorrestein & K.E.Quesenberry. W.B.Saunders, Philadelphia.
HEARD, D.J. (1997b) Avian anesthesia: Present and Future Trends In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
KING, A.S. & McLelland, J. (1984). Birds, their structure and function. 2nd
ed. Baillire Tindall, London.

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MCLELLAND, J. (1989) Anatomy of the lungs and air sacs. In Form and
Function in Birds. Vol 4 (eds. A.S.King and J.McLelland). Academic
Press, London.
LAWTON, M.P.C. (1996a) Anaesthesia. In Manual of Psittacine Birds.
(eds.P.H.Beynon, N.A.Forbes and M.P.C.Lawton). BSAVA, Cheltenham.
LAWTON, M.P.C. (1996b) Anaesthesia. In Manual of Raptors, Pigeons and
Waterfowl. (eds.P.H.Beynon, N.A.Forbes and N.Harcourt-Brown).
BSAVA, Cheltenham.
LAWTON, M.P.C. (1997). Anaesthesia. In: Core Day Proceedings of the
4th Conference of the European Committee of the Association of
Avian Veterinarians. EAAV,1997. London.
MANDELKER, L. (1972) Ketamine hydrochloride as an anaesthetic for
parakeets. Veterinary Medicine/Small Animal Clinician 67, 55.
MANDELKER, L. (1987) Anesthesia and surgery. In Companion Bird
Medicine (Ed. E.W.Burr) Iowa State University Press, Ames.
PAUL-MURPHY, J. (1997) Evaluation of analgesic properties of butorphanol and buprenorphine for the psittacine bird. In: Proceedings of
the Association of Avian Veterinarians Annual Conference,
Reno.1997. AAV, Lake Worth.
PHALEN, D.N., LAU, M.T. & Filippich, L.J. (1997) Considerations for
safely maintaining the avian patient under prolonged anesthesia. In:
Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
SINN, L.C. (1994) Anaesthesiology. in Avian Medicine: Principles and application. (eds.B.W.Ritchie, G.J.Harrison, and L.R.Harrison).
Wingers, Lake Worth.

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89

SCIVAC EXOTIC ANIMALS STUDY GROUP

Diagnostic techniques for birds


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary
Avian medicine has developed rapidly in the last 10
years, improved analytical techniques have improved the
applications for blood biochemistry. DNA techniques have
been applied for the determination of sex, and then for various diagnostics. Improvements in anaesthesia have lead to
the extension of endoscopic sexing into the taking of endoscopically guided biopsy samples.

In avian medicine laboratory workups are extremely


valuable in diagnosis. Much is best sent to specialist laboratories since bird blood is significantly different - not least the
nucleated erythrocytes! Avian haematology requires specialist training and a good throughput to produce consistent and
meaningful results. In-house testing has a major role for referral practices where quick results are valuable in stabilising patients while specialist lab tests are in the post. Appropriate samples should be taken, if necessary speak to the
lab while you still have the patient! Lane (1992a) has covered some of the problems of sampling. Spenser (1994) and
Carpenter (1996) are recommended).

is found running down the middle of the neck, in psittacines


there is usually a featherless apterylae over it making visualisation fairly simple. In small birds it is often the only vein
large enough for venipuncture. This is my preferred route.

Blood tests
Haematology
Haematology is a very valuable tool in avian medicine,
blood can be collected into heparin and EDTA. Microtainers
are preferred since the larger tubes contain too much EDTA
which may cause cell lysis. EDTA should not be used with
corvids, ratites, cranes, penguins or kookaburras as it causes
erythrocyte lysis.
A blood smear should be made at the time of collection
for a differential leucocyte count using blood which has not
been exposed to any anticoagulant.
Making full use of avian haematology really calls for experienced technicians and clinicians. Stress haemograms occur but vary between species. In cockatiels, african greys,
cockatoos and macaws the stress haemogram is heterophilic,
whilst in amazons it appears lymphocytic.
Summary of changes

Blood sampling
Blood can be collected from the brachial/cutaneous ulnar
vein (running across the ventral surface of the humero-radial joint - under the wing) in many species including pigeons,
raptors and waterfowl. The vessel is quite small and mobile
and blood collection will often result in haematoma formation. It is often necessary to pluck the site and poor restraint
may result in wing damage.
The metatarsal vein is often used in waterfowl and
ratites, although some avian veterinarians like the site for
routine use in a wide range of species. The vessel is on the
medial aspect of the intertarsal joint, venipuncture is usually carried out proximal to the joint, first plucking a few
feathers. If the vein is accessed through the scaled area the
bleeding may be difficult to stop. Exponents of the brachial
and metatarsal routes suggest not drawing blood with the syringe plunger, rather let the blood flow by capillary action.
Avian blood clots slowly so blocked needles are rarely a
problem.
The right jugular vein is a larger less mobile vessel and

CELL TYPE

COMMENTS

Heterophils

Band cells - rise in severe inflammatory disease


such as clamydiosis toxic heterophils - especially
in chronic equilibrated disease degranulated seen in low grade or chronic conditions

Eosinophils

These are rare, seen with Giardia in cockatiels,


and with worms in other species

Basophils

Rare, some in respiratory infections

Lymphocytes

Large - cf. monocytes, small predominant cell


type in amazons

Monocytes

Chronic illness esp. Chlamydia, lead poisoning,


Aspergillosis

Serology
At present there are not many useful serological tests for
birds in Europe. In the USA there are now tests for poly-

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4th European FECAVA SCIVAC Congress

90

4th European FECAVA SCIVAC Congress

omavirus, Pachecos disease, Aspergillus, chlamydia. There


are a number of chlamydia serology tests available. In UK
PMV serology is available. Serum iron assays can be useful
in toucans.
Biochemistry
Biochemistry tests are widely available and can be extremely valuable. In-house systems such as VetTest 8008 can

be used, even though some doubt has been cast on the validity of the results but their great value is that results are
available quickly. Plasma or serum can be used, gel-separation tubes are very useful to prevent haemolysis when samples must be sent to distant laboratories.
Specialised PCR / DNA tests
Sex determination by DNA probe single drop of blood

TEST

COMMENTS

ALT

Although useful for assessment of liver disease in mammals this is of no value in avian work.

AST / SGOT

Used as an indicator of liver damage, although it is non-specific sources of AST are liver, skeletal and cardiac muscle.
When it is elevated by hepatocellular damage and eventually returns to normal this does not indicate that liver function has
returned to normal. Bile acids may give a better prognostic measure for liver function.

Bile acids

Birds excrete biliverdin, not bilirubin (they lack bilirubin reductase), so bilirubin measurements are meaningless.
Unconjugated biliverdin does not accumulate in tissues, discolouration of avian plasma (or skin) is more likely to be due
to carotenoids than pathological changes). Samples should be tested within 24 hours. Post-prandial levels are higher than
pre-prandial since they are reabsorbed after eating

Calcium

This is an important parameter to measure in many birds. Low levels can be associated with breeding failure, egg binding
or fractures. Never collect samples into EDTA.

Cholesterol

This can be a useful measure in cases of hepatic lipidosis, hypothyroidism, atherosclerosis and in assessing obese birds on
high fat diets.

Creatinine

Not considered to be a useful test in birds. Has been seen to rise associated with high protein foods.

CK / CPK

This is found in all muscle tissue and c an be found at high values associated with activity, fights, fits etc. Rough technique
in capture and blood sampling can result in elevation. It is useful in helping to interpret raised AST levels, ie a raised AST
with normal CPK is strongly indicative of liver damage.

GLDH

This is fairly liver specific (within the hepatocyte mitochondria), there is reported to be some present in kidney.

LDH

This is non-specific, found in liver, muscle, kidney and erythrocytes. Limited value, prone to elevation due to haemolysis.

Phosphorus

In theory an elevation can be associated with renal failure, but in practice changes are not seen very often.

Protein

Changes in albumin and globulin levels are not well documented in birds, although direct parallels have been drawn with
mammalian results. Dry chemistry systems are said to be unreliable for measurement of avian albumin.

Triglycerides

These can be a useful indicator in investigating egg related peritonitis, elevations will also be seen during starvation.

Urea

Birds manufacture very little urea and it is not a useful test, elevations may occur with pre-renal dehydration.

Uric acid

Used as a guide to renal function, but is not absolute. It is synthesised in the liver and excreted by the medullary nephrons
independent of urine flow rate, dehydration etc. Raised uric acid levels do not indicate dehydration, they rise when renal
function is reduced to less than 30% of normal. A rise is seen with prolonged fasting 48-72 hours due to catabolism.

TEST

COMMENTS

Sex determination

Can be carried out on blood samples or feathers.

Parrot Circovirus
(Psittacine Beak & Feather Disease)

Infected birds appear to remain viraemic (except for a small number which appear to eliminate the
virus) and so blood samples will provide suitable target DNA in the majority of cases. Clinical cases
are often immunosuppressed so feather pulp should be included since such cases can be negative on
blood test. Feather pulp or 1 drop of blood in the collection vial. Fixed material or paraffin embedded tissues can also be used.

Avian Polyomavirus
(Budgerigar Fledgling Disease)

This test can only detect virus from birds which are actively shedding the virus, birds do not remain
viraemic. In the clinical situation this is particularly likely at times of stress such as moulting or
breeding, or following transportation. Cloacal swabs or faeces from live birds appear to be the most
reliable sample for detection of this virus. Fixed material or paraffin embedded tissues. Or fresh liver, spleen or kidney tissue from post mortems in collection medium. Blood samples have been rather
unreliable until recently but improved molecular techniques are now showing that these might well
be suitable for carrier detection.

Chlamydiosis / Psittacosis

This test can detect organisms when even very few are being shed, developments in molecular
echniques are making this suitable for examining blood.

required. PCR diagnostics for PBFD and Polyomavirus.


It is recommended that before any samples are sent veterinarians should speak to the laboratory and ensure that the
collection materials are appropriate. Special media may be
required.

Faecal tests
There is a lot of useful evidence in a simple examination
of the droppings in the cage. A normal dropping will contain a coiled, semi-solid faecal component, a white/creamy
urate component and some liquid urine. Diet will influence
faecal colour and consistency considerably, seed diets usually produce compact, green faeces, formulated diets tend to
produce bulkier brown coloured faeces. Items such as beetroot, blueberries and pomegranate will also cause alarming
changes. Apparent haematuria is a feature of lead (or other
heavy metal) poisoning in amazon parrots. This topic has
been reviewed by Bauck 1995. Consistent discolouration
green or yellow discolouration of urine or urates is cause for
concern and investigation.
Microbiology
In-house microbiology in my opinion is often of very
limited value, in my experience few practice laboratories do
it thoroughly enough, cutting corners with media ranges to
keep costs down. Lane (1992b) gives a review of techniques
for the practice laboratory.
Gram stains
Although referred to often as faecal gram stains it is
more useful to look at cloacal smears, these can be useful at
a basic level for assessing levels of yeasts, presence of
megabacteria or the gram positive/gram negative (GP/GN
ratio). Small passerines usually have no gram negative organisms present while psittacines have very few. In general
megabacteria will be seen if clinically significant, the organism is difficult to find in carriers. Microbiological culture is
suggested on birds with more than 10% gram negative organisms, observations by Brown (1996) suggest poor correlation between staining and culture. Choanal smears are also examined by grams stains, there are often more gram negative organisms in choanal than cloacal samples.

Endoscopy
Direct visualisation of organs is an extremely useful
technique, the 2.7mm rigid endoscope used routinely for
surgical sexing of birds can be utilised in a range of approaches. Taylor and Harrison 1997 have produced a superb
reference work on CD-ROM showing anatomy and surgical
approaches for all of the organs. This also covers the necessary approaches for endoscopically guided biopsy.

Biopsy
Crop biopsy has proved a useful means of obtaining a diagnosis in cases of proventricular dilatation (Doolen, 1994).

91

Endoscopic guided biopsy techniques have become popular and the Stortz system has been designed specially for
the purpose. Hunter and Taylor (1992) describe a technique
for lung biopsy, they stress that this is not a routine procedure but one which is valuable in cases where a diagnosis
cannot be made otherwise. Renal biopsy has also been investigated (Murray & Taylor,1997) since renal disease is difficult to assess by blood sampling techniques, this is a more
routine procedure than lung biopsy, most haemorrhage is
minor and self limiting.
Specialist Laboratories
DNA sexing, PBFD, Polyomavirus and Chlamydia PCR
tests.
University Diagnostics Ltd, South Bank Technopark, 90
London Rd, London, SE1 6LN.
Tel: 0171-401-9898, fax: 0171-928-9297

References
BAUCK, L. (1995) Abnormal droppings and their workup. In: Proceedings
of the Association of Avian Veterinarians Annual Conference.1995.
AAV, Lake Worth.
Carpenter, J.W. (1996) Ed. Avian and exotic parasitology. In. Seminars in
Avian and Exotic Pet Medicine. 5, (2).
DOOLEN, M. (1994) Crop biopsy - a low risk diagnosis for neuropathic
gastric dilatation. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1994. AAV, Lake Worth.
GRIMES,J.E. (1993) Interpretation of avian host Chlamydial titers using
various serologic methods. In. Seminars in Avian and Exotic Pet
Medicine. 2, (4).
HUNTER, D.B., & TAYLOR, M. (1992) Lung biopsy as a diagnostic technique in avian medicine. In: Proceedings of the Association of Avian
Veterinarians Annual Conference, New Orleans.1992. AAV, Lake
Worth.
JOYNER, K.L. (1991) The use of gram stain results in avian medicine. In:
Proceedings of the Association of Avian Veterinarians Annual Conference, Chicago.1991. AAV, Lake Worth.
LANE, R.A., (1992a). Microbiology practical tips. In: Proceedings of the
Association of Avian Veterinarians Annual Conference. New Orleans.1992. AAV, Lake Worth.
LANE, R.A., (1992b). Sampling procedures: Dos & Donts. In: Proceedings of the Association of Avian Veterinarians Annual Conference.
New Orleans.1992. AAV, Lake Worth.
MURRAY, M.J., & TAYLOR, M. (1997). The use of endoscopy and endoscopic biopsy as aids in the diagnosis. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV,
Lake Worth.
Niagro, F.D., Ritchie, B.W., Latimer, K.S., Lukert, P.D., Steffens, W.L., and
Pesti, D. (1990) Polymerase chain reaction detection of PBFD virus
and BFD virus in suspect birds. In Proceedings of the Annual Conference of the Association of Avian Veterinarians. Phoenix: 25-37,
1990.
SCOTT, P.W. (1993). DNA Technology: Practical applications for the avian
veterinarian. in Proceedings of the 1993 European Conference on
Avian Medicine & Surgery. Utrecht, Netherlands. European Committee of the Association of Avian Veterinarians. 178-190.
SPENSER, E.L. (1994) Ed. Clinical Pathology: Blood testing. In. Seminars
in Avian and Exotic Pet Medicine. 3, (1).
TAYLOR, M., & HARRISON, G.J. (1997). Diagnostic Application of
Avian Endoscopy. Wingers Publishing Multimedia Series, Lake
Worth, Florida.
WORELL, A. (1991) Serum iron levels in Ramphastids. In: Proceedings of
the Association of Avian Veterinarians Annual Conference, Chicago.1991. AAV, Lake Worth.

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95

From pharmacokinetics clinical application


Empirical antibiotic treatment in infections diseases
David Aucoin

Summary
Avoiding antimicrobial failure involves initially ensuring
that the patient has treatable infection. Antimicrobial selection can be based on probabilities and input from flexible
labeling guidelines. A clinician who is familiar with the efficacy of each antimicrobial can avoid therapeutic failure and
use therapy as a diagnostic tool.

Treatment failure can be regarding in two different


lights. On one hand, true antimicrobial failure results from
using an inappropriate agent, incorrect dosage and or duration of treatment. However, a much greater reason for failure, is absence of a treatable infectious pathogen. Our perchance to use antibiotics frequently in situations where antibiotics have no efficacy or in situations where infectious
pathogens are not even present leads to our greatest failures.
Even though most patients receiving antibiotics get better
during treatment, it is this inappropriate use of antibiotics
that has lead many lay people to call for greater restrictions
on antimicrobial use, especially in animals.
This paper will address the specific issues regarding
true antimicrobial failure in a patient with treatable infectious disease as well as address more social issues regarding appropriate antimicrobial use and avoiding misuse on
antimicrobial.

Patient selection
The presence of an antimicrobial responsive infectious
disease is usually readily apparent. Localizing signs, history
and a good physical examination are often sufficient. Fever
has been the most frequent indication for antimicrobial use,
however, there is little indication that most fevers seen in the
dog or cat are caused by bacterial or rickettsial infections.

Moreover, most fevers associated with upper respiratory


or gastrointestinal infection sin the cat are viral infections.
These common infections do not require a fever to be diagnosed but do point out that fever of unknown diagnosis is
not likely, based on more common infections, to result in a
fever. The point is most practitioners use antibiotics because
there MAY be a bacterial cause.
Herein lies the problem: If you are trying to rule out a
bacterial infection the choice of antimicrobial agent must be
based on predictable efficacy against the most probable
pathogen(s) you are trying to rule out. Terms such as broad
spectrum are of little use in this situation since spectrum
does not indicate efficacy within that spectrum. The tetracyclines have a broad spectrum of activity from bacteria, mycolplasma, rickettsiae and chlamydia.
However, their efficacy against rickettsial species is excellent while against most common gram negative bacteria
theyre fair to poor. Its appropriate using tetracyclines to
rule out an unexplained fever caused by rickettsiae but
would be inappropriate to use it to rule out any bacterial infection.
Ampicillin is a broad spectrum antimicrobial with excellent activity only against streptococci. Using it to rule out a
possible bacterial infection would be illogical. It would only eliminate a systemic streptococcal infection. A rare disease in the dog or cat. To use an antimicrobial with a higher
degree of success depends on two principals.
If an infection is readily apparent (pyoderma), then antimicrobial choice, dose and duration is important in avoiding failure. If an infection is possible but not apparent (i.e
fever of unknown origin), then an antimicrobial(s) must be
selected to rule out a wide variety of pathogens.
Again, selection, dose and especially duration of therapy is important here but very different, since the antimicrobials are being used as a diagnostic tool as well as potential
therapy.

Table 1. Presence (+) or absence (-) of fever in the presence of common infections.

Pyoderma

Otitis
Externa

Lower
UTI

Upper
Respiratory

Lower
Respiratory

Gastrointestinal

Canine

+/-

+/-

Feline

+/-

+/-

+/-

MAIN PROGRAMME

DVM, Dip ACVCP


Santa Monica, California - USA

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4th European FECAVA SCIVAC Congress

Antimicrobial selection

Antimicrobial dosing

Selection in a known infection should be based on that


antimicrobial which has a high degree of predicable efficacy
against the most common pathogens at that site.
Again, it can be appreciated that even in the most commonly infected body sites, the infection is not always bacteria and rationale antimicrobial use against these infections is
impossible.
Selecting an antimicrobic with excellent predicted efficacy against these pathogen at these sites is the first step. It
is illogical in my opinion to use an agent that usually
works only to confront that owner again after failure to then
prescribe an agent that will work.
Treatment failure is very costly to the owner, the pet and
to your practice.
Table 3. Is based solely on in vitro efficacy and does not
take into account costs, toxicity, ease of use or in vivo factors which may favor one family vs. another.

The advent of flexible label dosing in the USA has finally made antimicrobial use more rational. Antimicrobial activity may be over a wide concentration range. Enrofloxacin is
effective against most Pasteurella spp at <0.006 ug/ml while
requiring 1-2 ug/ml to have similar in vitro efficacy against
90% of P. aeruginosa. Thats a 300 fold difference in effective concentrations! It would only be logical to assume the
dose for treating pasteurellosis would be lower than treating
a Pseudomonal infection. Antimicrobial like enrofloxacin
now have flexible dosing labels, however, all antimicrobial
should be dosed according to pathogen requirements.
Frequency of dosing depends on whether an antimicrobial in vivo activity is better correlated with its peak serum
levels (Concentration dependent) or time during a dosing interval serum levels are above the inhibitory concentration
(MIC) of the pathogen (Time Dependent). B-lactams (like
amoxi-clav and cephalexin) are time dependent while
quinolones and aminoglycosides (enrofloxacin, mar-

Table 2. Most common bacterial pathogens at commonly infected sites.

Pyoderma
Canine

Staphylococci

Feline

Otitis
Externa

Lower
UTI

Upper
Respiratory

Lower
Respiratory

Proteus/
Pseudomonas

Coliforms

Not
Predictable

Coliforms

Not Usually
Bacterial

Not Usually
Bacterial

Usually
Viral

Anaerobes
Pasteurella

Not Usually
Bacterial

Pasteurella

Gastrointestinal

Table 3. Antimicrobial families with excellent predicted in vitro efficacy (> 90%) against these pathogens.
Staphylococci
Antimicrobial

Coliforms

Pseudomonas

Anaerobes

Rickettsia

Cephalosporins
Quinolones
Potentiated, Penicillins

Quinolones

Quinolones
Aminoglycosides

Metronidazole

Tetracyclines
Quinolones

Table 4. Author suggested dosing guidelines based on pathogens and maximizing in vivo activity.
Amoxicillin
clavulanate
Staphylococci
Streptococci
Pasteurella
Coliforms
Pseudomonas
Anaerobes
Rickettsiae

10-15 BID
10 BID
10-15 BID
15-30 TID

Enrofloxacin

Marbofloxacin

Cephalexin

Gentamicin

5 SID

2 SID

6 SID

5 SID
5-10 SID
10-15 SID

2 SID
2-4 SID
4-8 SID

10-15 BID
10 BID
10-15 BID
15-30 TID

10-15 BID

10-15 BID
5 SID

4 SID
6 SID
8 SID

4th European FECAVA SCIVAC Congress

Antimicrobial dosing duration


Duration of treatment is empirical and based upon how
well the patient responds. However, to short a treatment period does increase the emergence of resistant bacterial
strains and too long a treatment increases unnecessary costs
and may delay alternative treatments or diagnostics.
Acute treatments should be continued 3-5 days past clinical cure which usually respond quickly with 5-10 days of
treatment adequate. If no clinical response is noted within a
few days it is unlikely a response will be seen in after 10
days. Treating acute infections for 2-3 weeks awaiting a response is illogical and the patients needs to be reevaluated.
Chronic infections can be treated for 2- 6 weeks. Length
of treatment is designed to keep bacteria from colonizing
and replicating while local tissues heal and normal antibacterial defenses are operational. Without local healing, it will
be impossible to prevent further bacterial infections. Many
pyoderma and lower UTIs are frequently recurrent requiring
frequent treatments. I prefer pulse therapy, treating these patients for short periods but frequently.

Ruling out a treatable bacterial infection


Antimicrobial can be used as diagnostic tools. A therapeutic trial is only effective if the response to therapy gives
high probability of a yes or no answer. Selecting an antibiotic depends on the rule outs (rickettsia vs. bacteria) and the
probability of knowing which pathogen is present. A post op
patient following a bowel resection is likely to coliforms,
enterococci and anaerobes present if leakage is suspected
while a dog with an aspiration pneumonia could have any
number of potential pathogens.
Select an antimicrobial with an excellent activity rating
against the suspected pathogens administer at a dose to maximize its effect. Observe for positive changes in clinical
signs which should occur within 24 hours. If no effect is observed after 48 hours it is unlikely that he patient has treatable bacterial infection. The patient may have peritonitis or
pneumonia but antibiotics alone will not likely be efficacious. Changing antibiotics is illogical and has a high degree
of failure.
If the pathogen(s) are known, use a four quadrant approach to effectively choose agents that are effective against
all gram positive and gram negative aerobes and anaerobes.
Combining a fluoroquinolone with a potentiated penicillin
or an aminoglycoside with a penicillin are effective protocols. If no clinical response is noted within 24-36 hours, it is
highly unlikely that the patient has treatable infection and
further diagnostics are warranted.

MAIN PROGRAMME

bofloxacin and gentamicin) are concentration dependent.


Simply put, to maximize a time dependent antimicrobic you
must give it more frequently (not just higher dose) while for
a concentration depend antimicrobic increasing its dose is
more efficacious than increasing its frequency of delivery.

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99

Cataracts in dogs: etiology, development


and clinical findings
Ellen Bjerks

Summary
The definition of cataract is any light-scattering opacity
in the lens, regardless of the initial cause, but not necessarily with any demonstrable effect on vision. This definition
may also be extended to include opacities of the lens capsule. The end result of cataract formation is destruction of
lens tissue with loss of transparency, either partially or completely. Developmental cataracts initially affects cortical fibres, while nuclear cataracts are most often congenital. The
nucleus may, however, be affected in more extended developmental cataracts as well. A special form of nuclear
cataract is the pulverulent type.
Causes of primary cataract include congenital malformations, nutritional deficiencies, toxins, radiation, UV-light,
trauma, inheritance and ageing. Secondary cataracts may
be caused by systemic diseases as well as other diseases
within the eye.

Definition of cataract
The word cataract is derived from the greek word katauraktos which means waterfall.
The definition of cataract is any light-scattering opacity in
the lens, regardless of the initial cause, but not necessarily
with any demonstrable effect on vision. This definition may
also be extended to include opacities of the lens capsule1.

Development of the lens - malformations


In early embryogenesis, the optic vesicle comes in contact with the surface ectoderm, stimulating the ectoderm to
form the lens vesicle. The lens vesicle later separates from
the ectoderm. In fetal life the lens is surrounded by a plexus
of vessels, the tunica vasculosa lentis, which normally disappears shortly after the puppy is born2. Remnants of the tunica vasculosa lentis may occasionally be visible on the posterior lens capsule. The primary vitreous and tunica vasculosa lentis may also be hyperplastic, this condition is termed
PHTVL/PHPV (persistent hyperplastic tunica vasculosa
lentis/persistent hyperplastic primary vitreous). PHTVL/PHPV is seen as an inherited condition in some dog breeds, the
dobermann being most frequently affected. The changes
range from only small pigmented dots on the posterior lens

capsule, not affecting vision, to major changes of the lens including lenticonus (a bulging of the posterior lens capsule),
cataract and intralenticular hemorrhage3-5.
In front of the lens the mesodermal tissue will differentiate to form the eyelids, conjunctiva, cornea, anterior chamber and the iris. Defective differentiation of the structures
may lead to many forms of malformations, including persistent pupillary membranes (PPM) which may attach to the
anterior lens capsule and cause opacities6.
Other malformations affecting the lens include: aphakia no lens at all, microphakia7-abnormally small lens, anomalies
of the lens shape (colobomas, lenticonus and lentiglobus)8
and congenital cataract. Congenital cataract may be present in
an otherwise normal eye, or may be associated with other
malformations, most commonly microphthalmia.

Lens anatomy and physiology


The normal lens is a clear structure, the oldest part being
the nucleus. The lens is surrounded by a collagenous lens
capsule freely permeable to water, ions and other small molecules. This lens capsule forms the basement membrane of
the lens epithelium. The lens epithelial cells which cover the
anterior part of the lens are a simple layer of cells, lying side
by side, but not tied together by tight junctions. Thus,
there is no major barrier across the epithelium into the extracellular spaces between the lens fibres. This is of potential importance to the effects on the lens of drugs delivered
topically to the eye, and also to changes in the composition
of the aqueous9.
The germinative zone of the epithelium is in the periphery, at the equator, and mitoses here give rise to new rows of
cells. These differentiate into secondary lens fibres (cortical
fibres) by elongation and loss of their nucleus. The layer of
secondary lens fibres is termed the lens cortex. The cortical
fibres meet and form suture lines anteriorly and posteriorly.
The anterior suture lines form an Y, whereas at the posterior
pole they form an Y upside down.
The lens steadily grows throughout the whole life of the
animal, adding layers of cortical fibres to the already existing lens tissue. The lens can only expand to a very limited
extent, therefore the result of this growth is that the lens fibres become more densely packed with increasing age, giving the lens a blueish appearance. The increased density of
the lens is termed nuclear sclerosis and is a normal age

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

100

change which should not be confused with cataract. True senile cataracts with loss of transparency may occur in dogs as
in other species, however.
The cortex is the most metabolic active part of the lens,
and cataractogenic factors are most likely to influence the
cortical fibres initially. In comparison, congenital abnormalities will more probably affect the nucleus which after birth
is far less metabolic active than the cortex.
The aqueous transports nutrients to the lens. Glucose is
the main source of energy, with certain amino acids providing an additional source. Glucose enters the lens by simple
diffusion and is mainly metabolized by anaerobic glycolysis. The glycolysis route is regulated by the enzyme hexokinase, which is found in a limited supply within the lens and
thus serves as a rate limiting step for glycolysis. A small
amount of glucose is also metabolized by the hexose
monophosphate shunt which also depends on hexokinase for
control rate. Excess glucose is shunted into other pathways,
mainly the sorbitol (polyol) pathway. The sorbitol pathway
converts glucose to sorbitol which is a sugar alcohol. Normally, the sobitol pathway accounts for only about 5% of the
lens metabolism. Hyperglycemia causes more glucose to enter this pathway. The accumulation of sorbitol within lens
cells causes an osmotic gradient that draws water into the
lens fibres10.

The biochemical causes of cataract


The lens fibres are normally held in a relatively dehydrated state. This is important to provide the organized structure of the lens proteins (crystallins). The normal intracellular protein structures are maintained mainly by certain essential amino acids like methionine and cysteine. Low levels of these essential amino acids may therefore lead to destruction of the protein structures and cataract formation11.
This is not a condition normally seen in dogs, but may occur
in other animal species as well as humans in the third world.
In short, it can be said that the biochemical cause of
cataract is both water entrying the cells, and the unfolding of
the regular protein structures, thus enabling the proteins to
form aggregates. Both factors may cause rupture of cell
membranes with destruction of lens fibres and production of
cellular debris. The result of these structure alterations is
scattering of light. The effect of the protein aggregates is especially of significance in cortical cataracts.
A major cause of damage to the lens is oxidative stress,
and ascorbate, vitamin C, plays an important role in protecting the lens from oxidative damage 1. This is also the reason
why vitamin C eyedrops have been tried as cataract treatment, without any effect, however. Another anti-oxidant is
glutathione which is present in high concentration in the lens
and which acts co-operatively with ascorbate. A third antioxydant which has aroused interest is vitamin E, since in vitro administration of vitamin E on lenses has been shown to
slow cataract progression12. Topical administration of vitamin E in vivo has not shown any effect, though.

4th European FECAVA SCIVAC Congress

Morphologic changes
Regardless of the initial cause of cataract formation, the
end result is destruction of lens tissue with loss of transparency, either partially or completely. When a cataract develops in previously clear mature lens fibres, there are a limited number of forms that the opacity can take. These forms
are determined by the anatomy of the lens fibres and their
arrangement within the lens, so-called fibre-based cataracts.
Thus, when fibres within a particular perinuclear cortical fibre shell are affected, a lamellar cataract is formed. When
limited groups of fibres are affected, the appeareance is that
of spokes13. This is seen for instance in the late form of developmental cataract in the Boston terrier14. If the tips of the
fibres are affected, the opacity forms the branching pattern
of the sutures as the fibre tips enter the suture lines. Such
opacities are usually subcapsular and situated at the posterior pole.
Lens vacuoles are often found in connection with
cataract and are considered to represent early changes of
lens fibres. Transient vacuoles have been reported in humans15 and may well be occurring in dogs as well. However, in dogs they will most often just represent a stage of
cataract development, indication that the cataract is progressing.
In addition to the described changes of the originally
normally developed lens fibres itself, the epithelium may
loose the ability to produce normal lens fibres. This may be
the explanation of posterior polar cataracts in dogs, and also
of radiation cataracts in humans. Abnormal fibres first appear in the posterior subcapsular region of the lens periphery, where the changes may be difficult to detect. The abnormal fibres then move axially in the direction normally
taken by the growing lens fibres. Eventually they will form
a subcapsular cataract around the posterior pole.
At a later stage of cataract development, fibrous metaplasia of epithelial cells may also occur. There may also be
proliferation of the epithelial cells, which gives rise to abnormally shaped bladder cells.
Nuclear cataracts are most often congenital, but the nucleus may also be affected in more extended developmental cataracts as well. A special form of nuclear cataract is
the pulverulent type, the name borrowed from human ophthalmology. Early changes occur early in life as small
opacities along the suture lines, just behind the fetal nucleus. At the age of 4-5 years, a ball of small opacities appear in the nucles, giving the nucleus a candy-floss appearance. The changes do not involve the whole nucleus,
the outer adult nucleus is unchanged. This type of cataract
has been described in the Norwegian buhund 16, but occurs
also in other breeds, like the German shepherd and the
Leonberger.

Description of cataract
Cataracts can be divided into primary and secondary
cataracts. Secondary cataracts occur because of other
changes within the eye. These include uveitis, glaucoma,
lens luxation and retinal degeneration. Cataract may also be

4th European FECAVA SCIVAC Congress

Description according to localization of the changes:


- nuclear cataract
- anterior/posterior polar cataract
- equatorial cataract
- cortical cataract
- complete cataract
- subcapsular cataract
- capsular cataract

Causes of cataract
Malformations (see above).
Nutritional deficiencies, not as important in dogs as in certain other animal species.
Toxins. Cataract is a common indicator in toxicity studies18. Long-term topical administration of steroids has been
proven to cause cataract in humans and in laboratory animals19. The effect in dogs is uncertain.
Radiation. UV-light is one factor causing cataracts in humans. The effect of UV-light and oxidative damage on the
dog lens has not been thoroughly studied.
Trauma. The changes in traumatic cataract depend on the
type of injury. Blunt trauma to the eye may cause complete
cataract that does not become obvious until a couple of
weeks after the accident, since the initial changes are subtle and difficult to observe. Smaller injuries, like a stab by
a cat claw through the lens capsule may result in only a focal opacity, especially if the capsule seals rapidly after the
injury and the destruction of lens fibres is limited.
Inheritance (see below).
Ageing
Secondary cataracts
Systemic diseases. These will be covered in a separate
lecture.
Other diseases within the eye.

Hereditay cataract
Hereditary cataracts are of particular importance in dogs,
and there is a long list of breeds with cataracts proven or suspected to be inherited. Despite a considerable number of affected dogs within certain breeds, establishing the modes of
inheritance has proven difficult. Evidence for autosomal recessive inheritance are convincing in the two types of
cataract in the miniature schnauzer and in cataract in the
Afghan hound. Otherwise convincing information on modes
of inheritance is lacking. There is also limited knowledge as
to what is actually inherited, that is whether it is the lens
changes per se or some initiating factor.
Criteria for classifying cataract changes as hereditary
cataracts17:
Hereditary cataract has previously been described in the
breed.
The age of appearance and the localization of the lenticular changes correspond to those described in this breed.
The cataract occurs bilaterally (there may be exceptions).
The cataract is progressive, although slowly in certain cases.
The problem arises when cataract is diagnosed in a
new breed. The advise would be not to breed the affected
animal(s). Re-examination of the dog for signs of progression of the cataract, as well as examination of littermates,
offspring and parents should be performed. Unilateral
cataracts suspected to be hereditary may also be difficult to
evaluate, and affected animals should be re-examined at a
later stage for signs of bilateral involvement. Examination of
the colsest family of the affected dog is also advised.
As the genetic lines within breeds differ from country to
country, there will be variation in the cataract incidences. Information on affected breeds and cataract incidence can be
obtained from the national eye panels for inherited eye diseases in each respective country20-21.

Secondary cataracts
Other eye diseases may cause secondary cataracts. These
diseases include uveitis, lens luxation, glaucoma and retinal
disease. The cause of cataract is the change in composition
of the aqueous, with the presence of inflammatory or other
products acting toxic to the lens. In addition, there may be a
direct effect on the lens capsule of the adherence of iris to
the lens in uveitis.
Ocular signs, including cataract, secondary to systemic
disease will be covered in a separate lecture.

Lens induced uveitis


Leakage of the smallest crystallins (d crystallins)
through the lens capsule occurs to a minor degree in normal
eyes, but the rate of leakage is increased in the presence of
cataract22. The reason for this is that breakdown of the fibre
membranes can release crystallin sub-units or proteolytic
fragments of appropriate size to leak into the aqueous. These
substances are considered foreign material by the eye and
will cause an inflammatory reaction.

MAIN PROGRAMME

associated with microphthalmia. Primary cataracts develop


in an eye otherwise normal.
Cataracts can be described according to stages of development17:
Incipient cataract describes focal opacification(s) of the
lens and/or its capsule. Vision is not impaired. This cataract
may or may not progress.
Immature cataract. The opacity is more or less diffuse, but
the fundus can still be examined. Vision may or may not be
impaired. The changes are mostly progressive.
Mature cataract. The fundus cannot be inspected, as the
opacification is complete and dense. Vision is severely impaired. If a mature cataract takes up fluid and swells it is
referred to as intumescent.
Hypermature cataract. Dissolving of the cataract may occasionally occur. The content of the lens capsule is more or
less liquefied. Lens protein can be resorbed, leading to
shrinkage of the lens with wrinkling and dimpling of the
capsule. The nucleus will dissolve to a lesser extent and
may migrate inferiorly in the capsular bag to form what is
termed a Morgagnial cataract.

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Clinical signs of lens-induced uveitis are those of a lowgrade chronic uveitis:


- red eye
- moderately lowered intraocular pressure
- moderately miotic pupil
- darkened iris
Lens-induced uveitis is treated with anti-inflammatory
therapy. The inflammation should preferably be controlled
before attempting cataract surgery.

10.

References

13.

8.

9.

11.
12.

14.
1.
2.
3.

4.

5.

6.

7.

Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann


Ltd, Oxford, 91-132.
Glaze MB, Carter JD, (1995), Veterinary Pediatrics, WB Saunders
Philadelphia 1995: 297-336.
Boev MH, van der Linde Sipman T, Stades FC, (1988), Morphogenesis of persistent hyperplastic tunica vasculosa lentis and persistent hyperplastic primary vitreous, Invest Ophthalmol Vis Sci, 29:
1076-1086.
Boev MH, Stades FC, van der Linde-Sipman, Vrensen GFJM,
(1992), Persistent hyperplastic tunica vasculosa lentis and primary
vitreous (PHTVL/PHPV) in the dog: A comparative review, Progr Vet
Comp Ophthalmol, 2: 163-172.
Leon A, Curtis R, Barnett KC, (1986), Hereditary persistent hyperplastic primary vitreous in the Staffordshire bull terrier, J Am Anim
Hosp Assoc, 22: 765-774.
Strande A, Nicolaissen B, Bjerks I, (1988), Persistent pupillary
membrane and congenital cataract in a litter of English cocker
spaniels, J Small Anim Pract, 29: 257-260.
Molleda JM, Martin E, Ginel PJ, et al, (1995), Microphakia associated with lens luxation in the cat, J Am Anim Hosp Assoc, 31: 209-212.

15.
16.
17.

18.

19.
20.
21.
22.

Narfstrm K, Dubielzig R, (1984), Posterior lenticonus, cataracts and


microphthalmia; congenital ocular defects in the cavalier king charles
spaniel, J Small Anim Pract, 25: 669-77.
Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann
Ltd, Oxford, 53-90.
Basher AW, Roberts SM, (1995), Ocular manifestations of diabetes
mellitus: diabetic cataracts in dogs, Vet Clin North Am, Small Anim
Pract 25: 661-676.
Whikehart DR, (1994), Biochemistry of the eye, Butterworth-Heinemann Ltd, Oxford, 1-30.
Kojima M, Shui YB, Murano H, Sasaki K, (1996), Inhibition of
steroid-induced cataract in rat eyes by administration of vitamin-E
ophthalmic solution, Ophthalmic Res 28: 64-71.
Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann
Ltd, Oxford, 133-160.
Curtis R, (1984), Late-onset cataract in the Boston terrier, Vet Rec,
115: 577-578.
Brown N, (1971) The visibility of transparent objects in the eye by
retro-illumination, Br J Ophthalmol 55: 517-524.
Bjerks E, Haaland M, (1995), Pulverulent nuclear cataract in the
Norwegian buhund, J Small Anim Pract, 36: 471-474.
Peiffer RL, Petersen-Jones SM, (1997), Small animal ophthalmology: a problem-oriented approach, WB Saunders, Philadelphia, 85165.
Martin CM, Christmas R, Leipold HW, (1072), Formation of temporary cataracts in dogs given a disophenol preparation, J Am Vet Med
Assoc, 161: 294-301.
Urban RC, Cotlier E, (1986), Corticosteroid-induced cataracts, Surv
Ophthalmol, 31: 102-110.
Rubin LF, (1986), Inherited eye diseases in purebred dogs, Williams
& Wilkins, Baltimore.
ACVO Genetics committee (1996), Ocular disorders presumed to be
inherited in purebred dogs.
Van der Woerdt A, Nasisse MP, Davidson MG, (1992), Lens-induced
uveitis in dogs: 151 cases (985-1990), J Am Vet Med Assoc, 201:
921-926.

4th European FECAVA SCIVAC Congress

103

Ocular signs of systemic diseases in dogs


Ellen Bjerks

Summary
Ocular change is a prominent feature of many systemic
diseases. The ocular signs may accompany changes elsewhere in the body, or may be the only present sign of systemic disease. Thus, a complete history and a thorough clinical examination of the whole animal are essential in all
dogs presented with eye disease. The age of the animal
should also be considered. Malformations, as for instance
portosystemic shunts causing hepatic encephalopathy, affect
young animals, whereas other diseases, like diabetes mellitus, usually occur in middle-aged animals.
Systemic diseases causing ocular signs may be divided into:
Infectious diseases
Immune-mediated diseases
Metabolic diseases
Diseases of the cardiovascular system
Neoplasias
Nutritional deficiencies

Ocular change is a prominent feature of many systemic


diseases. The ocular signs may accompany changes elsewhere in the body, or may be the only present sign of systemic disease. Thus, a complete history and a thorough clinical examination of the whole animal are essential in all dogs
presented with eye disease. The age of the animal should also be considered. Malformations, as for instance portosystemic shunts causing hepatic encephalopathy, affect young
animals, whereas other diseases, like diabetes mellitus, usually occur in middle-aged animals.
Systemic diseases causing ocular signs may be divided into:
Infectious diseases
Immune-mediated diseases

CAUSE OF DISEASE

Metabolic diseases
Diseases of the cardiovascular system
Neoplasias
Nutritional deficiencies
The initial ophthalmic signs of systemic disease may be
divided into two main groups: Red eyes and visual disturbance. Red eyes are caused by inflammation, either of the
extraocular or the intraocular structures. Inflammation of extraocular structures is associated with conjunctival hyperemia, while inflammation of deeper structures is also associated with episcleral hyperemia. One should always remember that the eye is highly susceptible to inflammation
which may lead to loss of vision. Thus, a correct diagnosis
both of the ocular disease as well as of the possible underlying cause is of importance. Unilateral ocular manifestations
do not exclude the presence of a systemic disease.
Some diseases may initially cause inflammation, with
later progression to blindness. In some infectious diseases
the age of the animal when infected determines the ocular
signs. Canine herpesvirus is an example of this, as puppies
infected perinatally may develop retinal dysplasia, while
adults only develop mild conjunctivitis1.
Sudden blindness may occur because of ocular change,
but one should always also remember that diseases of the
brain can cause visual disturbance. Changes in the innervation of intraocular and extraocular structures, presenting
with ocular signs, may also be a result of damage to the brain
as well as to the actual cranial nerve.
Below there is a detailed list of common and less common systemic diseases associated with ocular signs. The
most important of these diseases will be discussed in the
lecture.

OCULAR SIGNS

Infections
Virus
Canine distemper2
Infectious canine hepatitis2

Conjunctivitis, KCS, chorioretinitis, optic neuritis. The end-stage of a slowly progressing multifocal chorioretinitis may resemble PRA. Blindness may
also be associated with encephalitis.
Uveitis. Corneal edema due to endothelial damage, blue eye, is a prominent feature. This may also occur after vaccination with live hepatitis virus.
Some breeds are reported to be more susceptible than others: Afghan hound,
basset hound, Siberian husky and St.Bernard.

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

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4th European FECAVA SCIVAC Congress

Canine herpesvirus1

Conjunctivitis, keratitis, uveitis. Usually mild signs in adults. More serious


signs including retinal dysplasia in perinatal infection.

Rabies2

Chorioretinitis, optic neuritis. Central blindness.

Bacteria
Leptospira spp.3

Episcleral injection, yellowing of the sclera due to icterus, conjunctival petechia, uveitis.

Brucella canis3

Uveitis. Ocular signs are rare.

Clostridium tetani4

Enophthalmos, protrusion of the third eyelid.

Borrelia burgdorferi5

Uveitis, chorioretinitis. Ocular signs are rare in dogs.

Sec. to systemic bacterial disease3

Uveitis, endophthalmitis. Examples of bacterial diseases: Pyometra, prostatitis, severe otitis externa.

Protozoa
Toxoplasma gondii2

Uveitis, chorioretinitis. More common in cats, but should be considered in


chorioretinitis.

Leishmania donovani5,6

Blepharitis (spectacle blepharitis) with skin surface desquamation and hair


loss. Keratoconjunctivitis, keratouveitis. Endemic disease in Southern Europe.

Babesia spp.2

Chorioretinitis. Rare.

Neospora caninum7

Uveitis, chorioretinitis.

Rickettsia
Rickettsia rickettsii8
(Rocky Mountain spotted fever)

Conjunctivitis, keratitis, uveitis, petechial (Rocky Mountain spotted fever)


retinal hemorrhage.

Ehrlichia canis9
(tropical canine pancytopenia)

Conjunctivitis, conjunctival hemorrhage, hyphema, uveitis, keratic precipitates, retinal detachment. Widespread in Europe.

Fungi and algae3


Blastomyces dermatitidis10
Cryptococcus neoformans
Histoplasma capsulatum
Coccidioides immitis
Aspergillus fumigatus11
Prototheca
Parasites
Toxocara canis12

Granulomatous uveitis and chorioretinitis Cryptococcus neoformans Systemic mycoses are more common in America than in Europe.

Visceral larvae migrans may cause choroidal granulomas, intraretinal hemorrhage and retinal necrosis. End-stage may present as generalized retinal
degeneration.

Dirofilaria immitis4

Uveitis, vitritis, larvae may be visible in the anterior chamber. Death of larvae within the eye may cause severe uveitis resulting in blindness.

Fly larvae, Cuterebra, Oestrus, Hypoderma13

Uveitis, vitritis, larvae may be visible in the anterior chamber. Occasionally


reported.

Demodex canis3

Non-pruritic blepharitis with periocular hair loss. Most common in young


animals.

Immune-mediated diseases
Uveodermatologic syndrome14

Uveitis, depigmentation of uvea. Pigment loss of the skin on eyelids, lips,


paws and occasionally elsewhere on the body as well as depigmentation of
hair in the same regions. Breed predisposition in the Akita inu, Samoyed,
Siberian husky, also reported in other breeds. Comparable with Vogt-Koyanagi-Harada syndrome in humans.

Pemphigus complex15

Ulceration of mucocutaneous areas, including eyelids. KCS.

4th European FECAVA SCIVAC Congress

105

Systemic lupus erythematosus15

Ulceration of mucocutaneous areas, including eyelids. KCS, uveitis.


Glomerulonephritis may cause hypertension (see cardiovascular diseases).

Immune-mediated thrombocytopenia15

Petechiae in conjunctiva, hyphema, retinal hemorrhage.

Atopy15

Blepharitis, conjunctivitis, chemosis

Metabolic diseases
Cataract, bilateral. Rapid development may cause swelling of the lenses and
lens induced uveitis. Diabetic retinopathy is rare in dogs.

Hypoparathyroidism (hypocalcemia)17

Linear cataract reported in a few dogs.

Hypothyroidism18

Corneal deposits, KCS, signs of hyperlipoproteinemia. Facial paralysis may


cause secondary exposure keratitis.

Hyperlipoproteinemia19

Primary or secondary. Lipemia of ocular blood vessels, corneal opacities,


lipemic aqueous.

Hyperadrenocorticism (Cushings disease)20

Sudden acquired retinal degeneration (SARD)? An association with SARD


has been found in some patients.

Ceroid lipofuscinosis (CL)21


(lysosomal storage disease)

Hereditary diseases. Deposits of lipofuscin (lysosomal storage disease) in


ganglion cells and RPE cells. Secondary retinal degeneration. CL diagnosed
in many breeds, not all of them show ocular changes. Affected English setters have normal retinas. Retinal changes described in the Tibetan terrier and
the Polish owczarek nizinny.

Other lysosomal storage diseases22

Group of hereditary storage diseases. Corneal opacities, CNS signs.

Hepatic encephalopathy (liver failure)22

Central blindness.

Ehler-Danlos syndrome23

Rare congenital disease. Corneal edema, KCS, cataract, lens luxation.

Diseases of the cardiovascular system


Hypertension24

Primary or secondary to other systemic disease, most commonly chronic renal failure. Mildest signs often not noticed: tortuosity of retinal vessels,
cotton wool spots due to ischemia of vessels in the nerve fibre layer of the
retina. More severe changes include retinal hemorrhage, retinal detachment
and edema of the optic nerve head. Dogs are most often presented with acute
loss of vision.

Coagulopathies (deficency of clotting factors)25

Conjunctival hemorhage, hyphema, retinal hemorrhage. Also see immunemediated thrombocytopenia.

Hyperviscosity syndrome26

Tumors producing plasma cells may cause monoclonal gammopathies


which lead to increased levels of plasma immunoglobulins and increased
viscosity of the blood. Distention of retinal vessels, retinal hemorrhage, retinal detachment, hyphema.

Neoplasias (metastases)
Malignant lymphoma /
malignant fibrous histiocytoma27,28

Tumor infiltration in lymphoid tissue in conjunctiva. Tumor infiltration of


uvea. Uveitis, retinal detachment, retinal hemorrhage.

Other tumors29

Metastases from other tissues. Adenocarcinomas from the mammary glands


most common.

Nutritional deficiencies
Vitamin A deficiency2

Rare in dogs. KCS, keratomalacia, retinal changes. Nyctalopia.

Riboflavin (vitamin B) deficiency2

Keratitis. (Retinal degeneration reported in fish).

MAIN PROGRAMME

Diabetes mellitus16

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Vitamin E deficiency (experimental)30

Ophthalmoscopic changes of the retina similar to central PRA. Affection


of pigment-epithelial cells.

Zinc deficiency33

Dry, scaly skin, blepharitis. Siberian husky reported to be especially susceptible. (Cataract reported in fish).

References
1.

2.
3.
4.
5.
6.

7.

8.

9.
10.

11.
12.

13.

14.

15.
16.

Albert DM, Lahav M, Carmichael LE et al, (1976), Canine herpes-induced retinal dyplasia and associated ocular anomalies, Invest Ophthalmol 15: 267-278.
Ettinger SJ, (1997), Textbook of Veterinary Intenal Medicine, 4th edition, Saunders, Philadelphia, 524-533.
Gelatt KN, (1991), Veterinary Ophthalmology, 2nd ed, Lea and
Febiger, Philadelphia, 357-395.
Morgan RV, (1992), Handbook of small animal practice, 2nd ed,
Churchill Livingstone, New York, 1119-1123.
Roze M, (1997), Les uvites, Prat Med Chir 32 (suppl): 129-147.
Gothe R, (1990), Leishmaniosen des Hundes in Deutschland: Erregerfauna und -biologie, Epidemiologie, Klinik, Pathogenese, Diagnose, Therapie und Prophylaxe, Kleintierpraxis, 36: 69-84.
Dubey JP, Koestner A, Piper RC, (1990), Repeated transplacental
transmission of Neospora caninum in dogs, J Amer Vet Med Assoc
197: 857-860.
Davidson MG, Edward BB, Nasisse MP, (1989) Ocular manifestation
in Rocky Mountain spotted fever in dogs, J Amer Vet Med Assoc,
194: 777-781.
Woody BJ, Hoskins JD, (1991) Ehrlichial diseases of dogs. Vet Clin
North Am Small Anim Pract 21: 75-98.
Bloom JD, Hamor RE, Gerding PA, (1996), Ocular blastomycosis in
dogs: 73 cases, 108 eyes (1985-1993), J Amer Vet Med Assoc, 209:
1271-1274.
Gelatt KN, Christmas CL, Samuelson DA, et al, (1991), Ocular and
systemic aspergillosis in a dog, J Am Anim Hosp Assoc, 27: 427-431.
Johnson, BW, Kirkpatrick CE, Whiteley HE et al, (1989), Retinitis
and intraocular larval migration in a group of border collies, J Am
Anim Hosp Assoc, 25: 623-629.
Gwin RM, Meredith R, Martin CL, (1984), Ophthalmomyiasis interna posterior in two dogs and a cat, J Am Anim Hosp Assoc, 20: 481486.
Murphy CJ, Bellhorn RW, Thirkill C, (1991), Anti-retinal antibodies
associated with Vogt-Koyanagi-Harada-like syndrome in a dog, J Am
Anim Hosp Assoc, 27: 399-402.
Ettinger SJ, (1989), Textbook of Veterinary Internal Medicine, 3th
edition, Saunders, Philadelphia, 2283-2327.
Basher AW, Roberts SM, (1995), Ocular manifestations of diabetes

17.
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mellitus: diabetic cataracts in dogs, Vet Clin North Am, Small Anim
Pract 25: 661-676.
Mannerfelt T, (1997), Primr hypoparathyroidism hos hund, Sv Vet T,
49: 473-478.
Crispin SM, Barnett KC, (1978, Arcus lipoides corneae secondary to
hypothyroidism in the Alsatian, J Small Anim Pract, 19: 127-142.
Crispin SM, (1993), Ocular manifestations of hyperlipoproteinaemia,
J Small Anim Pract, 34: 500-506.
van der Woerdt A, Nasisse MP, Davidson MG, (1991), Sudden acquired retinal degeneration in the dog: Clinical and laboratory findings in 36 cases, Progr Vet Comp Ophthalmol, 1:11-18.
Wrigstad A, Nilsson SEG, Dubielzig R, Narfstrm K, (1995), Neuronal ceroid lipofuscinosis in the Polish owczarek nizinni (PON) dog.
A retinal study, Doc Ophthalmol, 91: 33-47.
Oliver JE, Lorenz MD, (1993), Handbook of veterinary neurology,
Saunders, Philadelphia, 322-373.
Barnett KC, Cottrell BD, (1987), Ehler-Danlos syndrome in a dog:
ocular, cutaneous and articular abnormalities, J Small Anim Pract, 28:
941-946.
Bartges JW, Willis AM, Polzin DJ, (1996), Hypertension and renal
disease. Vet Clin North Am- Small Anim Pract, 26: 1331-1345.
Ettinger SJ, (1989), Textbook of Veterinary Intenal Medicine, 3th edition, Saunders, Philadelphia, 2246-2279.
Lane IF, Roberts SM, Lappin MR, (1993), Ocular manifestation of
vascular disease: hypertension, hyperviscosity and hyperlipidemia, J
Am Anim Hosp Assoc, 29: 28-36.
Krohne SG, Henderson NM, Richardson RC, Vestre WA, (1994),
Prevalence of ocular involvement in dogs with multicentric lymphoma: prospective evaluation of 94 cases. Prog Vet Comp Ophthalmol, 3: 152-157.
Scherlie PH, Smedes SL, Feltz T, et al, (1992), Ocular manifestation
of systemic histiocytosis in a dog, J Am Vet Med Assoc, 201: 12291232.
Dubielzig RR, (1990), Ocular neoplasia in small animals. Vet Clin
North Am. Small Anim Pract, 20: 837-849.
Riis RC, Sheffy BE, Loew E, et al, (1981), Vitamin E deficiency
retinopathy in dogs, Am J Vet Res, 42: 74-86.
Van Den Brock AHM, (1988), Diagnostic value of zinc concentrations in serum, leukocytes and hair of dogs with zinc-responsive dermatosis. Res Vet Sci, 44: 41-44.

4th European FECAVA SCIVAC Congress

107

Ocular signs of systemic diseases in cats


Ellen Bjerks

Summary
In cats, many systemic diseases show ocular manifestations. The importance of a complete work-up in cats presented with diseases of the eye or adnexa should therefore
not be under-estimated. When examining the animal, one
must determine whether there are signs of concurrent systemic disease. Conversely, if a cat is presented with a systemic disease that is frequently associated with ocular
changes, a careful examination of the eyes is necessary to
detect changes which should be treated.
Uveitis with or without chorioretinitis is one of the most
frequent and significant ophthalmic diseases in cats.The
most important causal agents are coronavirus (feline infectious peritonitis), feline leukemia virus, Toxoplasma gondii
and feline immunodeficiency virus, but other factors may also cause uveitis. The other important group of systemic diseases causing ocular changes is the infectious upper respiratory tract diseases.

In cats, many systemic diseases are associated with ocular manifestations. The importance of a complete work-up in
cats presented with diseases of the eye or adnexa should
therefore not be under-estimated. When examining the animal, one must determine whether there are signs of concurrent systemic disease. Conversely, if a cat is presented with
a systemic disease that is frequently associated with ocular
changes, a careful examination of the eyes is necessary to
detect changes which should be treated.

Uveitis
Uveitis with or without chorioretinitis is one of the most
frequent and significant ophthalmic diseases in cats. In recent reports, between 38% and 70% of the cats with uveitis
have concurrent systemic disease1. The most important
causal agents are coronavirus (feline infectious peritonitis),
feline leukemia virus, Toxoplasma gondii and feline immunodeficiency virus2,3.
Feline herpesvirus is also a suspected cause of uveitis,
since diagnostic tests (polymerase chain reaction -PCR) has
revealed herpesvirus-DNA in the aqueous of a number of
cats with so-called idiopathic uveitis.
FIP may present in a granulomatous (dry) and a produc-

tive (wet) form. The granulomatous form of FIP, which is


caused by a partial cell-mediated immune response, is most
often associated with ocular signs, and uveitis may even be
present without concurrent signs of systemic disease.
Ocular changes linked to FeLV are related to the ability
of the virus to induce immunosuppression, hematologic
changes and tumor formation4. Ocular signs include retinal
dysplasia, tumor formation, retinal hemorrhages and pupillary changes. Perinatal infection can result in retinal dysplasia, which occurs seconday to diffuse retinal inflammation.
Spontaneous retinal hemorrhage is the result of anemia-induced hypoxia of small retinal vessels followed by increased
capillary fragility and rupture of the vessels. Abnormalities
in pupil shape include spastic pupil, D-shaped pupil and reversed D-shaped pupil5. These changes probably represent
FeLV infection of the autonomic ganglia for the parasympathetic portion of the third cranial nerve which delivers one
branch to each of the two pupillary constriction muscles of
the iris.
Feline immunedeficiency virus may cause a mild uveitis
that can be aggravated by co-infection with Toxoplasma
gondii. The prevalence of toxoplasmosis has been difficult
to determine, but the demonstration that IgM titers to the organism can be found in many uveitis-affected cats has led to
heightened interest in toxoplasmosis as a cause of feline
uveitis6.

Upper respiratory tract infections


The other important group of systemic diseases causing
ocular changes is the upper respiratory tract diseases. By tradition, four infectious agents have been associated with conjuntivitis: Feline herpesvirus, Chlamydia psittaci, Calicivirus and Mycoplasma spp.
Mycoplasma is a common finding in the normal conjunctival flora of cats7. This may suggest that mycoplasma
species are rarely pathogenic unless the animal is immunosuppressed or very young.
Calicivirus-infection has also been associated with conjunctivitis. Experimental inoculation with calicivirus in cats
has not produced ocular signs as response to infection, however2. The significance of this virus in conjunctivitis may
therefore be worth further studies.
Chlamydia psittaci is a primary conjunctival pathogen in
cats, and spread to other cats within a household is not un-

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

108

4th European FECAVA SCIVAC Congress

common8. After infection, organisms are shed for a long period of time. Although different from the human strain, there
are similarities enough for the feline strain to cause infections in humans. The zoonotic aspect should therefore be
considered when treating affected anmals. Perinatal chlamydial infection is also considered a cause of ophthalmia
neonatorum in cats.
Feline herpesvirus (FHV-1) is a very common pathogen,
studies in the USA have shown that abut 75% of the adult cat
population is seropositive. Latency is established in the
trigeminal ganglia, and a chronic carrier state develops with
intermittent virus shedding9. Recurrence is common, especially with stress or other systemic disease.
Newborn kittens may develop ophthalmia neonatorum
if infected before the eyes are opened. The infection may
also progress to affect the cornea and cause a keratitis
which may result in corneal perforation, endophthalmitis
and phthisis.
Older kittens develop a serous conjunctivitis with
chemosis and subsequent conjunctival epithelial necrosis.
Corneal changes are seen as superficial branching ulcera, socalled dendritic ulcera. These changes are often too superficial to be diagnosed by staining with fluorescein, however staining with rose-bengal may show the corneal

DISEASE

changes. Symblepharon formation (adhesion of conjunctiva


to itself or to the cornea) is not an uncommon sequela of primary FHV-1 infection. The ability of herpesvirus to produce
epithelial necrosis is presumably responsible for the symblepharon formation in young cats.
Older cats with signs of recrudescent herpesvirus-infection show only moderate signs of systemic disease. The ocular changes are often more severe than in primary infection,
however. Corneal changes are often unilateral and present as
superficial keratitis with dendritic or geographic epithelial
defects due to virus replication, or as stromal keratitis. Stromal keratitis is probably not caused by active viral replication, as virus is rarely isolated from these ulcers. The
changes of the corneal stroma may, however, be the result of
a hypersensitivity reaction to viral antigens in the stroma.
Corneal sequestration (corneal necrosis - black body) is a
non-specific response to keratitis, but FHV-1 is considered a
contributing factor in many cats. Chronic conjunctivitis may
cause keratoconjunctivitis sicca because of obstruction of
the lacrimal gland ducts.
Below there is a detailed list of both common and less
common systemic diseases which may cause ocular
changes. The most important of these diseases will be discussed in the lecture.

OCULAR SIGNS

Infectious diseases
Virus
Feline herpesvirus2

Perinatal infection: ophthalmia neonatorum. Young kittens: serous conjunctivitis, conjunctival epithelial necrosis, dendritic corneal ulcera, symblepharon. Recurrent infection: superficial or stromal keratitis, corneal sequestration, KCS, uveitis (?)

Calicivirus2

Conjunctivitis. Significance?

Coronavirus (Feline infectious peritonitis)10

Granulomatous uveitis, chorioretinitis, keratic precipitates.

Feline Leukemia virus2

Tumor cells in uvea, uveitis, retinal hemorrhage, keratic precipitates, change


in pupil shape. Retinal dysplasia in perinatal infection.

Feline immunodeficiency virus2,11

Any ocular change, serious eye changes probably due to secondary problems caused by immunosuppression.

Panleukopenia virus12

Conjunctivitis, chorioretinitis. Fetal or perinatal infection: retinal dysplasia,


optic nerve hypoplasia.

Borna disease virus (staggering disease)13

Central blindness.

Pox virus2

Blepharitis, conjunctivitis.

Bacteria

Bacteria

Mycobacterium tuberculosis14

Uveitis, chorioretinitis, retinal detachment.

Chlostridium tetani

Protrusion of third eyelid.

Chlamydia psittaci2

Conjunctivitis, chemosis. Ophthalmia neonatorum.

Mycoplasma spp.7

Conjunctivitis, chemosis. Significance?

4th European FECAVA SCIVAC Congress

109

Rickettsia
Hemobartonella felis15 (feline infectious anemia)

Anemic retinopathy, retinal hemorrhage.

Protozoa
Toxoplasma gondii16

Uveitis, chorioretinitis.

Fungi
USA. Occurs occasionally also in other parts of the world. The most common of the systemic mycoses in cats, but systemic mycoses are generally
rare in this species. Uveitis.

Histoplasma capsulatum4,18

Endemic disease in temperate and tropical regions. Uveitis.

Blastomyces dermatitidis4

America, Africa. Uveitis.

Coccidioides immitis4

America. Uveitis.

Microsporum spp.2

Blepharitis.

Parasites2
Notoedres cati

Blepharitis, pruritic.

Demodex spp.

Non-pruritic periocular hair loss.

Toxocara cati

Intraretinal hemorrhage, retinal necrosis, choroidal granulomas.

Dirofilaria immitis

Uveitis, vitritis, larvae may be visible in the anterior chamber.

Fly larvae, Cuterebra, Oestrus, Hypoderma

Uveitis, vitritis, larvae may be visible in the anterior chamber.

Thelazia californiensis

Conjunctivitis, nematodes found in conjunctiva.

Immune-mediated diseases2
Pemphigus complex

Ulceration of mucocutaneous junctions.

Allergies (especially food allergies)

Blepharitis.

Metabolic diseases
Diabetes mellitus19

Ocular manifestations are rare in cats. Cataract and diabetic retinopathy


have been reported.

Hepatic encephalopathy (liver failure)20

Central blindness.

Renal failure

See hypertension.

Hyperthyroidism

See hypertension.

Hyperparathyroidism21

Cataract.

Hyperlipemia, familial hypercholesterolemia22

Lipemia retinalis, lipemic aqueous.

Lysosomal storage diseases23

Corneal opacity, accumulation in ganglion cells, retinal lesions, central


blindness.

Chdiak-Higashi syndrome2

Color dilution, cataract.

Diseases of the cardiovascular system


Hypertension24,25

Primary or secondary to chronic renal failure or hyperthyroidism. Mildest


signs often not noticed: Tortuosity of retinal vessels, cotton wool spots

MAIN PROGRAMME

Cryptoccus neoformans4,17

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4th European FECAVA SCIVAC Congress

due to ischemia in vessels in the nerve fibre layer of the retina. More severe
changes include retinal hemorrhage, retinal detachment and edema of the
optic nerve head. Animals are most often presented with acute loss of vision.
Feline infectious anemia (Hemobartonella felis)

Retinal hemorrhage, hyphema. Also listed under infectious diseases.

Coagulation disorders2

Hyphema, conjunctival hemorrhage, retinal hemorrhage.

Hyperviscosity syndrome2

Tumors producing plasma cells may cause monoclonal gammopathies


which lead to increased levels of plasma immunoglobulins and increased
viscosity of the blood. Distention of retinal vessels, retinal hemorrhage, retinal detachment, hyphema.

Periarteritis nodosa2

Fibrinoid necrosis of small arteries, formation of granulation tissue leads to


vascular occlusion. Exudate in anterior chamber, uveitis.

Diseases of the nervous system


Dysautonomia26

Dilated pupils, KCS.

Feline spongiform encephalopathy27

Central blindness. Retinitis in other species.

Haws syndrome

Bilateral protrusion of third eyelid. Secondary to infectious diseases.

Nutritional deficiencies
Taurine deficiency28

Feline central retinal degeneration progressing to complete retinal degeneration.

Thiamin deficiency29

Mydriasis, peripapillary edema.

Arginine deficiency30

Cataract.

References
1.

2.
3.

4.
5.
6.

7.

8.
9.

10.
11.

12.
13.

Gmensky A, Lorimer D, Blanchard G, (1996), Feline uveitis: a retrospective study of 45 cases. Transactions Am Coll Vet Ophthalmol, 27:
49.
Gelatt KN, (1991), Veterinary Ophthalmology, Lea and Febiger,
Philadelphia, 529-575.
Heider HJ, Pox C, Loesenbeck G, Egberink H, (1997), Ophthalmologische Befunde im Zuzammenhang mit verschiedenen Virusinfektionen der Katze, Kleintierpraxis, 42: 887-900.
Barnett KC, Crispin SM, Feline Ophthalmology, (1998), Saunders,
London.
Gelatt KN, (1991), Veterinary Ophthalmology, Lea and Febiger,
Philadelphia, 706-743.
Chavkin MJ, Lappin M, Powell CC, Roberts SM, (1993), Seroepidemiologic and clincal observations of 93 cases of uveitis in cats, Prog
Vet and Comp Ophthalmol, 2: 29-36.
Nasisse MP, Guy JS, Stevens JB, et al, (1993), Clincal and laboratory findings in chronic conjunctivitis in cats: 91 cases (1983-1991), J
Am Vet Med Ass, 203: 834-837.
Dorin SE, Miller WW, Goodwin JK, (1993), Diagnosing and treating
chlamydial conjunctivitis in cats, Vet Med, 325-330.
Weigler, BJ, Babineau CA, Sherry B, Nasisse MP, (1997), High sensitivity polymerase chain reaction assay for active and latent feline
herpesvirus-1 infections in domestic cats, Vet Rec, 140: 335-338.
Davidson MG, Nasisse MP, English RV et al, (1991), Feline anterior
uveitis: a study of 53 cases, J Am Anim Hosp Assoc, 27: 77-83.
Loesenbeck G, Drommer W, Heider H-J, (1995), Augenbefunde bei
serologisch FIV (felines Immundefizienzvirus)-positiven Katzen,
Dtsch Tierrztl Wschr, 102: 348-351.
Percy D, Scott F, Alberts D, (1975), Retinal dysplasia due to feline
panleukopenia virus infection J Am Vet Med Assoc, 167: 935-937.
Lundgren AL, Borna disease virus infection in cats. On the etiopathogenesis of feline non-suppurative meningoencephalomyelitis (staggering disease), (1995), Academic thesis, Swedish University of
Agricultural Sciences, Uppsala.

14.
15.
16.

17.
18.
19.
20.
21.
22.
23.

24.

25.
26.
27.
28.

29.

Formston C, (1994), Retinal detachment and bovine tuberculosis in


cats, J Small Anim Pract, 35: 5-8.
VanSteenhouse JL, Millard JR, Taboada J, (1993), Feline hemobartonellosis, The Compendium, 15: 535-544.
Chavkin MJ, Lappin MR, Powell CC, et al., (1991), Seroepidemiologic and clinical observations of 93 cases of uveitis in cats, Prog Vet
Comp Ophthalmol, 2: 29-36.
Gerds-Grogan S, Dayrell-Hart B, (1997), Feline cryptococcosis: A
retrospective evaluation, J Amer Anim Hosp Assoc, 33: 118-122.
Peiffer RL, (1979), Ocular manifestations of disseminated histoplasmosis in a cat, Feline Practice, 9: 24-29.
Peiffer RL, Gelatt KN, (1974), Cataracts in the cat. Feline Pract, 4:
34-38.
Oliver JE, Lorenz MD, (1993), Handbook of veterinary neurology,
Saunders, Philadelphia, 322-373.
Stiles J, (1991), Cataracts in a kitten with nutritional secondary hyperparathyroidism, Prog Vet Comp Ophthalmol, 1: 296-298.
Crispin SM, (1993), Ocular manifestations of hyperlipoproteinaemia,
J Small Anim Pract, 34: 500-506.
Aguirre G, Stramm L, Haskins M, (1983), Feline mucopolysaccharidosis VI: general ocular and pigment epithelial pathology, Invest
Ophthalmol Vis Sci 24: 991-1007.
Stiles J, Polzin DJ, Bistner SI, (1994), The prevalence of retinopathy
in cats with systemic hypertension and chronic renal failure or hyperthyroidism, J Amer Anim Hosp Assoc, 30: 564-572.
Sansom J, Barnett KC, Dunn KA et al., (1994), Ocular disease associated with hypertension in 16 cats, J Small Anim Pract, 35: 604-611.
Blaxter A, Gruffydd-Jones TJ, (1987), Feline dysautonomia, Feline
Pract, 9: 58-61.
Gruffydd-Jones TJ, Galloway PE, Pearson GR (1991), Feline spongiform encephalopathy, J Small Anim Pract, 33: 471-476.
Sturman JA, Gargano AD, Messing JM, Imaki H, (1986), Feline maternal taurine deficiency: Effect on mother and offspring, J Nutr 116:
655-667.
Ettinger SJ, (1997), Textbook of Veterinary Intenal Medicine, 4th edition, Saunders, Philadelphia, 524-533.

4th European FECAVA SCIVAC Congress

111

Acute renal failure: from emergency to patient


stabilisation
Claudio Brovida

Summary
Acute renal failure: from emergency to patient stabilisation.
Acute ranal failure (ARF) may be recognized by an
abrupt onset of azotemia or oliguria, rapidly progressive
azotemia or sudden onset of clinical signs of uremia in a previously healty patient. Several life threatening complications
may occur in patients with ARF, they are hyperkalemia,
metabolic acidosis, severe anemia, volume depletion, sepsis.
Patients may die of the diseases process which initiated
ARF (e.g.: acute pancreatitis, sepsis, shock, hypercalcemia,
ethylen glycol intoxication) rather than from ARF or its
complications. Therefore diagnosis and initiation of specific
therapy for diseases which may have precipitated ARF
should be a high priority. The history, physical examination
and urinalysis are usually sufficient to rule out pre-renal and
post-renal causes of azotemia.
Although therapy designed to eliminate the cause(s) of
ARF will not directly result in repair of renal lesions, it will
minimize the severity and extent of renal damage. Symptomatic and supportive therapy designed to minimize deficits
and excesses in fluid, electrolyte, acid-base and nutritional
balance, will often allow life to be sustained until the body
can restore adequate renal structure and function.

Acute renal failure (ARF) is a rapid onset of azotemia


over hours to days (two weeks), or pathologic oliguria which
could not have been present for more than a few days, that
indicates rapid deterioration or loss of renal function. While
ARF may not by itself constitute an emergency, its causes
(hypovolemia, shock, urinary obstruction, sepsis, etc.) often
are life threatening. In addition, the potential for enhancing
reversibility of renal lesions and return of renal function may
be lost if therapeutic intervention is delayed. In contrast to
CFR, rapid diagnosis and initiation of therapy may greatly
enhance a favourable prognosis in ARF.
ARF may result from diverse renal diseases and injuries.
The syndrome of acute tubular necrosis (ATN) accounts for
the majority of cases. With ATN there is a rapid reduction in
GFR resulting from an ischemic or toxic renal insult. Reduced GFR is thought to result from a combination of vascular and tubular effects.
The clinical course of oliguric ATN may be characterized
by three sequential phases:

1) initiation and development,


2) maintenance,
3) diuresis (recovery).
The initiation phase begins with onset of renal injury and
continues through onset of oliguria (reduction in urine output below 0.5-1 ml/kg/hour). Glomerular filtration rate may
begin to fall immediately following the renal insult (as in the
case of shock), or it may be delayed for hours to days (as in
the case with exposure to nephrotoxic drugs).
The duration is highly variable, but it usually persists
about 1 or 2 weeks.
The oliguric phase is characterized by predictable fluid
and electrolyte imbalances including alterations in hydration, hyponatremia, hyperkaliemia, metabolic acidosis and
hyperphosphatemia.
Clinical signs typically develop during the oliguric phase
of ATN, including gastrointestinal, hematological and neurological manifestations. Gastrointestinal disorders are common and include anorexia, vomiting, mucosal ulceration and
hemorrage.
This hemorrage results primarily from defective platelet
function, but may also be associated with thrombocytopenia,
decreases in various coagulation factors and defects in capillary function.
Progressive anemia and neurological disorders characterized by lethargy, depression, stupor and coma may occur
during the oliguric phase.
Transition from the oliguric to the diuretic phase heralds
the onset of re-establishment of tubular continuity, dissolution and/or mobilisation of intratubular casts, and return to
near normal patterns of renal perfusion.

Diagnosis of acute renal failure


ARF may be recognized by an abrupt onset of azotemia
or oliguria, rapidly progressive azotemia, or sudden onset of
clinical signs of uremia in a previously healthy patient.
A preliminary diagnosis of ARF is based on evidence
from medical history, previous data concerning renal function and lack of phisical evidence of CFR (e.g. weight loss,
poor haircoat condition, rubber jaw, growt retardation in
puppies).
Usually, physical examination of patients with ARF typically reveals good nutritional status.
Diagnostic plans should be directed toward:

MAIN PROGRAMME

Med Vet
Private Practitioner, Moncalieri - Italy

112

1) identifying life-threatening complications,


2) localizing the cause of ARF (e.g. pre-renal, post-renal or
primarly renal failure),
3) determining urine volume,
4) differentiating ARF from CRF,
5) determinig the etiology of ARF,
6) monitoring patient response to therapy.
It is particularly important to obtain an urine sample for
analysis and culture before initiating fluid therapy because
fluid therapy may cause concentrated urine to become dilute, making diagnosis of prerenal azotemia difficult. In addition, fluid therapy may alter the urine sediment causing erroneous interpretation.

4th European FECAVA SCIVAC Congress

to less than 7.10, acidosis may:


1) reduce cardiac contractility and the inotropic response to
catecholamines,
2) predispose to ventricular arrhytmias,
3) promote neurologic signs ranging from lethargy to coma.

Volume depletion
At the time of diagnosis, most patients with ARF have
some degree of volume depletion. Although volume depletion can usually be detected by physical examination, physical changes can be subtle, particularly when fluid loss has
occurred quickly and recently.

Medical emergencies in ARF


Infection
Several life threatening complications may occur in patients with ARF, they are hyperkaliemia, metabolic acidosis,
severe anemia, volume depletion, sepis.

Hyperkalemia
Hyperkalemia is a common complication of oliguric
acute primary renal failure and urinary tract obstruction. It is
less commonly associated with non-oliguric acute primary
renal failure and is rarely associated with prerenal azotemia
unless prerenal azotemia results from Addisons disease. Detection of bradycardia or other cardiac dysrhytmias should
alert one to the possibility of hyperkalemia.
Hyperkalemia is confirmed by determination of serum
potassium concentrations; however, electrocardiography
provides a rapid means of detecting hyperkalemia. Typical
electrocardiographic changes observed with mild to moderate hyperkalemia include tall, peaked T waves, slowing of
the heart rate, flattening of P waves and prolongation of the
P-R intervals and QRS complex.
Patients with azotemia, hyperkalemia, hyponatremia
may have hypoadrenocorticism (Addisons disease), in this
case the major disadvantage of administering hormone replacement therapy for ARF is that the catabolic effect of corticosteroid administration may increase the magnitude of
azotemia.

Metabolic acidosis
Metabolic acidosis is a relatively common finding in
ARF. The magnitude of renal dysfunction appears to be a
poor predictor of metabolic acidosis.
Acidosis may be more common in patients with oliguric
ARF than nonoliguric ARF, but not all patients with oliguric
ARF have significant metabolic acidosis.
Therefore diagnosis of metabolic acidosis should be
based on evaluation of blood bicarbonate (or total CO2) concentration and, if available, blood pH. Urine pH is not reliable guide to systemic acid-base status.
Clinical effects of acidosis are usually minimal unless
blood pH is less than 7.20U. However, when blood pH drops

Infection may be a cause or complication of ARF. Dilute


urine, oliguria, anuria and urinary obstruction predispose to
urinary tract infection. Furthermore uremia is characterized
by reduced immunocompetence. Because of these factors,
infection is an important cause of morbidity and mortality in
uremic patients.
Often infections are related to invasive diagnostic and
therapeutic procedures such as vascular and expecially urinary catheterisation. Careful attention to detail and intelligent decisions regarding application of use of catheters and
invasive diagnostic and therapeutic procedures will dramatically reduce the incidence of infection-related mortality.
Examination of urinalysis, urine culture, and a complete
blood cell count are indicated to rule out infection as a cause
or complication of ARF. When fever, physical examination,
or laboratory findings indicate the probability of infection,
its location and cause should be vigorously sought so that
the most appropriate and least nephrotoxic antimicrobial
therapy may be initiated.

Underlying disease processes


Patients may die of the diseases process which initiated
ARF (e.g. acute pancreatitis, sepsis, shock, hypercalcemia,
ethylene glycol intoxication) rather than from ARF or its
complications. Therefore, diagnosis and initiation of specific therapy for diseases which may have precipitated ARF
should be a high priority.
The history, physical examination and urinalysis are usually sufficient to rule-out prerenal and postrenal causes of
azotemia.

Renal biopsy
Renal biopsy may help to differentiate acute from chronic renal failure. In addition, it may provide an etiologic diagnosis and allow assessment of the potential reversibility of
renal injury. However, since renal biopsy is an invasive procedure which entails several risks, it should not be performed unless necessary. Not every patient with ARF re-

4th European FECAVA SCIVAC Congress

Prognosis of acute renal failure


The prognosis for dogs and cats with acute primary renal
failure has been generally considered poor. It is best determined by response to therapy. However, the outcome may
not become apparent for days to weeks following diagnosis.
While it is often difficult to offer an accurate prognosis
early in the course of acute primary renal failure, severe,
progressive hyperkaliemia, metabolic acidosis and uremic
symptoms are negative prognostic indicators. In absence of
these factors, patient treatment and monitoring should be
continued, even if azotemia continues to increase.

Treatment of acute renal failure


Although therapy designed to eliminate the cause(s) of
ARF will not directly result in repair of renal lesions, it will
minimize the severity and extent of renal damage. Symptomatic and supportive therapy designed to minimize deficits
and excesses in fluid, electrolyte, acid-base and nutritional
balance, will often allow life to be sustained intil the body
can restore adequate renal structure and function.
Because many of the complications of ARF are medical
emergencies, it is often necessary to initiate therapy before
diagnostic evaluation can be completed. Furthermore, treatment of ARF should be modified according to patient response to therapy, that is assessed by comparing pre-treatment and serial post-treatment data.
Patient with severe metabolic disturbances may require
frequent laboratory and clinical evaluation, whereas patients
with less severe disturbances generally require less frequent
monitoring.

Fluid therapy
Most patients with ARF are volume depleted before induction of therapy. However, the decision to administer fluid therapy should be based on clinical assessment of hydration, in order to correct volume depletion, regardless of urine volume.
Because hypovolemia and hypotension cause oliguria
and may contribute to the genesis of ATN or predispose to
further renal damage, volume depletion should be rapidly
corrected. Patients should be rehydrated with replacement
fluid via an aseptically placed intravenous catheter.
In most cases, cristalloids, like lactated Ringers solution
are satisfactory. However, if a large amount of fluid has been
lost, in order to help the increase of the blood oncotic pressure, it is advisable to administer plasma-expanders solution
(colloids), up to 20 ml/kg of body weight.
Urine volume and other contemporary losses (e.g. vom-

iting and diarrea) greatly influence fluid requirements during


the maintenance and recovery phases of ARF. Measurement
of urine volume may provide a particularly useful guide to
fluid therapy during the diuretic phase of ATN. Patients are
predisposed to dehydration during this phase because involuntary urine losses are often great. In order to prevent dehydration, the volume of parenteral fluids administered and
oral fluids, should consider also the amount of urine volume,
contemporary fluid losses and insensible fluid losses (about
20 to 25 ml/kg/day).

Therapy of potassium and acid-base


imbalance
Hyperkaliemia is commonly associated with oliguric
ARF and may cause skeletal muscle weakness, reduce cardiac contractility and cause a variety of cardiac conduction
disturbances.
If serum potassium concentration exceed 8.0 mEq/l, or if
serious cardiotoxiticy occurs, therapy with sodium bicarbonate, glucose, with insulin, or calcium gluconate should
be considered. Of these drugs, sodium bicarbonate (0.5 to
1.0 mEq/kg body weight over 15 minutes) is commonly
used first because many hyperkalemic patients also require
this drug for treatment of concurrent metabolic acidosis. Administration of glucose (20% at the dose of 0.5 to 1.0 gm/kg
body weight) and insulin (1 unit each 3 grams of glucose administered) or calcium gluconate (10% solution, not exceed
0.5 to 1.0 gm/kg body weight) are indicated primarily for
rapid correction of severe hyperkalemic cardiotoxicity.

Oliguria versus non oliguria


Therapy specifically designed to convert oliguria to nonoliguria should be considered only for oliguric patients unresponsive to fluid volume replacement. In this case use of
diuretics alone or associated with vasoldilators should be
considered.
Furosemide has been the most commonly used diuretic
in canine and feline patients. Initially it should be administerd intravenously at the dose of 1-2 mg/kg body weight. If
no substantial diuresis develops within one hour after administration, the dose may be doubled (4 mg/kg). If this dose
also fails to induce diuresis, the dose may be further increased to 6 mg/kg body weight.
If diuresis still does not occur, the combination of
furosemide and dopamine may be considered.
Mannitol is an osmotic diuretic commonly used to treat
oliguric ARF. Mannitol has at least three theoretical advantages over furosemide:
1) it may enhance renal function by minimizing renal tubular cell swelling via its osmotic properties,
2) mannitol exerts its diuretic effects along the entire
nephron and therefore may directly affect the proximal
tubule,
3) mannitol may expand the extracellular fluid volume.
The major disadvantage of mannitol is the potential for
vascular overload if oliguria persists. Therefore it should be

MAIN PROGRAMME

quires renal biopsy.


Today, with the use of automated biopsy instruments
guided by ultrasound inspection of the kidney and a correct
anesthesia protocol and technique, kidney biopsy may be
performed within a very acceptable margin of safety for the
patient.

113

114

avoided in overhydrated oliguric patients. Mannitol (20% 25% solution) is administered intravenously over 5 to 10 minutes at a dose of 0.25 to 0.5 g/kg body weight. If substantial
diuresis ensues, administration of mannitol can be repeated
every 4 to 6 hours, or administered as maintenance infusion (8
to 10% solution) during the initial 12 to 24 hours of treatment.
Because reduced renal flow may contribute to the pathogenesis of ARF, vasodilators are the logical therapy for patients with ARF. Dopamine, a precursor of norepinephrine,
has been suggested for patients that are unresponsive to osmotic and/or loop diuretics. Infusion of low doses of
dopamine reduces renal vascular resistance and increases renal flow, particularly to the inner renal cortex. Dopamine
should be administered by intravenous infusion at the rate of
1 to 3 g/kg body weight/min, using an intravenous fluid administration pump or under close supervision to assure accurate fluid delivery rate.

Dietary management
Clinical manifestations of uremia are improved by combination of a correct dietary protein amount and pharmacologic control of uremic gastritis and vomiting. It limits the
catabolic effects of starvation and may be performed also using enteral or parenteral feeding.

4th European FECAVA SCIVAC Congress

Control of uremic vomiting


Uremic gastritis is a major cause of vomiting in patients
with renal failure.
Cimetidine and ranitidine have been recommended for
control of uremic hemorragic gastritis because they block
gastrin-stimulated gastric hyperacidity. For dogs in uremic
crises, cimetidine is given intravenously at an initial dose of
10 mg/kg body weight every 12 hours (5 mg/kg for cats) and
ranitidine is administered at 2 mg/kg.
Once uremic gastritis has been controlled and oral
medication may be tolerated, cimetidine can be administered orally at a dose of 5 mg/kg every 12 hours for 2 to 3
weeks.
The dosage is reduced to 5 mg/kg given once daily for 2
to 3 weeks before being withdrawn. Dosage recommendations for cats are approximately one-half of the canine dose.
Because uremic vomiting may also result from stimulation
of the chemoreceptor trigger, intravenously administered
centrally-acting antiemetics may be useful in controlling
vomiting. However, hypotension and sedation are potential
pitfalls associated with antiemetic therapy. Chloropromazine
(0.5 mg/kg), prochlorperazine (0.13 mg/kg q 6 hrs),
trimethobenzamide (3 mg/kg q 8 hrs) are centrally-acting
antiemetics which may help to control nausea and vomiting
in uremic patients.

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115

Surgical treatment of most common diseases


of tortoises
Leonardo Brunetti

Carapace and plastron fractures


Living in home gardens tortoises are subject to injuries
caused by mowers, cars, electric gates, children and pets. As
for turtles they can easily fall down from their enclosures or
from the balconies.
These fractures have to be stabilized as soon as possible,
so its necessary to advise the owner, even over the phone,
how an emergency bandage can be done, that is by binding
up the shell with some sticky tape and keeping the animal
away from further traumas.
As soon as it reaches the veterinary practice, an inspection of the fracture and a clinical examination must be done,
to establish the reptiles general health.
If we are in front of prostrate and dehydrated subjects,
first we must give some fluids by intraperitoneal or intrabone injection.
When it is necessary we must treat the shock and the internal haemorrhage. As a cover, an antibiotic therapy is always advisable.
The success of the operation largely depends on the timeliness with which the patient is taken to the veterinary practice. Contaminated but recent fractures (1-4 hours) have a
better prognosis than the ones with a small bacterial infection but having taken place a longer time before (>4 hours).
The most frequent situation for tortoises living in gardens is when the fracture has happened 1 or 2 days before.
In this case its better to wait some days before proceeding
with orthopaedic treatment, in order to stabilise the patient
and control the infection.
Before the re-establishment, the patient must be washed
with an antiseptic solution (i.e. a soap solution of iodine
povidone). Any foreign material (soil, grass, stones) must be
removed. We can use an elevator and the anatomic forceps
to lift carefully the carapace and the plastron, where its possible, spraying the under part with a warm sterile physiologic solution.
After having removed the largest foreign materials, the
patient must be washed again with an antiseptic solution.
Every part of the patient, including the ones not interested in the fracture must be submitted to a surgical scrub, because it will be necessary to handle the whole body of the
patient, especially the smallest subjects, in the re-establishment treatment.
It may be useful to do an X-ray on the entire animal, to
highlight possible fractures on the spine and /or on bones of

the limbs.
The X-ray examination may also reveal the presence of
foreign materials.

Linear composed fractures


These are usually the easiest to treat. After having made
a careful curettage in the above described way, we stabilise
the fracture trying to keep up some pressure between the
ends of the fracture. If the displacement is small or absent, it
may be sufficient to put a cerchage wire all around the patient (Fig. 1).
However, if between fracture ends there is a certain
looseness, its possible to put a cerchage wire on detached
points along the fracture line (Fig. 2).
A different approach is necessary when the composed
linear fracture is placed on zones where the animals movement operates a particular traction on the edges of the frac-

Figure 1

Figure 2

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Med Vet
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4th European FECAVA SCIVAC Congress

ture, as for example it happens when there is a fracture between the humeral and the pectoral scutes of the plastron. In
this case its necessary to join the two techniques: 1) the detached suture stitches by cerchage wire and 2) the application of the cerchage all around the carapace. Once the fracture is stabilized, we can apply some acrylic resin for dental
use(with catalyst), or some two components vitrified stucco,
normally used for small repairs on boats and cars. This proceeding is necessary to reinforce the structure and to obtain
the impermeability of the interested zone.

Decomposed multiple fractures


We often must treat subjects with multiple fractures both
on the carapace and the plastron. In this case we must behave as if being in front of a puzzle, trying to preserve and
put together again the different pieces, in the best way, along
the fracture lines. The depressed fragments must be kindly
lifted by elevators, and the ones not connected with the vascular system removed. When the mosaic is composed, we
can go on putting the single pattern wire suture along the
fracture line trying to stabilize the structure. The cerchage
wire must be passed through two holes, previously made by
a drill, along the edges of the shell bits to be rebuilt with the
help of a wire passer or with a suitable diameter needle put
in one of the two holes to work as a guide.
In this case too, at the end of the rebuilding surgery we
must put on some resin or some other suitable material to
give a mechanical help to the shell and to keep up impermeability and asepsis in the coelomatic cavity.

loss of matter from the shell, we can hope in a complete recovery of the animal.
We use the following technique to repair the matter loss:
a surgical sponge is put inside the sinus caused by the trauma, then a piece of X-ray film is put on the sponge. This film
has already been exposed, passed in autoclave and cut according to the necessity. Some small cuts will be made along
the edges of the film to allow it to fit the shape of the tortoise
shell (Fig. 5).
The piece of film has to be longer than the shell zone to
be recovered and it will be glued along its edges by a histocompatible cianoacrylic glue or by two components epossidic resin glue. The edges of the film are then covered by
some acrylic resin (with catalyst) for dental use or vetrified
stucco (with hardener) or with a glue containing two components to keep impermeability and asepsis inside the treated area.
As an alternative we have used successfully acetate
sheets, in place of X-ray film. The desired rebuilding materials are those which offer a low heating, a strong mechanic
resistance and a low price.

BRACHIAL PLEXUS

Fractures with loss of matter


Shell lesions with loss of matter caused by mowers are
among the most frequent ones among home tortoises.
A complete neurological examination should be performed, in addition to the examination first described, because in chelonians, vertebrae are fused with dermal bones,
(Fig. 3) and a dorsal fracture of the carapace can interest the
spinal cord and the brachial and lumbosacral plexuses (Fig.
4). If the spinal cord is safe, even in front of an important

Figure 4

CORNEAL
SCUTE DERMAL
BONE
NEURAL
ARCH

LATERAL
PROCESS
CENTRUM
SPINAL
CORD

Figure 3

Figure 5

LUMBO SACRAL PLEXUS

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117

Turtles will have to remain in dry zone for weeks or


months, until they are healthy again; they are put in a clean
water pool only to eat.
Tortoises can go back to their gardens a few days after
the operation.
A chelonian having such an important trauma must not go
into hibernation during the first winter following the lesion.
Figure 6

Its necessary to cut the plastron to reach the coelomic


cavity in chelonians.
The usual approach is through abdominal and femoral
scuti but may also be cranial or caudal or lateral, depending
on the organs we have to reach and / or possible present
fractures.
A rectangular wedge must be done on the plastron by a
cutting blade. To enable the wedge to turn over, the bone and
horny layers of three sides must be completely cut, while the
ones of the fourth side must be cut only in some parts, preserving the vascolarization.
During the cutting it is vital to cool the plastron by a cold
sterile physiological solution dripping on the part.
When the bone is drifted and the periostium is taken
away the underlying abdominal musculature is showed
clearly. Now it is the moment to make an incision on the
coelomic membrane, where two venous sinuses run down on
each side of the middle line.- Be careful to save the venous
sinuses (only for drastic measures one of them may be cut).
Celiotomy may be used for a lot of procedures: dystocia,
cystotomy for cystic calculi, gastro-intestinal foreign bodies
removal, lesions of the coelomic cavity organs following
shell fracture traumas. In this particular case we always try
to reach the coelomic cavity trough the fracture lines in order to avoid further damage on the patients stiff structure.
When the surgery is finished and the wedge is placed
back in the original position some acrylic resin for dental use
has to be put on the surface of the plastron.

Surgical treatment of penis prolapse


Penis prolapse is rather frequent both for turtles and tortoises. Normally the organ prolapsed for physiologic or
pathologic causes may have an oedema with a probable consequent paraphimosis.
If we are lucky and the animal is taken in time to the veterinary practice, so that the paraphimosis interested tissues
are in good condition, it is possible to place back the penis.
At first it is necessary to wash carefully the wounded
area with a chlorhexidine soap solution, then the organ has
to be sprayed with a sterile physiologic solution. Now we
proceed with a compressive manual pressure to reduce the
oedema and contemporaneously we have to push the penis
inside the cloaca. This operation is often difficult, but it is
necessary to repeat it many times until we are successful.
When the organ is replaced we have to put one or two sutures on the cloaca opening to tishten it, in order to avoid another prolapse (Fig. 6). The residue opening cloaca has to be

sufficient to permit the passage of fecal and urinary product.


The suture will be left in situ for 2-3 weeks. During this period the original causes of prolapse must be found and resolved.
When the patient is taken too late to the veterinary practice and there are some ulcerated and necrotic areas on the
surface of the prolapsed penis, it is necessary to cut the organ off. This amputation doesnt cause any urinary problems
because a reptiles penis has only a copulative function and
it doesnt contain the urethra.
The surgical technique is rather easy: the organ which
has a seminal groove, being kept in physiological position,
is held by an assistant and a continuous pattern mattress suture is applied on its base, then the suture has to be tightened. At this point it is possible to cut off the necrotic part
but there are some devices to consider:
1) the suture must be done with very close sutures to control
the haemorrhage caused by the resection of penis sinus
bodies.
2) an end of suture material must be left to hold it by a mosquito, so as not to lose the organ in the cloaca when we
are replacing it back and to control possible haemorrhages of the penis remaining part.

Surgical treatment of cloacitis


Female tortoises living in small gardens together with a
lot of males often present some cloacitis for the too frequent
coupling.
Cloacal lesions are often complicated by miasis.
The surgical treatment of cloacitis consists in removing
necrotic tissues and every larvae by an accurate curettage.
Then we have to reconstruct the cloacal orifice.
The suture material used is nylon monofilament. Sometimes an anal scutes plastronectomia is necessary, to have
easy access to the cloacal zone.
Sutures will be left in situ between 20 days and two
month, depending on the recovery time.
It is opportune to keep only one male with 4-5 females in
the same garden to prevent this usual pathology.

Surgical treatment of abscesses


Abscesses are rather usual in chelonians where they appear as firm lumps under the skin or under muscles in various zones, especially in the auricular regions (turtles) and in
axillary, inguinal and pericloacal zone (tortoises).
Surgical treatment is necessary because, unlike mam-

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Celiotomy

118

mals, neutrophili granulocytis are not able to colliquate the


pus, permitting a spontaneous draining outside.
The abscess will be completely removed, being careful
to cut off the capsula. We make an incision on the skin above
the lump, and we isolate the lump after drying up the surrounding tissues. The remaining cavity will be sutured with
nylon monofilament and the sutures will be removed 2 or 3
weeks after.

4th European FECAVA SCIVAC Congress

If some delicate structure is present near the lump, we


can use an alternative technique. After cutting the skin above
the lump we take away the infected solid matter with a
Wolkmanns spoon or other adequate instrument. Then we
wash the cavity with a solution composed of hydrogen peroxide, iodopovidone (or chlorhexidine) and physiological
solution, 1-2 times a day for some days. In this case, it can
be unnecessary to suture the remaining cavity.

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119

Ultrasonography in the diagnosis of the urinary tract


diseases in dogs and cats
Claudio Bussadori

The ultrasound examination is a rapid and secure technique, which allows a valuation of the position, dimension
and the parenchyma morphology of the organ in exam.
This methodic by now is large diffused and constitutes
the preferential techniques of imagine of the urinary apparatus, as it reveals, respect to the radiology, a major sensibility and specificity in the diagnostics of the urinary and
nephrological pathologies.
The ultrasound examination can be also used to guide the
withdrawal of bioptic samples through percutaneous way,
which permits histological examinations in a bloodless manner.
The observed pathology alterations can be classified in
many standards: in this specific case we applied the classification on the ground of the structural modifications which
are pointed out in ecografy, considering the different pathologies who can determine them. Since there are not described
some pathology aspects of ultrasound examinations, these
are been located in the classification on the ground of the
macroscopic or microscopic modifications and the analogy
with other pathologies which echografic aspects are known.

tern. The echogenicity is correlated to the cellular type,


which are involved, to the vascular system, to the grade of
haemorrage and to the presence of necrotic phenomenons.
The solid uniform hyperechoic masses can have an aspect
similar to the cysts, without demonstrating lateral acoustic
shades and posterior reinforcement, but with an evident survey of the internal echoes increasing the gain. The lesion of
the lynphosarcoma, the tumor most common of the cat is
characteristic of a weak vascular system, are ipoecogen. The
hypoechoic lesion has a connective tissue or mineral deposit: among these are part of it, the calcification, the infarct,
the fibrous zone and the gathering of gas.
The type of complex mass lesion shows a mosaic of different echogenic areas: in differential diagnosis we can distinguish tumors, granulomas, organized haematoms recent
infarcts. The most tumor types, described with vary echopattern in small animals are haemangiosarcoma, renal blastoma, adenocarcinoma, condrosarcoma, cancer or papilloma
of transit cells.

Diffused lesions
KINDNEY
Parenchyma modification of the kidneys.
Focal cyst lesion
The cystic renal lesion includes a group of hereditary and
acquired diseases, often verified on occasion. The renal cyst
are most roundish with thin and regular walls and the contains without echo frames; they are characterized by the
presence of artificials which are the reinforcement of the
posterior walls and the refraction.
The distinction treated from the human medicine between polycystic autosomic recessive or infantile renal disease and policystic autosomic dominant renal disease or of
the adult can be adapted in veterinary medicine to the feline
species in which this pathology is frequent.
Other tumors localized with characteristics alike the
cysts are the haematomas and the abscesses.

The solid focal lesion


This kind of lesion can have an hyperechoic, hypoechoic
or isoechoic aspect with a regular or subtle sonographic pat-

The renal cortex can present itself hypoechoic, like the


lynphosarcomatic infiltration or iperechogenic, like the Ethylene Glycol Toxicity, in the interstitial and glomerular
nephritis, in the acute tubular necrosis, in the nephrocalcinosis, and in the renal sclerosis.
It has also been signalized in the lynphosarcoma of cats
and the infective peritonitis.
Sonographic findings includes focal hyperechoic of the
corticomedullary junction but it is considerated a characteristic lesion of the Ethylene Glycol toxicity (medullar rim
sign). We can also observe it in the vasculitis due to the
FIP, in acute tubular necrosis and in interstitial chronic
nephritis.

Volume decreasing Sclerosis


- With loosing of the distinction between the cortical and the
medullar.
We observe it in the renal displasia, which is the result of
a disorganization of the organogenesis probably for a hereditary autosomic recessive character.

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Med Vet, Dipl ECVIM


Private Practitioner, Milan - Italy

120

In the policystic kidney with microcysts the presence of


lots of little interfaces can determine a diffused hyperechogenicity without any distinction between cortical and
medullar.
- With decrease of the cortical-medullar correlation.
We find it in pathologies with a progressive course, like
the tubule-interstitial nephropathology of the Norvegian
Elkhound and the Fanconi del Basenji Syndrome.

PELVIS
The ultrasound examination is certainly indicated as the
gold standard examination when there is a suspect of pathology of the first part of the urinary duct.
It is possible to find physiologic symptoms of pyeloectasia (how it happens in the diuresi caused of drugs or pathologic symptoms (how it happens in the case of traumas, obstruction of the urine flow, infective pathologies).
An other frequent pathology in cats and dogs is the hydronephrosis, or rather the dilatation of the pelvis and the calyx secondary to the urinary accumulation caused of obstructions: it is important to distinguish the renal vein in the
presence of a possible extended urinary duct (control the expectoration of the vena cava).
To be able to distinguish the pyeloectasia caused of an
obstruction from a pyeloectasia which has not an origin obstructive, like the obstructive pyelonephritis, it has been estimated in the dog the use of the resistivity index (RI) or
Pourcelot index (you reach out to it dividing the difference
between the systolic top speed with less diastolic speed multiplied with the systolic top speed measured out at the level
the arcuate artery): recently the results are pointing out a low
sensibility and specificity with an high percent of falsehood
negatives, even if it is spotted that the falsehood negatives
could be lower in to 24 hours after the obstruction.
It is possible to express a diagnosis of pyelonephritis
when there are present contemporary two or more of the following signs: dilatation of the pelvis or the proximal part of
the urinary duct, presence of an hyperechoic bed in the
pelvis or in the proximal part of the urinary duct, hypo or
hyperechoic areas in cortex or medullar, loss of the differentiation corticomedullar.

URINARY BLADDER
The bladder for its anatomical position and for its anechoic contents is fit for an ultrasound examination. In the
condition of physiological or artificial fullness, constitutes
an excellent acoustic window and besides represents an important point of reference.

4th European FECAVA SCIVAC Congress

mally indicative of cystitis. We can see urinary polyps in the


bladder wall, typical of the polypoid cystitis or else a neoplasm eziology: these proliferations have to be differentiated
from blood clots adherent to the wall, trying to determinate,
with a patient rotation, with localized abdominal wall compression with the sonographic sound or with a bladder washing with sterile saline a neoplasm shifting that happens if it
is an haematomic agglomerate. In case of neoplasm it can be
associated a certain disorganization of the wall architecture.
Its important that the wall investigation is done accurately, to evidence localized thickness (usually cranioventral) that means cystitis and parietal diverticul presence:
these can be hereditary or acquired, have to be accurately analyzed to find the presence of neoplasm or calculus inside
the diverticolo. Since infect the diverticulum wall is deprived of the muscular component it results an almost always partial emptiness, favoring the persistence of oncogenic stimulus contact to the diverticolar urothelial mycoses
or easier the appearance of chronicle or recidivist infection
of the urinary ways.
The convex bladder wall determinates the appearance
of an artificial due to the sound refraction that simulates a
continuous interruption that disappears changing the sound
orientation.
The vegetating forms appear as solid and homogeneous
structures, with an echogenecity lower than the echogenecity of the bladder wall, with plant base such large to interrupt the continuity of the bladder inside jetting out into
the inside of the viscera.
For now infiltrating neoplasm determinate a thickness
and a rigidity of the bladder wall with an alteration of the
echografic structure: these can present a redoubt component
of the bladder lumen and are difficult to identify.
The possibility to evidence a neoplasm depends essentially of the dimension (the sonographic threshold to evidence a neoplasm are 5 millimeter) and of its seat (the neoplasm which are localized in the neck of the bladder are difficult to identify). Its easier to find the neoplasm localized
in the caudal part of the urinary bladder and trigone, rarely
in the cranial part of the urinary bladder.
If we examinate the cranial part of the trigone sometimes
its possible to recognize the intraparietal part of the urethras
which can be confused with neoplasm, because it appears
like a little convex form with regular walls: for that it is useful to observe if there are coupled structures and to point out
the turbulence created by the urinary peristaltic waves by
coming out the uretery outlets. The persistent uraco that goes
to the umbilicus can appear as a diverticulum or as an anechogic tubular structure cranial to the bladder; the uracal
cysts usually cranial of the bladder have thin walls and anechoic contents.

Contens
Bladder wall
The bladder wall appears as a reflecting line without any
discontinuity, whose thickness varies with the state of fullness: it is important to considerate pathologic only a substantial increasing of thickness in an expanded bladder nor-

Normally the urine is, as said, anechoic: presence of


blood or other fine urinary sediment can generate inside diffused, pointed formed echoes, which go slowly to sediment.
This phenomenal must not be confused with artificial due to
the wrong position in the bladder lumen of echoes borned

outside of the ultrasound bunch periferic portions structure:


this artificial shows as an echigenic band parallel to the dorsal bladder wall, similar to sediment deposit, which is not
possible to resupend shaking or balloting the bladder, which
doesnt move changing animal position and modifies itself
with the sound orientation.

121

The gas inside the bladder normally hyatrogen origin, is


hyperechoic, creates reverb and moves itself to an higher position: if the animal is in a dorsal recumbence it can be confused with the proximal sound reverb; in this case it can be
used a spacer or easier it has to be reexamined the animal in
standing position.

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123

Pathophysiology and treatment


of pericardial diseases
Claudio Bussadori
Med Vet, Dipl ECVIM
Private Practitioner, Milan - Italy

Anatomy and functions of the pericardium


The pericardium holds the heart and is composed by an
external part or lamina parietalis pericardii and an internal
part or lamina visceralis pericardii: the pericardial space
contains normally a small amount of serous liquid (0.5-15
ml in the dog). Although it is not an essential anatomic
structure, it is able to perform important functions: containment and protection of the heart, limitation of the acute dilatation, maintenance of the cardiac geometry and of the
ventricular compliance, modulation in the ventricular diastolic refilling phase, protection of the heart from infections
or adhesions, increasing of the diastolic relation between the
two ventricles.
The measurements of the intrapericardial pressure of a
normal heart is, unfortunately, not easy to obtain: this value is nevertheless very important in the study of pericardial
diseases. At this subject it is important to remember that
the transmural pressure of each ventricle is obtained by the
difference between the diastolic intracardiac pressure and
the intrapericardial and is independent from gravity. The
intrapericardial pressure is strictly connected to the right
atrial pressure and is comparable to the filling pressure of
the right ventricle when in a range between 0 and 20
mm/Hg. This value emerged from the utilization of intrapericardial balloon catheter (Santamore) which have
been demonstrating how, in a normal heart, the catheters
with open lumen were underestimating the values of the
pericardial pressure.
Moreover the pericardial pressure is not homogeneous in
each cardiac segment, but is higher at the level of the free
wall of the left ventricle (Hoit). It is not the pressure of a liquid which has to be equal in various regions, but it is a contact surface pressure, which means the pressure of a liquid
plus its deformation powers.

Etiology of pericardial diseases


The pericardial diseases in the dog are distinguished in
congenital (pericardial agenesia, periton-pericardio-diaphragmatic hernia) or acquired: this last ones can be classified depending on the type of effusion, which can be transudative (congestive heart failure, cysts, hypoalbuminemia
or other reasons of increased vasal permeability), exudative: infectious diseases, particularly bacterial and mycotic,
while the viral pericardial pathologies are more common in
bovine and feline species, the pericarditis in uremic syndromes are more frequent in the human species. Bleedings
occur in neoplasm: cardiac tumor, tumor of the heart base,
hemangiosarcoma, receptoma, pericardial celioma, lymphosarcoma, in idiopathic benign pericarditis, external trauma or heart rupture.
In the dog the major causes of pericardial effusion are the
neoplasm forms and the benign idiopathic pericarditis. The
definition benign is refereed to the human pathology while
in the dog this pathology frequently causes heart tamponade:
the etiology of this form is unknown in both species, even if
hyphotesis suggest an immunological genesis in both species.

Pathophysiology
The haemodynamic effects of the pericardial effusion are
related to the volume of the fluid, the compliance of the myocardium and the time that occurs. The physiological intrapericardial pressure in dogs varies around the values of atmosphere pressure (from -3.8 to 3.8 mm/Hg): this condition
enables the cardiac filling especially in the inspiratory
phase. After the gathering of fluid in the pericardial cavity
the intrapericardial pressure increases, joining first the atmosphere pressure and then further on to higher values,
while in the meantime there is an increasing of the right ventricle diastolic pressure.
The cardiac tamponade is a clinical syndrome, which
generates a cardiac emergency: it develops from an uncontrolled increasing of the intrapericardial pressure, this limits
the ventricular compliance which causes a significant obstacle to diastolic filling.
The pericardium is extremely resistant to acute stretching, while it is able to extend in a progressive way if the
stretching is continued. So this is the reason why even a
small increase of pericardial fluid developing suddenly can

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The author describes pathophysiology and the more


common causes of pericardial diseases furthermore are described guidelines for clinical and Echo-Doppler diagnosis
and staging of pericardial tamponade.
For treatment are described the most utilized medical
therapy and the technique of percutaneous pericardiotomy
using balloon catheter.

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lead to a severe cardiac tamponade, while an effusion of two


or more liters which accumulates slowly can associate only
with a small increase of intrapericardial pressure causing
better tolerated haemodynamic effects.
In slowly developing effusions we have at first only clinical signs of right cardiac failure and only in the following
phases of the process we have the clinical signs of emergency. The intrapericardial pressure increases then until it
causes a critical compression of the outside of the cardiac
walls, able to induce a diastolic collapse of the right atrium
and ventricle and the reduction of the ventricular volume followed by a systolic deficit of the left ventricle, inducing an
hypertension of the venous district and a hypotension of the
arterial district with severe compromise of cardiac output.

Clinical signs
The symptoms depend on the seriousness of the cardiac
tamponade. Slight tamponade in its initial phase can be
asymptomatic.
During an acute tamponade the clinical signs are particularly severe. We can have the lost of the cardiac impulse at
the palpation of the thorax, at the auscultation we have either
paraphoniac tones or tones that can not be detectable, noises
caused by preexistent murmurs, which sonorous is muffled
from the sonorous vibration caused by the passage through
the pericardial fluid.
A typical symptom is the paradox pulse, a huge decreasing (> 10 mm/Hg) of the arterial systolic pressure during inspiration. This phenomenon follows the reduction of the systemic venous drainage and the filling of the right ventricle
followed by reduction of the left filling and output. Central
venous pressure can, on the contrary, increase in the inspiratory phase determining a huge distention of the jugular veins.
To this clinical signs we can have the symptoms of a
backward heart failure like the enlargement of liver and
spleen and hepatojugular reflux. The decreased cardiac output causes also a secondary peripheral vasoconstriction,
with pallor mucosae, delay in the capillary filling, cold extremities (forward heart failure).

Electrocardiography
Electrocardiogram alteration are not pathognomic, but
are anyway significative if coupled with clinical signs and
enables the doubt of pericardial effusion. We can have voltage reduction of the ventricular complex (R<1 mV in D2)
associated to a normal a wave upper level of the ST segment
with under level of the P-R tract when even the atriums are
compromised. We can also observe phenomenon of electrical alternations, or cyclic variations of the QRS amplitude
due to the swinging of the heart inside the overdistended
pericardium (swinging heart).

Radiology
Moderate or massive pericardial effusions determinate

particular radiological alterations: the cardiac silhouette


shows an increasing of the transverse diameter without enlargement of the heart base. The profile of the cardiac shadow assumes a globular aspect without any sign of the auricles or of the atrioventricular junctions. The increased size
of the cardiac silhouette with its characteristically pumpkin shape is not proportional to the amount of liquid contented in the pericardium; in the same time the detection of
pleural effusions and hepatomegalia suggest a chronic
process. At the radiological examination of the thorax we
can also see the signs of the venous congestion and of the
low range, we can observe evident dilation of the caudal vena cava and the pulmonary veins while the pulmonary arteries are decreased and the lung appears hypovascular and radiolucent.
Before the advent of the echocardiography there was a
radiological method, called the diagnostic pneumopericardium, in this method there was the introduction, after pericardiocentesis, of atmospheric air or carbon dioxide in the
amount of half or less of the drained fluid, in that way it was
possible to obtain a good negative contrast for a radiological
study of the silhouette. This diagnostic proceeding can be
very helpful when there is a suspect of an effusion due to a
tumors etiology.
In those cases the association of a non selective angiography enables us to evidentiate the profile of the cardiac
chambers and of the big vessels, to better define the intrapericardial structure and their anatomical belonging.

Echocardiography
The echocardiogram is surely the technique that better
shows diagnostic utility, because it is highly specific and
sensible in the detection of pericardial effusion. In normal
conditions the pericardium is not visible as a distinct structure: if there is an effusion we have an anaechoic space between the echo reflected from the visceral pericardium and
the one reflected from the parietal pericardium, while they
normally reflect a single echo together.
Besides the detection of an effusion, echocardiography
consent to see the entity, the distribution and the grossly
physical characteristics of the fluid examined (for example
corpuscolated material). But an evaluation of the echodensity of the fluid within the pericardium depends too much on
the regulation of the echocardiographic instrument to be fully reliable, while the evidence of a lacertus fibrosus suggest
chronic inflammatory effusions or sometimes pericardial tumors like celiomas. A solid granular figure can lead to an intrapericardial hematoma, solid masses adherent to one of the
layer or infiltrating suggest tumors effusions. Echocardiography also grants an accurate evaluation of the level of the
haemodynamic commitment.
An important echocardiographic find is represented by
an excessive diastolic relation or a variation in concomitance
with the respiratory acts and the kinetics of the interventricular septum: the septum in the inspiratory phase, moves towards the left ventricle and in the espiratory phase, towards
the right ventricle. In other words, during the inspiration the
right ventricular cavity enlarges its volume, due to the in-

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Constrictive pericarditis
The diagnosis of chronic cardiac compression presents
great difficulties what allows to think that this pathology is
in effect more common of what it is believed, and that often
it is not identified, but it is important to identify this illness
because also if it has a particular severe prognosis in most of
the cases, it is surgically treatable. In this illness the clinical
signs of a commitment of the systemic and pulmonary venous drainage are evident as in the cardiac tamponade, but
only the echocardiography allows an non invasive diagnosis
of chronic cardiac compression, the bidimensional exam
shows a hyperlucent and a thickened pericardium, although
in truth, this report is extremely dependent from the operator, instead there is always an evidenced biatrial enlargements with normal seized ventricles. With the M-mode the
left ventricle shows a backward movement of the septum in
early diastole (early diastolic dip) and a fast early diastolic
excursion of the posterior wall; this aspect of the early diastolic phase shows that the left ventricle suddenly fills in protodiastole while subsequently the filling interrupts. We can
see a flattening of the posterior wall in mid and late diastole,
which represents the haemodynamic corresponding of the
square root sign.
The Doppler exam highlights a sharp deceleration of the
transmitral and transtricuspidal diastolic flows, this report is
common to restrictive cardiomyopathy, but in this last one
we do not have an inspiratory reduction of the flows which
is quiet evident in the constrictive pericarditis.

Treatment
The ultrasound tecnique enables a correct therapeutical
approach for the percutaneous pericardiocentesis, which
represents the procedure used for the stabilization of the patient in the acute phase and the resolution of the pericardial
tamponade. The method we use in those cases provides, if
the conditions of the patient allows it, the positioning of the
dog in a right lateral recumbency on a special table for
echocardiography, if the patient is not able to tolerate the recumbency this procedure can be performed with the animal
in a sitting or standing position. Under echographic guide a
needle of 18G is connected to a tube extension to a large syringe, the needle is introduced in the right forth intercostal
space under the costochondral junction, and through this
system it is possible to introduce physiological solution in
the pericardial sac in order to contrast the area containing the
tip of the needle. We chose the right approach because from
this side there is no risk of injury at the coronary vessels.
If this should be necessary, due to the relapse of the heart
tamponade, a second pericardiocentesis, can be considered.
In idiopathic pericarditis in order to obtain a radical resolution of the illness, and to avoid the evolution toward
chronic cardiac compression, we suggest a surgical subtotal
pericardiectomy, this can be executed in a traditional thoracotomy approach or through thoracoscopy.
In older dogs or animals in critical conditions, so that
they can not be subordinated to surgery we have used percutaneous pericardiectomy tecnique with a balloon catheter

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crease of the venous drainage in concomitance with the reduction of the left ventricular dimensions, the flattening, and
the dislocation of the septum towards the left ventricle. This
irregular movement is called the diastolic paradox septum.
Unfortunately it is not easy to measure this echocardiographic element and moreover it is not pathognomic for
pericardial effusion, but only for a diastolic compromising
of the left ventricle, which can occur also in other pathologies that causes an increasing of the right ventricular pressure like pulmonary hypertension, or pulmonary stenosis.
Better correlated to the relation between intrapericardial
pressure and right atrial pressure are the late diastolic collapse of the right atrium and the early diastolic collapse of
the right ventricle: with the increasing of the pericardial
pressure the right ventricle tends to remain longer in the diastolic phase. This echocardiographic signs are extremely
early and represent the beginning of the real cardiac tamponade, which start to express only when the intrapericardial
pressure, equalizing the diastolic pressure of the right atrium
causes its compression.
Another early echocardiographic sign of pericardial tamponade is the absence of the physiological reduction of the
diameter of the caudal vena cava during the inspiratory
phase, that should be around 50%: this phenomenon is
called vena cava plethora. This fact is strictly correlated
with the values of atrial pressure, index of vena cava collapsing lower than 35% is showing high values of right atrial pressure (Pepi).
The excursion of the caudal cava vein is appreciable and
measurable through a series of monodimensional scans, possibly obtained slowing the speed of sliding and detected at
the height of the diaphragmatic caval hiatus during the respiratory phases. The caval plethora is a very sensible echographic sign to point the venous drainage impediment, unfortunately not specific for cardiac tamponade, but only for
an important right diastolic dysfunction. Using the Doppler
method enables quantitative assessment of the inspiratory
reduction of the transmitral and transaortic speed of the fluid, associated to delayed opening of the mitral valve (in correspondence with the atrial systole) and a premature closing
of the aortic valve. (Appleton) (Schutzman).
Physiologically the aortic and transmitral flow have no
respiratory variation or if they have, only minimal (5%). In
the heart tamponade we can see respiratory reduction of the
mitral and aortic flow more than 25%, clear evidence of the
massive diastolic relation that occurs in the heart tamponade.
Analyzing the transmitral diastolic flow with the
Doppler, we can also highlight a reduction of the amplitude
and duration of the E wave, expressing a diastolic impediment in the first phase of the ventricular filling, or like in the
severe forms, were this only happens when we have the atrial contraction. In the massive forms the left ventricular filling is almost exclusively caused by the atrial contraction. In
physiological conditions the atrial contribution to the diastole is not higher than 25%, while in this cases it determinate
over the 50% of the diastolic volume: this phenomenon is
detected by the Doppler with a decreasing of the E/A ratio
and an increasing of the ratio between the A area and the integral of the whole transmitral flow. (Appellation).

125

126

(Cobb). This tecnique is executed under fluoroscopic control


with the dog in right lateral recumbence and after sedation.
With the help of the echographic guide the point were the
catheter will be introduced is chose, and in this point we
practice a local anesthesia, taking care to also include the
pleura parietalis. Then we introduce a needle of 16G through
the thorax wall to the pericardium, through this needle we
introduce in the pericardial sac a metal guide wire of 0.038
inches and 150 cm length, and through this guide we pass a
vascular dilator of 8 French until the pericardial sac, finally
removed the dilator, through the guide wire we introduce the
balloon catheter, the deflated balloon is placed through the
pericardial sac. For this use we need balloons that once inflated reach the diameter of 2-3 cm and the length of 4 cm.
The inflating of the balloon is executed with a 50% physiological solution and a contrast medium, the balloon is first
partially inflated, what enables us to highlight through fluoroscopy the depression on the balloon caused by the pericardial sac, if necessary we can move the balloon back and
forth. The balloon is then completely inflated until the waist
on it disappears, and kept like that for 2. This procedure has
given good results as a palliative therapy in tumors pericardial effusions, allowing the liquid formed in the pericardium
to pour in the thorax and to be reabsorbed.
In the benign idiopathic pericarditis with a possible immunological etiology there have been used many pharmacological therapies in order to reduce the immunitary response,
like corticoids, prednisolone 0.5-1 mg/kg. We experienced
(10 patients) the administration of azathioprine orally 1
mg/kg SID for a three months period after the first pericardiocentesis or in subjects which presented relapse after a
short time from the second pericardiocentesis.
During the treatment with Azathioprine we did not highlight secondary effects, besides a modest anemia and leu-

4th European FECAVA SCIVAC Congress

copenia. At this point of time in neither one of the subjects


treated there has been a relapse of important pericardial effusion.
The validity of this therapy surly needs further confirmations with treatments for a longer period of time and
groups of animals of greater numbers besides groups treated
with dummy.

Bibliography
Appleton C, Hatle L, Popp R: Cardiac tamponade and pericardial effusion:
respiratory variation in transvalvular flow velocities studied by
Doppler echocardiography. J.A.C.C. 1988;11:1020-1030.
Assanelli D, Lew W, Shabetai R, Le Winter M: Influence of the pericardium on right and left ventricular filling in the dog. J. Appl. Physiol.
1987; 63:1025-1032.
Cobb M.A. Boswood, G.M. Griffin and McEvoy F.J. Percutaneous balloon
pericardiotomy for the management of malignant pericardial effusion
in two dogs. Journal Small animal practice 1996; 37: 549-551.
Gibbs C, Gaskell CJ, Darke PGG, Wotton PR: Idiopathic pericardial hemorrage in dogs: A review of fourteen cases. J. Small Animal Pract.
23:483,1982.
Lopez-Sendom J, Garcia Fernandez M, Coma Canella I, Sotillo J, Silvestre
J: Mechanism of right atrial wall compression in pericardial effusion:
an experimental study in dogs; Journal Cardiovascular Ultrasonography 1988; 127-134.
Pepi M, Tamborini G., Barbier P., Doria E., Ecografia nello studio della fisiologia e della patologia del pericardio. Giornale Italiano di
Ecografia Cardiovascolare. Vol 4, N1 Marzo 1994.
Reed J.R. Pericardial diseases in Fox, Canine and Feline Cardiology
Churchill Livingstone 1988.
Santamore W, Constantinescu M, Little M: Direct assessment of right ventricular transmural pressure. Circulation 1987;75:744-747.
Schutzman J, Obarsky T, Pearce G, Klein A: Comparision of Doppler and
two-dimensional echocardiography for assessment of pericardial effusion. Am J Cardiology 1992; 70:1353-1357.
Sisson D, Thomas WP, Ruehl WW, Zinkl JG: Diagnostic value of pericardial fluid analysis in the dog. J Am Vet Med Assoc 184:51, 1984.

4th European FECAVA SCIVAC Congress

127

Disseminated intravascular coagulation:


State of the Art
Marco Caldin

Diagnosis of DIC, as well as many other aspects of this


fascinating intermediary mechanism of disease, is still a
rather complex phenomenon. We learned through the analysis of the DIC cases - as described in literature and through
ones we considered - that doesnt exist a single sign either of
laboratory or clinic, which can prove the existence of such a
clinical condition. Moreover often there are no correlation at
all between clinical-laboratory signs and autopsy findings.
That is why the diagnosis of DIC is a challenge for the internist who must evaluate critically clinical and laboratory
manifestations. For the clinical point of view in order to hypothesise the DIC, there must be a clinical entity able to
cause it. From the laboratory side the results must be evaluated in relationship with their sensibility and specificity towards the DIC.

then, exceeds the normal physiologic answers of compensation. Whereas in course of a low-grade DIC (compensatedchronic), the alterations are often only of the laboratory
kind, because the comsumption of the coagulant factors is
balanced by an increased production. Nevertheless the evolution from a phase to another, such as from normal to fulminant DIC, is very fast. This points out the dynamism of
the hemostatic balance.
Thrombotic manifestations, which are more difficulty visualized, bring to the production of microthrombes and
macrothrombes, that produce damages and sometimes a real
failure of the organs involved. Together with organ failure,
systemic signs of shock and metabolic acidosis appear deriving from a reduction in the tissue perfusion.

Laboratory features
Clinical features
Clinical signs deriving from DIC are generally those associated to the thrombohaemorrhagic disease. We must consider that it is quite easy for the physician to diagnose haemorrhagic events while it is more difficult to recognise the
thrombotic signs so our comprehension of the problem is only partial. We must add that the clinical picture shows also
the clinical signs deriving from the disease that has caused
the DIC. For that reason it is sometimes difficult to distinguish between cause and effect, that is to say between the
disease and its effects, i.e.,It is common the onset of liver
failure when there is a fulminant DIC, but it is also true that
liver failure is often the cause of the DIC.
The clinical signs combined with the haemorrhagic event
can be such as petechiae, ecchymosis, subcutaneous
haematomas, hemorrhagic diarrhoea and vomiting, hematuria, excessive post-traumatic (or post venipunctures)
bleeding.
According to our experience, hemorrhagic body effusions rarely are due to a DIC. When the clinician finds a hemorrhagic body effusion with laboratory signs of DIC
he/she must go on looking for the cause of it, since hemorrhagic manifestation depends from specific causes. In this
case the DIC emphasises the hemorrhagic events. Tipical example is the spleen hemangiosarcoma with abdominal effusion. Hemorrhagic manifestations are more frequent when
there is a fulminant DIC (decompensated-acute), when the
dynamic of the coagulation process first, and hemorrhagic

Data base (hemogram-biochemical profile-urynalisis) are


essential tools for a interpretation of the coagulative alterations. The data base often point out causes and the effects in
the DIC. As we said above, there is no single test able to diagnose the DIC. Nevertheless the laboratory tests are very important to evaluate the existence of the DIC. Unfortunately, as
far as we know, in veterinary licterature they are seldom considered in relation to their sensibility and specificity towards
the DIC. Besides the increasing number of the diagnostic
markers make us evaluate critically not only the new tests but
also the more traditional ones which have been revalueted in
the light of what we know. The data here reported refer to 71
DIC cases, analysed by one of the authors (M.C.).

Prothrombin time (PT)


Prothrombin time represents a global test which measures
the extrinsic pathway1 and the common pathway. It represents a direct measure of the factors I, II, V, VII, and X. When
one or more of these coagulation factors goes down to an
amount considerated critical (50-60 %), there in an increase
in PT. In the DIC the PT gets longer for different reasons:

Attualmente la divisione in due cascate coagulative ritenuta sorpassata


data la ormai comprovata relazione tra fattore VII e IX.

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Med Vet
Senior Lectures, Faculty of Veterinary Medicine, University of Padua - Italy

128

A. consumption of the factors involved in the extrinsic pathway and specially in the common pathway (fibrinogen).
B. Inactivation of the factors V and IX caused by the plasmin
C. Interference with fibrin monomer polymerization caused
by the FDP.
Sometimes in the DIC we assist also to a shortening of
the PT, because of the activated coagulation factors (thrombin and Xa).
In our research the PT has demonstrated a sensibility of
29% on 71 cases and it has also demonstrated a specificity
of 30%, showing the tendency to be alterated in the fulminant DIC together with the fibrinogen and platelets.

Activated partial thromboplastin time


(aPTT)
Activated partial thromboplastin time represents a global test which measures the intrinsic pathway 1 and the common pathway. It represents a direct measure of the factors
XII, XI, IX, VIII, prekallikrein, HWMK and more approximately of the factors I; II, V and X. In the DIC the lengthening and the shortening of the aPTT occurs for the same
reasons described for the PT. In our study the aPTT has
demonstrated a remarkable sensibility (73%), in spite of a
low specificity (30%), with the tendency to be alterated either in the fulminant DIC or in the low grade DIC. The great
sensibility of this test is probably due to the fact that the
aPTT evaluates in a more detailed way the intrinsic pathway,
which is mainly involved in the consumption of the coagulation factors.

Fibrinogen
During the DIC there is the consumption of fibrinogen
by the activation of the coagulation system which leads to its
trasformation to fibrin with diffuse thrombosis. Even if this
event occurs almost steadily, many times it does not determine a recognizable hypofibrinogenemia. This is due to a
considerable capacity of the hepatic synthesis in an acute or
chronic inflammatory process, when the liver increases the
synthesis of this coagulation factor concealing the consumption process. Furthermore collocation of fibrinogen to the
acute phase proteins may trasform this coagulant factor in a
protein sensible to other events different from the coagulation.When the fibrinogen level reduced at 75-100 mg/dl,
there is a lengthening of the PT and aPTT, and the PT seems
more sensible than aPTT to the hypofibrinogenemia. In our
series of 71 cases of DIC, fibrinogen appears of low sensibility (11%) but with a fairly good specificity (80%). Probably this depends by the low number of diseases that can reduce it (e.g. liver failure). Hypofibrinogenemia becomes evident during the fulminant DIC and it occurs a short time before the platelets consumption. If -in order to measure this
coagulation factor- we use a laboratory method based on
trasformation of fibrinogen to fibrin it can happen that artificious low values are recorded. This is due to the interference of the FDP in the conversion of fibrinogen into fibrin.

4th European FECAVA SCIVAC Congress

Thrombocytopenia/thrombocytopathia
In the DIC the low platelet count is due to the activation
of the coagulation process that causes the formation of microthrombes in the vascular bed. However as in the fibrinogen model,the presence of the inflammatory processes causing the DIC, or developping together with the DIC, can produce a reactive thrombocytosis that conceals the low level of
platelets.
High levels of platelet factor 4 and beta-thromboglobulina, document this fact, also if these markers are not pathognomonics. The alteration of the functional platelet is another aspect following the DIC.This is caused by the FDP coating of platelet membranes or the partial release of platelet
procoagulant material. Tests performed to document this fact
(bleeding time and platelets aggregation), have a unfavourable relationship between cost and benefit. In our series of 71 cases of DIC, a low platelets count shows a 13%
sensibility and a specificity of 90%, with the tendency to appear in fulminant DIC together with hypofibrinogenemia.

Schistocytes
Schistocytes, or red cell fragments, are end result of the
mechanical damage of the plasmatic membrane of eritrocytes against intravascularly fibrin strands. This event its
well documented by Bull and coworkers and it is more frequent in low-grade DIC. In fulminant DIC, often, the
process its so fast that there is not enough time to create a
extensive damage of the red cells.Other conditions that can
produce schistocytes are Heinz body anemia, iron deficiency, and laboratory artifacts.
In our series the sensibility of this test has been 20% and
the specificity 90%.

Fibrin(ogen) degradation products (FDP)


Plasmin degradation of the fibrin and the fibrinogen produces the FDP. The appearance of these products of degradation in blood shows the presence of plasmin. The FDPs
are constituted by the fragments X, Y, D and E. These fragments D and E are the most important from the diagnostic
point of view, and the commercial kit (thrombo-wellcotest)
which is generally used for FDP, measures these two fragments only.
The FDP are important not only for their diagnostic
meaning, but also for their anticoagulant activity that is responsible, together with the consumption of coagulant factors, of the haemorraghic syndrome that appears during the
DIC. They are considered ones of the most important inhibitors in blood. The derivation from fibrinogen, other than
fibrin, makes this diagnostic test less specific towards the
DIC. Nevertheless the DIC represents the clinical condition
that more frequently causes an increase of the FDP. There are
some other conditions that can produce a high level of FDP
through an increased production or a reduced elimination:
A. insufficiency of the mononuclear phagocytice system
which removes these products.

4th European FECAVA SCIVAC Congress

D-Dimers
The D-Dimers are the products of fibrins degradation.
They are the direct witness of the fibrinolytic activation, secondary to a coagulation process.
The D-Dimers are the most specific test to diagnose a
DIC, since they come only from the fibrin and not from the
fibrinogen as it happens to the fragments X, Y, D and E.
With regard to the DIC on 71 cases of DIC our research
has demonstrated a 82% sensibility and a 95% specificity.
We believe that, as in human medicine, also in dogs, the
D-Dimers appears to be the test most likely to be alterated in
confirmed DIC.

Antithrombin III (AT III)


The AT III, together with protein C, protein S, and components of the fibrinolytics system are physiologically the
most important naturally occuring anticoagulants proteins
The AT III regulates the blood haemostasis and defends the
organism against intravascular thrombosis2. It is an alpha-2globulin, produced by the liver (systemic action in blood)
and, to a lesser extent, it is produced by the vascular endotelium (local action). It inactivates thrombin and other
serine proteases in a progressive, irreversible manner. Antithrombin also inactivates other serine proteases, including
factors Xa, IXa, Xa, XIIa, and kallikrein, although with less
efficiency than for the inhibition of the thrombin.The rate of
AT III-mediated inactivation clotting factor is markedly enhanced by heparin (i.e., 2,000 folds compared to thrombin).
In DIC there is an increased consumption and consequently
a low level of AT III in blood. Diseases that can cause a low
level of AT III, besides the DIC are:
A. liver failure (reduced production).
B. Nephrotic syndrome (increased loss).
C. Protein loosing entheropathies (increased loss).
From a diagnostic point of view the AT III is less specific because there are quite many diseases which can influence
it. The low diagnostic aid from the AT III levels in diagnosing the DIC is related to the function of the molecule which
belongs to the acute phase proteins. Consequently, the AT III
levels undergo to fluctations in relationship to the entity of
the process. Since the AT III measures the patients anticoagulant capacity it must be considered as an indirect test for
the diagnosis of the DIC. In our DIC dogs, the sensibility
and specificity were respectively 48% and 60%. The AT III
levels might have great importance mostly in fulminant
DIC, where the consumption is greater than hepatic synthesis. The AT III is a good prognostic indicator. The prognosis
is guarded as much as the levels of AT III are reduced in
blood.

A list of suggested readings (MS Word97 or html format)


will be e-mailed by the authors if requested to
sanmarco@iperv.it

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B. Corticosteroids.
C. Liver failure.
D. Disfibrinogenemia (fibrinogens molecules not coagulated in test tube, cross-react with the policlonal antibodies
towards the fragments D and E).
E. Primary hyperfibrinolysis (clinical entity poorly described in veterinary medicine).
F. Artifacts deriving from the failing separation of the fibrinogen from fragments D and E cause a cross-reaction
with policlonal antibodies and the fibrinogen.
Besides positives in a clinical condition, different from
the DIC, you can find also some false negatives:
A. in the DIC with low activation of the fibrinolysis are produced only X fragments in the very early phase of plasmin degradation, which are not measured out by the traditional assays for FDP.
B. In the coagulation process which takes place in the testtube the D and E fragments can be trapped in the clot and
they can be present in a small quantity in the serum.
C. Excessive release of collagenase and elastase, originated
in leukocytes, which degrades the FDP producing false
negatives.
In spite of these difficulties, in the current veterinary literature the FDP are considered the mainstay of the diagnosis of the DIC.
In our study on 71 cases the FDP has demonstrated a
64% sensibility against a 55% specificity.

129

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131

Claw diseases in dogs and cats


Didier-Nol Carlotti

Summary
A figure of the anatomy of the canine claw is first presented. The clinical aspects of claw alterations and the diseases which cause such alterations in dogs and cats are reviewed, with emphasis on particular conditions: trauma,
bacterial infection, fungal infection, parasitic diseases, allergies, auto-immune diseases, Raynauds disease, keratinization disorders, genodermatoses, naevus and idiopathic
onychogryphosis, neoplasia. Claw diseases are often diagnostic and therapeutic challenges. A detailed case history, a
thorough physical examination and appropriate complementary examinations are required to establish a diagnosis of
claw diseases in dogs and cats. Therapy must be specific. In
all cases appropriate follow-up is most important.

Introduction
Nail disorders are relatively rare in companion animals,
particularly in comparison with nail disorders in man1,2,3,4,5,6.
In man, nail disorders are numerous and related to various
causes7. These include hereditary nail dystrophies, trauma,
bacterial infection, candidiasis, dermatophytosis, psoriasis,
eczema, lichen planus, nail disorders observed in systemic
diseases, Raynauds disease, arteritis, frost-bite.

Anatomy
Figure 1 shows the anatomy of the canine claw unit1,8,9.
The nail, or claw, is made of a thick stratum corneum. Claws
have prehensile, locomotor and offensive/defensive functions3,4. A fibro-myxoid body with an ovoid shape has been
discovered between the claw and the third phalanx in dogs
and cats9.

nail fold. Usually the area looks erythematous and oedematous. Oozing, crusting, and - less common - erosion and ulceration may be present (e.g. in auto-immune mediated dermatoses). In chronic cases, scaling, alopecia, lichenification
and hyperpigmentation may be observed.
Onychoschisis means fissuration (splitting) of the nail. It
can be caused by many inflammatory processes which alter
the nail structure and by trauma.
Onychorrhexis is the breaking of a nail which has become brittle for pathological reasons.
Onychogryphosis is a deformation of the claw. It appears
to be elongated and distorted. Usually this is caused by the
inflammation of the digit extremities, coupled with a perionyxis.
Onychomadesis is the sloughing off process for nails, it
is usually multiple.
Claw fracture is sometimes called onychoclasis.
Onyxis can affect only one nail (trauma, idiopathic onychogryphosis, neoplasia, and often dermatophytosis, although the latter can affect a few digits, not necessarily all
on the same foot). On the other hand multiple onyxis is observed in bacterial infections, leishmaniasis, allergic diseases, auto-immune disorders, Raynaud-like diseases, and
keratinization disorders.
Pruritus is rarely observed in cases of onyxis. It mainly
appears in cases of allergic dermatitis. Pain is more common,
particularly in cases of severe perionyxis, onychoschisis,
onychorrhexis and onychomadesis, particularly in bacterial
infections and immune-mediated disorders. It can be acute in
the case of nail fracture. It will only appear belatedly in cases of neoplasia. However, neither pruritus nor pain will be
noticeable in many cases, such as onychogryphosis (e.g. dermatphytosis, leishmaniasis, keratinization disorders, idiopathic onychogryphosis and the early stages of neoplasms).

Consideration of particular
diseases1,2,3,4,5,6,9,11
Clinical signs1,2,3,4
1 - Traumatic onyxis
Onyxis (or onychia) is by definition the disease of the abnormal looking nail. Often, but not always (e.g. trauma, neoplasia), an inflammatory process is responsible for the nail
alteration. Onyxis can be proximal (usually at the onset of
the disease), distal, or it may involve all the nail.
Perionyxis (or paronychia) is the inflammation of the

This is a very common disease in the dog. It usually affects only one nail, in particular the thumbnails (digit 1) on
the hind legs. The nail is more or less distally broken and pain
is usually observed. Diagnosis is clinically obvious. Therapy
consists in promptly removing the distal part of the nail with

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Med Vet, Dipl ECVD


Private Practitioner, Bordeaux - Merignac, France

132

forceps. A bandage is then applied for a few hours. If this is


done a few days after the fracture, systemic antibiotics should
be used for a week to prevent secondary bacterial infection.

4th European FECAVA SCIVAC Congress

serology and/or a parasitological examination (skin and/or


bone marrow cytology). Comprehensive therapy
(Lomidine, Glucantime, amphotericin B, allopurinol) and
a strict follow-up are mandatory.

2 - Bacterial onyxis
5 - Onyxis of canine ankylostomiasis
This disease exists in the dog but is much rarer in the cat.
In the latter, it is usually associated with an immunodeficient
state (FeLV and/or FIV infection, diabetes mellitus etc...). In
the dog it may be idiopathic or secondary to an underlying
disease (such as hypothyroidism, or even Cushings disease). Perionyxis, onychoschisis, onychorrhexis and onychomadesis are usually seen on several nails, with pain as
the primary complaint.
Diagnosis is made by cytology - which reveals a bacterial pus (degenerated neutrophils, phagocytosis), bacteriology and the response to therapy. Treatment must be based on
the removal of broken nails, topical antibacterial therapy and
long term systemic antibiotic therapy (based on bacterial
cultures and sensitivity testing, Staphylococcus sp. and
Gram negative rods often being cultured). Months of careful
therapy are needed, until the distal abnormal part of the nail
has disappeared. In all cases, and particularly in chronically
relapsing ones, an underlying disease should be suspected
and, if found, treated.
Bacterial pododermatitis, whatever the cause, often leads
to bacterial onyxis. Good examples are interdigital pyodermas due to demodicosis and allergic skin diseases. Perionyxis is a prominent feature in such cases. Therapy appropriate to the causal pododermatitis will cure the nail problem
if carried out for long enough.

3 - Dermatophytic onyxis
This is a rare cause of onyxis and perionyxis in the dog,
usually with one or a few digits being affected. In Aquitaine,
Microsporum gypseum and Microsporum canis have been
found to be the dermatophytes which most frequently cause
fungal onyxis. Alopecia of the corresponding digit is often
observed. Diagnosis is made by Woods light examination
which may reveal the fluorescence of the hair of the digit involved, direct examination and fungal culture of this hair,
and histopathology of the nail itself. Skin biopsy and the removal of the third phalanx are unnecessary. PAS staining of
the nail is mandatory and reveals the invasion of the nail keratine by the fungal hyphae.
Long-term antifungal therapy (griseofulvine, ketoconazole, itraconazole) is necessary until the abnormal part of the
nail disappears distally. This may take several months. Other
cutaneous lesions should be topically treated simultaneously.
Dermatophytic onyxis appears to be extremely rare in the cat.
The author has never made such a diagnosis in a feline.

4 - Onyxis of leishmaniasis
Onychogryphosis is a classic symptom of canine leishmaniasis. In the the enzootic area such a complaint justifies

Onychorrexis and onychomadesis can be seen in chronic


cases of pododermatitis caused by ankyostomiasis12. Diagnosis is made by cutaneous histopathology and coproscopy.

6 - Onyxis of allergic dermatites


An inflammatory skin disease of the digits (pododermatitis) is observed clinically in canine atopic dermatitis and
food allergy or intolerance. Onychogryphosis is frequent, often associated with perionyxis and redness of the hair on the
digits. The nails may appear reddish in dogs whose nails are
normally white.
A diagnosis is obviously reached by evaluating all the
symptoms observed in these diseases, by skin-testing, serology and elimination diets. Therapy includes allergen eviction, hyposentitization and symptomatic treatment (systemic
glucocorticoids, antihistamines, essential fatty acids, topical
antipruritic agents etc.).

7 - Onyxis of auto-immune dermatoses


These diseases usually affect several digits.
A - discoid lupus erythematosus/symmetrical lupoid onychodystrophy.
Discoid lupus erythematosus is a not so uncommon
cause of onyxis in the dog3,9,13. In fact, as the disease is symmetrical, as focal thickening and smudging of the basement
membrane zone are not seen and as direct immunofluorescence testing is negative, Danny Scott named this disease
Symmetrical Lupoid Onychodystrophy in 199511. Onychorrhexis and onychogryphosis are the main features of the
disease. Other lesions may be seen in other areas of the
body, but this is not always the case. Perionyxis is not always pronounced and skin biopsies of the nail bed area may
be unrewarding. Amputation of the third phalanx is often the
only way to reveal the typical hydropic and lichenoid interface dermatitis. Immuno-suppressive doses of glucorticoids
(prednisolone) may control the disease. Vitamin E and essential fatty acids (omega-3/omega-6 commercial compound) have been reported to be effective in some cases3,11.
B - pemphigus vulgaris.
Nails and nail beds may be affected in pemphigus vulgaris. Onychogryphosis and onychomadesis can be observed.
Severe perionyxis is also present, with erosions around the
nail bed which are a source of pain. Diagnosis is made by
histopathology either by skin biopsies around the claw or alternatively by amputation of the third phalanx. Biopsies of lesions in other body areas may be diagnostic. Only a guarded
prognosis should be made. Immunosuppressive therapy
should be carried out (glucocorticoids, azathioprine).

4th European FECAVA SCIVAC Congress

8 - Raynaud-like disease
In Man, Raynauds disease is due to a spasm of digital
arteries due to cold, which may be either secondary (e.g. to
SLE) or idiopathic. It is a cyanotic/hyperhaemic and painful
disease. Three female dogs (2 Boxers of 3 and 4 years of age
and a 5 year-old mongrel) were suspected by the author to
have a Raynaud-like disease. The patients were in severe
pain from several digts which from time to time looked
cyanotic. Onychogryphosis was prominent. Skin biopsies
were performed in 2 dogs around the claws and showed non
specific superficial dermatitis and a few Malassezia in the
stratum corneum in one dog. Direct immunofluorescence
testing was negative for IgG and C3. ANA test was negative
in the 3 dogs. Long term therapy with isoxsuprine, a vasodilatator, at the dose of 1mg/kg/day, was very helpful.

9 - Keratinization diseases
The author has seen severe mutiple onychogryphosis in
cases of canine ichthyosis. However, generalized skin lesions were prominent and histopathology of the lesions con-

firmed the diagnosis. Many cases responded partially to


retinoid therapy.
Some cases of zinc responsive dermatosis observed in
nordic dogs involve several digits. Two cases restricted to
the digits, with a prominent perionyxis and above all onychorrhexis were observed by the author in Malamutes (of 10
and 12 months of age respectively). Diagnosis was made by
histopathology, with biopsies taken around the nail bed.
There was a dramatic response to zinc sulfate supplementation (150 mg/kg BID) whereas zinc methionine had not been
very helpful.
Several cases of idiopathic nosodigital hyperkeratosis in
the older dog may be associated with mild multiple onychogryphosis.

10 - Genodermatoses
Ichtyosis is a hereditary keratinization disorder.
Onychogryphosis can be seen in canine dermatomyositis
(Collies, Shetlands, Beaucerons) and epidermolysis bullosa
(Beaucerons)14. Glucorticoids, vitamin E and pentoxifylline
are helpful. A similar hereditary condition could exist in the
cat, with onychomadesis15.

11 - Linear nevus and idiopathic


onychogryphosis
A case of congenital linear epidermal nevus ending in the
paw of a hindleg was diagnosed by the author in a 3 year old
Pyrenean shepherd, with a prominent onychogryphosis on 2
digits (and a secondary demodectic pododermatitis as well).
The nevus responded well to retinoid therapy (etretinate 1
mg/kg/day during 18 months followed by acitretin, at the
same dosage, during 8 months).
The author has seen multiple inverted papillomas in a 7
year old mixed French Spaniel associated with a severe onychogryphosis of only one digit. Papillomas can cause the development of cutaneous horns and potentially this claw alteration was linked to the skin disease.
Idiopathic onychogryphosis is observed in dogs. It usually affects one digit. Diagnosis is made by the elimination
of other possible causes. Regular removal of the nail affected is advisable.

12 - Neoplasms
Neoplasia of the nail fold is a common cause of onyxis
and onychomadesis in the old dog. Squamous cell carcinoma (which is often misleading since it looks like a non-healing wound), melanoma, and mast cell tumour are relitavely
frequent. However keratoacanthoma, inverted papilloma,
and eccrine adenocarcinoma may also be observed3. These
tumours affect only one digit usually, and necessitate agressive excision therapy. Melanoma and mast cell tumour may
metastase, although squamous cell carcinoma has a better
prognosis than usually believed if excision is carried out at
an early stage. Swelling is often prominent and pain is acute.

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C - pemphigus foliaceus and/or erythematosus.


Onychogryphosis and perionyxis can be observed in canine pemphigus foliaceus, particularly in severe forms of the
disease. When pemphigus foliaceus is exclusively confined
to the foot pads onychorrhexis is often observed. The author
has seen 2 cases of pemphigus erythematosus confined exclusively to the footpads, with onychorrhexis.
Diagnosis can be made by histopathology. In the extensive forms of the disease, biopsy of the skin lesions may be
diagnostic. In the localized forms, biopsy of the foot pads
and/or an amputation of the third phalanx may be diagnostic. Immunosuppressive therapy is necessary.
In the cat, pemphigus foliaceus is a possible cause of severe perionyxis. A thick pus is discovered in the nail bed.
Diagnosis is usually made by skin biopsy of the other skin
lesions. Glucocorticoid immunosuppressive therapy is
helpful.
D - bullous pemphigoid-like skin disease.
Severe multiple onychomadesis and/or severe onychogryphosis with ulcerative perionyxis may be seen in the
bullous pemphigoid group skin disease (a group of auto-immune disorders with subepidermal clefting as a common
feature). They may even be the prominent features of this
disease, making it a most painful one. Diagnosis is made by
biopsy of the skin lesions, particularly of the digits, if there
is ulceration around the nail bed. Alternatively, amputation
of the third phalanx of an affected digit may be the only way
to diagnose such a condition if only nail disease is present.
In one case, the author had the luck to establish a diagnosis
of bullous pemphigoid by removing nails from a dog with
onychomadesis; a small amount of skin tissue still attached
to the claw displayed the typical lesions of dermal-epidermal
clefting.
Therapy is not easy. Glucorticoid immunosuppression is
not always helpful.

133

134

4th European FECAVA SCIVAC Congress

Diagnosis is made by histopathlogy of the removed tumour


and radiographs of the digits often reveal bone lysis.
Multiple squamous cell carcinomas are seen in black
dogs, affecting several digits, with a slow growth rate. Excision therapy is mandatory.
Nail bed tumours are rarer in old cats. Those that do occur are squamous cell carcinoma, hemangiosarcomas, and
metatasis of primary lung carcinomas3.

inations are required to establish a diagnosis. The latter include cytology, bacteriology, mycology, histopathology (skin
biopsy around the nail bed or even third phalanx amputation,
sometimes very helpful) and immunological tests such as
skin-testing and elimination diets. Therapy must be specific.
In all cases appropriate follow-up is most important.

References
1.

Conclusion
Claw diseases in dogs and cats are often diagnostic and
therapeutic challenges. A detailed case history, a thorough
physical examination and appropriate complementary exam-

2.
3.
4.
5.
6.

DORSAL
EPIDERMIS
3rd PHALANX

DORSAL
MATRIX

7.
8.
9.
10.

11.

12.
13.
14.

VENTRAL
FOOTPAD
MATRIX
NAIL
VENTRAL
EPIDERMIS

15.

16.
Figure 1 - Anatomy of the canine claw

Scott DW, Miller WH, Griffin CE (1995), Muller and Kirks Small
Animal Dermatology, 5th edition, WB SAUNDERS Company,
Philadelphia.
Foil CS (1987), Disorders of the feet and claws, Proc. 11th KAL
KAN Symposium, 23-32.
Scott DW, Miller WH (1992), Disorders of the claw and clawbeds in
dogs, Compend Contin Educ Pract Vet, 14: 1448-1458.
Scott DW, Miller WH (1992), Disorders of the claw and the clawbeds
in cats, Compend Contin Educ Pract Vet, 14: 449-457.
White SD (1989), Pododermatis, Vet Dermatol, 1: 1-18.
Guagure E, Hubert B, Delabre C (1992), Feline pododermatitis, Vet
Dermatol, 3:1-12.
Du Vivier A (1980), Atlas of Clinical Dermatology, Gower Medical
Publishing Ltd, London.
Mueller RS, Sterner-Kock A, Stannard AA (1993), Microanatomy of
the canine claw, Vet Dermatol, 4: 5-11.
Carlotti DN (1995), Affections des griffes chez le chien et le chat,
Prat Md Chir Anim Comp, 30: 235-247.
Delabre C, Guagure E, Magnol JP (1993), Mise au point dune technique de coupe histologique de doigts de carnivores - applications
pratiques, Proc. 8es Journes du GEDAC, St-Malo.
Scott DW, Rousselle S, Miller WH (1995), Symmetrical Lupoid Onychodystrophy in Dogs: A retrospective Analysis of 18 Cases (19891993), J Amer Anim Hosp Ass, 31: 194 - 201.
Gross TL, Ihrke PJ, Walder EJ (1992), Veterinary Dermatopathology,
Mosby Year Book, St-Louis.
Remy I, Fontaine J (1992), Lupus rythmateux discode localisation unguale chez un chien, Proc Congrs CNVSPA, Paris, 314.
Fontaine J, Remy I, Clerxc C (1992), Epidermolyse bulleuse jonctionnelle familiale chez les chiots Bergers de Beauce, Proc Congrs
CNVSPA, Paris, 313.
Johnstone I, Mason K, Sutton R (1992), A hereditary junctional
mechanobullous disease in the cat, Proc 2nd Word Congress of Veterinary Dermatology, Montral, 1992, 111-112.
Goldschmidt MH, Shofer FS (1992), Skin tumors of the dog an the
cat, Pergamon Press, Oxford.

4th European FECAVA SCIVAC Congress

135

Its a coagulopathy. But couldnt it be ehrlichiosis?


C. Guillermo Couto

Summary
Spontaneous bleeding disorders are common in dogs.
Because canine ehrlichiosis can result in thrombocytopenia,
thrombopathia, and other coagulopathies, it frequently leads
to spontaneous bleeding.

Etiology and epidemiology


Canine ehrlichiosis (CE), also known as tracker dog disease, tropical canine pancytopenia, and canine hemorrhagic
fever, is caused by Ehrlichia canis, an obligated parasite of the
mononuclear cells, and it is distributed worldwide. It appear
that in German Shepherd dogs and Dobermann Pinschers, the
disease is more severe than in other breeds. This disease became prominent after a large number of military dogs developed CE during the Vietnam war. A neutrophilic strain of
ehrlichia has also been identified in dogs. Also, E. risticii (the
Potomac horse fever agent) may result in seropositivity without clinical signs in dogs. Recently, it was demonstrated that
E. risticii can result in seropositivity and transient fever, lymphadenopathy, and diarrhea in experimentally inoculated cats.
Another ehrlichia organism, E. platys, prevalent only in
the southeastern United States, can result in cyclic thrombocytopenia in dogs.
The vector and main reservoir of E. canis is the common
brown dog tick (Rhipicephalus sanguineous), which can
transmit the organisms for more than 5 months after engorgement with infected blood; the incubation period varies
from 7 to 21 days. The brown dog tick also can harbor
Babesia and Hepatozoon spp. This organism can also be
transmitted through blood transfusions.

Clinical features
Three common clinical phases are recognized for CE:
acute, subclinical, and chronic. The acute phase is common
in enzootic areas, and rare in other regions. It lasts approximately two to four weeks and consists of mild to severe clinical signs, secondary to lymphoid hyperplasia, pyrexia, and
cytopenias. Clinical signs and physical examination findings
include presence of ticks, pyrexia, depression, weight loss,
evidence of primary hemostatic bleeding, reactive lymphadenopathy and hyperplastic splenomegaly, dyspnea or

exercise intolerance due to pneumonitis, and occasionally,


central nervous system (CNS) signs. During this phase, the
titer may be negative, since it takes one to two weeks to develop sufficient antibody production (see below).
The subclinical phase occurs after the acute phase, may
last years, and is usually asymptomatic, although clinicopathologic abnormalities such as cytopenias and hyperglobulinemia may occur. An immunocompetent dog usually
eliminates the organism during this phase.
The chronic phase develops in dogs who cannot eliminate the organism, and is common in the non-enzootic areas.
Clinically, it is also characterized by lymphoreticular hyperplasia, cytopenias, and hyperglobulinemia. The clinical
signs begin one to four months post-inoculation, are variable
in severity, and include weight loss, pallor, evidence of primary hemostatic defects, generalized reactive lymphadenopathy, hyperplastic splenomegaly with extramedullary hematopoiesis, ocular changes (chorioretinitis,
anterior uveitis, hyphema, retinal hemorrhages), limb edema, and occasionally, CNS signs.

Clinicopathologic features
The hematologic and serum biochemical findings consist
mainly of cytopenias and hyperproteinemia due to hyperglobulinemia. During the acute phase thrombocytopenia due
to peripheral destruction of platelets (ie; presumptively immune-mediated), regenerative anemia (due to immune hemolysis), leukocytosis with monocytosis, and a hypercellular bone marrow constitute common hematologic abnormalities; hyperproteinemia is present in a variable percentage of
cases, and it usually worsens with time.
Hyperglobulinemia and increased liver enzyme activities
(with or without hyperbilirubinemia) are the main serum
biochemical abnormalities during this phase.
During the chronic phase, clinicopathologic changes are
dominated by bi- or pancytopenia (with a hypocellular bone
marrow), lymphocytosis (up to approximately 15,000 lymphocytes/l), hyperglobulinemia and hypoalbuminemia due
to a polyclonal (or more rarely, monoclonal) gammopathy,
and proteinuria due to interstitial, lymphoplasmacytic
nephritis; in addition to hypocellularity, bone marrow aspirates usually reveal increased numbers of plasma cells. Occasionally, dogs with chronic ehrlichiosis and normal
platelet counts experience episodes of primary hemostatic

MAIN PROGRAMME

DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

136

bleeding; in those cases, a platelet dysfunction appears to be


the cause of the bleeding. Polyarthritis has also been recognized in dogs with chronic ehrlichiosis.

Diagnosis
A confirmative diagnosis of CE can be obtained by either: a) identifying the organism on cytologic specimens of
lymph node, spleen, or bone marrow; or b) obtaining a positive serology for E. canis. Ehrlichia organisms are rarely
identified in cytologic preparations, even retrospectively,
once a diagnosis has been confirmed by serology. Serology
for E. canis is usually performed by means of indirect immunofluorescent antibodies (IFA), a technique which is
highly sensitive and specific. Some degree of cross-reactivity with other ehrlichia organisms occurs, mainly E. equi, E.
risticii, and E. sennetsu, but no cross-reactivity exists with
Rickettsia rickettsi, the RMSF agent. Titers of 1:10 (the lowest dilution used by most laboratories) are considered diagnostic for infection, and may persist even after successful
treatment. Because detectable antibody titers do not occur
until after 7 to 21 days post-inoculation, paired serum titers
may be necessary in order to diagnose acute CE. Polymerase
chain reaction (PCR) is now widely used to diagnose CE.
Canine ehrlichiosis, as lymphoma and systemic lupus
erythematosus (SLE), can mimic a variety of disorders.
However, the main differential diagnoses in dogs with
chronic CE include multiple myeloma, lymphoma, chronic
lymphocytic leukemia, and SLE. Oftentimes, in a dog that
presents with a chronic history of weight loss, splenomegaly,
generalized lymphadenopathy, bi- or pancytopenia, bone
marrow plasmacytosis, and a monoclonal gammopathy, the
only one to differentiate between CE and multiple myeloma
is by obtaining a positive serology for E. canis. The same
holds true for dogs with chronic weight loss, mild lymphadenopathy and hepatosplenomegaly, lymphocytosis, and
a monoclonal gammopathy. Another disorder that is commonly mimicked by acute CE is immune-mediated thrombocytopenia (ie; isolated thrombocytopenia and increased
numbers of megakaryocytes in a bone marrow smear); in
these cases, immunosuppressive corticosteroid treatment
should be initiated in conjunction with tetracycline or doxycycline, until the results of the serology become available.

Treatment and prevention


Even though the clinical signs in dogs with CE can be
quite severe, response to treatment is usually remarkably
good. A notable exception is that of dogs with severe

4th European FECAVA SCIVAC Congress

chronic CE, in which response to treatment may be minimal. Recovery in dogs with acute forms and in dogs with
mild chronic forms occurs in 24 to 72 hours; complete recovery in dogs with chronic infection may take up to four
months. As discussed above, elevated titers (and a monoor polyclonal gammopathy) may persist for months or
years.
Tetracycline, and its derivative doxycycline, constitute
the mainstay of treatment (Table 1). They should be administered for 10 to 21 days and usually result in complete resolution of the clinical signs. However, serum titers may persist for several months (or even years).
Most textbooks recommend using tetracycline as the first
line of treatment; however, since a less expensive generic
doxycycline is available, we routinely use it to treat dogs
with CE at doses of 5 to 10 mg/kg, PO, SID to BID. Moreover, it appears to be more effective than tetracycline, and it
causes less yellowing of the teeth in pups than its parent
compound (tetracycline).
Doxycycline can also be used intravenously in dogs with
severe clinical signs or vomiting.
Chloramphenicol can also be used successfully to treat
CE. However, given its potential for marked hematologic
toxicity it is not the drug of choice for a cytopenic dog.
If treatment with tetracycline, doxycycline, or chloramphenicol fails to induce clinical or hematologic remission,
imidocarb dipropionate, and anticholinesterase agent not
available in the United States should be used.
It is administered as a single subcutaneous or intramuscular injection (5 mg/kg), which can potentially be repeated
in 2 to 3 weeks. It usually causes transient vomiting, diarrhea, shivering, and coughing, which resolve within minutes
to hours of the administration. As a general rule, intramuscular administration of drugs should be avoided in dogs with
thrombocytopenia or thrombocytopathia.
Supportive treatment in dogs with CE include administration of fluids and/or blood products, and possibly, corticosteroids to treat the underlying immune mediated disorder.
Immunosuppressive doses of corticosteroids, equivalent to
2-4 mg/kg of prednisone daily, do not appear to adversely affect the course of the disease when used concomitantly with
tetracycline or doxycyline. Anabolic steroids may be used in
attempts to stimulate hematopoiesis.
Prevention of CE centers around tick control, for which
a variety of products are available. Hunting dogs should be
tested and treated, since asymptomatic carriers can be a
source for continuous infection from ticks.
Prophylactic treatment with tetracycline (3 mg/kg, PO,
SID) or doxycycline (2-3 mg/kg, PO, SID) during tick season may prevent infection. All canine blood donors should
be tested for E. canis by serology.

4th European FECAVA SCIVAC Congress

137

Practical chemotherapy
C. Guillermo Couto
DVM, Dipl ACVIM
Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

Chemotherapy is commonly used in small animals with


malignant tumors. The basic principles, indications, contraindications, and practical applications of this treatment
modality will be discussed using case examples.

Cell and tumor kinetics


The mammalian cell cycle has 2 apparent phases: mitosis and resting phase. The resting phase is indeed composed of 4 phases:
synthesis phase (S): DNA synthesis occurs
gap 1 phase (G1): synthesis of RNA and enzymes needed
for DNA production occurs
gap 2 phase (G2): synthesis of the mitotic spindle apparatus occurs
gap 0 phase (G0): true resting phase.
The mitosis phase is termed M phase.
Several terms need to be defined prior to discussing
chemotherapy. Mitotic index (MI) refers to the percentage
of mitoses in a tumor mass. Growth fraction (GF) refers to
the proportion of proliferating cells within a tumor. Doubling time (DT) refers to the time required by a tumor mass
to double in size. In dogs they range from 2 days (for
metastatic osteosarcoma) to 24 days (for metastatic
melanoma), while in humans they range from 29 days (for
malignant lymphomas) to 83 days (for breast cancer). The
DTs depend upon the time spent in mitosis, cell cycle duration, GF and cell loss from death or metastases. Given our
knowledge on tumor kinetics, by the time a pulmonary
metastatic nodule is visualized on radiographs, it has
200,000,000 cells and weighs less than 150 mg (and it has
already divided 25 to 35 times).
As a general rule, most non-neoplastic tissues (with the
exception of bone marrow stem cells and intestinal crypt
epithelium) have low GF, low MI, and prolonged DT,
while most neoplastic tissues have high MI, high GF, and
short DT.
Surgical cyroreduction (debulking) of a tumor that
reached a plateau of growth will decrease the total number
of cells, thus increasing the MI and GF, and shortening the
DT. This will turn the neoplasm more susceptible to chemoor radiotherapy.

Indications and contraindications


of chemotherapy
Chemotherapy is primarily indicated for patients with
systemic (eg; lymphoma, leukemias) and metastatic neoplasms, although it can also be used for nonresectable,
chemoresponsive neoplasms which have been historically
refractory to radiotherapy or hyperthermia (primary
chemotherapy). It can also be used as an adjuvant treatment
following partial surgical debulking of a neoplasm (eg; partial excision of an undifferentiated sarcoma), and is indicated for control of micrometastatic disease following surgical
excision of a primary neoplasm (eg; cisplatin therapy after
limb amputation in dogs with osteosarcoma; VAC for dogs
with hemangiosarcoma). As a general rule, chemotherapy
should NEVER be used as a substitute for surgery, radiotherapy, or hyperthermia, or in patients with severe underlying multiple organ dysfunction (the latter will increase the
possibility of developing systemic toxicity).

Mechanism of action of anticancer drugs


The effects of anticancer drugs on a neoplastic cell population follow first order kinetic principles (ie: the number
of cells killed by a drug or drug combination is directly proportional to one variable, the dose used). Anticancer drugs
kill a constant proportion of cells, rather than a constant
number. Therefore, the efficacy of a drug or drug combination will depend upon the number of cells within a given tumor [eg; a drug combination that kills 99% of the cells in a
tumor containing 100,000,000 (109) cells will leave
1,000,000 (106) viable cells]. It should also be kept in mind
that different types of anticancer drugs kill tumor cells by
different mechanisms (see below).

Types of anticancer drugs


Anticancer agents are classified in the following categories:
alkylating agents
antimetabolites
antitumor antibiotics
plant alkaloids (or mitotic inhibitors)
hormones
miscellaneous

MAIN PROGRAMME

Summary

138

Alkylating agents cross-link DNA, thus preventing its


replication. Since they mimic the effects of radiotherapy
they are also referred to as radiomimetics. These drugs are
active during several phases of the cell cycle (ie; they are
cell cycle-nonspecific drugs). Alkylating agents commonly
used in pets with cancer include:
cyclophosphamide (Cytoxan)
chlorambucil (Leukeran)
melphalan (Alkeran)
cisplatin (Platinol) [DO NOT USE IN CATS!]
Antimetabolites exert their activity during the S phase of
the cell cycle (cell cycle phase-specific drugs). These drugs
are structural analogues of naturally occurring metabolites
(fake metabolites) that substitute for normal purines or
pyrimidines. The following antimetabolites are commonly
used in small animal cancer patients:
cytosine arabinoside (Cytosar-U)
methotrexate (Methotrexate)
5-fluoruracil (5-FU) [DO NOT USE IN CATS!]
6-thioguanine (6-TG)
6-mercaptopurine (PuriNethol)
azathioprine (Imuran)*
Antitumor antibiotics act by several mechanisms, the
most importants of which appear to be cross-linking of DNA
and inhibition of protein synthesis. They include:
doxorubicin (Adriamycin)
bleomycin (Blenoxane)
actinomycin D (Cosmegen)
mitoxantrone (Novantrone)
Plant alkaloids are derived from the periwinkle plant
(Vinca rosea) and the May apple plant (Podophyllum peltatum ). They disrupt the mitotic spindle and are therefore cell
cycle phase-specific (active during M phase). Commonly
used plant alkaloids include:

*Commonly used as an immunosuppressive drug.

4th European FECAVA SCIVAC Congress

vincristine (Oncovin)
vinblastine (Velban)
etoposide or VP-16 (VePesid)
Hormones are commonly used for the treatment of hemolymphatic malignancies or endocrine-related tumors.
Commonly used hormones include:
prednisone
testosterone
estrogens
progestagens
With the exception of corticosteroids, the use of hormones is not recommended since they are associated with
significant side effects in animals.
Finally, miscellaneous agents include drugs whose
mechanism of action is either unknown or different from the
ones listed above. Miscellaneous agents commonly used in
small animal cancer patients include:
DTIC (DTIC)
l-asparaginase (Elspar)

References
Bech-Nielsen S, Reif JS, Brodey RS: The use of tumor doubling time in
veterinary clinical oncology. J Amer Vet Radiol Soc 17:113-116,
1976.
Couto CG: Principles of chemotherapy. In Proceedings 10th Annual Kal
Kan Symposium for the Treatment of Small Animal Diseases. 1986,
pp 29-36.
Couto CG: Practical chemotherapy. In Nelson RW and Couto CG: Essentials of Small Animal Internal Medicine. St. Louis, Mosby-Yearbook,
1992, p 842-846.
Dorr RT and Fritz WL: Cancer Chemotherapy Handbook. New York, Elsevier, 1980.
Helfand SC: Principles and applications of chemotherapy. Vet Clin North
Amer 20:987-1013, 1990.

4th European FECAVA SCIVAC Congress

139

Complications of chemotherapy
C. Guillermo Couto

Summary
Chemotherapy is commonly used in small animal practice. Although this treatment modality is associated with a
high prevalence of adverse effects in people, toxicity in dogs
and cats is minimal and they usually preserve excellent quality of life. This lecture will discuss the common toxicities of
chemotherapy, emphasizing recognition and management.

Most anticancer agents are relatively nonselective in that


they not only kill rapidly dividing neoplastic tissues, but also some of the rapidly dividing tissues in the host as well
(eg; villal epithelium, bone marrow cells). In addition, they
are similar to other commonly used agents (eg; digitalis glycosides) in that they have low therapeutic indices (ie; narrow
therapeutic-to-toxic ratios).
Because anticancer agents follow first order kinetic principles (ie; the fraction of cells killed is directly proportional
to the dose used), increasing the dose of a particular drug
will increase the proportion of neoplastic cells killed, but it
will also enhace its toxicity. This is commonly seen when a
tumor relapses and higher doses of a previously used drug
are utilized.
Because toxicity is generally directed against rapidly dividing tissues, given the short turnover rate of bone marrow
and villal epithelial cells, myelosuppresion and gastrointestinal signs are the most common toxicities encountered
in practice. Other rare complications of chemotherapy include anaphylactoid (or anaphylactic) reactions, dermatologic toxicity, pancreatitis, cardiotoxicity, pulmonary toxicity, neurotoxicity, hepatopathies, and nephropathies. Table 1
lists anticancer drugs commonly used in small animals and
their toxicities.
In addition to the direct effects of the drugs on different
organ systems, rapid killing of certain neoplastic cells (ie;
lymphoma cells) can lead to rapid metabolic derangements
that result in acute clinical signs which mimic those of drug
toxicity (ie; depression, vomiting, diarrhea). This syndrome
is referred to as acute tumor lysis syndrome (ATLS).
Overall, the prevalence of toxicity of different
chemotherapy protocols is considerably lower in dogs and
cats (approximately 5% to 40%) than in humans (75% to
100%) treated with similar drugs or combinations. A recent
survey of owners whose pets had been treated with a variety
of chemotherapy protocols at The Ohio State University Vet-

erinary Teaching Hospital revealed that over 80% of those


questioned considered their pets quality of life to be equal
to or better than that prior to initiating chemotherapy.

Hematologic toxicity
The high mitotic rate and growth fraction (ie; 40 to 60%)
of the bone marrow cells predispose this organ to toxicity
from anticancer drugs. Hematologic toxicity represents the
most common toxicity of chemotherapy, and oftentimes results in temporary or permanent discontinuation of the offending agent/s due to severe (and often life-threatening) cytopenias. Agents commonly implicated in this type of toxicity are listed in Table 1.
When one considers the bone marrow transit times and
circulating half lives of blood cells, it is easy to anticipate
which cell line will be affected. For example, the bone marrow transit time and circulating half life of RBCs in the dog
are approximately 7 days and 120 days, those of the platelets
are 3 days and 4 to 6 days, and those of granulocytes are 6
days and 4 to 8 hours, respectively. Therefore, it is anticipated that neutropenia will occur first, followed by thrombocytopenia; anemia induced by chemotherapeutic agents is
extremely rare in dogs and cats, and, if it occurs, is of a late
onset (3 to 4 months after initiation of therapy). Other patient (eg; malnutrition, old age, concurrent organ dysfunction) and tumor factors (eg; bone marrow infiltration, widespread parenchymal organ metastases) can also effect the
degree of cytopenia.
Although thrombocytopenia is probably as common as
neutropenia, it is rarely severe enough to cause spontaneous
bleeding, and it will therefore not be discussed at length. In
general, in most dogs and cats with chemotherapy-induced
thrombocytopenia the platelet counts remain above 50,000
cells/l; spontaneous bleeding does not usually occur until
platelet counts fall below 30,000/l. Thrombocytosis is
common in cats and dogs receiving vincristine.
Neutropenia usually constitutes the dose-limiting cytopenia and occasionally leads to life-threatening sepsis. For
most drugs, the nadir usually occurs 5 to 7 days after treatment, and the neutrophil counts return to normal values
within 36 to 72 hours of the nadir. Patients with neutrophil
counts under 2,000 cells/l should be closely monitored for
the development of sepsis, although overwhelming sepsis
rarely occurs with neutrophil counts of 1,000/l.

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

140

4th European FECAVA SCIVAC Congress

Table 1. Toxicity of anticancer agents commonly used in dogs and cats


Drug
A.

B.

C.

D.

E.

Hematologic

GI

Anaphylaxis

Dermatologic
Pancreatitis

ALKYLATING AGENTS
Busulfan (Myleran)
Chlorambucil (Leukeran)
Cyclophosphamide (Cytoxan)
Melphalan (Alkeran)

++
+/++/+++
++

+/++
+/-

+/- A1
+/-A
+A
+/-A

?
?
?
?

ANTIMETABOLITES
Cytosine arabinoside (Cytosar-U)
5-Fluoruracil (5-FU)
6-Mercaptopurine (Purinethol)
Methotrexate (Methotrexate)
6-Thioguanine (Thioguanine)
Azathioprine (Imuran)

++/+++
++
+/++
+/+++
+/++
+/+++

+/+/++
+/++
+/+++
+
+/++

+A
+A +/-H2
+A
+/++A
+/++A
+A

+/?
+/++
?
?
+/++

ANTITUMOR ANTIBIOTICS
Doxorubicin (Adriamycin)
Bleomycin (Blenoxane)

++/+++
-

+/+++
-

+/++
-/+

++AH +++S3
+H

+/++
?

+
+/+/++

+++4

+A ++S
+A ++S
+A

?
?
?

PLANT ALKALOIDS (MITOTIC INHIBITORS)


Vincristine (Oncovin)
+/++
Vinblastine (Velban)
++/++
Etoposide (VePesid)
+/+++

+/+++

+/-

(see other)
-

++
?

MISCELLANEOUS
Dacarbazine (DTIC)
Cis-platinum (Platinol)

++/+++
+/-

++/+++
++/+++

+A
+A

+/++
?

L-asparaginase (Elspar)
Hydroxyurea (Hydrea)

F.

HORMONES
Prednisone
Estrogens

+/+/+++

+/+/-

+++
-

+/+++A

Other

Cystitis

Liver?

Cardiac
Lungs

+++
?

Cushings

Renal
Lung5

1A: alopecia; 2H: hyperpigmentation; 3S:perivascular sloughing; 4 when administered IV; 5 in cats.

The pathogenesis of sepsis in neutropenic patients is as


follows: chemotherapy-induced death and desquamation of
gastrointestinal crypt epithelial cells occurs simultaneously
with myelosuppression; enteric bacteria are absorbed
through the damaged mucosal barrier into systemic circulation; the numbers of neutrophils in circulation are not sufficient to phagocytose and kill the invading organisms; as a
consequence, microbial colonization of multiple organs occurs, and death ensues unless the patient is treated appropriately.
From the clinical standpoint, it is important to identify
the septic neutropenic patient, since the cardinal signs of inflammation (ie; redness, swelling, increased temperature,
pain, and abnormal function) may be absent due to insufficient numbers of neutrophils available to participate in the
inflammatory process. The same holds true for radiographic
changes compatible with inflammation; for example, dogs
with neutropenia and bacterial pneumonia diagnosed on the
basis of cytologic and microbiologic findings in transtracheal washes, oftentimes have normal thoracic radiographs.

As a general rule, when a severely neutropenic patient (neutrophil count <500/l) presents with marked pyrexia (T
>104), the pyrexia should be attributed to bacterial pyrogens
until proven otherwise, and the patient should be treated aggressively with empirical antimicrobial therapy (see below).
In addition, neutropenic patients with severe constitutional
signs (eg; depression, vomiting, diarrhea) and normal or low
body temperature should be regarded as septic and treated
aggressively. At the VTH-OSU, every neutropenic dogs and
cat with fever or nonspecific clinical signs is considered to
be septic until proven otherwise.
All patients undergoing chemotherapy should be current
on their immunizations. However, hematologic monitoring
the patient on chemotherapy constitutes the most effective
way to prevent severe, life-threatening sepsis secondary to
myelosuppression. Complete blood counts (CBCs) should
be obtained weekly or every other week when using myelosuppressive protocols, and the myelosuppressive agent/s
should be temporarily discontinued (or their doses decreased) if the neutrophil count is below 2,000 cells/l or if

the platelet count is below 50,000 cells/l. Discontinuing the


offending agent/s for 2 or 3 administrations is usually sufficient for the cell counts to return to the normal range. When
therapy is reinstituted, it is recommended that only 75% of
the initial dose be used, escalating doses over 2 to 3 weeks
until the initially recommended dose (or a dose which does
not result in marked cytopenias) is reached.
Clinically, neutropenic patients can be classified as
febrile or afebrile. Neutropenic febrile patients should be approached aggressively, since they are usually septic. Thus,
fever in a neutropenic patient constitutes a medical emergency. The following protocol is currently used in neutropenic febrile patients at the VTH-OSU (Table 2). The patient undergoes a thorough physical examination in search of
a septic focus, an indwelling intravenous catheter is placed
aseptically and intravenous fluids are administered as required. All anticancer agents with the exception of corticosteroids are discontinued at once (corticosteroids should be
discontinued gradually, since patients on chronic steroid
therapy can develop episodes of acute hypoadrenocorticism
when the drug is abruptly discontinued). Blood samples for
CBC; serum electrolyte, blood glucose, and blood urea nitrogen (BUN) concentrations are obtained immediately; a
urine sample for urinalysis and bacterial culture is also obtained. Two to three sets of aseptically collected blood samples can be obtained for aerobic and anaerobic bacterial cultures and antibiotic susceptibility tests at 30 minute intervals
(this is usually not necessary, since the bacterial isolates are
quite predictable - see below). After collecting the second
set of samples for blood cultures, therapy with an empirical
bacteriocidal antibiotic combination is instituted. We prefer
a combination of gentamicin (2.2 mg/kg, IV, TID) or
amikacin (6-10 mg/kg, IV, TID) and cephalothin (40 mg/kg,
IV, TID) since most bacterial isolates in these patients are
Enterobacteriaciae and staphylococci, organisms commonly
susceptible to these agents. Once the neutrophil count returns to normal and the patient is clinically normal (usually
within 72 to 96 hours), the antibiotic combination is discontinued and the patient is released with instructions to administer sulfadiazine-trimethoprim (ST) at a dose of 13-15
mg/kg, PO, BID for 5 to 7 days.
Neutropenic afebrile asymptomatic patients can be
treated as outpatients with discontinuation of the drug/s as

Table 2. Management of neutropenic febrile


dogs and cats
search for septic focus (PE, rads, US)
IV catheter
blood for CBC and biochemical profile
LRS solution (40-60 ml/kg for dogs and 20-30 ml/kg for cats)
discontinue chemo drugs (except for corticosteroids)
antibiotics
cephalotin 40 mg/kg, IV, tid
gentamicin 2.2 mg/kg, IV, tid or amikacin 6-10 mg/kg, IV, tid*
after patient stabilizes, decrease rate of IV fluids to 60-90
ml/kg/day
* if the patient is oliguric or anuric, do not administer aminoglycoside until
after the urinary bladder is palpable (ie; there is diuresis).

141

above plus ST (15 mg/kg, PO, BID); if the patients is


afebrile but has constitutional signs, he/she should be considered to be septic and treated as described above. If the
neutropenia is not severe (ie; 2,000 cell/l), no therapy is
needed, and the patient should only be monitored by the
owner. Owners should be instructed to monitor their pets
rectal temperature twice daily, and call the veterinarian if
pyrexia develops, in which case the patient is treated as neutropenic and febrile. Sulfa-trimethoprim combinations eliminate the aerobic intestinal flora, but preserve the anaerobic
bacteria, which are an important component of the local defense system, due to their ability to produce local antibiotic
factors. In addition, ST is active against a large number of
pathogens isolated from cancer patients, provide therapeutic
blood and tissue concentrations, and also provide high intragranulocytic concentrations.
Myelosuppression may be alleviated by using lithium
carbonate (10 mg/kg, PO, BID), granulocyte colony stimulating factor (G-CSF) at a dose of 5-10 g/kg SQ bid, or
products which stimulate release of endogenous G-CSF (eg;
bacterial products).

Gastrointestinal toxicity
Although less frequent than myelosuppression, gastrointestinal toxicity is a relatively common complication of cancer chemotherapy in pets. From the clinical standpoint two
major types of gastrointestinal complications can occur:
nausea/vomiting and gastroenterocolitis.
Although controlled studies are not available, nausea and
vomiting are not apparently as common in pets as in humans
(when using similar drugs and dosages). Drugs associated
with nausea and vomiting in dogs include DTIC, cisplatin,
doxorubicin, methotrexate, and actinomycin D; doxorubicin
and cyclophosphamide frequently result in nausea/vomiting
in cats (Table 1).
Acute nausea and vomiting caused by injectable drugs
can be alleviated by administering the offending agents by
slow intravenous infusions. If they persist despite slow administration, the use of antiemetics such as metoclopramide
(Reglan) at a dose of 0.1 to 0.3 mg/kg, IV, SQ, or PO TID,
or prochlorperazine (Compazine) at a dose of 0.5 mg/kg,
IM, BID to TID is indicated.
Gastroenterocolitis from anticancer agents is rare. Drugs
which occasionally cause mucositis include methotrexate,
5-fluoruracil, actinomycin D, and doxorubicin; it occurs
rarely with other alkylating agents such as cyclophosphamide. Of the drugs listed above, only doxorubicin (Adriamycin) and methotrexate (Methrotrexate) appear to be of
clinical importance. In my experience, Collies and Collie
crosses, Old English Sheepdogs, and West Highland White
terriers appear to be extremely susceptible to doxorubicininduced enterocolitis.
Doxorubicin-induced enterocolitis is characterized by
the development of hemorrhagic diarrhea (with or without
vomiting), primarily of large bowel type, 3 to 7 days after
administration of the drug. Supportive fluid therapy (if necessary) and treatment with therapeutic doses of bismuth subsalicylate-containing products (Pepto Bismol, 3 to 15 ml or

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4th European FECAVA SCIVAC Congress

142

1/2 to 2 tablest PO, TID to QID) are usually effective in controlling the clinical signs, which usually resolve in 3 to 5
days. Although anecdotal, if the patient is at risk for gastroenterocolitis (ie; one of the breeds mentioned above, prior history of this toxicity), administration of Pepto-Bismol
from days 1 to 7 of the treatment may alleviate or prevent
these signs. Gastroenteritis associated with oral methotrexate administration usually develops after the patient has been
receiving this drug for a minimum of two weeks.

Hypersensitivity reactions
Acute type I hypersensitivity reactions occasionally occur in dogs receiving parenteral l-asparaginase (Elspar) or
doxorubicin (Adriamycin), and are common in dogs treated with etoposide (VePesid). The reaction to doxorubicin
does not appear to be a true hypersensitivity reaction, since
this agent can induce direct mast cell degranulation independently of IgE mediation. Etoposide can be safely administered orally to dogs. Hypersensitivity reactions to anticancer agents are extremely rare in cats and will not be
discussed.
Clinical signs in dogs with hypersensitivity reactions are
primarily cutaneous and gastrointestinal. Typical signs begin
during or shortly after administration of the agent, and include head shaking (due to ear pruritus), generalized urticaria and erythema, restlesness, occasional vomiting, and
(rarely) collapse due to hypotension.
Most systemic anaphylactic reactions can be prevented
by pretreating the patient with H-1 antihistamines (ie;
diphenhydramine, 1-2 mg/kg, IM, 20-30 minutes prior to administration of the drug) and by administering certain drugs
(such as l-asparaginase) by the subcutaneous, intramuscular,
or intraperitoneal route, rather than intravenously. If the
agent cannot be given by any other routes (ie; Adriamycin),
it should be diluted and administered by slow intravenous
infusions. At the VTH-OSU we routinely pretreat dogs (but
not cats) with diphenydramine prior to administering doxorubicin or l-asparaginase.
Treatment of acute hypersensitivity reactions includes immediate discontinuation of the agent, administration of H-1
antihistamines (ie; diphenhydramine, 0.2-0.5 mg/kg, slow
IV), intravenous dexamethasone sodium phosphate (1-2
mg/kg), and fluids, if deemed necessary. If the systemic reaction is severe, the administration of epinephrine (0.1-0.3 ml of
a 1:1,000 solution, IM or IV) is indicated. Once the reaction
subsides, the administration of certain drugs such as Adriamycin may be continued. Intravenous H1 antihistamines
should be used with caution in cats, since they can cause
acute CNS depression leading to apnea.

Dermatologic toxicity
Dermatologic toxicity is rare in small animals. Three
types of dermatologic toxicities can occur: local tissue
necrosis due to extravasation, delayed hair growth or alopecia, and hyperpigmentation.
Local tissue necrosis due to extravasation of vincristine,

4th European FECAVA SCIVAC Congress

vinblastine, actinomycin D, or doxorubicin is occasionally


seen in dogs receiving these drugs; however, it is rare in cats.
Although the pathogenesis of this toxicity is poorly understood, these drugs are extremely caustic when given perivascularly, causing marked tissue necrosis 1 to 15 days after the
injection (earlier with the vinca alkaloids, and later with
doxorubicin and actinomycin D). As a consequence of this,
every effort should be made to ensure that these drugs are
administered intravascularly.
In order to prevent or minimize extravascular injection
of caustic drugs, they should be administered through a
small gauge (22 G to 23 G) indwelling intravenous catheter
(I prefer over-the-needle catheters such as the Terumo Surflo) or 23 G to 25 G butterfly catheters. I use the former for
doxorubicin and the latter for vinca alkaloid administration;
in cats, it is safe to administer doxorubicin through a butterfly catheter. Caustic drugs should be properly diluted prior
to administration (ie; vincristine to a final concentration of
0.1 mg/ml and doxorubicin to a concentration of 0.5 mg/ml),
and patency of the catheter should be assured by intermittently aspirating until blood appears in it. If the catheter is
not patent, it should be placed in another vein.
Despite careful intravascular injection, some dogs develop mild to moderate local tissue reactions (eg; erythema,
moist desquamation, and alopecia). This is common in
Golden Retrievers receiving vincristine, vinblastine, actinomycin D, or doxorubicin, and is believed to be due to selfinflicted damage after developing mild phlebitis or thrombophlebitis. These patients are managed as discussed below.
Recommendations for management of extravascular injections are listed in Table 3.
If despite these precautions a local tissue reaction occurs,
it will develop in approximately 1 to 7 days after perivascular injection of vinca alkaloids, and 7 to 15 days after actinomycin D or doxorubicin extravasation. Tissue necrosis is
far more severe with doxorubicin, since it is extremely caustic and it persists in the tissues for several weeks to months.
Clinical signs include pain, pruritus, erythema, moist dermatitis, and necrosis of the affected area; severe tissue
sloughing usually occurs. If mild local tissue reactions develop, they can be treated as described in Table 4.
In dogs and cats undergoing chemotherapy delayed hair
growth is more common than alopecia. This is in contrast
with human patients, in which severe scalp alopecia is a predictable complication of therapy. Excessive shedding is also
a common occurrence.
Alopecia appears to occur predominantly in wooly
(coarse) haired dogs such as poodles and Kerry blue terriers.
In short haired dogs and cats, it affects primarily the tactile
hairs. Although the exact reason why wooly haired dogs develop chemotherapy-induced alopecia is unknown, a prolonged anagen phase and synchronous hair growth, comparable to that existing in human scalp hair may make these
dogs prone to this toxic effect. Drugs commonly associated
with delayed hair growth or alopecia include cyclophosphamide, doxorubicin, 5-fluoruracil, 6-thioguanine, and hydroxyurea. Alopecia and delayed hair growth usually resolve
shortly after discontinuation of the offending agent.
Hyperpigmentation induced by anticancer agents is
rare in dogs and extremely rare in cats. Cutaneous hyperpig-

Table 3. Recomendations for the management


of perivascular injections of caustic anticancer drugs
in cats and dogs
1. Do not remove the IV catheter.
2. Administer 10 to 50 ml of sterile saline solution through the
catheter (in an attempt to dilute the agent).
3. With a 25 G needle administer 10 to 20 ml of sterile saline solution subcutaneously (SQ) in the affected area.
4. Inject 1 to 4 mg of dexamethasone sodium phosphate SQ in the
affected area (in an attempt to stabilize lisosomal and plasma
membranes).
5. Apply cold compresses or ice packs to the area for 48-72 hours
(to cause vasoconstriction and prevent local dissemination of the
drug, and to decrease local tissue metabolism).

Table 4. Recommended treatment for dogs that received


a perivascular injection of a caustic anticancer agent
1. Apply an antibiotic ointment (with or without corticosteroids) to
the affected area.
2. Bandage the area (and replace bandages daily).
3. Prevent the patient from causing self mutilation by using an elizabethan collar or a muzzle.
4. If there is no bacterial contamination (ruled out on the basis of
negative bacterial cultures or cytology), DepoMedrol can be injected subcutaneously (10 to 20 mg) in the affected area to alleviate pruritus and inflammation.
5. If severe necrosis or gangrene due to anaerobic contamination
occurs the area should be surgically debrided.
6. In severe doxorubicin-induced soft tissue necrosis, amputation
of the affected limb may be required.

mentation affecting the face, ventral abdomen and flanks is


quite common in dogs receiving doxorubicin-, actinomycin
D, and bleomycin-containing protocols.

Cardiotoxicity
Cardiotoxicity is a relatively rare complication of doxorubicin therapy in the dog, and appears to be extremely rare
in the cat. Two types of doxorubicin-induced cardiac toxicity are observed in dogs: an acute reaction during or shortly
after administration, and a chronic cumulative toxicity.
Acute doxorubicin toxicity is characterized by the development of cardiac arrhythmias (mainly, sinus tachycardia) during or shortly after administration. This phenomenon is
thought to be related to doxorubicin-induced histamine-mediated catecholamine release, since the sinus tachycardia
and hypotension can be prevented by pretreatment with H1
and H2 antihistamines. Several weeks or months after repeated doxorubicin injections, persistent arrhythmias, including ventricular premature contractions, atrial premature
contractions, paroxysmal ventricular tachycardia, second
degree AV blocks, and intraventricular conduction defects
develop. These rhythm disturbances are usually associated

143

with the development of a dilated cardiomyopathy, similar


to that seen spontaneously in large breed dogs and Cocker
Spaniels.
The hallmark of chronic doxorubicin toxicity in the dog is
the development of dilated cardiomyopathy after surpassing a
total cumulative dose of approximately 240 mg/m2. The cumulative cardiotoxic dose in the cat is unknown, but it appears
to be approximately 150 to 170 mg/m2. Clinical signs of toxicity in dogs are those of congestive heart failure (usually leftsided). Therapy consists of discontinuation of the drug and
use of cardiac drugs such as digitalis glycosides or non-glycoside inotropic agents. Once cardiomyopathy develops, the
prognosis is poor, since myocardial lesions are irreversible.
For a detailed discussion of treatment of dilated cardiomyopathy please refer to a standard internal medicine textbook.
Monitoring dogs receiving doxorubicin is critical to prevent the development of fatal cardiomyopathy. In this respect, dogs and cats with underlying rhythm disturbances or
impaired myocardial contractility, as determined by decreased fractional shortening on M-mode echocardiograms
should not receive doxorubicin. It is also recommended that
patients receiving doxorubicin undergo M-mode echocardiographic evaluation every three doxorubicin cycles (9
weeks) to assess myocardial contractility, and that administration of the drug be discontinued if decreased fractional
shortening occurs. The use of endomyocardial biopsies to
monitor cardiac toxicity from doxorubicin is impractical in
dogs and cats.
Several protocols have been devised in an attempt to
minimize doxorubicin-induced cardiomyopathy. Unfortunately, only three protocols have shown promise. Of these,
weekly low dose doxorubicin showed a significantly lower
frequency of histologic changes when compared to the conventional 3-weekly schedule in humans. I have been able to
administer total cumulative doses of 500 mg/m2 to two dogs,
when using 10 mg/m2 weekly. However, recent evidence
suggests that this schedule is not as effective in dogs with
lymphoma. A new compound termed ICRF-187 (or ADR
259) offers a promising means of reducing the chronic cardiotoxicity induced by doxorubicin; using this compound,
doses in excess of 500 mg/m2 have been administered to
dogs without significant cardiotoxicity. Unfortunately, this
compound is not commercially available. At the VTH-OSU
we administer doxorubicin as a slow bolus (20-30 minutes)
of a 0.5 mg/ml solution intravenously. This results in a relatively low peak plasma concentration of the drug, and decreases the risk of developing cardiotoxicity. Using this protocol we evaluate approximately one dog every 18 months
with clinical evidence of doxorubicin-induced cardiomyopathy; for reference, we administer approximately 4 gm of
doxorubicin per year, and a 70 lb dog receives an average
dose of 30 mg.

Urotoxocity
The urinary tract is rarely involved in adverse reactions
to anticancer agents in small animal patients. Only two specific complications are of clinical importance in pets with
cancer: nephrotoxicity and sterile hemorrhagic cystitis.

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144

Transitional cell carcinomas (TCCs) of the urinary bladder


associated with cyclophosphamide (CTX ) therapy can also
occur in dogs.
Nephrotoxicity is rarely observed in dogs and cats undergoing chemotherapy. Although several potentially
nephrotoxic drugs are commonly used in these species, only
doxorubicin (primarily in the cat), cisplatin (in the dog), and
intermediate- to high-dose methotrexate (in the dog) are of
concern to the clinician. Doxorubicin may be a potent
nephrotoxin in cats, and the limiting cumulative toxicity in
this species may be renal, rather than cardiac. Doxorubicin
may cause nephrotoxicosis in dogs with preexisting renal
disease, and in those concomitantly receiving other nephrotoxins, such as aminoglycoside antibiotics.
Sterile hemorragic cystitis is a relative commmon complication of chronic CTX therapy in dogs, but it is extremely rare in cats. Although rare, hemorrhagic cystitis may also
occur acutely or peracutely after the first dose of CTX.
Three dogs treated in our clinic with 100 mg/m2 of CTX IV,
and 4 dogs receiving 300 mg/m2 of CTX PO developed
acute clinical signs and urinalysis changes compatible with
sterile hemorrhagic cystitis after the first dose. Sterile cystitis apparently results from the irritating effects of one of
CTX metabolites (acrolein). Approximately 5% to 25% of
dogs, and 1% to 3% of cats treated with oral CTX develop
sterile hemorrhagic cystitis, which usually occurs after 18
weeks. Furosemide administered concomitantly with CTX,
appears to decrease the prevalence of cystitis.
Forced diuresis appears to prevent or minimize the frequency of this complication. I usually recommend administering the CTX in the morning, allowing the pet to urinate
frequently (if he/she is an indoor dog), salting the food, and
administering prednisone on the same day that the patients
receive the CTX (if the protocol calls for prednisone administration).
Clinical signs of serile hemorrhagic cystitis are similar to
those of other lower urinary tract disorders, and include pollakiuria, hematuria, and dysuria. Urinalyses are character-

4th European FECAVA SCIVAC Congress

ized by the presence of blood, with mildly to moderately increased numbers of white blood cells, and absence of bacteria. Treatment of this complication is aimed at discontinuing
the offending drug, forcing diuresis, diminishing inflammation of the bladder wall, and preventing secondary bacterial
infections. Discontinuation of CTX results in resolution of
the cystitis in most dogs within one to four months. In addition to discontinuing the drug, I administer furosemide
(Lasix), at a dose of 2 mg/kg, PO, BID for its diuretic effects; prednisone, at a dose of 0.5-1 mg/kg, PO, SID for its
antiinflammatory (and diuretic) effect; and a sulfadiazinetrimethoprim combination (Tribrissen), at a dose of 13-15
mg/kg, PO, BID to prevent secondary bacterial contamination. If despite this approach the clinical signs worsen, instillation of 1% formalin solution in water into the bladder
can be attempted. In two dogs thus treated, gross hematuria
resolved within 24 hours and did not reoccur. Intravesical infusion of a 25% to 50% DMSO solution may also alleviate
signs associated with cystitis in dogs.

References
Couto CG: Management of Complications of Cancer Chemotherapy. Vet
Clin North Amer 20:1037-1053, 1990.
Couto CG: Complications of cancer chemotherapy. In Nelson RW and
Couto CG: Essentials of Small Animal Internal Medicine. St. Louis,
Mosby, 1992, p 847.
Crow SE, Theilen GH, Madewell BR et al: Cyclophosphamide-induced
cystitis in the dog and cat. J Am Vet Med Assoc 171:259,1977.
Harvey HJ, MacEwen EG, Hayes AA: Neurotoxicosis associated with use
of 5-fluoruracil in five dogs and one cat. J Am Vet Med Assoc
171:277, 1977.
Knapp DW, Richardson RC, DeNicola DB, Long GG, Blevins WE: Cisplatin toxicity in cats. J Vet Internal Med 1:29, 1988.
Laing EJ, Miller CW, Cochrane SM: Treatment of cyclophosphamide-induced hemorrhagic cystitis in five dogs. J Am Vet Med Assoc
193:233, 1988.
Weller RE: Intravesical instillation of dilute formalin for treatment of cyclophosphamide-induced cystitis in two dogs. J Am Vet Med Assoc
172:1206, 1978.

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145

Fever of unknown origin in dogs


C. Guillermo Couto

Summary
Persistent fever in a patient in which a diagnosis cannot
be obtained is relatively common in practice. Fever of unknown origin can be due to infectious, immune-mediated,
neoplastic, or miscellaneous causes. The diagnostic and therapeutic approach to a patient with FUO will be discussed.

The term fever of undetermined (or unknown) origin


(FUO) is used quite liberally in veterinary medicine to describe a febrile syndrome for which a diagnosis is not evident. In human medicine, the term FUO refers to a febrile
syndrome of more than 3 weeks duration, which remains
undiagnosed after one week of thorough in-hospital evaluation. If the term FUO is used as recommended in the human
literature, very few dogs and cats will actually fit in that category. Therefore, this chapter will discuss the approach to a
dog with fever, which does not respond to antibacterial antibiotic treatment, and for which a diagnosis is not obvious
after obtaining a minimum data base (i.e.; CBC, serum biochemical profile, urinalysis).
In general, the clinician tends to assume that a dog with
fever has an infection, until proven otherwise. This appear to
be true in practice, since a large proportion of dogs with
fever respond to nonspecific antibacterial treatment. In most
of those patients, because the fever responds so promptly to
treatment, no clinicopathologic evaluation is performed.

Disorders associated with FUO


In humans, certain infectious, neoplastic, and immunemediated disorders are commonly associated with FUO. Approximately one third of the patients have infectious diseases; one third have cancer (mainly hematologic malignancies such as lymphoma and leukemia); and the remaining
one third have immune-mediated, granulomatous, or miscellaneous disorders. Ten to 15% of the patients with FUO remain undiagnosed despite intensive efforts to obtain a definitive answer.
However, to my knowledge, prospective or retrospective
studies of dogs with FUO are lacking in the veterinary literature. Based on the patients evaluated in our clinic and in reports from the literature, the most common cause of FUO
appear to be infectious diseases, followed by immune-medi-

ated, miscellaneous, and neoplastic disorders (Table 1). It


should be remembered that despite aggressive evaluation,
the cause of the fever cannot be determined in approximately 10% to 15% of the patients.
Table 1. Causes of fever of undetermined origin in dogs
Infectious
Bacterial
subacute bacterial endocarditis
brucellosis
tuberculosis
Lyme disease
suppurative infection
abscesses (liver, pancreas, stump pyometra)
prostatitis
diskospondylitis
pyelonephritis
peritonitis, pyothorax
septic arthritis
Rickettsial
ehrlichiosis, Rocky Mountain spotted fever, Salmon poisoning
Mycotic
histoplasmosis
blastomycosis
coccidioidomycosis
Protozoal
hemobartonellosis
babesiosis
hepatozoonosis
Chagas disease
leishmaniasis
Immune-Mediated
polyarthritis
vasculitis
meningitis
systemic lupus erythematosus
immune-hemolytic anemia (IHA)
steroid-responsive fever
Neoplastic
acute leukemia
chronic leukemia
lymphoma
malignant histiocytosis
multiple myeloma
necrotic solid tumors
Miscellaneous
metabolic bone disorders
drug-induced (tetracycline, enrofloxacin, penicillins, sulfa)
tissue necrosis
hyperthyroidism
idiopathic

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

146

Approach to the patient with FUO


A patient with FUO should be approached in a systematic fashion. In general, a three stage approach is used in our
clinic (Table 2). The first stage consists of a thorough history and physical examination, and a minimum data base. The
second stage consists of additional noninvasive and invasive
laboratory tests. The third stage consists of a therapeutic trial, and is instituted when no diagnosis is obtained after completing the second stage.
History and physical examination. Once a febrile patient fails to respond to antibacterial treatment, a course of
action must be formulated. A thorough history should be
obtained, and a complete physical examination should be
performed. The history rarely provides clues regarding the
cause of the fever; however, a history of ticks may suggest
the possibility of a rickettsial or hemoparasitic disorder, administration of tetracycline (mainly to cats) may suggest
the possibility of a drug-induced fever), and traveling to areas where systemic mycoses are endemic should prompt
further investigation by means of cytology, serology, or
fungal cultures.
During a physical examination, it is important to evaluate
the lymphoreticular organs, since a number of infectious and
neoplastic diseases affecting these organs (eg; ehrlichiosis,
RMSF, leukemia, systemic mycoses) may result in fever. An
enlarged lymph node or spleen should be evaluated cytologically by means of a fine needle aspiration (FNA); a sample
can also be obtained for bacterial and fungal culture and susceptibility through FNA, if the specimen is cytologically compatible with infection/inflammation. Any palpable mass/es or
swelling/s should also be evaluated by means of FNA.
The oropharynx should be inspected and palpated thor-

Table 2. Diagnostic evaluation of the dog with FUO


First Stage
CBC
Serum biochemical profile and thyroxine
Urinalysis
Urine bacterial culture and susceptibility
FNA of enlarged organs, masses or swellings
Second Stage
Thoracic and abdominal radiography
Abdominal ultrasonography
Echocardiogram
Serial blood cultures
Immune tests (ANA, RF)
Serum protein electrophoresis
Serology (see Table 1)
Arthrocentesis (cytology and culture)
Biopsy of any lesion or enlarged organ
Bone marrow aspiration (for cytology and bacterial/fungal culture)
Cerebrospinal fluid analysis
Leukocyte scanning
Exploratory celiotomy
Third Stage
Therapeutic trial (antipyretics, antibiotics, corticosteroids)

4th European FECAVA SCIVAC Congress

oughly, searching for signs of pharyngitis, stomatitis, or


tooth root abscesses. The bones should also be thoroughly
palpated, particularly in a young dog, since metabolic bone
disorders such as hypertrophic osteodystrophy, can result in
fever associated with bone pain. Palpation and passive motion of all joints is also indicated, in search of mono-, oligo,
or polyarthritis. A neurologic examination should be conducted to detect signs compatible with meningitis or other
CNS lesions.
The thorax should be ausculted carefully in search of a
murmur, which could indicate the presence of bacterial endocarditis. A thorough ocular exam may reveal changes suggestive of a specific etiology (eg; chorioretinitis in dogs with
ehrlichiosis).
Laboratory evaluation. A minimum data base consisting of a CBC, serum biochemical profile, urinalysis, and
urine bacterial culture and susceptibility should always be
obtained in dogs and cats with persistent fever. The CBC
may provide important clues regarding the cause of the fever
(Table 3). A serum biochemical profile is rarely diagnostic in
patients with FUO, although it provides indirect information
on parenchymal organ function. However, hyperglobulinemia and hypoalbuminemia may suggest an infectious, immune-mediated, or neoplastic disorder. Pyuria in a urinalysis is suggestive of a urinary tract infection (UTI); however,
lower UTIs rarely result in fever.
Finally, when a definitive diagnosis has not been obtained, a therapeutic trial of specific antibacterial/antifungal
agents or immunosuppressive doses of corticosteroids can
be initiated (see below).
If a dog presents with chronic fever and severe neutropenia, it must be determined if the neutropenia is the
cause or the consequence of the pyrexia (i.e.; which one
came first). Several clues from the physical examination and
CBC are helpful in establishing this. If the patient is severely ill, and the neutrophils in the blood smear are toxic (or
there is a pronounced left shift), the neutropenia is probably
the consequence of the fever (i.e.; there is neutrophil consumption due to bacterial infection, that initiated the fever).
If a dog is healthy (other than the fact that he/she has a
fever), and if the neutrophils do not exhibit toxic changes,
the most likely explanation is that the fever is secondary to
the neutropenia. The latter patients are likely to have steroidresponsive neutropenia.

Treatment
If a definitive diagnosis is obtained, a specific treatment
should be initiated. The problem arises when a definitive diagnosis cannot be arrived at. In these patients, changes in the
CBC usually represent the only laboratory abnormality
(Table 3). That is, results of bacterial and fungal cultures,
serology, imaging, and FNAs are negative (or the studies are
normal). If the patient has already been treated with a broad
spectrum bactericidal antibiotic, a therapeutic trial of immunosuppressive doses of corticosteroids is warranted.
However, prior to instituting this treatment, the owners
should be informed of the potential consequences of this approach (mainly, if the dog has an undiagnosed infectious dis-

Table 3. Hematologic changes in dogs with FUO


Hematologic change

Compatible with

Regenerative anemia

immune-mediated, hemoparasites,
drugs
infection, immune-mediated, tissue
necrosis, malignancy, endocarditis
infection, immune-mediated, tissue
necrosis, malignancy, endocarditis
leukemia, immune-mediated,
pyogenic infection, bone marrow
infiltrative disease, drugs
infection, immune-mediated, tissue
necrosis, lymphoma, endocarditis,
histiocytosis
ehrlichiosis, Chagas disease,
leishmaniasis, chronic lymphocytic leukemia
hypereosinophilic syndrome,
eosinophilic inflammation, lymphoma
rickettsiae, leukemia, lymphoma,
drugs, immune-mediated
infectious (chronic),
immune-mediated

Nonregenerative anemia
Neutrophilia with left shift
Neutropenia

Monocytosis

Lymphocytosis

Eosinophilia

Thrombocytopenia
Thrombocytosis

147

ease, death could occur from systemic dissemination of the


organism after initiating immunosuppressive treatment). In
patients with immune-mediated (or steroid-responsive)
FUO, the pyrexia and clinical signs usually resolve within
24 to 48 hours of initiating treatment; in that case, the patient
is treated with maintenance immunosuppressive therapy.
If no response to corticosteroids is observed, two courses of action remain. First, to release the patient on antipyretic drugs, such as aspirin (10-25 mg/kg, PO, BID in dogs and
10 mg/kg, PO, every third day in cats), with instructions to
return to the clinic for a complete reevaluation in one to two
weeks. Antipyretics should be used with caution, since as
discussed above, fever is a protective mechanism (i.e.; lowering the body temperature may be detrimental in a patient
with an infectious disease. Moreover, drugs such as dipyrone and banamine, can result in significant hypothermia,
which may have adverse effects for the patient. It should also be remembered that most nonsteroidal antiinflammatory
drugs, in addition to their ulcerogenic effects, can cause
blood cytopenias and result in tubular nephropathy when the
patient becomes dehydrated or receives other nephrotoxic
drugs. Second, antibiotic trials can be continued, using a
combination of bactericidal drugs (eg; a cephalosporin and
an aminoglycoside) for a minimum of 5 to 7 days.

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149

Recurrent infections in dogs


C. Guillermo Couto

Summary
Recurrent or persistent infections are usually the result of
congenital or acquired abnormalities of the immune system.
Some breeds appear to be at high risk for congenital immunologic defects. This lecture will discuss the diagnostic and therapeutic approach to dogs and cats with recurrent infections.

Recurrent or persistent infections are usually the results


of congenital or acquired abnormalities of the immune system. Although canine clinical immunology is not a well developed speciality, great progress has been made over the
past decade in elucidating the underlying immunologic abnormalities in dogs with recurrent infections.
Congenital immunodeficiency syndromes in dogs can
affect the humoral, cellular, or phagocytic systems, either
singly or in combination. Humoral immunodeficiency syndromes include IgA deficiency in beagles, Shar-pei and, possibly, German shepherd dogs; IgM deficiency in Doberman
pinschers (not well documented); C3 deficiency in Brittany
spaniels; and transient hypogammaglobulinemia in
Samoyeds. These dogs usually suffer from recurrent upper
and lower respiratory tract infections, dermatitis, and enteritis; some beagles with selective IgA deficiency also experienced grand mal seizures.
Cellular immunodeficiency syndromes are apparently
less common; a T-cell abnormality has been documented in
Weimaraners with pituitary dwarfism and in Bull Terriers
with lethal acrodermatitis. The disease in Weimaraner pups
was characterized by retarded growth and recurrent respiratory and gastrointestinal infections. Necropsy findings in the
affected dogs included hypoplastic thymuses with absence
of thymic cortex. Several related Bull Terriers with growth
retardation, progressive acrodermatitis, chronic pyoderma
and paronichia, pneumonia, and diarrhea exhibited significantly decreased lymphocyte blastogenesis in response to
PHA stimulation. Other diseases with inconsistent cell-mediated immunologic abnormalities include Pneumocystis
carinii infection in Dachshunds, systemic aspergillosis, generalized demodicosis, and protothecosis.
Abnormalities in the phagocytic system have been well
documented in dogs. They may occur as a consequence of
decreased numbers of circulating phagocytes (ie; in grey
collies with cyclic hematopoiesis), or as a consequence of
abnormal phagocytic function (ie; defective neutrophil ad-

hesion in Irish setters with granulocytopathy syndrome; defective bactericidal capacity in Doberman pinschers with recurrent respiratory infections). Setters with deficiency of
surface adhesion proteins have recurrent episodes of omphalophlebitis, gingivitis, lymphadenitis, pyoderma, respiratory infections, pyometra, and fulminant sepsis. Affected
Dobermans exhibited recurrent episodes of rhinitis and
pneumonia that responded transiently to antibiotic therapy.
Immunodeficiency syndromes affecting more than 1 arm
of the immune system have been documented in a family of
Basset Hounds, and in several related Weimaraners. In the
former, severe growth retardation and early death were associated with low serum IgG and IgA concentrations, and
with abnormal lymphocyte blastogenesis in response to
PHA. In the latter, recurrent sytemic or multifocal infections
were associated with low serum IgG and IgM concentrations
and with impaired neutrophil chemiluminescence.
Acquired immunodeficiency syndromes include canine
distemper virus and parvovirus infections, and generalized
demodicosis. In addition, the use of systemic anticancer
agents may result in variable degrees of immunosuppression.
The type of infectious agent and the pattern of infection
are usually determined by the nature of the defect. For example, defects in the humoral immunity usually result in infections with pyogenic organisms affecting one or more
sites; defects in T-cell function result in viral, fungal, or protozoal infections that are usually widespread; abnormalities
in the phagocytic system may result in skin, respiratory,
meningeal, or systemic infections with pyogenic or enteric
organisms. Therefore, the type and pattern of infection will
dictate what test/s should be used in these patients.
Several diagnostic tests can be used in the evaluation of
dogs with suspected immunodeficiency. Some of these tests
(ie; neutrophil function tests; lymphocyte blastogenesis) require fresh blood samples (ie; need to be done within 4
hours) and specialized laboratory equipment; they are therefore of limited use to general practitioners and are limited to
teaching or research institutions. Other tests, however, can
be done of serum samples and can therefore be mailed to referral laboratories.
The following are some of the tests that can be used to
evaluate patients with recurrent infections:
humoral immunity: serum protein electrophoresis, immunoelectrophoresis, radial immunodiffusion for Ig levels, complement levels;
cellular immunity: lymphocyte blastogenesis in re-

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

150

sponse to ConA, PWM, and PHA; enumeration of circulating T-cells; NK cell assays;
phagocytic system: nylon wool adhesion; migration under agarose; phagocytosis of bacteria, yeasts, or latex;
phagocytosis of opsonized particles; chemiluminescence;
nitroblue tetrazolium reduction test; bacterial killing assay.
Clinical management of these patients includes use of
the appropriate antimicrobial drugs on the basis of identification of the etiologic agent. If an infectious agent cannot be
isolated and the patient appears to have a bacterial infection,
bacteriocidal antibiotics that attain high intraleukocyte concentrations (ie; sulfa-trimethoprim) should be used.

4th European FECAVA SCIVAC Congress

References
Felsburg PJ: Immunodeficiency. In Kirk RW (ed): Current Veterinary Therapy IX. WB Saunders, Philadelphia. 1986, pp 439-444.
Degen MA, Breitschwerdt EB: Canine and feline immunodeficiencies Part I. Comp Cont Educ 8:313-323, 1986.
Degen MA, Breitschwerdt EB: Canine and feline. immunodeficiencies Part II. Comp Cont Educ 8:379-386, 1986.
Couto CG, Giger U: Congentital and acquired neutrophil function abnormalities in the dog. In Kirk RW (ed): Current veterinary Therapy X.
WB Saunders, Philadelphia. in press.
Guilford WG: Primary immunodeficiency diseases of dogs and cats. Comp
Cont Educ 9:641-650, 1987.

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151

Emergency care of pet birds


Lorenzo Crosta

Summary
Emergencies are still frequent with avian patients. Pet
bird owners must understand the importance of preventive
medicine, but they should also be educated by competent
professionals. Even more important is for veterinarians and
technicians to be trained to deal properly with avian emergencies. This paper takes into consideration the general aspects of these cases, like staff education, patient stabilization
and fluid therapy. Afterwards a short list of equipment and
tools for avian emergencies is given. Finally the most frequent emergencies in avian medicine are considered.

Introduction
Avian medicine is one of the latest veterinary specialization, and the progress and developments in this field have
been remarkable in the past few years. What still differentiates avian medicine from other veterinary specializations, is
preventive medicine with all those regular appointments,
like vaccinations, check-ups and others, which make the relationship between veterinarian and bird owner more constant, therefore increasing the chances for a sub-clinical or
still inapparent disease, to be diagnosed. To make matters
worse birds have a peculiar way of hiding symptoms of disease; this seems to be a necessity for birds to look healthy to
any possible predator. If this attitude is an advantage in the
wild, it makes it very difficult to understand how serious a
birds disease can be, so symptoms seem to appear and develop very suddenly and birds presented to a veterinarian are
often emergencies.
Obviously many emergencies, like traumas and toxicosis, do not have any relation with preventive medicine, but if
the owners of some of these patients could have been trained
on good bird management, their pets would not have needed
the veterinarians help.

Staff training
As weve just seen with avian emergencies time is often
so short that a proper training of all the clinics staff is really making the difference. The veterinarian should understand all the physiological and pathophysiological aspects of
the avian patient, furthermore she/he must have a good

knowledge of pharmacodynamics in birds, at least of the


drugs most frequently used in these emergencies. Technicians should know how to act rapidly and with certain ease
with these particular patients, without creating any risk for
the bird. Everybody should also know perfectly where all
the emergency equipment is located; all these points help
achieve the first aim of emergency medicine: patient stabilization. It is also very important for a technician to complete
a detailed form regarding the patients history.
Last but not least, considering the zoological variety of
the avian patients, the practitioner should be able to taxonomically locate the presented bird. This could be very important, as the same symptom can have a different diagnostic meaning in different bird species. So while the veterinarian waits for tests results and the chance to make a sure diagnosis, she/he can make a presumptive one, which must
take into consideration the patients species.

Patient stabilization
Stabilization of the avian patient follows the same procedures as those of emergency treatment in mammals, but
we must not forget that birds are easily stressed and this
could depend on the fact that they are always prey to a
predator bigger than themselves. This continous condition of
vulnerabilty induces a bird to appear healthy, especially
when faced with a potential predator like man. For these reasons during emergencies, before handling the bird it is very
important to observe it in its enclosure, as this will make it
feel less threatened. A first important step is to observe carefully the depth and rate of breathing: a rapid and superficial
breathing may show a critically ill and hypothermic bird, as
so happens during septicemia; while dyspnoea or laboured
breathing may indicate a disease which involves the respiratory system directly. In these cases it is always better to put
the patient in a heated cage supplied with oxygen, allowing
the bird to rest and calm down before handling. In the meantime, if it has not already been done, a complete clinical history of the bird can be compiled. If the bird can be weighed
or we already know its weight, we can be able to calculate
the exact dose of the drugs we intend to use; otherwise the
birds weight can be estimated according to the ideal weight
of that particular species. If the bird can be handled it is better not to stress it with forced restraint, but to anesthetize it
with isoflurane: this will allow us to proceed without risk, to

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dress wounds, temporarily fix fractures, collect blood, swabs


and other diagnostic specimens, and administer the preliminary drug therapy.

Fluid replacement therapy


Fluid therapy is a very important tool in the case of avian
emergencies, but we must pay attention to some facts that
differentiate birds from mammals: normally, a healthy birds
water intake varies from 5 to 30% of its body weight, according to the birds species, body weight and type of food.
Theoretically this determines a degree of variability in the
fluid requirements of sick birds, too. Anyway, as a general
rule, the mean fluid need of a bird can be estimated at 50
ml/kg b.w./day. It is important to assess the dehydration degree of the patient, expressed in percent, together with its
ideal body weight, which will allow a good estimation of the
fluid requirements per day. Lactated Ringers solution is
generally used, warmed to 100.4 to 102.2 F (38 - 39 C),
while the route of administration may change according to
many factors.
Oral route: this is the easiest way of fluid or drug administration to birds, but it is not suitable for emergencies.
Severely sick birds might regurgitate fluids and suffocate.
Subcutaneous route: birds do not have much subcutaneous tissue and their skin is not as elastic as that of mammals. However, the subcutaneous route is used to replace
fluids in moderately dehydrated birds. Small fluid amounts
can be injected in different sites on a birds back, or bigger
amounts can be injected in the axilla or flank region, where
we are less likely to inject fluids in an air sac. For these reasons subcutaneous administration is used primarily for
maintenance fluid therapy.
Intravenous route: this is the most direct route for administration of fluids in birds too, in a word it is definitively the emergency route of fluid administration. The most
used vessels for this purpose are the right jugular vein, the
ulnar vein and the medial metatarsal vein. Blood vessels of
birds are easily visible, but they are very fragile and lack
elastic fibers, therefore placing an intravenous catheter in
bird is simply done, but to leave it in place for long periods
may be difficult. Consequently intravenous catheters are
placed during isoflurane anesthesia or in very depressed patients. In this way sufficient fliud volumes can be administered quickly (10 ml/kg b.w. over the first five minutes, to be
repeated every 3 - 4 hours for the first 12 hours, then every
8 hours for the following 48 hours). In very calm birds it is
possible to leave an intravenous catheter in the ulnar vein;
while the medial metatarsal vein is preferred in Anseriformes (ducks and geese), in Columbiformes (pigeons and
doves), in various long-legged birds and in some birds of
prey. This last vein, if cannulated, can be managed as the
cephalic vein of dogs and cats.
Intraosseous route: in birds it is considered a very good
alternative to intravenous administration; furthermore to
leave an intraosseous catheter in place, in a bird, is more
easy than to leave an intravenous one. The way to place intraosseous catheters in avian patients is the same as used in
mammals; the bones of choice are the ulna and the tibiotar-

4th European FECAVA SCIVAC Congress

sus: in the first bone a distal access is used, in the latter a


proximal one. To avoid the bone cortex blocking the needle
channel, spinal needles are preferred. As happens in mammals, the major risk of this procedure are bone infections;
furthermore often an infusion pump is often needed to help
the fluid pass through the intraosseous catheter.

Equipment for avian emergencies


- Incubators
- Gram scale
- Fluid warming chamber
- Nebulizer
- Circulating warm-water blanket, Heat lamps
- Towels for restraint
- Isoflurane anhaestesia machine
- Face masks for anhaestesia induction
- Respiratory monitor
- Small endoscopes, flexible and rigid
- Small endotracheal tubes
- Sterilized air sac tubes
- Radiosurgical unit
- Leg band cutter
- Haemostatic sticks
- Intravenous catheters, 20 - 24 G
- Variety of spinal needles
- Infusion pump
- Microdrip IV administration sets
- Parrot mouth speculums
- Vetwrap like bandages, cut into small sizes
- Slides and cover slips
- Heparinized microhematocrit tubes
- Blood smears stains
- Microbiology swabs

Common avian emergiences


- shock (septic, toxic, traumatic)
- toxicosis
- seizures
- major wounds
- oiled birds
- frostbite
- head trauma
- open fractures
- haemorrhagiae
- hypoglicemia
- hypocalcemia
- tight leg band
- apnoea
- acute dyspnoea
- tracheal foreign bodies
- beak fractures
- tongue lesions
- crop wounds
- crop burns
- g.e. foreign bodies
- gastric impaction

- cloacal prolapse
- egg binding
- oviduct prolapse
- phallus prolapse

Literature
Crosta L, (1992), Uccelli e inquinamento da petrolio e derivati, metodi di
trattamento e rilascio. Ob. e Doc. Veterinari, 12: 27 - 32.
Crosta L, (1997), La visita clinica del paziente aviare: principali punti di
repere, contenimento manuale e farmacologico e dosaggio di alcuni
farmaci di comune impiego. Veterinaria, 11 (2): 115 - 129.

153
Degernes LA: Trauma Medicine. In: Ritchie BW, Harrison GJ and Harrison
LR, (1994), Avian Medicine: Principles and Application, Wingers
Publishing, Lake Worth, pp. 417 - 433.
Heidenreich M, (1997), Birds of Prey, Medicine and Management. Blackwell Science Ltd, Oxford, pp. 98 - 101.
Jenkins JR: Avian Critical Care and Emergency Medicine. In: Altman RB,
Clbb SL, Dorrestein GM and Quesenberry K, (1997), Avian Medicine
and Surgery, W.B. Saunders Company, Philadelphia, pp. 839 - 863.
Quesenberry K and Hillyer EV: Supportive Care and Emergency Therapy.
In: Ritchie BW, Harrison GJ and Harrison LR, (1994), Avian Medicine: Principles and Application, Wingers Publishing, Lake Worth,
pp. 382 - 416.
Redig PT: Management of medical emergencies in raptors. In: Redig PT,
(1993), Medical Management of Birds of Prey, 3rd ed, St. Paul, pp.
13 - 21.

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155

Emergency care and medical stabilisation


of reptiles
Stephen John Divers

Summary
The veterinary care of reptiles has progressed a great
deal over the past decade or so. Current practice has built
upon the foundations laid down by pioneers such that the
veterinary surgeon is now able to offer a comparable level
of care for reptiles as has been available for the more domestic animals for many years. However, with increasing
skill comes increasing expectations, and reptile clinicians
are now being increasingly asked to deal with critically sick
animals. This paper hopes to introduce the clinician to the
important aspects of providing emergency care for reptiles.
Emphasis is made of the importance of a through history and
clinical examination, diagnostic investigations and medical
stabilisation including parenteral fluid therapy. Some common emergency scenarios are also discussed.

Introduction
Reptile emergencies do occur; the tortoise attacked by a
dog, the iguana with hypocalcaemic tetany, the septicaemic
python. The basic approach to emergency reptile medicine
follows along similar lines to domestic animal medicine,
however reptile medicine also throws up a number of other
problems1. Reptiles are ectothermic and have a metabolic
rate comparable to 1/7 that of mammals. Their slower metabolism generally results in the slower clinical manifestations
of disease. Therefore, the clinician will often be presented
with a moribund reptile that was in apparently good health
the previous day. Some of these cases are true medical emergencies but many represent the terminal presentation of a
chronic illness.

History
In cases of true emergency, it may be essential to admit
and commence treatment (e.g. oxygen therapy) prior to taking a complete history, but in such cases a history should be
taken by a veterinary nurse or the veterinarian at the earliest
convenience. The importance of a detailed history must never be overlooked and may actually help in determining
whether the current situation is truly acute or merely the terminal stage of chronic disease2. Historical details of interest
include:

temperature and thermal environment (power cuts,


heater malfunction, electrocution, breeding programme).
Lighting (sunlight, artificial UVB lights, how old, lightreptile distance, electrocution).
Hide-outs, substrate (wet, mouldy), furniture (fallen
rocks or branches).
Recent changes in husbandry (last 6-12 months).
Other reptiles in direct contact with current patient (their
health, clinical signs).
Recent additions to collection (last 6-12 months, quarantine).
Appetite and food intake (reduced, increased, slow deterioration, complete anorexia, duration, food types, supplements).
Water intake and humidity (observed drinking, increase
or decrease, unknown).
Changes in behaviour (courtship, mating, egg
laying/birth, tremors, depression, lethargy).
Owners records (weights, snout-vent measurements,
Jackson ratio, ecdysis, routine treatments, other medications.)

Clinical examination
In cases of true emergency, it may be essential to admit
and commence treatment prior to performing a complete examination. Nevertheless a thorough clinical exam is always
indicated and should be performed as soon as possible2. The
examination should be systematic and cover all available
systems. Traumatised areas including severe burns, fractures
and wounds must be handled carefully to avoid further damage. During the examination;
Confirm species, sex and age.
Obtain an accurate weight and length, and an appreciation of overall body condition (pelvic limb and tail muscle
coverage, poverty lines).
Obtain an appreciation of respiratory and cardiovascular
function; head extended and open mouth breathing, glottal
discharge, increased respiratory efforts at rest and when unrestrained, buccal mucous membrane colour, demeanour
(active or lethargic), auscultation or Doppler for heart rate
and peripheral pulse rate.
Obtain an appreciation of metabolic disturbances and hydration; tremors, seizures, moribund, urate tophi in mucous
membranes of mouth, reduced skin elasticity, skin tenting,
swollen limbs/jaw, pyramiding or saddle-like shell.

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The Exotic Animal Centre - Essex - United Kingdom

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Obtain an appreciation of the integument; abscessation,


swellings and discharges, erythema and petechial haemorrhages, burns, lacerations and penetrating injuries.
Obtain an appreciation of the gastro-intestinal tract; buccal cavity, cloaca, coelomic palpation.
Obtain an appreciation of the urogenital system; if possible palpate kidneys, coelomic cavity for bladder stones and
eggs.
Obtain an assessment of the musculoskeletal system;
limbs, jaw, swellings, fractures, muscle loss, cachexia.

Trauma
In cases of severe and continued bleeding haemostasis
can be achieved by the application of local pressure bandages. Identified vessels may be permanently or temporarily ligated using nylon or vascular clips, or repaired under
isoflurane or local anaesthesia to maintain important vascular supplies. The application of calcium or adrenaline impregnated swabs and radiosurgery are also useful in the control of haemorrhage.
Prolapses of gastrointestinal tract through penetrating
coelomic wounds should be cleaned and replaced as long as
the intestinal segment is viable and has no lacerations that
will lead to the leakage of gut contents. The wound is then
packed with sterile swabs soaked in dilute povidone-iodine
solution or metronidazole solution (Torgyl, 5 mg/ml, Rhone
Merieux) and bandaged using plastic film. In cases of intestinal laceration, the site should be packed with moist sterile swabs, maintaining the intestine outside the coelomic
cavity and the whole area bandaged as before until surgery
can be undertaken.
Cloacal, penile, colonic and bladder prolapses should be
replaced if at all possible. If surgery is thought necessary
the area can be bandaged using moist swabs and plastic
film to prevent dehiscence until the operation can be safely
undertaken.
Traumatised soft tissues including limbs, tail, flanks and
shell should be treated in much the same way as for domestic animals. If medical stabilisation is required before
surgery then immobilising the area, covering with sterile
gauze and bandaging will prevent further damage and contamination. Burns are particularly prone to infection and the
liberal use of topical silver sulphadiazine cream (Flamazine,
1%, Smith and Nephew) cream is recommended.
Bite wounds tend to be superficial lacerations but deep
penetrating wounds should not be sutured, but treated as infected wounds.

Drowning
Tortoises kept in garden enclosures seem particularly
prone to drowning and may not be recovered from the pond
for several hours. These animals are often presented in a
moribund state. In very unresponsive cases (no deep pain response or corneal reflex) it is wise to obtain e.c.g. evidence
that the reptile is still alive before proceeding. Whatever the
species, position and tape an endotracheal tube in place, and

4th European FECAVA SCIVAC Congress

hold the animal head down. Pump the limbs of chelonia,


massage the thorax of lizards or lung field area of snakes to
aid evacuation of water. This should encourage voiding of
any fluid remaining within the lung fields. Inflate the lungs
with either air or pure oxygen and give intravenous
doxapram (Dopram-V, 20 mg/ml, Willows Francis) at 5-10
mg/kg i.v. to help stimulate respiration. Until spontaneous
breathing returns (which may take minutes or hours) the reptile should be maintained on a respiratory monitor and given intermittent positive pressure ventilation 2-4 times every
minute. Cases of drowning in freshwater seldom require fluid therapy unless severe cardiovascular or respiratory compromise continues. However, cases of drowning in marine
water will often lead to rapid water loss from the lungs and
dehydration. In these cases fluid therapy is recommended.
The prophylactic use of broad spectrum antibiotics is advisable as secondary pneumonia is not uncommon.

Hypothermia and hyperthermia


Severe hypothermia can result from heating failure or
more commonly delayed national and international transportation. Slow sustained warming is essential as too rapid a
rise in core temperature may cause further compromise.
Gradual increase in environmental temperature to the
species-specific POTZ (preferred optimum temperature
zone) over 4-24 hours depending on degree of hypothermia
is usually sufficient. In severe cases fluid therapy using
warm fluids may also be beneficial.
Hyperthermia is less common than burns, however, constant exposure to temperatures above the POTZ and approaching the species-specific critical high temperature (often 35-45C) will lead to heat stress. Open mouth breathing,
increased respiratory effort and collapse are common signs.
Immediate reduction of the environmental temperature to
the lower end of the species specific POTZ is required. In severe cases, fluid therapy using cooler but not refrigerated
fluids (20-30C) may be beneficial.

Intestinal obstruction and constipation


Gastro-intestinal obstructions may be due to gravel,
stones, bark, balls, rubber suction devices, elastic bands, abscesses, neoplasia, intussusception, ileus, renal enlargement,
cloacitis, faecoliths and parasites. Characteristic signs include regurgitation, tenesmus and diarrhoea, and less commonly blood in faeces or vomitus. Coelomic palpation may
reveal discernible masses within the gastro-intestinal (or reproductive) tract.
In such cases electrolyte and fluid imbalances should be
corrected. Faecal analysis may reveal parasites that should
be treated. In cases of constipation, it is important to consider predisposing factors including renal disease, but until the
reptile is stable and a thorough investigation can be undertaken, the use of oral laxatives or water enemas may be tried.
Once stable, radiography and endoscopy should be used
to diagnose the problem and appropriate measures can then
be taken where necessary.

Pneumonia
Reptiles lack a functional diaphragm and therefore have
great difficulty in coughing. In cases of pneumonia, infectious exudates tend to accumulate reducing the functional
area of lung. Once the functional pulmonary reserve has
been exceeded the reptile will present with increased respiratory effort at rest, and a possible glottal discharge. Providing a high oxygen environment will help alleviate the signs.
In severe cases with confirmed radiographic fluid lines, it is
often helpful to insert a small catheter down the trachea into
the lung fields and aspirate as much exudate as possible. The
exudate should then be submitted for laboratory analysis. In
moribund lizards sedation or isoflurane anaesthesia is seldom necessary for lung exudate aspiration.

Medical stabilisation
Assessment of dehydration,
metabolic disturbances and fluid therapy
Hydration status can be assessed in much the same way
as other animals, including reduction in skin elasticity, dull
and wrinkled skin. This must not be confused with normal
ecdysis (skin shedding). Pre-treatment blood samples are
very useful in evaluating hydration status and biochemical
derangements in reptiles. Although there is relatively little
published data on observed haematology and serum/plasma
biochemistry values, serial blood samples offer the best assessment of hydration status and response to therapy.
Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Avoid the hemipenes of
males.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25 g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapinsDorsal tail vein; A 5/8 21-25 g needle is angled at 45-90
and placed, as cranial as possible, in the dorsal mid line of

157

the tail. The needle is advanced while maintaining a slight


negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species.
Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with neostigmine), and it may be necessary to use large spinal needles (3-8) to reach the vein.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90 in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Larger crocodilians (over 1.5 m)
may require chemical restaint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with
neostigmine).
Intramuscular injections can be given into the epaxial
muscles of snakes and proximal forelimb muscles of chelonia, lizards and crocodilians.
The daily water requirements for reptiles have not been
conclusively determined. Published literature suggests that
reptiles may be rehydrated by providing fluids at a rate of
10-50 ml/kg/day, but 15-30 ml/kg/day appears more appropriate for the vast majority of species5,6,7. Rehydration can
take several days to a week or more and it is wise to rehydrate slowly.
Dehydration in reptiles may be characterised as isotonic,
hypotonic or hypertonic5. Hypotonic dehydration is most
commonly associated with prolonged anorexia and hypertonic dehydration associated with water deprivation or an inability to drink. Isotonic dehydration can occur following
haemorrhage, emesis, diarrhoea and tissue damage. Water
balance in reptiles differs from that of mammals as, per unit
body weight, reptiles have a higher percentage of total body
water (63.0-74.4%) and a higher percentage intracellular
water (45.8-58.0%).8 These values appear to be highest in
freshwater species, lower in terrestrial reptiles and lowest in
marine reptiles, with the concentration of isotonic saline in
non-marine reptiles being 0.8%9. This has led to the recommendation that standard 0.9% normal saline solutions be

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4th European FECAVA SCIVAC Congress

158

slightly diluted for use in reptiles to facilitate the intracellular diffusion of water. Four suggested fluid solutions for parenteral administration in reptiles are:
1) Two parts 2.5% dextrose in 0.45% sodium chloride and
one part Ringers or equivalent electrolyte solution5.
2) One part 5% dextrose in 0.9% sodium chloride, one part
lactated Ringers and one part sterile water.
3) Nine parts 0.9% sodium chloride and one part sterile
water.
4) 0.18% sodium chloride and 4% glucose.
All fluids given by any route must be warmed to the
species-specific PBT (often 30-35C) prior to administration.
Bathing, oral, subcutaneous and intracoelomic fluid administration must not be overlooked, however intravenous
or intraosseous routes offer the best fluid therapeutic approach in emergency situations. Intravenous catheterisation
is not easy in reptiles and cut-down procedures are often required under local or isoflurane anaesthesia. In large lizards,
cephalic and abdominal vein catheterisation has been employed, while the right jugular is most accessible in the chelonia. In snakes, the right jugular can be catheterised using a
cut-down technique. The incision site is located 12 abdominal scales cranial to the heart and two lateral scales to the
right. A 2-3 cm incision reveals the jugular just medial to the
ribs, which can then be catheterised with a 50-100 mm (24) 20-23 g catheter. In larger snakes it is possible to place
an intracardiac catheter. The heart is located and immobilised as described previously for blood sampling, and a 2575 mm (1-3) 22-23 g catheter is inserted just caudal to the
heart apex and advanced cranially into the ventricle. In all
cases of venous catheterisation, the catheter must be securely sutured to the skin and bandaged in place. Fluid infusion
is best controlled by a syringe driver. Most intravenous
catheters can be left in place for up to 72 hours, or up to 36
hours in the case of intracardiac catheters.
Intraosseous infusion is an easier technique that is available for use in lizards, small crocodilians and chelonia. In
lizards and small crocodilians a 19-38 mm (3/4-11/2) 20-25 g
spinal needle (or 16 mm 5/8 25 g hypodermic needle for
very small species) is inserted into the proximal tibia. The
limb is flexed and the tibial tuberosity located. The needle is
inserted distally while holding the body of the tibia. Correct
positioning can be verified by the aspiration of bone marrow,
low resistance to flushing with heparinised saline, or radiography. Greater care must be exercised when dealing with osteodystrophic lizards as limb fractures are a potential complication. In chelonians, the intraosseous needle can be inserted into the distal tibia or the medullary cavity of the vertical shell that connects the carapace and plastron. Intraosseous needles are taped in position using zinc oxide
tape, incorporating a loop of the extension line to reduce
catheter tension. Syringe drivers are used to control the infusion rate. The author has used this intraosseous technique
in reptiles as small as 75 grams and considers it the parenteral route of choice.
Infusion rates for intravenous and intraosseous administration are similar. As a general guide 0.8-1.4 ml/kg/hour is
suitable for rehydration purposes, but in cases of severe dehydration, shock or during surgery the author has used 5
ml/kg/hour for up to 3 hours without ill effect.

4th European FECAVA SCIVAC Congress

Haemorrhage
In cases of severe haemorrhage a PCV evaluation is warranted. If the PCV is below 0.05L/L then a single whole
blood transfusion may be indicated. Blood should only be
collected from healthy reptiles preferably of the same
species and from the same collection to avoid cross-colony
infection. However, the author has taken blood from Hermanns tortoises (Testudo hermanni) for transfusion into a
leopard tortoise (Geochelone pardalis), and has taken blood
from a green iguana (Iguana iguana) for transfusion into a
common tegu (Tupinambis teguixin) without obvious ill-effects. Cross matching does not appear necessary, at least for
a one-off transfusion. The donor reptile can provide 7 ml/kg
blood which can be collected into a heparinised syringe for
immediate administration to the recipient. Alternatively,
blood may be collected into citrate-phosphate-dextrose and
administered later. Catheterisation of the right jugular of
donor and recipient tortoises facilitates blood collection and
transfusion. In lizards, collection and transfusion via the
ventral tail vein appears to work well. In snakes a jugular
catheter or cardiac catheter should be utilised. Blood has also been administered via an intraosseous catheter in iguanas.
Reptiles are able to cope with much greater blood loss than
mammals, and so blood transfusion is only required in dire
circumstances when the animal is very depressed following
acute and severe haemorrhage. Usually, the administration
of intravenous or intraosseous fluids is acceptable. Colloids
are less frequently used in reptiles because much of the water loss is from the intracellular space rather than plasma, but
in cases of acute haemorrhage their use is commendable.

Laboratory investigation
Basic biochemistries can be run on many in-house practice laboratories (e.g. Vettest 8001) with a reasonable degree
of accuracy. Uric acid must always be undertaken as a level
of over 1000 umol/l in an anorexic reptile tends to indicate
severe azotaemia (pre-renal, renal or post-renal). Above
1487 umol/l uric acid may start to precipitate out and cause
gout. However, post-prandial elevations of uric acid can occur normally in many species, particularly snakes, and so
short-term elevations of uric acid may not carry such a poor
prognosis. Consistently high or rising uric acid levels above
1500 umol/l, despite intensive fluid therapy, tend to carry
the worst prognosis. Urea and creatinine are poor indicators
of dehydration and renal disease and are not considered
clinically useful. PCV and total protein are useful for assessing dehydration and are relatively inexpensive permitting serial assessments at a viable cost. The inclusion of glucose in parenteral fluids may be important in supporting
cachexic reptiles and should certainly be used in cases of severe hypoglycaemia. Another metabolic disorder, severe
hypocalcaemic tetany, will benefit from the inclusion of calcium in the infusion fluid. However, it is important to consider concurrent control of any pre-existing hyperphosphataemia (diuresis, phosphate binders) to avoid soft tissue
mineralisation.

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159

Observed serum biochemistry ranges used to assess dehydration and biochemical imbalances in selected reptiles
(Adapted from references 3 and 4, and the authors unpublished observations)

PCV (%)
TP (g/l)
Urea (mmol/l)
Creatinine (mmol/l)
Uric acid (umol/l)
Glucose (mmol/l)
Calcium (mmol/l)
Phosphorus (mmol/l)
Sodium (mmol/l)
Chloride (mmol/l)
Potassium (mmol/l)

Gila
monster

Tortoise
(Testudo sp)

Box
tortoise

Boa
constrictor

Rat snake

Caiman

25-38
50-78
0-0.7
42-80
70-140
9.4-16.0
2.2-3.5
1.5-3.0
140-183
102-125
1.3-5.2

25-30
60-85
na
na
100-1000
2.5-6.0
2.2-3.5
1.4-2.9
150-190
114-130
4.1

19-40
50-75
0.25-6.70
20-150
75-200
2.6-5.2
2.7-3.6
0.8-1.5
120-158
98-128
4.0-7.0

20-38
40-50
na
na
100-200
2.0
2.5-3.5
0.9-1.7
130-149
104-108
4.6-4.7

20-32
46-80
0-1.67
0-26.5
75-250
0.6-4.0
2.5-5.5
0.8-1.6
130-152
104-124
3.0-5.7

20-30
40-70
na
na
75-250
na
2.5-6.3
2.1-3.1
130-160
125-147
4.1-5.2

26
50-65
na
na
175
4.1-6.3
2.3-3.8
1.3-2.9
139-150
109-132
3.8-7.9

Electrolyte imbalances will usually resolve as renal perfusion and function is restored, however if carefully monitored the correction of acid-base and electrolyte imbalances
may be attempted in a similar manner to mammals.
A complete blood count takes time and may well be beyond the capabilities of a practice laboratory, especially outside normal office hours. Nevertheless, a haematocrit tube
can provide a PCV, semi-quantitative estimate of total white
blood cell count and an idea of plasma colour and character.
In a full haematocrit tube, the first 1% of the buffy coat represents approximately 10109/L and every additional 1%
adds a further 5109/L. This is obviously not very inaccurate
but will provide an idea of whether a reptile has a WBC of
5109/L or 50109/L. In addition, a fresh blood smear
stained with DiffQuik will also permit the rapid assessment
of a white blood cell differential, with particular reference to
heterophils, azurophils and lymphocytes along with any
leukocyte toxic changes.
Any discharges, fluids or superficial tissues can be sampled for impression smear cytology using DiffQuik stains. It
is important to submit blood, tissues and aspirates for culture
and sensitivity before commencing broad spectrum antimicrobial therapy. Enrofloxacin and ceftazidime are safe,
broad antibiotics that are commonly employed. In cases of
suspected septicaemia, i.v. or i.o. ceftazidime and amikacin
may be employed but beware of the nephrotoxic effects of
aminoglycosides.

Hospitalisation
Once the acute emergency is over and the animal is on
continuous fluid therapy it is vital that the reptile is maintained in a suitable thermal environment, at the species-specific POTZ (often 25-35C). All metabolic and physiological processes are dependent upon environmental temperature and all your hard work will be undone if the animal is
left overnight in a cold kennel with a hot water bottle! Oxygen therapy can continue in the hospital vivarium and monitoring using peripheral pulse oximetry is useful.

Nutritional support is usually secondary to rehydration,


but in cases of severe starvation complete parenteral nutrition
can be attempted. The oral route is preferred although the intravenous administration of lipid emulsions may be feasible.
The author prefers Critical Care Formula (Vetark) as an initial oral electrolyte and maltodextrin, protein and amino acid
mixture. This can later be replaced by Hills a/d for carnivores
and insectivores or commercial human baby foods (vegetable
and fruit varieties lacking dairy products) for herbivores.
More recently, the use of Pretty Pets complete herbivorous
reptile diets (tortoise and iguana) have been utilised with apparent success by simply adding warm water and mixing into a thick slurry. It must be stressed that such exclusive diets
should only be used on a short term basis and that once the
reptile has started to improve, efforts must be made to provide a more varied, natural diet. Most reptiles will be very
weak and therefore food material should be placed directly
into the stomach using feeding needles or stomach tubes. The
head should be kept elevated for a prolonged period using
foam or sand bags to avoid regurgitation.
Once stabilised further investigation (radiography, ultrasonography, endoscopy etc.) and surgery can proceed.

Key words
Reptile, emergency, trauma, shock, haemorrhage,
drowning, gastro-intestinal obstruction, hypothermia, hyperthermia, pneumonia, fluid therapy.

References
1.
2.
3.

4.

Boyer, T.H. (1994). Emergency care of reptiles. Semin Avian Exotic


Pet Med 3:210-216.
Divers, S.J. (1996). Basic reptile husbandry, history taking and clinical examination. In Practice 18:51-65.
Stein, G. (1996). Hematologic and blood chemistry values in reptiles.
In: Reptile Medicine and Surgery, p473-483 (Ed. D. R. Mader). WB
Saunders, Philadelphia.
Divers, S.J., Redmayne, G. and Aves, E.K. (1996). Haematological

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Green
iguana

160

5.

6.

4th European FECAVA SCIVAC Congress


and biochemical values of 10 green iguana (Iguana iguana). Veterinary Record 138:203-205.
Jarchow, J.L. (1988). Hospital care of the reptile patient. In: Exotic
Animals. (Eds. E.R. Jacobson and G.V. Kollias). Churchill Livingstone, New York.
Klingenberg, R.J. (1996). Therapeutics. In: Reptile Medicine and
Surgery, p 299-321 (Ed. D. R. Mader). WB Saunders, Philadelphia.

7.

8.
9.

Pokras, M.A., Sedgwick, C.J. and Kaufman, G.E. (1992). Therapeutics. In: Manual of Reptiles. (Eds. P.H. Beynon, M.P.C. Lawton and
J.E. Cooper). BSAVA, Cheltenham.
Thorson, T.B. (1968). Body fluid partitioning in the Reptilia. Copeia
3:592.
Marcus, L.C. (1981). Veterinary Biology and Medicine of Captive
Amphibians and Reptiles. Lea and Febiger, Philadelphia.

4th European FECAVA SCIVAC Congress

161

Hemogram interpretation revisited


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Time spent critically reviewing all aspects of the complete hemogram is diagnostically rewarding. This, coupled
with newer automated technology better enables clinicians
to detect sample errors and potential errors as well as
graphically depicting cells. Automated technology also improves the identification of appropriate and abnormal cells,
and may reduce labor time as well as providing more objective quantitative information about blood samples.

Introduction
The following is considered a COMPLETE hemogram:
Examining red blood cells
1. Red blood count
2. Hemoglobin concentration
3. Packed cell volume or hematocrit
4. Mean cell volume
5. Mean cell hemoglobin
6. Mean cell hemoglobin concentration
7. Reticulocytes
8. Reticulocyte production index
9. Metarubricytes
10. Red cell morphology and cytograms
11. Histogram of red cell volume distribution
12. Total protein
Determining inflammation
12. Fibrinogen
13. Sedimentation rate
Examining platelets
14. Platelet count
15. Mean platelet volume
16. Platelet morphology
Examining leucocytes
17. White blood cell count corrected for metarubricytes
18. Differential white blood cell count in absolute values
Immature forms
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Degenerated cells
Unidentifiable cells

19. White blood cell morphology


20. Leucocyte cytogram

The relationship between hemoglobin,


hematocrit, and the red cell indices plus
the histogram of red cell volume
distribution
The hemoglobin concentration is probably the most accurate (and the red cell count the least accurate) of the three
analytes needed to calculate the red cell indices. The packed
cell volume is the number derived from packing red cells by
centrifugation in a glass tube. It is similar to but not necessarily the same as the hematocrit which is a calculated number. If the red cell indices are within the reference interval
(this is the new jargon for normal range), then the relationship between hemoglobin and hematocrit is steady. That is to
say, the hemoglobin multiplied by 3 should approximate the
hematocrit or the hematocrit divided by 3 should approximate the hemoglobin. Any significant departure from this ratio suggests laboratory error. If the red cell indices are not
within the reference interval the ratio is not valid.
It is important to recall the red cell indices are MEAN
values. Therefore it takes a lot of abnormally sized cells to
move the MCV out of range. It takes a significant decrease
in hemoglobin production to drop the MCHC. Abnormal indices provide free useful information. However normal indices require further examination of the hemogram. Responsive anemias, responsive to hemolysis or blood loss, usually
become macrocytic and hypochromic. Macrocytic normochromic anemias suggest aberrant red cell maturation and
are often the first signs of impending marrow dysplasia or
neoplasia. Most clinical anemic presentations are normocytic and normochromic requiring additional examination of
the hemogram and, perhaps, additional testing. Microcytic
hypochromic anemias suggest blood loss. In younger animals this often is associated with parasitism. In older animals ulceration and/or neoplasia is suggested. Histograms of
red cell volume distribution is a relatively new measurement
allowing visualization of erythrocyte volume variability.
Disturbances of red cell production that result in altered
red cell size are more readily detected. These histogram abnormalities alert the technologists or clinicians to the presence of unusual red cell volumes when the mean values of
the red blood cell indices are within the reference interval.

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Summary

162

Reticulocytes and nucleated red cells


Reticulocytes are an index of marrow erythroid production and effective delivery to the vascular space. Reticulocytes are observed in blood smears stained with vital
stains. Polychromasia, virtually the same as reticulocytes,
is observed in Romanowsky (Wrights) stained smears.
Reticulocytes, to be interpreted properly, in dogs and cats,
must be adjusted for packed cell volume and erythropoietin
production. The reticulocyte production index is one attempt at understanding how responsive is bone marrow
erythropoiesis.
Metarubricytes are the only nucleated red cells that
should ever be observed in peripheral blood smears. Red cell
precursors younger than these often suggest marrow dysplasia or neoplasia. Since nucleated red cells inflate the white
cell count, whenever nucleated red cells are present the
white cell count should be corrected. Nucleated red cells are
never an indication of red cell response unless accompanied
by reticulocytes in numbers exceeding nucleated red cells
(sans unitage).
Clinicians should be capable of developing a diagnostic
differential scheme for the presence of nucleated red cells
and/or reticulocytes in nonanemic patients as well as anemic
patients.

Red cell morphology


It is almost too mundane to think of red cell morphology
in only terms such as polychromasia, poikilocytosis, anisocytosis and occasional spherocytosis. There are many red
cell shapes and sizes that are diagnostically useful. A few include codocytes and stomatocytes which also may be observed in immune-mediated hemolysis, burr cells in advanced glomerulonephritis, acanthocytes in some forms of
cholestatic disease, schistocytes associated with disseminated intravascular coagulation, Heinz bodies when hemoglobin is oxidized, and blister cells observed in hypersplenic
diseases. There are many more helpful red cell changes...

Red cell cytograms


The typical erythrocyte cytogram plots each red cell by
the size of the cell and the hemoglobin content. The cytogram is compared to appropriate cytograms for the species
in question. This technology allows for the earlier detection
of iron deficiency anemia and documentation of active erythropoiesis. These are just several examples.

Total protein, fibrinogen, erythrocyte


sedimentation rate, icterus index
The only way red cell mass can be viewed critically is
with total protein quantitation. Dehydrated patients may
mask mild anemias. Blood loss is often clinically obvious
and is supported by lowered proteins. Younger animals have
lower proteins (less immunoglobulins) than do older ani-

4th European FECAVA SCIVAC Congress

mals. Fibrinogen and erythrocyte sedimentation rate are


helpful additions to our diagnostic armamentaria as regards
inflammation. They often increase, preceding changes in the
leucogram and return towards normal before the leucogram
does. Decreases in fibrinogen are associated with disseminated intravascular coagulation. Marked increases in fibrinogen quantitation and erythrocyte sedimentation rate are
associated with renal or neoplastic diseases.
Icterus index is a way of making an objective assessment
of patient jaundice. Plasma color is compared to potassium
dichromate standards and given a number value. Comparative aspects become evident on patient reexamination or
when speaking to a colleague about the patient. Regularly
inspecting plasma color and clarity often reveals free hemoglobin or lipemia.

Platelet count, platelet morphology,


and mean platelet volume
Platelet numbers should be critically assessed. It is simply not enough to receive a report that platelet numbers are
increased, adequate, or decreased. In patients that have
primary hemostatic defects, diagnostic and therapeutic decisions must be based on absolute numbers. In addition, large
platelets suggest young platelets. Platelet granularity is observably affected by some diseases and some drugs. Oval to
cigar-shaped platelets often suggest occult bleeding. Mean
platelet volume (MPV) is a new measurement designed to
enable us to view platelet size distribution. The detection of
microthrombocytosis in immune mediated thrombocytopenia is but one example of the advantage of determining
MPV. Another example is the detection of macrothrombocytes and active response to thrombocytopenia.

White cell count, distribution,


and morphology
White cells counts must be corrected for increased numbers of nucleated red cells. Additionally, the white cell count
is use to calculate absolute numbers of individual cell types.
Percentage distribution is not informative and often leads to
misdiagnoses. Included among the categories of cells in the
white cell differential should be cells called unclassifiable
and degenerated. These additional categories are an alert
to the presence of neoplastic cells and/or toxic cells.
The difference between a stress leucogram - mature neutrophilia, monocytosis, lymphopenia, and eosinopenia - and
an inflammatory leucogram - left shift - must be grasped.
Regenerative and degenerative left shifts are useful diagnostic academic terms which affect therapies.
The neutrophil to lymphocyte ratio is 3:1 in dogs and 2:1
in cats. These differences allow quantification of response
comparatively between the two species. Dogs often mount
an elegant response to a lesion or process. Cats, given the
same degree of insult, mount a lesser response. Ratio inversions are significant.
Nonspecific evidence of systemic toxicity is revealed
when neutrophil morphology changes. Vacuolation, toxic

4th European FECAVA SCIVAC Congress

granulation, and hypersegmentation, when observed, require


additional patient examination in order to determine the
cause of these morphological changes.

163

detect toxicity, detect modest eosinophilias, and detect blast


cells in early leukemic patients.

Recommended reading
There are several leucocyte cytograms now available.
These are the peroxidase cytogram and the basophil cytogram. The peroxidase cytogram plots each leucocyte by
cell size and peroxidase activity and the computer draws
lines around cell clusters that are distinctly different from
each other and allows an automated leucocyte differential
count. The basophil cytogram strips away leucocyte cytoplasm and plots naked leucocyte nuclear size and density. Interpretation of the basophil cytogram is based on the shape
of the cell cluster. The shape can determine individual leucocyte types and numbers, detect left shifts automatically,

Tvedten H. Advanced hematology analyzers interpretation of results. Vet


Clin Path 1993; 22:72-80.
Weiser MG. Sizing of animal erythrocytes using sulfate-based diluent. Vet
Clin Path 1985; 14:7-9.
Weiser MG. Modification and evaluation of a multichannel blood cell
counting system for blood analysis in veterinary hematology. J Amer
Vet Med Assoc 1987; 190:411-415.
Northern J, Tvedten HW. Reports of retrospective studies. Diagnosis of microthrombocytosis and canine immune-mediated thrombocytopenia
in dogs with thrombocytopenia: 68 cases (1987-1989). J Amer Vet
Med Assoc 1992. 200: 368-372.
Kocher WD. Autoimmune hemolytic anemia in: Atlas of automated cytochemical cytology. Edited by Simson, Ross, Kocher. Tarrytown NY,
Technicon Instruments 1988. 26-27.

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Leucocyte cytograms

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165

Special hematology diagnostics


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Leucocyte cytograms

Hemogram
Red cell cytograms
Mean platelet volume and cytogram
Leucocyte cytograms
In-house blood typing
Feline transfusion medicine
Detection of antibodies on red cells
Use of erythropoietin
Use of granulocyte-colony stimulating factor
Hemostasis
Primary hemostasis - the buccal mucosal bleeding time
Secondary hemostasis - PIVKA
Tertiary hemostasis - D-Dimer

There are several leucocyte cytograms now available.


These are the peroxidase cytogram and the basophil cytogram. The peroxidase cytogram plots each leucocyte by
cell size and peroxidase activity and the computer draws
lines around cell clusters that are distinctly different from
each other and allows an automated leucocyte differential
count. The basophil cytogram strips away leucocyte cytoplasm and plots naked leucocyte nuclear size and density. Interpretation of the basophil cytogram is based on the shape
of the cell cluster. The shape can determine individual leucocyte types and numbers, detect left shifts automatically,
detect toxicity, detect modest eosinophilias, and detect blast
cells in early leukemic patients.

HEMOGRAM

In house blood typing

Red cell cytograms

A simple in-house card test for feline red cell antigens


A, B, and AB and canine DEA 1.1. The dog has eight different blood types identified as dog erythrocyte antigens (DEA)
1.1, 1.2, 3, 4, 5, 6, 7, and 8. The use of DEA 1.1 and 1.2 positive blood products that are crossmatch incompatible may
cause hemolysis. Controversy exists as to whether DEA 7 is
an important determinant in canine transfusion reactions.
Ideally canine blood negative for DEA 1.1, 1.2 and 7 should
be used as it conforms with the concept of universal donor
blood. In random source, first time canine transfusion of
noncrossmatched or typed blood the transfusion reaction
rate is approximately fifteen percent. Again, transfusion reaction indicates that the materials transfused are not effective and are causing a physiologic burden on an already burdened patient - reasons to blood type and crossmatch. Recently there has been suggestions that the only significant
canine antigen is DEA 1.1. Donors blood products negative
for DEA 1.1 that are crossmatch compatible have a much reduced chance of transfusion reaction.

The typical erythrocyte cytogram plots each red cell by


the size of the cell and the hemoglobin content. The cytogram is compared to appropriate cytograms for the species
in question. This technology allows for the earlier detection
of iron deficiency anemia and documentation of active erythropoiesis. These are just several examples.

Mean platelet volume


Platelet numbers should be critically assessed. It is simply not enough to receive a report that platelet numbers are
increased, adequate, or decreased. In patients that have
primary hemostatic defects, diagnostic and therapeutic decisions must be based on absolute numbers. In addition, large
platelets suggest young platelets. Platelet granularity is observably affected by some diseases and some drugs. Oval to
cigar-shaped platelets often suggest occult bleeding. Mean
platelet volume (MPV) is a new measurement designed to
enable us to view platelet size distribution. The detection of
microthrombocytosis in immune mediated thrombocytopenia is but one example of the advantage of determining
MPV. Another example is the detection of macrothrombocytes and active response to thrombocytopenia.

Feline blood groups


and transfusion medicine
Three feline blood groups have been described: A, B,
and AB. The feline blood group system is different than that
in dogs because the occurrence of natural isoantibodies is

MAIN PROGRAMME

Special hematology diagnostics

166

common. Approximately 70% of all type B cats have anti-A


antibody in a high enough titer to cause decreased RBC survival and acute hemolysis. As little as 5 ml of incompatible
blood is enough to cause a fatal reaction. In 35% of all type
A cats anti-B is present but usually in low titer; reaction in
these animals is less frequent. Although the incidence of
type B cats in the United States is low, many purebred cats
(excepting the Siamese) such as the Cornish and Devon Rex,
British shorthair, Abyssinian, and Himalayan cats have a
high frequency of B blood types. Crossmatching is strongly
recommended for all cats about to receive blood or blood
products. The presence of natural isoantibody always result
in decreased RBC survival posttransfusion. Mean RBC survival is approximately 30 days in cats of the same blood type
and less than 10 to 14 days in cats with differing blood types.
Donor cats should be screened for red cell parasites,
heartworms and feline leukemia virus (FeLV), feline infectious peritonitis (FIP), and feline immunodeficiency virus
(FIV). At 2 week intervals 10 ml/kg can be collected. The
use of citrate-phosphate-dextrose-adenine (CPD-A1) is the
recommended anticoagulant. Heparin is contraindicated as
it activates platelets and antithrombin III and can result in
many unwarranted and disparate reactions including hemorrhage.
When delivering feline whole blood taken in a citrate anticoagulant care must be taken not to cause hypocalcemia,
which may be severe and even lethal. Citrate is a strong calcium chelator. Caution must also be used not to induce volume overload. Generally if less than 20% of blood volume
is delivered to a normovolemic but anemic feline patient
during an 8 hour period, volume overload does not occur. As
mentioned, cats have a normal blood volume of approximately 70 ml/kg.

Detection of antibodies on red blood cells


The ability to detect antibody in IHA will depend on the
characteristics of the antibody. Agglutination occurs readily
with IgM antibodies and poorly, if at all, with IgG antibodies. This is due to the fact that the larger IgM molecule can
span the distance imposed by mutually repulsive forces that
keep rbcs separated. When this happens IgM forms a lattice
and agglutination occurs. Additionally a sufficient amount
of antibody must be present for this phenomenon to occur.
The direct antiglobulin test (DAT; Coombs reaction) involves the species specific production of an antiantibody
thus allowing agglutination to occur in vitro. The majority of
autoimmune antibodies in human animals and nonhuman
small animals are IgG1 and the remainder are predominantly IgG3. The use of antiIgG and anticomplement 3 antisera
can aid in the determination the pattern of antibody or complement fixation in IHA. The antiglobulin test results are
then of four types:
a) antibody alone is fixed, generally antiIgG but no antiC3. In human animals this reaction is generally associated with specific blood groups and with specific
drug-induced IHA.
b) both IgG and C3 are found to be present on the rbc.
This indicates that IgG antibody is capable of fixing

4th European FECAVA SCIVAC Congress

complement. This pattern in human animals is seen in


SLE and in idiopathic IHA. This never occurs when
drugs are involved.
c) complement only is fixed; antiIgG does not cause agglutination. This kind of DAT reaction has several
causes. The antibody may not be IgG. The antibody
may have low affinity due to temperature. Papainization of the rbcs may result in a positive immmunoglobulin test because papain will increase the
ability of the antibody to interact with the rbc surface
antigen.
d) the test is negative. This results when the test is not
performed in both cold and warm environs, when the
affinity of the DAT antibodies is too low, when there
are too few antibodies or complement molecules on
the rbc surface, or when the DAT antibodies are too
avid resulting in the prozone phenomenon that is, too
many antiantibodies cover the antigens and lattice
structures are prevented.
WHAT YOU SHOULD DO! - As the handling clinician
you must ask your laboratory a series of questions. First is
the DAT being uses species specific? Do they run positive
and negative controls on each patient? Was the test run in
both cold and warm environs? What dilutions were used to
overcome potential prozone phenomena (generally dilutions
out to 1:16 will do this)?
OTHER MEANS OF DIAGNOSIS - There does not
seem to be a major age or sex predisposition to IHA in nonhuman animals. There does seem to be a breed predilection
with Cocker Spaniels, Old English Sheepdogs, Poodles,
German Shepherds and Doberman Pinschers predominating.
The presence of spherocytes helps but there is a caveat here.
Unless a trained technologist or cytologist is reviewing the
smears, spherocytes often are incorrectly identified. Conversely without training spherocytes are often missed. With
feline and equine rbcs spherocytosis is often missed because
of the small cell size. Spherocytosis is suggested when the
MCV is below normal or at the low end of the reference interval despite the large numbers of reticulocytes which often
accompany IHA and when the MCHC is above the reference
interval. This results when smaller cells (spherocytes) are
present (MCV) and have only lost membrane without loss of
intracellular content (MCHC). Slappendel from the State
University of Utrecht suggests that performing a standard
osmotic fragility test at half strength will reveal increased
osmotic fragility in IHA patients. Attempting to cause or disperse agglutination has been singularly unrewarding in this
authors hands.
Increased reticulocyte production indices without clinical evidence of bleeding and without hypoproteinemia suggests hemolysis. The caveat here is that nonimmune hemolysis can occur and spherocytosis can occur without IHA (hypophosphatemia often causes spherocytosis).

Use of erythropoietin (Epo)


Erythropoietin is synthesized primarily in the peritubular
cells located in the inner cortex and outer medulla of the kidney although small amounts are synthesized in the liver. Re-

4th European FECAVA SCIVAC Congress

combinant EPO has been produced and is commercially


available. Like the natural hormone, the recombinant product acts preferentially on the late differentiation of CFU-E.
In the clinical trials in dogs it has had remarkable effects.
Not only is the anemia of end-stage renal disease effectively treated but activity seems to ameliorate many of the other
effects of renal disease such as hypertension, hyperkalemia,
and thrombotic tendencies. EPO appears to be a true hormone, acting at a distance from its site of production.

167

and hemogram above. Specific examination of the primary


hemostatic reaction is accomplished with the buccal mucosal bleeding time (BMBT). The BMBT is accomplished
with a bleeding time device and has been described. The
BMBT is sensitive to platelet dysfunctional states primarily
and to vascular dysfunction secondarily. The BMBT is not
performed when thrombocytopenia is pronounced.

Use of granulocyte-colony stimulating


factor (G-CSF)
G-CSF is most well known in veterinary medicine. G-CSF
has a molecular mass of 18 to 22 kilodaltons and is released
from fibroblasts and activated monocytes. The effect of GCSF is more restricted than that of GM-CSF and IL-3. G-CSF
enhances the differentiation and neutrophil function. G-CSF
increases neutrophil killing of tumor targets by a mechanism
of antibody-dependent cellular cytotoxicity (ADCC), and also
enhances phagocytosis. In clinical trials, G-CSF has been
shown to shorten the period of dangerous neutropenia following chemotherapy for neoplasia and the number of days antibiotics must be used to treat some septic processes. G-CSF
produces remarkable increases in neutrophil numbers without
affecting the numbers of monocytes and lymphocytes.

HEMOSTASIS
Examination of primary hemostasis-buccal
mucosal bleeding time
Primary hemostasis consists of vascular constriction,
platelet adhesion and platelet aggregation. It must be distinguished from secondary hemostasis - coagulation (fibrin formation) and tertiary hemostasis (fibrinolysis). Primary hemostasis has been partially examined in the microhematocrit

The PIVKA test (proteins induced by or involved in vitamin K antagonism or absence) is a specific test of vitamin
K deficiency. In fact, the PIVKA test often prolongs as much
as 24 hours before clinical signs may be observed. The PIVKA plasma is deficient in three of the four vitamin K coagulation proteins, factors II, VII, and X. The test is simple and
reproducible. It can be accomplished in-hospital and requires only the deficient plasma and a hot water bath.

Examination of tertiary hemostasis D-Dimers


The reference interval assessed for D-dimer in normal
dogs was 0.01-0.25 mcg/ml (mean = 0.13 mcg/ml). In the 71
cases of DIC the D-dimer concentration ranged from 0.05 to
3.93 mcg/ml (mean = 0.73 mcg/ml). With a cut-off of 0.25
mcg/ml, the calculated. sensitivity for D-dimers in the DIC
group was 82 percent. D-dimer can be detected and utilized
diagnositically in clinical canine medicine. D-dimer concentrations appear to be useful in the assessment of uncompensated canine DIC. Further research is needed to determine
the usefulness of this analyte in cases where DIC is suspected but not supported by current laboratory testing protocols.

References available on request

MAIN PROGRAMME

Examination of secondary hemostasis PIVKA

4th European FECAVA SCIVAC Congress

169

Clinical approach to anemia


Bernard F. Feldman

Case examination
A nine month old West Highland White Terrier was presented for elective castration but, during physical examination, the mucous membranes were noted to be pale. Despite
this the patient was bright, alert, responsive and afebrile. A
biochemical profile was essentially unremarkable but the hemogram had some unusual findings:
WBC/L 14,400 (12,400 neuts; 500 monos; 1000 lymphs;
500 eos)
RBC/L 2,400,000 (MCV 79; MCHC 34; MCH 27)
PCV%
19
Hbg/dL 6.5
T.P.g/dL 6.1
NRBCs 5/100 wbcs
Retics% 10
Icterus Index - normal
ESR (corrected) - negative 12
Polychromasia ++++, Anisocytosis +++++, Poik +,
Target ++, Lepto ++, Spherocytes -, Stomatocytes -,
Bowls -, Knizocytes -, Schisto -.
Abnormal test(s)? _________________________________
Diagnosis? _______________________________________
Why? ___________________________________________

Anemia
I. Hypoproliferative (nonresponsive anemia)
II Hyperproliferative (responsive anemia)
III. Variable response anemia
Anemia is NOT a disease, simply a sign of disease.
The evaluation of the patient with anemia requires the usual
careful history and physical examination, followed by laboratory screening that provides a complete hemogram:
Examination of red blood cells
1. Red blood count
2. Hemoglobin (Hc) concentration
3. Packed cell volume or hematocrit
4. Mean cell volume
5. Mean cell hemoglobin
6. Mean cell Hb concentration
7. Reticulocytes
8. Reticulocyte production index
9. Metarubricytes and other NRBCs

10. Red cell morphology and cytograms


11. Histogram of RBC vol. distribution
12. Total protein
Determining inflammation
13. Fibrinogen
14. Sedimentation rate
Examination of platelets
15. Platelet count
16. Mean platelet volume
17. Platelet morphology
Examination of leucocytes
18. White blood cell count corrected for metarubricytes
19. Differential white blood cell count in absolute values
Immature forms, neutrophils, lymphocytes,
monocytes, eosinophils, basophils, degenerated cells,
unidentifiable cells
20. White blood cell morphology
21. Leucocyte cytogram
Red Cell Indices - While the red cell indices reflect abnormalities in red blood cell production, changes in the indices are slow to occur (remember, they are mean values!)
and often lag behind the pathologic process. Despite the fact
that most clinical anemias are normocytic and normochromic, macrocytic normochromic anemias usually reflect maturation abnormalities (vitamin B12, folate, myeloproliferative disease), microcytic hypochromic anemias
specifically suggest iron deficiency in small animals, and
macrocytic hypochromic anemias are associated with intense red cell regeneration.
Reticulocyte Count - The percentage reticulocyte count
requires, at least, conversion to absolute values. The reticulocyte count in the dog requires several conversions to account for the normal bone marrow response to erythropoietin, and the length of time of bone marrow reticulocyte
maturation which is correlated with the degree of anemia.
These two conversions are often called the reticulocyte production index (RPI).
Hypoproliferative (nonresponsive) anemia - Anemia
as a disease sign is placed into one of several categories.
Anemia of inflammatory disease is modest, often undetectable, and clinically insignificant. Anemia associated
with acute hemorrhage presents little diagnostic challenge
and in the early stages is characterized as nonresponsive.
Anemia associated with chronic hemorrhage is associated,
in general, with parasitism in young animals and ulceration
of bleeding neoplasms in older animals and in the early

MAIN PROGRAMME

DVM, PhD, Dipl ACVIM


Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

170

stages is characterized as nonresponsive. Microcytosis and


hypochromasia, however, are slow to occur. Anemia associated with decreased erythropoietin production suggests the
clinician examine renal function, thyroid function or adrenal function. Production deficits, manifested by anemia and
or bicytopenia or pancytopenia suggests anemia associated
with bone marrow disease.
Hyperproliferative (responsive) anemia - Hemolysis
or Hemorrhage
Hemolytic Anemia is caused by fragmentation, phagocytosis, or intravascular lysis. The most common canine hemolytic anemia is immune-mediated hemolytic anemia
(IHA), which may be defined as a premature breakdown of
red cells and in the case of immune-mediation, premature
breakdown of red cells associated with antibodies. Among
the implicated antibodies are immunoglobulin G (IgG) and
IgM. When associated with the red cell at 37 degrees they
are considered warm reacting. When temperatures are below
35 degrees and antibody is associated with red cell membranes, the reaction is considered cold reacting. Both of the
aforementioned immunoglobulins, and especially IgM, can
fix complement. Complement- and/or phagocyte-mediated
red cell membrane damage result in swelling (spherocytosis)
or lysis (hemoglobinemia). When hemolysis is active the
erythroid marrow becomes responsive in three to five days.
Anemia of hemorrhage also becomes responsive in three to
five days.
Variable response anemia, anemia which is unpredictable in terms of its reticulocyte response is a maturation
abnormality due, most often, to vitamin B12 or folate deficiency. Intrinsic marrow disease, also potentially a maturation abnormality may also present similarly in the early
stages.

Causes of anemia - a summary


1. Iron deficiency - always nonresponsive
2. Inflammation - always nonresponsive
3. Marrow damage - always nonresponsive
4. Decreased erythropoietin - always nonresponsive
5. Hemorrhage - nonresponsive early; responsive later
6. Hemolysis - nonresponsive early; responsive later
7. Maturation abnormality - usually nonresponsive but
unpredictable

4th European FECAVA SCIVAC Congress

Initial approach to the anemic patient


The reticulocyte count is the only index of effective erythropoiesis. Proper usage requires: 1) conversion to an absolute quantity; 2) adjustment for the reduced hematocrit;
and 3) correction for the effect of erythropoietin on marrow
reticulocyte release. THESE ADJUSTMENTS RESULT IN
CALCULATION OF THE ADJUSTED RETICULOCYTE NUMBERS OR THE RETICULOCYTE PRODUCTION INDEX (RPI).
First: figure out the absolute quantity of reticulocytes. If
the canine mean red cell count is seven million, one percent
reticulocytes is seventy thousand reticulocytes - the reference interval would be thirty-five thousand to one hundred
five thousand reticulocytes per microliter.
Second: correct for the reduced hematocrit. Multiply the
absolute reticulocyte count by the patients hematocrit and
divide the result by the mean species hematocrit.
Third: correct for the effect of erythropoietin on reticylocyte release.

Erythropoietin
Erythropoietin (Epo) is inversely correlated with the red
cell count (or hematocrit). The lower the hematocrit the
higher the concentration of erythropoietin (except in renal
failure). The effects of erythropoietin include:
1. commits uncommitted stem cells to the erythroid line;
2. decreases the marrow maturation time for red cell development;
3. increases individual cell hemoglobin synthesis;
4. causes premature release of reticulocytes from bone
marrow.

Adjusting the reticulocyte numbers


the reticulocyte production index (RPI)
The average time for reticulocytes to mature in the dog
or cat is four and one-half days, three days occur in the marrow and one day in peripheral blood if the hematocrit is appropriate:
In the dog:

The laboratory evaluation of anemia is initiated by examination of the red cell indices - MCV, MCHC, and MCH.
If these indices are abnormal, this is essentially free information and gives specific direction. Examples are macrocytic hypochromic anemia which invariably suggests red cell
response and microcytic hypochromic anemia which suggests (at least) iron deficiency. However if the indices are
normal, normocytic and normochromic, examination of the
degree of red cell response - specifically the appropriateness
of the reticulocyte response - must be considered.

In the cat:

Development
in Marrow

in Peripheral
Blood

45
35
25
15

Laboratory evaluation of anemia

Hematocrit

3.5 days
3.0 days
2.5 days
1.5 days

0.5 days
1.5 days
2.0 days
2.5 days

32
24
16
10

3.5 days
3.0 days
2.5 days
1.5 days

1.0 days
1.5 days
2.0 days
2.5 days

To correct for the effect of erythropoietin on reticulocyte


release, after converting reticulocytes to absolute values and
adjusting for the reduced hematocrit, divide the final figure

4th European FECAVA SCIVAC Congress

of 3.5 million/ul, the absolute value is approximately


170,000/ul.
170,000 22% (patients Hct)/ 45% (mean canine Hct)
= 85,000/2.0 = 42,500.
This corrected absolute reticulocyte number is within the
reference interval observed for dogs with appropriate hematocrits. Thus, this patient must be considered nonresponsive

Initial characterization of anemia is it responsive? nonresponsive?


A RPI less than 2.0 = nonresponsive anemia.
A RPI greater than 2.0 = responsive anemia i.e., hemorrhage or hemolysis.

References available on request

MAIN PROGRAMME

by the number of days the average reticulocyte will live as a


reticulocyte based on the patients hematocrit (see charts
above).
For example, to determine red cell production over
basal rate:
If a canine patients hematocrit is 22 percent (mean normal is 45 percent) and the patients reticulocyte percentage
is 5 percent, is this patient responding appropriately to the
reduced hematocrit?
5% 22% (patients Hct)/ 45% (mean canine Hct) =
2.5/2.0 = 1.27 basal rate.
If 1.0 is basal rate, 1.27 over basal rate is nonresponsive!
Only patients with a corrected reticulocyte count over 2.0
are considered responsive, i.e. are responding from either
hemorrhage or hemolysis.
For example, to determine corrected absolute reticulocyte counts:
If the reticulocyte count is 5 percent of a red cell count

171

4th European FECAVA SCIVAC Congress

173

Interpretation of the blood smear.


Morphologic alterations of red and white cells
Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Case 1 (C6) - Two year old, spayed female cat presented with anorexia, depression, and increased temperature.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

8
5
3.45
43.5
33.3
15.5
0
0
Heinz bodies
Doehle bodies
640

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

6.7
230
2.0
500
0
306
294
0
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

Case 2 (C8) - One year old intact male cat presented because of weight loss, anorexia and, hemorrhagic diarrhea.
On entry the PCV was 21%. These are data accumulated the next day.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

7
2.3
3.12
44.5
30.3
15.5
0
0
Heinz bodies
Doehle bodies
0

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

3.2
320
2.0
3100
0
2330
670
100
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

Case 3 (282) - Two year old Corgi-Cocker Spaniel spayed female was presented because of episodes of bleeding
for the past two weeks. There was gingival bleeding and some petecchiae on mucous membranes and on the abdomen.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul 38
Plat morph

23
8.0
3.2
117
25.7
36
4
4+ aniso, polychr
toxic granulation
(200-400)
megathrombocytes

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected)/ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Metamyelocytes
Myelocytes

6.7
250
2.0
43500
9000
21400
4100
2200
800
0
3500
2500

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

MAIN PROGRAMME

During this session we will examine a series of cases and discuss the morphologic alterations seen in blood and bone marrow preparations associated with those cases.

174

4th European FECAVA SCIVAC Congress

Case 4 (D13) - Six year old spayed femal Basenji dog presented because of chronic diarrhea.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul
Plat morph

32
10.5
5.4
64
32
21
1.0
4
slight anisocytosis
immature
988
variably sized

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Metamyelocytes
Myelocytes

6.1
450
3.0
28100
4100
19000
1100
1000
900
0
1500
500

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

Case 5 (289) - Neutered male Collie, 4.5 years of age presented because of nervousness, whining, crying, and pacing
(will not sleep).
PCV %
37
Hb g/dl
10.7
RBC x 106/ul
6.3
MCV fl
58.7
MCHC g/dl
28.9
MCH pg
16. 9
Retics %
4.8
Nrbcs/100wbc
28
RBC morph-slight aniso; polychr
WBC morph
normal
Plat x 103/ul
218
Plat morph
normal

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable
Damaged

6.2
200
3.5
9900
0
7500
1200
800
400
0
0
0

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

Case 6 (298) - Six year old neutered male toy Poodle presented because of persistent diarrhea.
PCV %
47
Hb g/dl
17
RBC x 106/ul
5.12
MCV fl
91.7
MCHC g/dl
36.1
MCH pg
33.2
Retics %
0
Nrbcs/100wbc
0?
RBC morph-retained nuclei?
WBC morph
hypersegmented
Plat x 103/ul
332

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

7.1
300
2.0
15100
151
8909
4454
755
831
0
0

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 7 (297) - Two year old neutered male mixed breed cat presented with an acute history of anorexia and depression.
Temperature was subnormal, pulse 200/minute and respirations 32/minute. Mucous membranes were pale.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

11
2.6
1.8
95.6
28.2
31
12
15
Heinz bodies
Doehle bodies
313

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

6.3
400
8.0
9400
0
8300
700
400
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

4th European FECAVA SCIVAC Congress

175

Case 8 (C15) - Six and one-half year old neutered male cat presented with a two week history of anorexia, two day history
of vomiting and diarrhea. Temperature was elevated, there was marked splenic enlargement on palpation and on radiography.
The patient was dehydrated approximately 5%.
(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells
Unclassifiable cells

7.8
450
10.0
33700
?
4000
700
?
0
0
0
29000

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 9 (C11) - Male intact mixed breed cat presented because of anorexia and depression.
Mucous membranes were pale and icteric. On palpation the cat had hepatomegaly and splenomegaly. Temperature was subnormal.
PCV %
10
Hb g/dl
3.2
RBC x 106/ul
2.1
MCV fl
65
MCHC g/dl
31
MCH pg
29
Retics %
few
Nrbcs/100wbc
12
RBC morph some bowl forms
WBC morph
Doehle bodies
Plat x103/ul low
Platelet morphology not done

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)
Unclassifiable cells

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

8.2
500
17.0
7900
?
1700
2500
?
0
0
0
3700

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 10 (C14) - Mixed breed neutered male cat presented because of lethargy and poor appetite.
Mucous membranes were pale. Temperature was subnormal.
PCV %
11
Hb g/dl
3.5
RBC x 106/ul
1.7
MCV fl
54
MCHC g/dl
34
MCH pg
26
Retics %
few
Nrbcs/100wbc
0
RBC morph aniso; megalo
WBC morph bizarre nuclei
Plat x103/ul low
Platelet morphology not done

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells
Unclassifiable cells

86.8
250
4.0
12000
200
9800
1500
300
200
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 11 (7 - 139339) - Two year old, mixed breed, spayed female dog presented because of persistent fever
and pale mucous membranes. On palpation and radiography abdominal fluid was found.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph normal
WBC morph
Plat x 103/ul

15
4.5
2.19
68.5
30
20.5
2.0
9

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

toxicity
44

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

8.6
400
2.0
3700
1739
370
370
74
0
0
1147

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

MAIN PROGRAMME

PCV %
12
Hb g/dl
4.0
RBC x 106/ul
2.1
MCV fl
64
MCHC g/dl
32
MCH pg
29
Retics %
0
Nrbcs/100wbc
14
RBC morph
normal
WBC morph
Doehle bodies
Plat x103/ul clumped
(300-800)
Platelet morphology not done

176

4th European FECAVA SCIVAC Congress

Case 12 (139930) An Irish Setter spayed female, seven years of age was presented because of a swollen right salivary gland
(or perhaps, submandibular lymph node).
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph normal
WBC morph
Plat x 103/ul

24
8.2
3.26
73.6
34.2
25.3
0.8
2.3

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

toxicity
213

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Meta- and myelocyte

7.0
700
2.0
20500
3588
8610
1435
3793
102
0
2358: 615

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 13 (140469) This patient, a Doberman Pinscher intact female, six years of age was referred because
of inappropriate reticulocyte numbers and leucocytosis.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul

35
4.6
2.03
74.9
32
23.9
4.8
3.5
normal
many immature
138

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

7.1
500
29900
2541
14203
3140
9419
149
0
0

(6.0-8.0)
(200-400)
3 (2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 14 (140682) Pomeranian, 12 year old intact female was presented for pyometritis. She was anorectic, depressed and weak.
Temperature was normal. Pulse was 180 per minute. The following data were obtained as a part of the presurgical screen.
PCV %
23
Hb g/dl
7.1
RBC x 106/ul
3.61
MCV fl
63.7
MCHC g/dl
30.9
MCH pg
19.7
Retics %
3.8
Nrbcs/100wbc
2
RBC morph poly; microcytes
WBC morph
many immature
Plat x 103/ul
456

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)
Progranulocytes
(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Blasts
Myelocytes; metas

7.3
500
2
123900
25400
73720
2478
6195
rare
rare
620; 15487

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(0)
(0)
(0)

4th European FECAVA SCIVAC Congress

177

Mycobacterial skin diseases


Luis Ferrer

Introduction
In general, mycobacteria are uncommon causes of skin
diseases. Three groups of mycobacterial skin diseases have
been recognized: cutaneous atypical mycobacteriosis, cutaneous tuberculosis and feline leprosy. In this lecture we will
focus predominantly in atypical cutaneous mycobacteriosis,
which is most prevalent in Europe.

Atypical mycobacteriosis
Etiology: most cases are due to rapidly growing mycobacteria included in Runyon group IV. These mycobacteria are nonchromogenic, rapidly growing, gram positive,
acid fast, aerobic, non-spore forming bacilli. Mycobacterium
fortuitum, M. phlei, M smegmatis and M. chelonei are the
most common species. They are ubiquitous in nature, specially in water, wet soil and intestines of ruminants, pigs and
other animals. They are non-pathogenic for animals under
normal circunstances. Infection is usually consequence of
trauma or fight wounds.1
Dogs and cats are quite resistent to infection by slow
growing atypical mycobacteria (Mycobacterium avium-intracellulare, M. genavense). They are classified as Runyon
group III and are acid fast, slender rods; non-chromogens.
Most reported cases have described disseminated disease
without cutaneous involvement, but cutaneous lesions have
been described in a few cases.2
Clinical signs: most patients present with a history of
trauma and non-healing lesions that have not responded to
antimicrobial therapy.
In atypical mycobacteriosis associated with rapidly
growing mycobacteria lesions consist in fistulous tracts and
purpuric macules and nodules that ulcerate. Ventral abdomen, inguinal region and legs are the most commonly affected body parts. Usually dogs and cats are systemically
unaffected and disseminated disease is rare.
In atypical mycobacteriosis due to slow growing mycobacteria (M. genavense, M avium-intracellulare) disseminated disease is rather uncommon. Cutaneous disease, when
exist, may present as nodules or diffuse subcutaneous
swellings. Anorexia, weight loss, lymphadenopathy,
splenomegaly and anemia have been reported in dogs and
cats with the disseminated form of the disease.3,4,5
Diagnosis: a complete physical examination and bichem-

ical evaluation (complete blood count, chemistry panel and


urinalysis) in patients suspected of mycobacterial infections
is recommended. If disseminated disease is suspected apropriate imaging techniques (RX, ultrasound) are recommended. In cat, FeLV and FIV infection should be investigated.
In most cases the definitive diagnosis is based on biopsy
plus culture or PCR. Histopathologic findings consist of
vatying degrees of granuloma formation, pyogranulomatous
dermatitis, cellulitis and panniculitis. Acid-fast bacteria are
observed in approximately 50% of cases. M. avium-intracellulare and M. genavense usually are present in larger numbers and are more commonly identified on cytology and
histopathology compared to the rapidly growing group IV
mycobacteria.
Polymerase Chain Reaction (PCR) is a very sensitive
and specific diagnostic tool. Most human hospitals run rapid
kits to detect mycobacteria in samples. There are also commercial kits to detect M. avium-intracellulare. The identification of other species can only be made in well equiped, experienced laboratories. The identification of the mycobacteria can also be made from paraffin embedded tissue samples
(after DNA extraction) allowing retrospective studies.
Treatment: prolonged courses of antibiotics and surgical
removal of infected tissue are the most effective treatments.
Antibiotic selection should be based, if possible, on culture
and senstivity results. Good choices while culture and sensitivity results are pending or lack include enrofloxacine and
clarithromycin.
Based on published reports fluoroquinolones, aminoglycosides, tetracyclines and clofazimine appear to be most effective.
Prognosis: guarded in all patients. Antibiotic resistance
in mycobacteria is becoming an increasing problem.

Cutaneous tuberculosis
Tuberculosis in dogs and cats has a worldwide distribution. The incidence of the disease, however, has decreased
with the decline of the disease in human beings and cattle.
Etiology: M. bovis or M. tuberculosis. In the case of M.
bovis dogs and cat contract the disease consuming infected
meat or milk. In the case of M. tuberculosis the disease is
contracted via airborne transmission from an infected human. Probably, the incidence is higher in cats than in dogs.
Clinical signs: respiratory and digestive systems are pri-

MAIN PROGRAMME

DVM, Dipl ECVD


Universitat Autonoma de Barcelona - Spain

178

marily affected. Cutaneous involvement is unusual but occasionly happens. Patients show draining tracts, noedules,
plaques, abscesses or ulcers. Patients usually are systemically ill with fever, weight loss and anorexia.
Diagnosis: history, clinical exam, biopsy, culture and
PCR. Biopsy specimens show nodular to diffuse pyogranulomatous dermatitis, with few acid-fast organisms. M. bovis
and M. tuberculosis are slow-growers and growth may take
up to 8 weeks. Intradermal skin testing with 0.1 ml of bacille
Calmette-Gurin or PPD is best performed on the inner surface of the pinna. At 48-72 hours, persistent erythema with
necrosis, crusts or ulceration is considered a positive test.
However, the test is not 100% sensitive and specific. Nowadays, PCR using exudates or biopsy tissue -fresh, frozen or
even paraffin-embedded-is the best diagnostic tool.
Treatment: because of the seriousness of the disease and
the public health hazard most patients with tuberculosis are
euthanized and treatment is usually not recommended.

4th European FECAVA SCIVAC Congress

winter months and the majority of case reported have been


in young cats between 1 and 3 year of age. Lesions are typically single or multiple firm to soft nodules in the skin and
subcutis. Lesions are most frequently found on the limbs,
head and trunk. Regional lymphadenopathy is common,
however, disseminated disease is rare.
Diagnosis: is made on the basis of clinical findings in
conjunction with the presence of large numbers of acid-fast
bacilli on cytology or histology and the absence of growth in
routine cultures for Mycobacterium.
Treatment: excisional surgery, if possible, is the treatment of choice. Systemic therapy with clofazimine (2-8
mg/kg/day) or dapsone (1 mg/kg/day) are the alternatives.
Spontaneous remission in one case of feline leprosy has
been described.6

References
1.

Feline leprosy
The disease is very rare in Euope (a few cases described
in United Kingdom). The prevalence is higher in Canada,
USA (NW states), New Zealand and Australia.
Etiology: unknown. Some authors believe that Mycobacterium lepraemurium, the causative agent for rt leprosy, is
responsible for the disease in cats. tranmission is thought to
occur thriugh the bite of infected rats.
Clinical signs: most cases appear to present during the

2.
3.

4.
5.
6.

White SD, Ihrke PJ, Stannard AA, et al., (1983), Cutaneous atypical
mycobacteriosis in cats, J Am Vet Med Assoc, 182: 1218-1222.
Lemarie SL, (1997), Mycobacterial diseases, Proceedings of the Annual Members Meeting AAVD & ACVD, Nashville, Tennessee.
Jordan HL, Cohn LA, Armstrong PJ, (1994), Disseminated Mycobacterium avium complex infection in three Siamese cats, J Am Vet
Med Assoc, 204: 90-93.
Walsh KM, Losco PE, (1984), Canine mycobacteriosis: a case report.
J Am Anim Hosp Assoc, 20: 295-299.
Shackelford C, Reed W, (1989), Disseminated Mycobacterium avium
infection in a dog, J Vet Diag Invest, 2: 273-275.
Roccabianca P, Caniatti M, Scanziani E, et al., (1996), Feline leprosy:
spontaneous remission in a cat. J Am Anim Hosp Assoc, 32: 189-193.

4th European FECAVA SCIVAC Congress

179

Cutaneous drug reactions


Luis Ferrer

MAIN PROGRAMME

DVM, Dipl ECVD


Universitat Autonoma de Barcelona - Spain

Paper not received

4th European FECAVA SCIVAC Congress

181

From proper preparation to interpretation


of the cytology smear
Corinne Fournel-Fleury
DVM, PhD
Laboratoire dImmunopathologie-Hmatologie-Cytologie, Ecole Vtrinaire de Lyon - France

2) Production of smears

The sampling method makes a preliminary distinction


between samples taken from solid masses and fluid samples.
The necessary equipment consists of slides with frosted ends,
a good microscope and a centrifuge.
For the cytology of fluids, the preferred equipment is a
cytocentrifuge. The principles common to all cytological
preparations are intended to favor the quality of the cellular
analysis rather than the quantity of material examined, and
to obtain a result that is as representative as possible of the
tissue sampled.
In the cytology of solid masses, fine-needle aspiration
takes precedence over scraping and imprint smears. In the
cytology of fluids, the centrifugate is spread according to the
blood smear technique, in the absence of cytocentrifuge.
Rapid air drying is most often used for stains of the Romanowsky type.
Other cytochemical and cytoenzymological stains, as
well as immunostainings, can also be carried out by cytological methods.
The quality and representativity of the samples are
looked at successively. A hierarchical analysis is then carried out on smears, always bearing in mind, first and foremost, the general cellular context, prior to the analysis at
the cellular level.
The search for neoplastic cells, as compared to reactive
cells, is based on criteria of cellularity and homogeneity or
heterogeneity. One must then be sure to determine the histological type of the neoplastic population: epithelial, mesenchymal, hematopoietic or melanocytic.
Finally, the analysis of the cytological criteria of malignancy is carried out first at the level of the cell population,
then at the cellular level.

Principles

I) METHODOLOGY
1) Equipment
Sampling: variable methodology, depending on the tissue aspirated
Smears: slides with frosted ends
Centrifuges / cytocentrifuges
Microscopes / objective lenses

There are some principles which are common to all


preparations intended for cytological examination. These are:
- to give preference to the quality of the cells collected,
rather than to their quantity; and
- to obtain, in a limited sample, material which is as representative as possible of the tissue collected.

Conditions
For the quality of the cellular analysis, it is indispensable
to obtain smears in single-cell layers, since clusters are undecipherable.
For the representativity of the material analysed, it is indispensable to carry out dispersed collections in the mass of
tissue to be analysed, and to avoid excessive dilution.

Means
For solid masses, it is necessary:
- to favor aspirations with a fine needle (22 to 24 G) in different directions and at different depths; this gives a limited, but representative, sample of material without causing
undesirable bleeding, and also makes it possible to produce
thin smears, correctly spread;
- as far as possible, in neoplastic cytology, to avoid scrapings, which select superficial inflammatory or hyperplastic
tissue, missing the underlying neoplastic process;
- not to omit to take imprint smears, in parallel with the histological examination of a nodule, using fresh sections;
this is a valuable complement to histological methods;
- to limit contamination of fluid or semi-fluid collections by
blood, and to end the collection as soon as any appears;
- to carry out the centrifugation before spreading a voluminous fluid sample;
- as far as possible, to spread the smears to their limits, so
as not to lose the largest cells or cell clusters that are drawn
to the borders by the spreading process; this means producing smears with a small quantity of the material collected, which in turn necessitates, in most cases, a prior
distribution of this material among several slides.

MAIN PROGRAMME

Summary

182

4th European FECAVA SCIVAC Congress

Techniques

Rapid staining of the Diff-Quik type

Spreading of fine-needle aspirates


Techniques for drawing out material between two perpendicular slides.
Techniques for drawing out material between two parallel slides.
Imprint smears using sections
These are produced after excision biopsy of a solid mass.
They involve making a clean, fresh section of the mass, wiping it by gentle application of a swab, then applying it firmly to the object slides in several successive imprints. Imprint
smears have the advantage of supplying an approximation of
the tissue architecture, and of producing no deformation of
cells. However, they often suffer from excessive density, and
an excess of exudate in the section.
Spreading of fluid collections
- A prior centrifugation should always be carried out if the
quantity of fluid collected is sufficient.
- In the case of classical centrifugations, the concentrate
is pipetted and spread according to the blood-smear
technique.
- In the case of a cytospin obtained with a cytocentrifuge, the
smear will be useless except if the disk is very hemorrhagic, in which case it should be spread by drawing out according to the given procedure.

This stain is to be avoided absolutely in cytology, since


it induces an artefactual densification of chromatin, and a
red-purple stain in cytoplasm, which preclude any fine cytological analysis.
In medullary hematological cytology particularly, it can
be a source of confusion between erythroid lineages and abnormal lymphoids.
Its only use is that it gives the clinician the possibility of
carrying out a rapid check on the richness and quality of one
of the smears on a control slide before dispatching the others, non-stained, to the cytology laboratory.

Reaction to Periodic Acid Schiff (PAS)


This method is used to reveal the constituents of the tissue types characterized by the neighbouring glycol and hydroxyamine groupings. Glycogen, mucin, hyaluronic acid,
fibrin, hyaline and other elements give a positive reaction
which can go from pink to crimson.
In cancer cytology it is essentially of interest in the cytology of effusions, and contributes to the differential diagnosis between histiocytes, mesothelial cells and mucoid-secreting carcinomatous cells.
Intracellular mucopolysaccharides give a more or less intense red stain, which may be diffuse, granulous or clumped.

3) Staining / cytochemistry /
cytoenzymology / immunostaining
Black Sudan B stain
May-Grnwald-Giemsa stain (MGG)
This is the basic stain for hematological cytology. By
comparison with its alternative in cytology, namely the Papanicolaou stain, its advantages are:
- considerably more rapid utilization, and a facility of preparation and conservation of reagents;
- an increase in the size of the cell and the nucleus;
- a much better analysis of the coloring characteristics and
the content of the cytoplasm, which is indispensable in
hematology.
It is inferior to the Papanicolaou stain as regards the evaluation of irregularities in the chromatin and the nucleoli, and
especially in terms of cell transparency, which makes it possible, if necessary, to evaluate the three-dimensional organization of cell clusters, by varying the micrometric screw.
This is particularly useful in the cytology of effusions, as a
way of differentiating certain three-dimensional carcinomatous clusters of the mesothelial layers.
The important thing is to be familiar with ones own particular reference stain.
NB: for thick smears, which are frequently understained, it would seem preferable:
- to carry out a primary stain, as above;
- after a primary examination, to stain the slide a second
time according to the same procedure, rather than to
choose arbitrarily, according to the appearance of the dry
smear, a higher concentration of the Giemsa stain.

This stain allows the revelation of lipids stained black by


Sudan B.

Fontana stain
This stain is used for revealing argentaffin substances,
and in particular melanin granules, stained black for the
identification of cells from weakly-differentiated
melanomas.

Perls stain
This stain is used, essentially in hematology, for the revelation of iron in macrophages and erythroblasts, and in particular for the revelation of sideroblasts in certain preleukemic myelodysplastic syndromes and hemosiderophages.

Enzymatic reactions for the differentiation


of blood and medullary cells
These stains are used for identifying weakly-differentiated acute leukemias. Only two of them are in routine use by
our laboratory.

4th European FECAVA SCIVAC Congress

Immunostainings
Principle
- Immunostainings reveal, through the utilization of specific
antibodies (Ab), the presence of an antigen (Ag) at the surface of, or inside, a cell, this Ag being characteristic of one
or more cell types.
Utilization
- In cancer cytology, immunostaining is mainly used to assist in the identification of:
- solid anaplastic cancers;
- undifferentiated acute leukemias;
- certain carcinomas, as opposed to mesotheliomas or
abnormal mesothelial hyperplasias, in the cytology of
effusions.
Numerous specific Ags can thus be revealed, provided
that one possesses the appropriate Abs for the species under
consideration. The range of Abs available is large in human
medicine, but it remains limited in veterinary medicine. The
procedure necessitates the obtention of polyclonal or monoclonal Abs which are specific to the species, or Abs which
are specific to another species (the human species in particular), but which present a cross-reactivity with the animal
species being studied.
The principal Abs are:
- anti-cytokeratin Ab, for the identification of carcinomas;
- anti-vimentin and anti-desmin Ab, for the identification
of sarcomas;
- anti-factor VIII Ab, for the identification of endothelial
cells and of the platelet lineage in hematology;
- anti-glycoprotein IIIa Ab, which is specific to the
platelet lineage;
- anti-lysozyme Ab, as a histocytic marker.
Finally, certain Abs are particularly used for the typing of lymphoid cells and the characterization of malignant lymphomas:
- the polyclonal pan-T anti-CD3 Ab;
- the anti-CD5, CD4 and CD8 monoclonal ABs;
- the anti-CD79a pan-B Ab (mb1);
- Abs which recognize the different immunoglobulins
(Ig), surface (sIg) or intracytoplasmic (cIg), and, respectively, the heavy chains ( or ) of the IgG and
IgM, and the light chains ( and );
- an Ab (MIB-1) which recognizes a nuclear proliferation Ag (AgKi67), signifying the entry of the cell into
the cycle of cellular division, and thus the blastic character of a cell.

Procedure
Most of the Ags detected are fragile, and cannot be subjected to fixation, or to prolonged storage.
It is thus necessary either:
- to carry out stains within one or two days on fresh smears
stored at laboratory temperature;
or
- to freeze the smears and the cytospin disks at -70C, with
a view to future immunostainings.

II) PRINCIPLES OF EXAMINATION


AND INTERPRETATION
1) Quantitative and qualitative analysis/
Principal artefacts
1) Evaluation of the richness of a sample
2) Evaluation of the quality of a smear
- excessive thickness
- excessive crushing
- excessive drawing out
3) Evaluation of the quality of the fixation and the stain
- insufficient staining (previous fixation with formalinbased fixatives)
- insufficient drying
- excessive basophilia (Romanowsky-type stains)
- defective staining of the nuclear chromatin, and of certain granules (notably in mast cells), by rapid staining
(e.g. the Diff-Quik type)
- deposits of stain
- absence of stain: exclusive presence of free fat
4) Evaluation of cell degeneration
- increased nuclear volume
- light staining of the nucleus
- thickening of the nuclear membrane
- increased nucleolar size
- abnormal mitosis (multinucleation)
- vacuolar cytoplasm
- effacement of cytoplasmic outline
5) Artefacts caused by superposition
6) Evaluation of the representativity of samples

2) Principles of analytic examination


1) Analysis at the level of cell populations
- overall cellularity
- resident and reactive populations / smear background
- inflammatory population
- neoplastic population
- mitoses
2) Analysis at the cell level
- cell size
- cell shape
- nucleus
number of nuclei
size
N/C ratio
shape

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Peroxidase reaction
This reaction is intensely positive in the granular lineage,
in the form of brown-black granulations, weakly positive in
the monocytic lineage, and negative in the lymphoid lineage.
It also has the great merit, for parallel morphological analysis, that it can be combined with an MGG counter-staining.
Non-specific esterase and specific monocytic reactions
Non-specific esterase (without fluoride treatment)
shows up as blue precipitates in monocytic and myeloid cell
lineages.
In the presence of fluoride, only myeloid esterase remains, monocytic esterase being inhibited.

183

184

position
chromatin
nucleoli:
.quantity: total nucleolar volume
.shape
.position in the nucleus
- cytoplasm
volume
shape
outline
stains
content
.granules
.vacuoles: secretion
phagocytosis
degeneration
3) Determination of the cell type of a neoplastic population
- epithelial
- mesenchymal
- round-cell
- melanocytic
4) Cytological criteria of malignancy
The determination of malignancy most frequently results
from the combination of a set of morphological criteria,
firstly general, for the suspect population examined, then detailed, at the cell level.
These criteria are applicable whatever the sample examined, and thus for cancer cytology as a whole. There is just
one factor that varies, according to the type of sample (various fluids or solid masses) and the tissue of origin
(hematopoietic organs, liver, serous membranes, nervous
system, etc.), and that is the difficulty of making a differential diagnosis for benign, resident or reactive populations
and, consequently, the number of criteria required for establishing a cytological diagnosis of malignancy.
Criteria of malignancy at the level of the cell population
The general appearance of a malignant population is
characterised by:
*abnormal monomorphism, by contrast with the polymorphism of the smear background, associated with aniso-

4th European FECAVA SCIVAC Congress

cytosis and, especially, anisocaryosis giving the impression


of a single lineage, but anarchical in its evolution;
*a tendency to the formation of voluminous cell layers
and three-dimensional clusters;
*numerous and, especially, abnormal mitoses (which is
the distinguishing feature of mitoses that occur within benign populations).
Criteria of malignancy at the cellular level
1) Nuclear anomalies
The most interesting nuclear criteria are:
- a high N/C ratio;
- a large amount of variability of shape;
- a configuration which is often abnormal;
- irregular chromatin, and occasionally a hyperchromatic nucleus;
- finally, the presence of voluminous nucleoli, of variable dimensions, and sometimes veritable nuclei within the nuclei.
2) Cell size
One often finds an overall increase in size, going all the
way to cellular gigantism. Malignant cells are sometimes
multinuclear but, unlike benign cells, are characterized by
the nuclear abnormalities already mentioned.
3) Cytoplasmic criteria
Cytoplasmic modifications, finally, are less specific, but
are frequently observed:
- excessive basophilia (aggressive basophilia);
- vacuolization, going all the way to signet-ring cells;
- the presence of abnormal granules or, conversely, the
disappearance of specific granules (dedifferentiation).
None of these criteria, taken in isolation, is either necessary or sufficient. Only an in-depth, thorough examination
of the smear as a whole, bringing together all the observations carried out, can be considered as conclusive.
Indirect criteria
Interpretation
- Metastatic cells: the importance of the identification of
cells from the original tumor
- Variability, according to the tissue sampled
- Variability, according to the smear background.

4th European FECAVA SCIVAC Congress

185

Corticosteroid therapy: an update


Tommaso Furlanello
Med Vet
Private Practitioner, Padova - Italy

Which diseases should be treated?

Corticosteroids are among the most frequently prescribed medications, but they often pose a profound
quandary for practitioners. These agents have many beneficial and sometimes live saving short-term therapeutic effects. However, they also have a veritable panoply of potential side effects that can involve virtually all organs. Thus,
the decision to prescribe corticosteroids is an important one
in small animal patient care and deserves due respect. The
aim of this short review is to present a balanced view of
steroid therapy in veterinary medicine, taking into account
efficacy and common side effects.

Apart from Addisons disease, steroid therapy is always


symptomatic and does not act on the causative agent. In the
near future, as scientific knowledge on pathophysiology of
many diseases of dogs and cats improve, space available for
symptomatic therapy should hopefully become more and
more restricted.
The main indication for steroid therapy are the following:
1) Addisons disease: in acute cases, IV administrations
are preferred. The drugs suggested are prednisolone sodium
succinate (5-10 mg/kg) or hydrocortisone hemisuccinate (5
mg/kg). The latter has considerable mineralcorticoid activity. After the addisonian crisis, mineralcorticosteroids should
be supplemented with parenteral desoxycorticosterone or
fludrocortisone acetate. Many dogs treated with mineralcorticoids need very small physiological doses of prednisone
(0.1-0.3 mg/kg/day) or could be even glucorticoid-free.
2) Inflammatory diseases: steroids are considered to be
the most potent anti-inflammatory drug. Some of the mechanisms are still poorly understood, but they are prominent as
inhibitions of phospholipase A2 and of cyclo-oxygenase
(COX-2), two critical steps in the pathogenesis of inflammation. Although clinicians are daily tempted to use corticosteroid in the treatment of inflammatory disorders (cutaneous, respiratory, enteric), often only short term responses
are obtained if the cause is not controlled or removed. For a
durable remission of the disease, longer therapy is sometimes required, with high incidence of adverse reactions.
The anti-inflammatory dosage for prednisone/prednisolone
is 1 mg/kg/day in dogs. Feline patients are presumed to be
corticosteroids resistant and it is stated to double the canine dosage. Their anti-inflammatory dose could be about 2
mg/kg/day.
3) Immune-mediated disorders: glucocorticoids are very
effective and used immuno-suppressive drugs, both in human and veterinary medicine. They act primarily on cellulardependent immunity. Humoral response is not primarily affected, but many of the pathological effects of an aberrant
immune activity could however be controlled. Some of the
most common disorders, in which steroids are used as a first
line of therapy, are immune-mediated anemia and thrombocytopenia, immune mediated joint disease, immune-mediated skin diseases and others. Although very few objective data are available, suggested immune-suppressive prednisone/prednisolone doses are 2-6 mg/kg/day in the dog and

Introduction
Although corticosteroids are widely used by clinicians,
scarce scientific information is available about therapeutic
protocols in dogs and cats. Also in textbooks, many indications are based solely on anedoctical and sometimes dated
information. The aim of this paper is to offer a short update
about the clinical pharmacology of corticosteroids and their
practical use.

Which preparation?
Although many GCS have been developed, the pharmacological activity of this class of drugs remains quite the
same. One can obtain the same immunosuppression in a case
of immune mediated anemia with 2 mg/kg of
prednisone/prednisolone and with 0.3 mg/kg of dexamethasone. If a more potent immunosuppression is required, is
enough to increase the b/w dose of prednisolone. It is a myth
to consider dexamethasone or other steroids as extra
strong; the real difference is only in a much longer activity
(days) and this in most situations is an unfavorable side effect. Both in human and veterinary medicine it is suggested
to use only prednisone or prednisolone, by mouth or in aqueous solutions. If PU-PD is a concern, metil-prednisolone PO
is an excellent substitute. If neuroprotection is required, the
steroids of choice are metilprednisolone sodium-succinate
or prednisolone sodium-succinate (see below). Long acting
steroids should be used only in very special cases.

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Summary

186

even more in the cat. Although suggested by some clinicians, the IV dexamethasone therapy is not supported by any
scientific evidence, but it is certainly linked to a much higher incidence of gastrointestinal adverse reaction. Practitioners prescribing high immuno-suppressive dose of steroids
are often faced with serious adverse reaction. Many other
immuno-suppressive drugs (e.g. cyclophosphamide, azathioprine, chlorambucil and others) are available and could
be used adjunct to steroids, with the aim of reducing steroid
dosages and/or to increase their therapeutic efficacy.
4) Antineoplastic therapy: steroids may be very effective
drugs in the treatment of canine and feline lymphoma, but
only for a short time. This use, if not scheduled together with
rational chemotherapy, should be hardly discouraged, because it induces strong chemo-resistance in the survivor neoplastic cells. Corticosteroids are effective against mastocytomas, in which a systemic action is required. Again,
steroids can be successfully utilized in the treatment of some
paraneoplastic disorders (primarly hypercalcemia and immune-mediated haematologic disorders). As in human medicine, its use should be also considered in selected situations
in which a palliative care of the patient is required, as temporary control of pain associated with cancer development,
emesis, cachexia, and others.
Spinal trauma: selected steroids are suggested both in
human and veterinary medicine in the treatment of acute
spinal trauma. Their use in neurotrauma has been based on
their theoretical abilities to inhibiy lipid peroxidation, stabilize lysosomal membranes, and modify edema production. This neuroprotective activity is based on the anti-oxidative fraction of the metil-prednisolone sodium succinate
(MPSS) molecule. This steroid must be used at a very high
dose, in a timely manner, and should not be substituted by
any other less expensive glucocorticoids, although a very
recent report suggests the alternative use of prednisone
sodium succinate (PSS). Although longer therapy is still
suggested in veterinary literature, it is wise to follow the
following popular protocol, extrapolated from human medicine. If spinal trauma has occurred in the previous 8 hours,
administer MPPS in an IV bolus of 30 mg/kg. In the following 23 hours the therapy could be maintained with a
constant-rate infusion at 5.4 mg/kg/hour, or with two other
boluses of 15 mg/kg after 2 and 6 hours from the first bolus
and again a constant-rate infusion at 2.5-5.4 mg/kg/hour for
18-42 additional hours. A newer protocol utilizes PSS at the
initial IV dose of 30 mg/kg, followed by the same amount
q6h, for a total of 36h. According to his neuroprotective activity, a single IV dose of MPSS is also by some suggested
before every myelography or spinal surgery. Apart from
laboratory trauma-models, wide clinical studies are lacking
in veterinary patients with regards to the true efficacy of
MPSS treatment. Considering human experience, any
steroid administered after 8h (and surely after 24h) from the
initial trauma, it is probably of little value. Steroids are no
longer recommended in acute head injuries, because of their
lack of activity against cerebral hypertension and the constant induction of hyperglycemia, very detrimental for traumatized neuronal tissues.

4th European FECAVA SCIVAC Congress

Steroids in critical care patients:


facts and myths
One of the most popular use of steroids rely on the treatment of the shock patient. In human medicine a completely
different vision has been elaborated in recent years and no
space for steroids is reserved in critical care patients, apart
from the acute Addisonians crisis. As an example, we would
report the statement reported in Goodman & Gilmans The
Pharmacological Basis of Ther., 9th ed. (1996), one of the
most authoritative textbook in clinical pharmacology (page
1457): while corticosteroids are often administered to patients in shock, there is no convincing evidence to indicate that
such therapy is efficacious. In the past steroids were suggested also in the treatment of septic shock, a common and
very severe disorder both in human and veterinary medicine.
In this regard, we would remember the statements of the Infectious Diseases of America (1992), which deny any role of
steroids in the treatment of sepsis and correlated syndromes.
Unfortunately shock it is a very complex disorder and
the beneficial activity of steroids could be of some help only if administered very early in the pathogenic process. This
goal is achievable only in experimental studies, the initiating
phenomena (trauma, hemorrhage, sepsis...) is provoked and
timed. No clinical studies are available on the use of steroids
in canine and feline spontaneous disorders in critical care
medicine. Unless newer and convincing data will be presented, the widespread use of any steroids in shock patients
should be discouraged, and dated guidelines and medical
propaganda ignored.

Adverse reactions of glucocorticoid


therapy
The toxicity of adrenocortical steroids is well know. In
this review we will only list the most important points to remember during any steroid therapy. The incidence and the
severity of most of these is proportional to the magnitude of
the dose and the length of the therapy and not lastly to the
molecule. As an example, dexamethasone is certainly much
more ulcerogenetic than other oral steroids such as prednisone/prednisolone and metilprednisolone.
1) Interference with diagnostic tests: although not a true
adverse effect, this often neglected point must be considered by any clinician. After a few days of steroid therapy, a
wide array of haemato-biochemical alterations will (??) become evident (leukocytosis, increase of the activity of liver
enzymes, hyperglycemia, reduction of the urinary special
gravity and many many others). Many diagnostic tests will
be difficult or impossible to be correctly performed (evaluation of the activity of adrenal or thyroid gland, ANA test,
Coombs test, intradermal skin test and others).
2) Iatrogenic Cushings Syndrome: medium or long term
steroid therapy could induce in some dogs classic biochemical and physically signs of the syndrome. The diagnosis could be gained with an ACTH stimulation test. This
form is potentially reversible and should not be treated.
3) Iatrogenic Addisons Disease: any dogs or cats receiving steroids enter in a sort of surrenal pause. In human pa-

4th European FECAVA SCIVAC Congress

increased activity of ALP rely on the normal hepatic


isoenzyme. After about 3-4 weeks, a new isoenzyme, called
steroid-induced AP (SIAP) is dosable. Some dogs are also
prone to hepatomegaly, caused by glicogen storage in hepatocytes. This potentially reversible hepatopathy can sometimes evolve into a severe disorder. The severity of SH is related to the length and dosage of drug administered, to the
kind of steroids utilized and maybe to an individual predisposition. The cat is much more resistant than dog to steroids
hepatic toxicity.

Conclusion
Corticosteroids are an incredibly useful class of drugs if
used in appropriately cases and with rational protocols. In
many situations steroids are absolutely indispensable (e.g.
immune-mediate diseases) and can be truly life-saving. The
right dose for every particular patient must be fixed according to the clinical situation, age, intercurrent or past disorders, and other therapy.
It is an obvious rule that the clinician administer the less
toxic preparation, for the shortest period of time and to taper
in a cautious manner, especially after long term administration. Critical reading of current veterinary guidelines is suggested, until newer information is not diffused into the scientific community.
A list of suggested readings (MS Word97 or html format)
will be e-mailed by the authors if requested to
sanmarco@iperv.it

MAIN PROGRAMME

tients this iatrogenic suppression of the HPA axis is also


common and is sometimes linked to various clinical problems, especially when corticosteroid therapy is stopped (corticosteroid withdrawal syndrome). This situation potentially
could occur also in veterinary patients, but it is more difficult to recognize.
4) Immuno-suppression: steroids facilitate the pathological action of viruses, bacteria, yeasts and parasites. The immuno-suppression is probably one of the most fearing side
effects of steroids. The danger is even increased by the
asymptomatic reaction of the patient (because of the anti-inflammatory activity of steroids) to pathogens colonization.
Classical sites of infections are urinary tract, skin and respiratory tract. In cats latent FeLV infections could be re-actived. The popular prophylactic association steroids plus antimicrobial must be evaluated as ineffective and constantly
leads to bacterial multidrug-resistance. Constant surveillance by the clinician, with regards to infectious complications of steroid therapy is mandatory. The only preventive
measure is to reduce any unnecessary use of steroids, or to
keep as low as possible the amount of drugs utilized.
5) Gastric and intestinal bleeding/perforation: the antiprostaglandin activity of corticosteroids, induce gastric lesions after few days of therapy. In this regard, any association with other gastro-toxic drugs as AINS must be absolutely banned. Spinal patients are also proned to colon
perforation. Misoprostol could protect against gastric hemorrhage, while H2-blocker are ineffective as a preventive.
6) Steroid Hepatopathy (SH): in dogs steroids easily induce a notable increase of the serum activity of AST, ALT,
GGT and ALP. In the initial phase of steroid liver action, the

187

4th European FECAVA SCIVAC Congress

189

Pigmented and non-pigmented


masses at the eye level
Adolfo Guandalini

Summary
This study takes into consideration all eye pigmented
and non-pigmented masses, observable during a clinical examination. At the eyelid level congenital (dermoids), inflammatory (hordeolum, chalazion) and neoplastic masses can
be detected. The conjunctiva may show cystic or neoplastic
lesions. The third eyelid can present acquired modifications,
involving the cartilage (eversion) or the gland with prolapse, cyst, neoplasia. The corneal limbus is usually affected by immuno-mediated (for instance, nodular granulomatous episclerokeratitis) or neoplastic formations (epibulbar
melanoma). The cornea sometimes presents congenital
masses (dermoids), the outcomes of inflammatory (exuberant granulation tissue) or ulcerative forms (descemetocele,
iris prolapse). Besides, can be seen other diseases which can
affect the corneal endothelium (bullous keratopathy), cysts
(inclusion cysts) or tumors.
The uvea may present cystic or tumoral affections, which
can be primary (melanoma, adenoma and adenocarcinoma)
or secondary (lymphoma).

Eyelid1,2
The dermoids or choristomas are congenital abnormalities, containing many of the skin components.
Dog dermoids may involve the eyelid, mainly the lateral
side, the conjunctiva and the cornea. However, they can be
observed in other sites. German shepherd, Dalmatian and St.
Bernard dogs are particularly prone to them.
Inferior eyelid colobomas associated to dermoids result
in some line of St. Bernard. Some lines of Birman cats are
genetically predisposed, as well as Burmese cats seem to get
affected on a hereditary basis.
The dermoids may appear pigmented or not, uni or bilateral, single or multiple. They are histologically made up of
ectopic, layered, squamous epithelium, subepithelial connective tissue and adnexal tissues.
The resolution is surgical.
The hordeolum is a purulent inflammation of the eyelid
glands normally linked to staphylococcal infections. The external hordeolum involves Zeis and Molls glands. It is detected in young animals, in the form of single or multiple abscesses on the eyelid margin.
The chalazion, (inner hordeolum) involves meibomian

glands and is usually found in middle-aged dogs.


The meibomian gland duct obstruction causes retention
of oily gland secretion which accumulates and spreads into
the surrounding tissues. This causes a foreign body reaction
resulting in a granuloma.
It is observed on the eyelid conjuncitval surface in the
form of a thick yellow-colored mass, perpendicular to the
eyelid margin.
The hordeolum is treated with hot pads and antibiotics
topically. The chalazion treatment is made by the incision of
the conjunctival surface and surgical curettage. Antibiotics
and steroids are postoperatively administered for 5-7 days.
The eyelid neoplasms in dogs are mainly represented by
adenomas, adenocarcinomas, both benign and malignant
melanomas and papillomas. These tumors account for 82%
of neoplasms, according to a study on eyelid tumors on
dogs. Sebaceous gland tumors, mainly benign, occurr with
45% incidence rate.
Histologically, malignant tumors are locally invasive but
hardly ever metastasize. They are found in elderly dogs.
Beagle, Syberian husky and English setter are breeds at high
risk to developing eyelid neoplasms.
Papillomas, observed in young subjects, are often selflimiting neoplasms or they can be subjected to surgical resection and then the surgical site is submitted to
cryosurgery. Histiocytomas are found in young dogs; they
are usually self-limiting. Pseudotumors are processes clinically hard to distinguish from neoplasms. After surgical resection, histological diagnosis is carried out (for instance:
nodular fasciitis).
Eyelid neoplasms are less frequent in cats, however more
malignant than in dogs. Data concerning the incidence rate
of these neoplasms have been recently reviewed.
Squamous-cell carcinoma is the most common, invasive
and potentially malignant. The symptoms are reddened and
eroded skin areas. The diagnosis is made with histological
examinations.
Other cat neoplasms are basal cell carcinoma, mast cell
tumor and fibrosarcoma.
A histological examination is always needed, as all eyelid tumors in cats are potentially malignant. Eyelid neoplasm
treatment, according to the tumor type, may range from the
mere observation, in self-limiting tumors, to surgical resection followed by cryosurgery, radiotherapy, chemotherapy.
In some cases blepharoplasty may be required.

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Med Vet
Private Practitioner, Roma - Italy

190

Conjunctiva1,2
Dogs can present inclusion epithelial cysts and conjunctival cysts originating from the third eyelid gland, lacrimal
gland and zygomatic salivary gland.
The conjunctiva neoplasms include the squamous cell
carcinoma, fibrosarcoma, papilloma, malignant melanoma3,
lipoma, adenoma, histiocytoma, lymphoma, hemangioma
and mast cell tumor. These tumors may be primary or secondary, originating from the cornea, the nasolacrimal system, the episcleral and scleral tissue. The diagnosis is made
with cytological and bioptic examinations. The treatment
consist in surgery, cryotherapy, radiotherapy, immunotherapy and chemotherapy.
The fat pad prolapse can be found in dogs, with underconjunctival tumefaction and enophthalmos. Surgery is the
treatment4.
Cats showing a symblepharon, can also be affected by
conjunctival cysts, that must be removed surgically. The
conjunctival chemosis associated to many conjunctival diseases sometimes grows noticeably. Several neoplasms may
involve the conjunctiva primarily (for instance, the squamous cell tumor and, rarely, benign and malignant
melanomas) and secondarily (for instance, the lymphoma).

The third eyelid1,2


Some conditions in dogs and cats are shown as nodular
masses on the third eyelid. Dogs in their early months, mainly if they are large breed dogs, may show an inward or outward deviation of the nictating cartilage. Bassethound,
Bloodhound, English setter, German shepherd, Pointer,
Great Dane, Irish setter, Irish wolfhound, Newfoundland
dog, Rhodesian ridgeback, St. Bernard dog and Weimaraner
are predisposed breeds.
Such cartilage deviation is associated to the third eyelid
malfunction and chronic conjunctivitis.
The treatment consists in the surgical resection of the
folded cartilage.
The third eyelid gland prolapse, so called cherry eye,
seems to be due to the weak anchorage fibrous system of the
gland to the periorbita.
Several dog breeds are prone to this disease such as Beagle, Bloodhound, Boston terrier, American cocker, Lahssa
apso, Napolitan mastiff, Newfoundland dog, St. Bernard dog
and Shar pei.
The surgical treatment of this disease has been reviewed
over the years. In the past, in fact, the prolapsed gland was
surgically excised. As this gland produces from 29% to 57%
of the total lacrimal amount, today the gland repositioning is
preferred. Several surgical techniques have been described5.
Sometime, it is possible to find cysts within the third
eyelid gland which must be removed surgically.
Nictitating neoplasms are rare. The third eyelid gland
adenocarcinomas can be aggressive and highly malignant.
If the tumor is extended, the whole third eyelid should be
removed.
The third eyelid gland prolapse is rare in cats. It was observed in two Burmese cats associated to the cartilage ever-

4th European FECAVA SCIVAC Congress

sion. Neoplasms are rare [squamous cell tumor, fibrosarcoma, mast cell tumor, lymphoma, third eyelid gland adenocarcinoma6]. Proliferations on the third eyelid external surface have been recently described, as possible manifestation
of the eosinophilic granuloma complex7.

Lacrimal apparatus
The masses observed can be dacryops8, canaliculops9
and granulation tissue within the lacrimal canaliculus10.

Cornea1,2
The dermoids are usually found within the lateral limbus
area; they extend also on the sclera; keratectomy is carried
out to remove them.
The stromal abscess is caused by the hoard of inflammatory cells within the corneal stroma. It is opaque, yellowwhite colored, slightly raised, at the corneal level. Stromal
abscesses are sterile or can contain an infective agent. They
are not common in pets. The diagnosis is made by means of
cytological examinations and cell culture. The treatment
consist in local antibiotics or keratectomy followed by conjunctival flap.
The descemetocele is a very deep ulcer, so that the Descemet membrane is involved. Sometimes such membrane
protrudes to the point that it can be observed from the ulcer
stromal margins. It requires emergency surgery.
The deep corneal ulcer or wound with perforation and
iris prolapse result in a brown-black mass at the corneal level, usually covered by coagulated aqueous humor. This condition requires immediate surgery. The prolapsed iris is
repositioned if the lesion happened less than 8 hours before
otherwise it is removed; then, the corneal lesion is sutured
and the anterior chamber is reconstructed at last.
Bullous keratopathy is an endothelial corneal disease,
secondary to inflammation, degeneration or glaucoma
which may induce chronic corneal oedema with subepithelial or stromal bullae bulging from the corneal surface. Secondarily, these lesions may turn in epithelial erosions or actual corneal ulcers sometimes even followed by corneal
perforation.
Cats may present a severe bullous keratopathy;
etiopathogenesis is unknown. Young subjects are affected
and the disease is usually bilateral. The lesions recover completely or, viceversa, develop in perforation. The application
of a pedicle conjunctival flap can be effective to prevent
from perforation, if it is carried out in a very short time11.
There is another kind of bullous keratopathy, secondary to
the stromal corneal dystrophy, observed in Manx cat, and
endothelial dystrophy, seen in domestic short-hair cats.
Exuberant granulation tissue can bulge into the cornea.
Thus a differential diagnosis is to be made to distinguish it from
any corneal neoplasia. If it does not decrease using steroids topically, the surgical resection is required (keratectomy).
Inclusion cysts mainly involve the epithelial layer and
get evident after flap or conjunctival grafts. Some epithelial
cells are trapped within the stroma where they develop and

4th European FECAVA SCIVAC Congress

Limbus1,2
The fibrous histiocytoma is a mass, invading into the
temporal cornea in dogs. Histologically it consists in histocytes, fibrocytes, plasma cells and lymphocytes. The therapy envisages the superficial keratectomy followed by the local and subconjunctival application of steroids. Azathioprine
is effective to keep under control such diseases.
The nodular fasciitis is a solid infiltrating mass, mainly
consisting in fibroblasts and reticulin fibres. Surgical resection is effective.
The epibulbar melanoma is a usually pigmented, although it can also be amelanotic, neoplasia. It is invasive in
young subjects (2-4 years), stationary in old ones (8-11
years). It mostly originates in the dorso-lateral quadrant. The
German Shepherd seems to be particularly prone to develop
it. Such form must be distinguished from an intraocular
melanoma transcleral extension. On this regard, a gonioscopic examination is recommended to avert any possible
intraocular neoplasia. The surgical treatment consist in a free
corneo-scleral graft, third eyelid cartilage graft, cryosurgery,
PTFE transplant13, photocoagulation14. The treatment is indicated in young subjects to protect the eyeball, while recurrent observations are recommended in old subjects. Epibulbar melanoma is rare in cats. The treatment is the same as in
dogs.
The granulomatous nodular episclerokeratitis (NGE) is
represented by single or multiple masses at the limbus level,
which spread into the surrounding corneal stroma. The third
eyelid is frequently involved. Breeds, such as Collie and
Shetland Sheepdog are particularly predisposed to develop
it. It is a chronic granulomatous inflammation. Histiocytes,
plasma cells, fibroblastic cells, reticulin fibres and neovascolarization with infiltration of polimorphonucleates are histologically evidenced. The treatment consist in Azathioprine
administered orally associated to topical steroids.
Episcleritis and scleritis: episcleral lesions are usually
nodular, painless and rose-colored single lesions. They are
mostly located in the temporal limbus. The American cocker and Golden retriever are particularly predisposed breeds.
These are granulomatous lesions, containing histiocytes,
lymphocytes, plasma cells, and an amount of reticulin fibres.
Scleritis becomes evident with painful and red eyes, with
lesions and concurrent intraocular inflammation at level of
the posterior segment. Histologically, it consists of necrotiz-

ing diffused granulomatous lesions, with a deep infiltration


of inflammatory cells (histiocytes, lymphocytes, plasma
cells)15.

Uvea1,2
Uveal cysts in dogs may be congenital or acquired. Acquired cysts can have a traumatic or inflammatory origin.
However, the cause is usually unknown. They can be either
uni or bilateral, single or multiple, oval or globe-shaped;
black or brown colored or sometimes transparent. They can
be found free in the anterior chamber, adherent to the pupillary margin or to the ciliary bodies. Uveal cysts can be transilluminated, and then distinguished from the uveal
melanomas. They have been recently found as the cause of
secondary glaucoma in Great Dane16. They are removed by
inspirating through a limbal incision or by means of photocoagulation.
Nevi are restricted melanocytic lesions appearing over
the iris surface. They are mainly observed among young
subjects (2 years or younger).
Most of melanomas involve the anterior uvea in dogs.
According to a study on melanomas the metastasis incidence
is 4%. They are more frequent in older dogs (8-10 years).
German Shepherd and Boxer seem to be particularly predisposed breeds. These are, usually, nodular in appearence.
They can originate from iris or ciliary bodies.
Ciliary body neoplasms can derive either from embryonal indifferentiated tissue (medulloepithelioma) or differentiated cellular tissue (adenoma and adenocarcinoma). German
shepherd and American cocker seem to be more predisposed
to them. Middle-aged and older dogs (8 years average age)
are the most affected. They can originate either from the pigmented or non-pigmented epithelium; it seems more likely
from the latter. Adenomas are most of times limited to the
ciliary body while adenocarcinomas are more invasive and
they can metastasize. Two approaches are usually adopted:
waiting or the neoplasia surgical removal17.
The most frequent secondary neoplasia is lymphoma. It
usually involves both eyes. The anterior uveitis is the most
frequent clinical sign. Conjunctival infiltrations, interstitial
keratitis, hyphema, retinal haemorrhage and glaucoma can
be observed.
In the cat the most common primary neoplasia is the iris
melanoma which differently from the dog shows a trend to
the infiltration rather than nodular aspect and adenomas and
adenocarcinomas of the ciliary bodies. Lymphosarcoma associated to the FeLV virus is the most common, among the
secondary neoplasias.

Orbita1
The zygomatic mucocele is originated by the saliva release with secondary fibrosis and inflammation. The cause is
mainly traumatic. A mass can be observed within the ventral
conjunctival fornix. Within the mass aspirate, the presence
of a viscous fluid containing no inflammatory cells is detected. Surgery is the treatment.

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create a cystic cavity, coated by non-keratinized squamous


epithelium. These isolated, white-rosed cysts are usually
unilateral. The origin seems to be traumatic. They are surgically removed with a superficial keratectomy12.
The squamous cell carcinoma takes origin directly
from the cornea and is classified as corneal intraepithelial
neoplasia.
It becomes evident as a white-rosed multilobulate mass.
The treatment consist in a superficial keratectomy combined
to cryosurgery or beta-radiation.
Papillomas are more frequent in young dogs. They are
surgically treated with keratectomy followed by cryosurgery
or beta-radiation.

191

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References
1.
2.
3.

4.
5.

6.

7.

8.

Gelatt KN, (1991), Veterinary Ophthalmology, Lea & Febiger,


Philadelphia.
Barnett KC, Crispin SM, (1998), Feline Ophthalmology, W.B. Saunders Company Ltd London.
Collins BK, Collier LL, Miller MA et al., (1993), Biologic Behavior
and Histologic Characteristics of Canine Conjunctival Melanoma,
Prog in Vet & Comp Ophth, 3, 4:135-140.
Boydell, Paterson S, Pike R, (1996), Orbital Fat Prolapse in the Dog,
J Sm Anim Practice, 37:61-63.
Guandalini A, Rovesti G, DAnna N, (1997), Retrospective Evaluation of 49 Cases of the Periorbital Rim Anchorage Technique for
Third Eyelid Gland Prolapse in the Dog, Veterinaria, 11, 4:7-11.
Komarony AM, Ramsey DT, Render JA et al. (1997), Primary Adenocarcinoma of the Gland of the Nictitating Membrane in a Cat, J Am
Anim Hosp Assoc, 33:333-336.
Keil SM, Olivero DK, McKeever PJ et Al (1995), Bilateral Nodular
Eosinophilic Granulomatous Inflammation of the Nictitating Membrane of a Cat, Vet & Comp Ophthalmology, 7, 4:258-262.
Grahn BH, Mason RA, (1995), Epiphora associated with dacryops in
a dog, J Am Anim Hosp Assoc, 31:15-19.

9.
10.
11.
12.
13.

14.

15.

16.

17.

Gerding PA , (1991), Epiphora associated with canaliculops in a dog,


J Am Anim Hosp Assoc, 27:424-426
Williams DL, Long RD, Barnett KC, (1998), Lacrimal Pseudotumor
in a young Bull Terrier, J Sm Anim Practice, 39:30-32.
Glover TL, Nasisse MP, Davidson MG, (1994), Acute Bullous Keratopathy in the cat , Vet & Comp Ophthalmology , 4, 2: 66-70.
Bedford PGC, Grierson I, McKechnie NM, (1990), Corneal Epithelial Inclusion Cyst in the Dog, J Sm Anim Practice, 31: 64-68.
Wilkie DA, Wolf ED, (1991), Treatment of Epibulbar melanocytoma
in a dog Using Full - Thickness Eyewall Resection and Synthetic
Graft, J Am Vet Med Assoc, 198: 1019-1022.
Sullivan TC, Nasisse MP, Davidson MG et al., (1996), Photocoagulation of Limbal Melanoma in dogs and cats : 15 Cases (1989-1993),
J Am Vet Med Assoc 208: 891-894.
Deykin A, Guandalini A., Ratto A, (1998), A Retrospective
Histopathologic Study of Primary Episcleral and Scleral Inflammatory Disease in dogs, Vet & Comp Ophthalmology, 7, 4: 245-248.
Spiess BM, Bolliger JO, Guscetti F et al., (1997), Multiple Ciliary
Cyst and Secondary Glaucoma in the Great Dane: A Report of 9 Cases, Trans ECVO Meeting, Birmingham.
Clerc B, (1996), Surgery and Chemotherapy for the Treatment of
Adenocarcinoma of the Iris and Ciliary Body in Five Dogs, Vet &
Comp Ophthalmology, 6, 4: 265-270.

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193

Abnormal new bone formation


Herman A.W. Hazewinkel

Summary
The practicing veterinarian can be confronted with a variety of orthopedic diseases characterized by new bone formation. Recognizing these diseases is the basis of making a
diagnosis and advising a diagnosis, based on the prognosis.
Development, nutrition, inflammation and tumor related diseases are discussed including craniomandibular osteopathy,
osteoporosis, metaphyseal spurs, panosteitis, hypervitaminosis A, hypertrophic osteodystrophy, osteochondroma,
hypertrophic osteopathy and medullary bone infarction.

Introduction
Skeletal growth and remodelling is a close interrelated activity of bone forming osteoblasts and bone removing osteoclasts. Osteoblasts originate from the periosteum and are
moved to the growth plates by ingrowing blood vessels allowing to form primary spongiosa. Osteoclasts are originating from stem cells which are formed in the bone marrow.
Osteoclasts are in particular active at the endosteal side (enlarging medullary cavity), metaphyseal area (decreasing the
metaphyseal diameter to the size of the diaphysis) and near
bony foramen (enlarging foramen allowing vessels and
nerves to pass). In case of increased activity of osteoblasts
and/or decreased activity of osteoclasts too much bone may
be the result. A variety of diseases characterized by abnormal
new bone formation will be discussed related to development, nutrition, inflammation or tumors, whereas new bone
originating from fracture healing, osteoarthrosis, malignancies, and in musculo-tendinous tissue are beyond the scoop.

Development related
1. Craniomandibular osteopathy
Craniomandibular osteopathy (C.M.O.) is also known
under the names mandibular periostitis, lion-, westy- or scotty- jaw, or after the describer of a human disease with some
similarities, Caffey Silverman-Syndrome.
CMO is most frequently described in terriers (including
West Highland White, Scottish, Cairn, Boston), Great
Danes, Retrievers, and other dogs of larger breeds of either
gender. First signs are seen at 3-8 months of age. In Scottish
and West Highland White Terriers retrospective investiga-

tion of pedigree makes an autosomal recessive inheritance,


with 25% affected pups, most likely. Others have also reported several dogs from one litter being affected. The
expression may be variable since some dogs have only
radiological but not clinical signs of C.M.O.
The first sign is reluctance to open the jaws. The dog
may be in bad condition with intermittent elevated body
temperature (to 40.5), pain reaction upon palpation of the
mandible on one or both sides, upon opening of the jaws.
Repetitive coughing, lethargy, atrophy of muscles of
mastication, enlarged mandibular lymph nodes and sometimes rhinitis, conjunctivitis, otitis externa and stomatitis
may be seen. Blood investigation may reveal increased or
decreased globulins, increased alkaline phosphatase, negative culture. The clinical signs may totally disappear at the
age of 11-13 months1.
Radiographs may show typical signs: enlargement and
broadening of the rami mandibularis due to periosteal new
bone formation, with or without obliteration of bullae tympanicae. Other bones of the skull (os occipitale, parietale,
frontale and maxilla) might be affected with or without
mandibulas involvement. In exceptional cases proliferations
of long bones of the appendicular skeleton are seen. New
bone formation is found lateral, ventral and medial to the
corpus mandibulae and caudal to the foramen mentalis. The
alveolar side is not involved. Bullae tympanicae are filled
with new bone and can triple in size, causing tracheal displacement.
Osteoclasts remove bone, which is replaced by immature, less mineralized woven bone. The medulla is replaced
by highly vascularized fibroblastic tissue. Inflammatory
cells invade newly formed bone and surrounding subcutis
and muscles are destroyed. A disturbance of the development of the immune system has been suggested, based on
the dysproteinemia and the infections found in these patients, although infections are extremely rare. Fewer and periods of pain coincide with periods of the presence of inflammatory cells in the area of new bone formation.
The more severe cases need fluid therapy and analgesics,
with corticosteroids in case non-steroidal analgesics do not
give sufficient improvement. According to some, corticosteroids will diminish the new bone formation. Surgical removal of new bone will not lead to permanent improvement,
only in case of joint involvement.
2. Osteopetrosis
In a variety of species osteopetrosis (or osteosclerosis

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DVM, PhD, Dipl ECVS


Dept. Clinical Sciences of Companion Animals
Faculty of Veterinary Medicine - Utrecht University - The Netherlands

194

fragilis, or marble bones) is known as an autosomal recessive disease. In this disease, excessive accumulation of bone
and mineralized cartilage occurs due to abnormal decreased
osteoclastic function, due to defective enzyme systems and
morphological abnormalities. In addition, osteoblastic activity is increased. The disease in characterized by bone pain
and pathological fractures of affected bones, due to the fact
that bone is very bridle. On radiographs affected bones are
radiodence at the medullary cavity and cancellous portions
of all bones of the axial and appendicular skeleton. The
shape of the bones remains normal, and the bones can be
normal in size; histologically the growth plates are normal,
and endochondral ossification is not disturbed. However, the
trabeculae of primary spongiosa extends from the growth
plates to the medullary cavity into the diaphyses where it
contacts diaphyseal bone formed by the periosteum which is
not removed to form a medullary cavity. Therefore,
hematopoesis can be disturbed, causing anemia in severe
cases.
In man, spleen or bone marrow infusion after irradiation to knock out the defence mechanism, results in osteoclastic activity2. Till this can be performed also in dogs and
cats with osteopetrosis, there is no cure for these animals
available.

Nutritional related
1. Spurs in the cut-back zone
The large width of the metaphyseal area should be decreased to diaphyseal width by osteoclastic activity. In
young dogs of large breeds, a roughening at the palmar margin of the distal ulnar metaphysis can be noticed on mediolateral radiographs, during the dogs rapid growth phase. This
can be seen especially in young dogs with excessive dietary
calcium intake, known to decrease osteoclastic bone resorption3. However, also in 16 Great Danes raised on food
formulated to meet the recommendations for dogs4, including 1.1% calcium on dry matter base [dmb], these spurs
were present in 80% of the cases, especially at the age of 15
weeks. These bony spurs disappear at the age of 6 months.
In addition, flattening or indentation of the distal ulnar
metaphyses or even cartilage cones were present in these
dogs at the age of 15 weeks, and even in 6 dogs still at 6
months of age. In the remaining dogs, a small cartilage cone
did not had clinical consequences5. In more severe cases, as
are described in research dogs raised on a food with excess
calcium (3.3% on dmb), these cartilage cones may exceed
2.5 cm and go together with a disturbed growth in length of
the ulna, leading to the radius curvus syndrome3. These findings have led to the conclusion that 1.1% calcium on dmb
might cause a too high calcium uptake in fast growing large
breed dogs. Although a bony spur in itself does not have
clinical consequences, it reflects decreased skeletal remodelling with major complications for young dogs of large
breeds. This can be prevented by recommending a commercial dog food specially designed for young, large breed dogs.
2. Panosteitis
Panosteitis is also known as enostosis or eosinophilic
panosteitis. In young dogs, a high calcium intake causes a

4th European FECAVA SCIVAC Congress

high calcium absorption, causing a hypoparathyroidism and


a hypercalcitoninism and thus a decreased osteoclastic activity. This causes a routing of calcium to the skeleton,
where it is stored to be used later. Chronic calcium excess in
young dogs causes an increased calcium accretion and a decreased skeletal remodelling, including a decreased adaptation to soft tissue growth. Blood vessels centrifugally running through canals in the diaphyseal cortex do not expend
proportionally together. This will result in oedema formation
inside the medullary cavity with ultimately new bone formation on the fibrous tissue formed.
Increased pressure and finally new bone formation is
first seen near the foramen nutritium. Oedema may accumulate underneath the periosteum and thus make the periosteum more vulnerable to pressure and pull and may cause
extra lamellar bone formation.
So far no other etiologies have been demonstrated but
cannot be ruled out. The disease is mainly seen in mediumsized and large-breed dogs, especially in German Shepherds,
starting at 6 months of age, and is characterized by a sudden
onset of shifting lameness. The lameness is seen in different
legs, will become increasingly severe in several days, and
can disappear or regress for some time. Dogs may receive
dog food supplemented or rich in calcium. Radiographs
demonstrate a blurring of the trabecular pattern in the metaphyseal area (especially the proximal ulna) and eventually
white areas starting near the foramen nutritium and extending throughout the medullary cavity. In some cases and with
special radiographic technique a well-defined subperiosteal
cortical thickening can be noticed6,7.
Analgesics can be necessary and a calcium-deficient diet for a limited period to increase osteoclastic activity can be
advocated, although is not proven to be beneficial yet. In
mature dogs, corticosteroids can be prescribed. The disease
is self limiting and is not diagnosed in dogs over 22 months
of age, till that age relapses can occur.
3. Hypervitaminosis A
Vitamin A is one of the fat soluble vitamins, required to
prevent a variety of abnormalities including reproductive
failure, disorders of epithelia (bronchi, salivary glands, haircoat) and retinal degeneration. Vitamin A is also required for
normal skeletal growth and development, especially osteoclastic activity. Vitamin A1 is, present in a variety of foodstuffs originating from terrestrial and seefish, whereas vitamin A2 (which is 30% less effective in mammals) is present
in fresh water fish. Since cats cannot transform carotene into vitamin A, they totally rely on vitamin A as present in animal food tissue or supplemented to the food. Dogs, unlike
cats, are able to form retinyl esters making the vitamin A biological inactive, as well as to excrete 15-60% of the daily
vitamin A intake as retinyl palmitate in the urine. Although
massive doses of vitamin A caused hypervitaminosis in kittens and puppies after several weeks, in companion animal
practice hypervitaminosis A will be seen especially in the
mature cat, starting between 2 and 5 years of age. In dogs the
history of massive supply of cod liver oil or vitamin supplements will help to make the diagnosis. In cats the diet has
not always been raw liver, fish or supplements: 4 out of 8 of
our patients and 3 out of 80 cats did not eat these foodstuffs,
reason why an individual predisposition is suggested.

Excessive amounts of vitamin A will reduce chondrocyte


proliferation in the growth plates, depress periosteal osteoblastic activity, and stimulate osteoclastic activity, causing osteoporosis in addition to a variety of lipid infiltrations
in parenchymal organs including the liver. New bone formation is especially seen at the insertion sides of the tendons of
the main muscles, and at the origin of ligament and joint
capsules. Periarticular pull-out forces in the osteoporotic
bone may induce this new bone formation, which is similar
to callus formation, eventually leading to ankylosis.
In adult cats the stiff neck and/or larger joints of front or
rear legs, dull haircoat, hyper- or hyposensitivity of the skin,
impingement of nerves causing function loss, as well as
anorexia and weight loss may be noticed. When both shoulder or elbow joint reveal ankylosis, the cat may unload both
front legs in a sitting position. When ankylosis of the cervical area occurs, the animal is unable to wash and groom itself. The diagnosis can be made on radiographs of the cervical or thoracal vertebrae and the large joints of the legs: new
bone formation without bone loss, leading to ankylosis of
vertebrae (at the dorsal or ventral side) and of the joints.
Although vitamin A is quit thermolabile and will be destroyed above 70C, cooking of the liver will destroy most
but nor all of its vitamin A. From studies in larger groups of
patients it revealed that prognosis improves when, after the
diagnosis was made, the diet of the animal was changed
completely. Corticosteroids may releave some nerve pain,
but can hinder a decrease in plasma vitamin A concentration.
Clinical and even radiological improvement is seen. Ankylotic joints will not regain their normal motion, but with
drastic change in diet, supportive analgetics when needed
and time to heal, a dramatic improvement can be expected.
Improvement can be seen 2-4 weeks after the start of the
therapy.

Inflammation related
1. Hypertrophic osteodystrophy.
Hypertrophic osteodystrophy (HOD) is also known under the synonyms of metaphyseal osteopathy, metaphyseal
dysplasia, osteodystrophy and, misleadingly, canine scurvy
and Mller-Barlow disease. Although first described in the
early thirties, its etiology is still not elucidated completely. It
was long hypothesized that hypovitaminosis C, causing inferior collagen formation in bone and blood vessels in primates and guinea pigs, was the cause of HOD in dogs. This
has not proven to be the case. Other dietacly factors, including copper deficiency, overfeeding and oversupplementation with minerals, are also proposed as causes, but become
less likely. HOD is seen in more than one dog of a litter
which does not exclude an inherited factor, but does not exclude environmental factors, either. Recently Mee et al.8
have demonstrated that RNA and mRNA of canine distemper virus were present in osteoblasts, osteocytes and bone
marrow cells of dogs infected with this virus. Osteoblasts
and osteoclasts within the affected metaphyses of dogs with
HOD also contained the virus. These findings all support the
finding of Grndalen that blood of dogs with HOD caused
clinical CDV infection in recipient dogs.

195

HOD is only seen in young dogs, especially of the larger (fast growing) breeds. Dogs can be depressed, have
anorexia, be painful during walking or even unable to stand.
Metaphyseal areas, especially of the distal radius and ulna,
are swollen. Rectal temperature can be above 40C. Littermates may also be affected. Often an episode of respiratory
or gastrointestinal disease preceded this disease, and the animal may be vaccinated recently against CDV.
Radiographic findings are pathognomonic for HOD and
include an irregular radiolucent line in the metaphyseal area
parallel to the growth plate but a few millimeters away from
it. In subacute cases new bone formation, originating from
the periosteum in the diaphyseal-metaphyseal area becomes
noticeable. In very severe cases, probably when the patient
is not kept extremely quit during the period of the disconnection in the metaphyseal area, these bony cuffs can become very massive. Not only in the distal radius ulna and
distal tibia, but at almost all metaphyseal area, new bone
formation becomes visible. In chronic cases this cuff will be
attached to the bone and will either be removed or partially
remodeled by osteoclastic activity.
The therapy includes good nursing and analgesics on effect. Either the animal will die due to (pain/viremia) shock
or will clinically improve within 3-6 weeks. In some dogs
the periosteal new bone formation will be remodelled and
not noticeable at older age.
2. Osteochondroma
Osteochondroma is a benign, solitary or multiple new
bone formation arising from cartilage and found to be attached to any bone that develops from cartilage. In dogs, an
osteochondroma is growing when the animal grows and is
seen predominantly in tibia and femur and vertebrae of large
breed dogs. In cats, osteochondroma appear at mature age
(>2 years) without predisposition for the bones or the breeds
involved, but may be positive for feline leukemia virus
(Pool, 1993). Lameness develops especially in case of
mechanical hindrance or nerve impingement. The osteochondroma in dogs stops growing when the animal is mature. When indicated, the cartilage cap should be removed
together with the new bone formation with good prognosis.
In cats, the prognosis is much poorer since the new bone formation might grow autonomously, multiple tumors can be
present and the primary viral infection can be fatal9.

Tumor related
1. Hypertrophic osteopathy
This fascinating disease was first described by Marie (in
1890) and Bamberger (in 1891), and is also known as hyperplastic osteoperiostitis, hypertrophic (pulmonary) osteoarthropathy. The disease is characterized by bilaterally,
symmetrically periosteal new bone formation. It often, but
not always, starts at the distal bone ends and looks like oedematous swelling of the feet. However on palpation it is hard
and not very painful upon deep palpation. Historically, in
human patients this new bone formation was most often seen
in combination with, or as a result of, a space occupying
process in the thoracic cavity like tuberculosis. In dogs it is
described in combination with (primary or secondary) pul-

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4th European FECAVA SCIVAC Congress

196

monary neoplasia, or abscesses and granulomata, however


also together with esophageal granulomas or neoplasias, intra-abdominal neoplasia including liver tumour, bladder tumour or pyometra.
The disease is more often seen in middle aged (>8 years),
larger breed dogs, with a an over-representation of females10.
Lameness and unwillingness to walk are the predominant
complains. The typical radiological appearance includes
spicules of periosteal newly formed bone perpendicular to
the cortex starting at the distal end of the legs (i.e., the
metacarpal/tarsal bones) and climbing up proximally including carpal bones, radius-ulna, humerus and scapula as well as
tarsal bones, tibia, femur and pelvis. Ribs and vertebrae are
less commonly and the skull is never affected. There is no
endosteal new bone formation although superposition may
suggest this. In less typical cases the periosteal bone formation is at the proximal end of the legs, more smooth and regular. Spicules are not formed in joint spaces, although joint
effusion and inflamed synovial tissue may be present.
The occurrence of the periosteal new bone formation is
explained by increased peripheral blood flow. Regression of
the newly formed bone is seen after thoracotomy, after
removal of the space occupying process and after a variety
of dissections (including vagotomy). The latter indicates a
nervous involvement. In literature it is described that first
clinical improvement is seen within a month, whereas
radiologically regression takes much longer10. Most cases
with diagnosed hypertrophic osteopathy have a bad prognosis and will not reach this stage.
2. Medullary bone infarction
This is a diseases which is characterized by lameness
since 3-20 weeks, pain upon deep palpation and radiologically irregularly demarcated areas of radiopacity in the
medullary cavities. It is often seen bilateral in both front and
hind limbs, often but not always in conjunction with primary bone tumors (osteosarcoma or fibrosarcoma). Osteosarcomas are in almost all cases solitary and are seen in middleaged, medium-large breed dogs. However, in the here described disease osteosarcomas are most often seen in multiple locations and in Miniature Schnauzers or other smaller
sized dogs. Histologically, intramedullary vessels (but no
other vessels in the body) are occluded by deposition of abnormal collagen in the vessel walls. The radiopaque lesions

4th European FECAVA SCIVAC Congress

correspond with abnormal proliferative osteoid on the endosteal bone surface, and bone necrosis in severe cases. The
changes can be explained by the occlusion of the nutrient arteries11.

Key words
Developmental bone diseases, orthopedics, excessive
calcium intake, hypervitaminosis A, panosteitis, bony spur,
hypertrophic osteodystrophy, hypertrophic osteopathy, osteopetrosis, medullary bone infarction, craniomandibular
osteopathy, osteochondroma.

Literature
1.

2.

3.

4.

5.
6.

7.

8.

9.

10.
11.

Riser WH, (1993) Canine craniomandibular osteopathy Ch 123 in:


Disease mechanisms in small animal surgery 2nd ed. Bojrab MJ (ed)
Lea & Febiger, Philadelphia pp. 892-899.
Woodard JC, Riser WH Hyperostosis and osteopenia Ch 122 in: Disease mechanisms in small animal surgery 2nd ed. Bojrab MJ (ed) Lea
& Febiger, Philadelphia pp. 879-891.
Voorhout G, Nap RC, Hazewinkel HAW (1993) The development of
the antebrachium in Great Dane pups, raised under standardized conditions, a radiographic study. Journal of Veterinary Radiology & Ultrasound 35, 271-276, 1994.
Hazewinkel HAW, Goedegebuure SA, Poulos PW, Wolvekamp
WThC (1985) Influences of chronic calcium excess on the skeletal
development of growing Great Danes JAAHA 21: 377-391.
National Research Council (1974), Nutrient requirements of dogs,
National academy press, Washington DC.
Hazewinkel HAW (1993) Nutrition in orthopedics Ch 149 in: Disease
mechanisms in small animal surgery 2nd ed. Bojrab MJ (ed) Lea &
Febiger, Philadelphia pp. 1119-1128.
Hazewinkel HAW, (1992) Skeletal disease Ch 22 in: The Waltham
book of Clinical Nutrition of the dog and cat, Wills JM and Simpson
KW eds Pergamon, Oxford, pp. 395-423.
Mee AP, Gordon MT, May C, Bennett D, Anderson DC, Sharpe PT
(1993) Canine distemper virus transcripts detected in the bone cells
of dogs with metaphyseal osteopathy. Bone 14(1):59-67.
Pool RR (1993) Osteochondromatosis Ch 116 in: Disease mechanisms in small animal surgery 2nd ed. Bojrab MJ (ed) Lea & Febiger,
Philadelphia pp. 821-833.
Brodey RS Hypertrophic osteoarthropathy in the dog, a clinicopathologic survey of 60 cases. JAVMA 159: 1242-1250, 1971.
Dubielzig RR, Biery DN Brodey RS (1981) Bone sarcomas associated with multifocal bone infarction in dogs JAVMA 179: 64-69.

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197

The role of nutrition in orthopedic diseases


Herman A.W. Hazewinkel
DVM, PhD, Dipl ECVS
Dept. Clinical Sciences of Companion Animals
Faculty of Veterinary Medicine - Utrecht University - The Netherlands

Clinical and radiological examination

This seminar will focus on a variety of diseases which


are more or less of clinical importance, but in all cases important for the every-day practice, since owners ask often
advise about the influence of nutrition on skeletal development. For that reason and as differential diagnosis both hypovitaminosis D and low calcium intake are discussed. In
addition the harm of excessive food and calcium intake is extensively presented.

The young animal will be raised on an unbalanced food,


especially meat or by-products, which are extremely low in
calcium content. This etiology explains the synonym of this
metabolic bone disease: all meat syndrom. Also food of
poor quality, binding calcium to phytate, may cause a chronic calcium deficiency especially in young dogs of large
breeds. The animal will reveal a reluctance to stand and
walk, abnormal bowing of the long bones and protuberances
(i.e. calcaneus, olecranon, tuber ischium) or will even be
paralyzed due to spinal compression by pathological fractured vertebrae. The animal will be in good health, but is not
willing or unable to stand and walk. Bowed legs, bowed
protuberances, kyphosis, pain upon skeleton palpation may
be obvious. Blood investigation will not reveal typical abnormalities except for sophisticated determinations (i.e. elevated PTH and calcitriol levels) which will both cost a lot of
money and time. Radiography may reveal thin cortices,
wide medullary cavities, folding fractures, bowing of protuberances by muscle pull, normal hight of growth plates
boarded by relatively white metaphyseal areas and compression fractures of cancellous bone of epiphyses and vertebrae. Biopsies will reveal normal mineralization but increased resorption and thus a thin cortex and thin cancellous
bone spiculae.

Introduction
Preventing skeletal abnormalities to occur, the dog
should not have the potential to develop unwanted skeletal
abnormalities (which is a breeding responsibility), should be
protected from trauma (the responsibility of the new owners)
and should have a proper nutrition. Aspects related to the latter are discussed here, to prevent a variety of skeletal abnormalities to develop.

I. Alimentary hyperparathyroidism
In case there is an insufficient calcium intake or absorption during a long period, parathyroid hormone (PTH) will
be increased synthesized and secreted. PTH has mainly three
actions i.e., increase osteoclastic activity (deliberate calcium
and phosphorus from the skeleton), increase calcitriol synthesis in the kidney out of 25 hydroxy vitamin D (and thus
increase calcium and phosphorus absorption in the intestine
and decrease phosphorus reabsorption in the renal tubuli
(and thus cause a hyperphosphaturia). Hyperparathyroidism
will normalize the calcium concentration in the extracellular
fluid, allowing a variety of extra- and intracellular processes
which are of vital importance (blood clothing, nerve action,
muscle contraction) to take place.
When the increase in absorption of calcium in the intestine is not sufficient for the daily requirements, which is
higher in fast growing animals (especially of large breeds),
than the only source of calcium is the skeleton. The cortex
will be resorbed at its endosteal surface. Cartilage mineralization and endochondral ossification (i.e., the process of
new bone formation in the metaphyseal area bordering the
growth plates) will be undisturbed.

Differential diagnosis
Calcium deficiency can be complicated with vitamin D
deficiency when solely lean meat (which is low in calcium
and vitamin D) is fed. Especially bone diseases due to an inborn error may resemble alimentary hyperparathyroidism
including osteogenesis imperfecta, mucopolysaccharidose
and other rare diseases.

Therapy
It is extremely important to carry the animal and give it
strict cage rest to prevent more pathological fractures (especially of the vertebrae) to occur. No bandages or splints can
be applied since the bone just proximal to the end of the
splint cannot carry the weight of the leg and will fracture.
The skeleton is to bridle for osteosynthesis at this stage.

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Summary

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Analgesics will facilitate early mobility which is not desirable. A normalization of the diet with a calcium content up
to 1.1% on a dry matter basis will allow the skeleton to mineralize within 3-4 weeks, since a calcium absorption of almost 100% will take place due to the hyperparathyroid induced high calcitriol activity. An extra amount of calcium as
calcium carbonate or calcium lactate (and not calcium phosphate or bone meal) at 50 mg Ca/kg body weight might even
accelerate osteoid mineralization. Corrective osteotomies
can be planned, when needed, after the skeleton is normally
mineralized. Even compression fractures of the spinal cord
may lead to full recovery.

II. Rickets
Pathogenesis
Hypovitaminosis D in young animals is known as rickets, whereas in adults it is called osteomalacia. Vitamin D is
absorbed by the intestine as one of the fat soluble vitamins
and transported to, and hydroxylated in the liver to 25 hydroxy-vitamin D. It is proven now that dogs and cats are not
able to synthesize vitamin D in their skin under the influence of sunlight, unlike many other species including man.
A second hydroxylation takes place in the kidney, either to
24,25 dihydroxy-vitamin D or to 1,25 dihydroxy vitamin D.
The latter, also known as calcitriol, is the active metabolite
which acts in the intestine to stimulate active absorption of
calcium (in the proximal intestine) and phosphorus (in the
distal intestine). A similar action of calcitriol takes care of
an increased reabsorption of calcium and phosphorus from
the pre-urine in the renal tubular cells. In addition, vitamin
D is necessary for osteoid and cartilage mineralization and
thus routes calcium and phosphorus from intestine and kidneys to the bone. The absorption and first hydroxylation of
vitamin D is loosely controlled, whereas the hydroxylation
into calcitriol is directly and indirectly influenced by serum
calcium and phosphorus concentration parathyroid hormone
and increased mineral need during growth, reproduction and
lactation.
When food deficient with vitamin D is fed at an early
age, the kitten or puppy will first metabolize the vitamin D
from maternal origin (placenta and milk) and will then develop hypovitaminosis. When food highly supplemented
with calcium will be fed to young puppies, a hypoparathyroidism will develop with as a result a shut down of calcitriol synthesis. Despite the high calcium and normal vitamin D
content of the food, the animal will develop the clinical signs
of rickets. These are especially demonstrated by the low
mineralization of newly formed osteoid (ground substance
formed by osteoblasts) and cartilage (formed by chondroblasts). Since osteoclasts and chondroclasts are only capable
of removal of mineralized bone and cartilage, a thickening
of the flared area of the bone (metaphyses) occurs. Hypovitaminosis D in adult animals may take place more often than
rickets is seen, but does not coincide with obvious clinical
signs. It might play a role in chronic renal insufficiency.

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Clinical and radiological examination


An unbalanced food (either low in animal fat or enriched
with calcium salts) is fed from an early age onwards. The animal has a reluctancy to walk and stand, but is otherwise
healthy. On inspection and palpation of the appendicular
skeleton bowed legs, bulging metaphyseal areas, painful and
even fractured long bones, deformed vertebrae and pelvis
bones can be noticed.
Radiographs of radius and ulna will demonstrate the thin
cortex, bowed and even fractured diaphysis, extremely
thickened growth plates. Plasma concentrations of calcium
can be normal or low-normal due to hyperparathyroidism.
This might also cause a hypophoshatemia together with a
hyperphosphaturia (see hyperparathyroidism), Determination of vitamin D and its metabolites is both very specialized
and extremely expensive. A decreased level of 25-hydroxy
vitamin D will indicate dietary deficiency, whereas normal
25- but low 1,25 metabolite indicates hypoparathyroidism or
renal disease. A bone biopsy of cancellous bone and growth
plate, for example a core biopsy of the greater trochantor,
will reveal a poor mineralization of osteoid, large number of
osteoclasts and enlarged columns of cartilage cells in the
growth plate.

Treatment
First the food will be changed to a commercial dog or cat
food of one of the mayor brands, known to contain sufficient
vitamin D to cure and prevent rickets (Hazewinkel, 1989).
After 3 weeks the patient should be radiographically evaluated: in case of dietary hypovitaminosis D a dramatic improvement will be noticed (i.e, mineralization of cortex, callus and growth plates). Only when not responding on diet
change and the diagnosis is certain, either after bone histological examination or determination of the major vitamin D
metabolites (i.e. 25, and 1,25 metabolites) extra vitamin D
can be recommended. Vitamin D injections carry the risk of
over supplementation, causing hypercalcemia and hyperphosphatemia with mineralization of soft tissues, heart
valves and kidneys and consequently the animals death.

III. Over nutrition


The excessive intake of energy can be harmful for young
growing dogs with a cartilaginous skeleton, as well as for
adult dogs with arthrotic joints. The increased intake of minerals has especially negative effects on skeletal development
since the absorption process is less well regulated in young
than in adult dogs. This chapter will focus on the orthopedic
effects of overnutrition in young dogs.

Pathophysiology
Cartilage surrounding secondary ossification centers, i.e,
the growth plate is organized in a structured way, starting
with a reserve zone and ending with the lost of chondrocytes

in the hypertrophic zone. The thickness of the growth plates


parallels growth velocity. Growth plate growth and closure
depend on age, breed, location, as well as on humoral and
nutritional factors. Over nutrition, as well as high calcium
intake, have been proven to be in a variety of standardized
and epidemiological studies, important in the etiology of osteochondrosis. Osteochondrosis is a disturbance in the
process of endochondral ossification of growth plates as
well as of joint cartilage. The latter will become clinical evident in case fissure lines cause a cartilage flap, i.e., osteochondritis dissecans.
In addition, excessive energy intake (either as excessive
carbohydrates, fat or proteins) may cause an increase in
body weight and thus an overloading of deformable parts of
joints, expecially of incongruent joints including the cartilaginous acetabular rim in case of hip dysplasia, and of coronoid process in case of too short radius (as in Bernese Mountain Dogs).

Clinical and radiological examination


Osteochondrosis is more often seen in males and faster
growing females during the fastest growth phase of large
(i.e., fast growing) breeds. The daily ration in these circumstances has great demands on quality and quantity. Not relative but absolute amounts intake per kg body weight (or per
kg metabolic body weight) have to be taken into account.
Large amounts of calcium (with of without phosphorus)
with restricted feeding is as harmful as large amounts of balanced food with as a result the same amount of calcium intake. One or both front and/or rear legs can be affected in the
major joints and/or distal growth plates.
Inspection of the front and rear legs may demonstrate
valgus deformation. Inspection and palpation of elbow, stifle and tibio-tarsal joints may demonstrate overfilling. Hyperextension or -flexion of these joints and/or of the shoulder joints (which are not palpable for effluation) may cause
pain reaction in case of osteochondritis dissecans.
Radiographs of growth plates (especially of the fast
growing distal ulna) may reveal retained cartilage cones. Radiographs of shoulder, elbow, stifle or tibio-tarsal joints may
reveal an abnormality in the alignment at the predilection
sides for osteochondrosis. Other imaging techniques including arthroscopy may support the diagnosis.

Treatment
Young dogs of large breeds should be raised with limited amounts of food, preferably a food of good quality and
containing ingredients according to the requirements of
growing dogs. Overfeeding and over supplementation must
be avoided. The protein and mineral content of good commercial adult dog food is sufficient for raising large breed
dogs.
In case of valgus deviation and thickening of cartilage
without detaching, a prompt correction of food intake may
support the healing process. Radius curvus syndrom or osteochondritis dissecans demand surgical intervention.

199

In osteochondrosis, maturation of the cartilage cells and


its intercellular substance does not allow mineralization to
occur. Therefore the cascade of events, including chondrocyte death, capillary ingrowth, osteoblast introduction and
bone formation, will not take place. This causes elongated
cartilage columns in articular cartilage as well as in growth
plate cartilage.
The disturbance in endochondral ossification can occur
in articular cartilage with osteochondritis dissecans as a consequence. In osteochondritis dissecans a part of the articular
cartilage is detached and may be fragmented, mineralized or
even ossified together with inflammation of the joint and the
endochondral bone in the area of the cartilage lesion.
The disturbance in endochondral ossification can also
occur in growth plate cartilage, with irregular growth plates
and even large cartilage cores and decreased growth in
length as a consequence. In addition, the disturbance in endochondral ossification can be manifest in a delay in ossification of the secondary ossification centers.
Osteochondrosis is a multi factorial disease in which inheritance and nutrition play a significant role. The disease is
frequently seen in a variety of breeds. There is a prevalence
for location of osteochondrosis in each breed affected with
this disease, although multiple affected animals are frequently seen. Although histologically osteochondrosis can
be diagnosed also in non-weight bearing growth plates like
that of the rib, micro trauma may play a significant role in
causing the fissures as can be concluded from the fact that
osteochondrosis dissecans is mostly seen on convex, weight
bearing areas. Disturbances in growth plates leading to clinical manifestation including bilateral radius curvus syndrome or rear leg exorotation are especially seen in giant
breed dogs. Also the detachment of the anconeal process of
the ulna or the supraglenoid process of the scapula can be
seen in this respect. Since osteochondrosis is so frequently
seen in large breed dogs, a variety of studies are performed
in different institutes to elucidate the role of nutrition in the
manifestation of osteochondrosis. The original study was
performed by Hedhammer et al., (1974) on 12 pairs of Great
Danes raised on food rich in protein, calcium, phosphorus
and energy. More frequently, skeletal diseases including osteochondrosis and delayed skeletal modeling where seen in
the dogs fed this formula ad libitum, whereas the restricted
(i.e., 2/3 of the amount of the ad lib. group) fed dogs revealed less severe signs. This opened a whole series of investigations performed by others. Overload, by over nutrition of a basal food enriched with rice or just by suggesting
high body weight by sand belts in the scapular region did aggravate the signs of osteochondrosis (Meyer, 1991). In a
controlled study in Great Danes with high food intake of
more balance commercial foods, the ad libitum fed dogs revealed more frequent osteochondrosis of the shoulder compared to the dogs fed 60% of the ad libitum amount (Lavelle,
1986). In a recent published study, performed in Great
Danes raised on food only high in protein, no differences in
occurrence nor severity of osteochondrosis occurred when
compared with the normal or low protein fed dogs (Nap,
1991). In studies in Great Danes where the food only differed in its calcium content (with or without a constant ratio
to phosphorus) more and more severe disturbances of osteo-

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4th European FECAVA SCIVAC Congress

200

chondrosis were seen in the proximal humerus as well as in


growth plates of long bones and of non-weight bearing (i.e.,
ribs) areas (Hazewinkel, 1985).
This leads to the practical conclusion that chronic intake
of food rich or enriched in calcium, with or without high
phosphorus, protein or energy content, plays a significant
role in the development and manifestation of osteochondrosis in dogs of large breeds. It was demonstrated in a study in
miniature poodles, raised on a food with high calcium content that minor changes of enchondral ossification occurred.
Different research groups investigated the influence of
nutrition on the manifestation of osteochondrosis. Ad libitum intake of food (rich in Ca) and high Ca intake alone augmented the signs of osteochondrosis. Increased body weight
(by adding of rise) but not high protein intake revealed the
same. (*calculated from list of contents). In addition, enforced growth in body weight as well as in height due to ad
libitum food intake of food rich in calcium (Hedhammer
74, Meyer 92, Lavelle 87) coincide with more frequent
signs of osteochondrosis in the dogs studied. In the study of
Hazewinkel the dogs had a high calcium, but not a high
caloric intake but revealed severe osteochondrosis.
In young dogs, calcium is absorbed in the intestine by
means of both uncontrolled passive diffusion and active,
controlled absorption. It has been demonstrated that Great
Danes raised on a food according to the Nutrient Requirements (i.e., 1.1% Ca) absorbed 45-60% of the ingested
amount of Ca, whereas dogs with triple that amount of Ca in
their diet, absorbed 23-43%. As a result the dogs with the
high Ca containing diet, absorbed considerably higher
amounts. Intake of food, and especially of Ca, causes the release of gastrointestinal hormones, some of which will cause
calcitonin (CT) release from the thyroid glands. The increased CT concentration prevents calcium release from the
skeleton by influencing the bone resorbing osteoclasts. The
calcium absorbed, will routed to the skeleton without prandially influencing the concentration of calcium in the extracellular fluid. In the fasting periods and periods in between
meals, this loosely deposited calcium is freed and used for a
variety of life saving processes. The series of studies in
Great Danes have demonstrated that daily food intake of a
diet rich in calcium leads to hyperplasia of CT producing
cells, a reduced osteoclastic activity and a disturbed enchondral ossification (Nunez, 1975, Hazewinkel, 1985). Although it is not fully understood if calcium plays a direct
role in disturbing chondrocyte maturation, or is mediated by
CT and/or a relative deficiency of other minerals at a cellular level, there is little doubt on the deleterious effect of high
Ca intake on enchondral ossification, with osteochondrosis
as a consequence.

Diagnosis
In case of osteochondrosis of articular cartilage, without detachment of cartilage, no specific complains will be
expected. In case cartilage becomes detached, i.e., osteochondritis dissecans, than osteoarthrosis and inflammation
of the subchondral bone will occur. Therefore osteochondritis dissecans coincides with lameness, pain reaction up-

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on (hyper)extension and flexion of the affected joint, joint


effusion and subchondral sclerosis boarding an indentation of the articular surface visible on radiographs. In addition, a variety of diagnostic methods (including paracentesis, arthroscopy and other imaging techniques) can
be employed.
Measurement of circulating concentrations of calcium
or phosphorus will not give a good insight in the dietary
contents or absorption rate of these elements. It will not
give any indication to support the diagnosis of osteochondrosis. This is based on the fact that plasma Ca concentration is very well kept between limits and phosphorus is related with the calcium homeostasis, although its level is
more reflected by its intake. Alkaline phosphatase will be
increased in case of high calcium deposition into the skeleton, but will be high in all young animals during the period of rapid growth. Ca regulating hormones, i.e., parathyroid hormone (PTH), calcitonin (CT) and vitamin D, can
only be determined in very specialized laboratories and
will only give insight when measured repeatedly. In summary, blood investigation will not be of great value to support the diagnosis in the acute phase of osteochondrosis development. In case of clinical suspected osteochondritis
dissecans, a thorough clinical and radiological investigation will suffice in most cases, with additional techniques
required in some. In case of osteochondrosis of growth
plates, no special complains will be expected when the cartilage core is small and/or temporarily. In longitudinal radiological studies of the distal growth plate of the ulna of
Great Danes a slight flattening or indentation were seen at
the age of five months. From clinical experience it can be
stated that most of these slight abnormalities will not cause
clinical disturbances. When a severe flattening of the metaphyseal area develops, or a deep cartilage core can be seen,
an impaired growth in length of the radius and ulna can be
expected. The short ulna, the curved radius together with
the valgus deformation of the feet complete the radius
curvus syndrome.

Prognosis
Osteochondrosis in articular cartilage will not develop
into osteochondritis dissecans in all cases. Based on controlled studies where both shoulder joints were radiographed, it can be concluded that, although 45-65% of the
dogs had disturbed radiological detectable abnormal contours of the humeral head, only 3-5% was clinically affected
on both sides. When detached, the period of lameness can be
shortened as well as most probable the secondary changes of
the joint minimized with surgical treatment (Van Bree,
1992).
In case of the radius curvus syndrome, severe shortening
of the ulna may cause the irreversible abnormal development of the carpus and/or the detachment of the anconeal
process. The latter is only possible when the longer radius
pushes the humerus against the still incomplete ossified anconeal process.

4th European FECAVA SCIVAC Congress

Based on skeletal diseases induced by calcium or vitamin D deficiencies, dog owners and some dog food manufacturers tend to oversupplement the daily ration with calcium, with or without a proportional increase of the phosphate
content. In young dogs, a high calcium intake causes a high
calcium absorption causing a hypoparathyroidism and a hypercalcitominism and thus a decreased osteoclastic activity.
This causes a routing of calcium to the skeleton where it is
stored to be used later. Chronic calcium excess causes a
chronic decreased osteoclast activity. In growing dogs however, osteoclast play an important role in skeletal maturation
in adapting the skeleton to new demands.

Anatomy & physiology


Especially in immature dogs, there is a large blood supply of the metaphyseal area, bordering the growth plates.
These network of arteriolae receive blood from branches of
the periosteal side (i.e. the epiphyseo metaphyseal arcade)
and the medullary arteries. The latter enter the bone mainly
in the foramen nutritium. The direction of efferent blood
flow is through the diaphyseal cortex, centrifugal from
medulla to periosteum, and run through rigid bone canals including Volkmanns canals. These course transversely
through the cortex, connecting adjacent traversian systems
and provide intercommunication between medullar and periosted vessels.

Ethiology
Chronic calcium excess in young dogs causes an increased calcium accretion and a decreased skeletal remodeling including a decreased adaptation to soft tissue growth.
Blood vessels centrifugally running through the diaphyseal
cortex do not expend proportional with blood vessel growth,
This will result in oedema formation inside the medullary
cavity with ultimately new bone formation on the fibrous tissue formed. Increased pressure and finally new bone formation is first seen near the foramen nutritium. Oedema may be
accumulate underneath the periosteum and thus make periosteum more vulnerable for pressure and pull and may
cuase extra lamellar bone formation. Degeneration of cytoplasm of adipose bone marrow may prelude the sequence of
events, being either primary of secundary.
Panosteitis is seen in different studies in Great Danes
with high calcium intake. So far no other ethiologies are
demonstrated but cannot be ruled out.

Clinical and radiological examination


The disease is mainly seen in medium-sized and
large-breed dogs, starting at 6 months of age and characterized by a sudden onset of shifting lameness. The lameness is
seen in different legs, will become increasingly severe in
several days and can disappear for regress for some time.
Dogs may receive dog food supplemented or rich with calcium. Clinical investigation reveals pain reaction upon deep
palpation of several long bones especially the lateral-proximal ulna, distal humerus and mid tibia. An increased body
temperature may be present. Blood investigation or culture
of blood or bone are negative. Radiographs demonstrate a
blurring of the trabecular pattern in the metaphyseal area
(especially the proximal ulna and eventually white areas
starting near the foramen nutritium and expending throughout the medullary cavity. In some cases and with special radiographic technique a well-defined subperiosteal cortical
thickening can be noticed.

Therapy
Since the disease is self limiting and is not diagnosed in
dogs over 22 months of age the treatment is limited to supportive therapy and nursing of the dogs. Analgesics can relief pain sufficiently for an episode. The owner should be
warned that other episodes will follow. When the dog is mature and other skeletal diseases, especially joint pathology, is
ruled out, corticosteroids at a initial dose of 1 mg/kg body
weight can be prescribed.
Dietary corrections includes a decrease in the amount of
calcium and vitamins to the minimal requirements for dogs.
A calcium-deficient diet for a limited period to increase osteoclastic activity can be advocated and thus may be considered, although is not proven to be beneficial yet.

Key words
Developmental bone diseases, orthopedics, excessive
calcium intake, panosteitis, osteochondritis dissecans, all
meat syndrome, hyperparathyroidism, hypercalcitoninism,
overnutrition, panosteitis.

Literature
Hazewinkel HAW (1993) Nutrition in orthopedics Ch 149 in: Disease
mechanisms in small animal surgery Lea & Febiger, London, pp.
1119-1128.
Hazewinkel HAW, Schoenmakers I (1995) Influence of protein, minerals
and vitamin D on skeletal development of dogs Veterinary Clinical
Nutrition 2, 93-99.

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Panosteitis
(= enostosis = eosinophilic panosteitis)

201

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203

Elbow dysplasia
Herman A.W. Hazewinkel

Summary
Practicing veterinarians are increasingly confronted
with young dogs suffering from front leg lameness due to developmental diseases. Screening in different countries
demonstrated that large percentages of different breeds including German Shepherd, Labrador, Rottweiler, and
Bernese Mountain Dog, suffer from different developmental
diseases of the elbow joint all resulting in osteoarthrosis of
this joint. These diseases include ununited anconeal process
(UAP), fragmented coronoid process (FCP), osteochondritis
dissecans (OCD), and elbow incongruity (INC), grouped together under the name of elbow dysplasia (ED) which
makes it easier to understand by dog breeders and owners.
Here will be discussed the clinical and radiological protocols for diagnosis of UAP, FCP, OCD, and INC; their surgical approaches and, new information on measurements to
prevent the occurrence of ED in different breeds.

Introduction
Elbow dysplasia (ED) is recognized by veterinarians and
breeders as a serious problem for certain populations. Depending on the specific sub-population and the method of investigation, elbow dysplasia is seen in 46-50% of the Rottweilers, 36-70% of the Bernese Mountain Dogs, 12-14% of
the Labradors, 20% of the Golden Retrievers, 30% of the
Newfoundlanders, and 18-21% of the German Shepherds1
but also in Great Danes, St Bernards, Irish Wolfshoud, Great
Pyrenees, Bloodhounds, Bouviers, Chow chows and chondrodystrophic breeds2,3.
ED can be separated into different disease entities including ununited anconeal process (UAP), fragmented coronoid process (FCP), osteochondritis dissecans (OCD) of the
medial humeral condyle and incongruities of the elbow joint
(INC). From recent studies it became clear that OCD and
FCP, and also INC and FCP are diseases with a different
hereditary background. They should be considered as different diseases, all causing lameness and osteoarthrosis. The
success rate of surgical treatment of elbow dysplasia depends on the complete diagnosis before surgery, the correct
surgical positioning and on atraumatic surgical approach as
well as the careful aftercare by the owner. Here the following topics will be discussed: 1) the clinical and radiological
protocols for diagnosis of UAP, FCP and OCD, 2) the later-

al approach to the elbow joint for the removal of the UAP


and ulnectomy for fusion of the anconeal process 3) the medial approach to the elbow joint for removal of FCP and
OCD, and 4) new information on measurements to prevent
the occurrence of ED.

Clinical and radiological investigation


The clinical investigation starts with registration of the
breed and age of the dog (lameness starts at 4-10 months of
age) and inspection of the dog in standing position; in almost
50% of the cases the paw of the affected leg is externally rotated and slightly abducted. On palpation, the elbow is effused. Effusion is usually most pronounced in case of UAP
than in FCP or OCD. Effusion of the elbow joint is felt at the
side of the anconeal muscle. With the dog in lateral recumbency, the range of motion (ROM) of the elbow joint is examined while the thumb is placed on the anconeal muscle to
register crepitation; attention is payed when pain is evoked.
In case of a UAP, there is in particular crepitation and pain
sensation at a firm hyperextension of the elbow joint. In case
of FCP and/or OCD, crepitation and pain reaction can be
evoked at prolonged hyperextension, in particular when the
radius and ulna are exorotated at the same time.
Diagnosis of ED can be confirmed by radiography. Bony
union between the anconeal process and the olecranon
should be complete at the age of 16-20 weeks3. When a radiolucent area is present at an older age it is suggestive of an
anconeal process which is not bony united, i.e., an UAP, due
to a partial or complete separation in the cartilage between
anconeal process and olecranon. On a mediolateral flexed
(MLflexed) view there is no superposition of the humeral
condyles over the fusion area between anconeal process and
olecranon, therefore this is the preferred view. Sclerosis at
the fracture site and osteophytes at the margins of the joint
can be visible at a later stage.
OCD of the medial humeral condyle is best assessed on
anterior posterior medial oblique (APMO) views, whereas
on anteriorposterior (AP) views one third of the cases will be
missed4. Is a small amount of the cases a carcified flap can
be seen located near the indentation of the contour of the
medial condyle. For screening elbow joints on the presence
of a FCP a variety of views is advocated, including the AP,
APMO, MLflexed, MLextended and the ML view with the
joint extended plus the exorotation of radius-ulna 15 de-

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DVM, PhD, Dipl ECVS


Dept. Clinical Sciences of Companion Animals
Faculty of Veterinary Medicine - Utrecht University - The Netherlands

204

grees4. In a survey, we studied the value and additional value of each of the first four mentioned views, using the complete set of four views as a golden standard. We demonstrated that the MLflexed and the APMO views had a limited value as a sole view, but their great value as an additional view.
False negatives of almost 20% when only a MLflexed view
is used in a screening program for FCP, may explain the difference in percentage of positive Bernese Mountain Dogs
between countries5,6. In addition, osteophytes and sclerosis
of the semilunar notch are taken into account for making the
diagnosis. Small osteophytes are especially visible on a
combination of at least 3 or 4 of the mentioned views. UAP
and FCP occurs bilaterally in 30% and more than 50% of the
cases, respectively, and therefore both elbow joints should
be investigated, even in case of unilateral lameness. In case
there are no radiographic abnormalities visibly, auxiliary
techniques (computed tomography, bone scintigraphy,
arthroscopy) may be of value.
The correlation between radiographic signs of elbow
dysplasia and clinical signs depends on the physical demands (working dogs vs. companion animals), the severity
of the lesions (FCP plus incongruity is more severe than
LPC or incongruity alone, low grade arthrosis does not necessarily goes together with lameness), the age of onset of
complaints (lameness at young age is more severe), and
breed. The clinical signs due to a comparable coronoid lesion in Retrievers are more severe than in Rottweilers. Read
et al (1997) reported that 57% of a group of 55 Rottweilers
in a prospective study developed radiographic signs of FCP
but only15% showed physical signs including joint effusion, pain and crepitation during examination and 10% developed lameness7.

Therapy
1. Ununited anconeal process (UAP)
Excision
The anesthetized dog, is positioned in lateral recumbency with the lateral side of the affected elbow joint upwards.
An imaginary line is drawn between the lateral epicondyle
and the cranial aspect of the olecranon, just cranial of the insertion of the triceps muscle, and the distance is divided in 3
equal parts8. The incision is made between the first and second part counting from cranial trough the skin, the subcutis,
the fascia of the anconeal muscle and the anconeal muscle itself. Care is taken not to undermine the skin. The elbow joint
is flexed and with a blunt forceps the anconeal process is
freed from the supratrochlear foramen, and with a pointed
bone forceps it is fixed and removed. Particularly in more
chronic cases the UAP may have migrated to the proximal
portion of the joint. The soft tissue attachment is cut in order
to remove the anconeal process completely. The joint is inspected for free bodies, the fracture line may be curetted and
the joint is flushed with saline. Fascia and muscle are closed
with interrupted resorbable sutures, the subcutis is closed
carefully without leaving dead spaces which may develop
into a seroma. The skin is closed routinely. An elastic ban-

4th European FECAVA SCIVAC Congress

dage is applied for 3 days starting at the toes and including


the elbow joint. Activity is restricted for 3 weeks, thereafter
leash activity is allowed for 3 weeks. When necessary, the
other elbow may be operated after 6 weeks. Arthrosis formation will continue to develop but probably slower than
when an irritating ununited anconeal process remains in
place9.

Reattach
Especially in case of a partial separation of the anconeal
process due to elbow incongruity (see the other contribution
in this proceedings), an osteotomy of the ulna (ulnotomy)
can be performed to allow the anconeal process to reattach.
The spontaneous restoration of elbow congruity after ulnotomy may be expected in dogs under 12 months of age, since
at an older age the interosseus muscle becomes to be to firm
thus preventing the ulna to shift proximally. The dog is in
lateral recumbency with the affected elbow facing upwards
and the hairs have been shaved from proximal of the elbow
joint till half way the length of the ulna. The skin and muscle fascia are incised at the caudolateral border of the ulna at
the level of the proximal and middle 1/3 of the ulna and the
ulna is exposed with Hohman retractors10. With an oscillating saw or an osteotome, the ulnotomy is performed perpendicular or in a slight oblique way (i.e., 45) to the axis of the
ulna. With the aid of two osteotomes the free movement of
the ulna is controlled. The oblique cut allows for less forward tilting of the proximal ulna by triceps pull, but an earlier healing of the osteotomy cap than in case of the perpendicular cut3. Forward tilting can be prevented by an intramedullairy pin, which is especially advocated to use in
chondrodystrophic breeds with a physiological flexed elbow
joint11. An additional lag screw with or without a K-wire can
be placed, which might accelerate re-attachment of the UAP
and thus diminish arthrosis formation12. Early healing can be
prevented by an ostectomy of half a centimeter and/or by
placement of autologous fat in the osteotomy gap3. Fascia,
subcutis and skin are closed in a routine fashion. An elastic
bandage or Robert Jones bandage is applied to stay in place
for 3 days. The dog is allowed to bear weight on the operated leg; analgesics are administered since joint congruity is
restored by frequent flexion and extension of the joint. Bony
union may be expected within 4-14 weeks3.

2. FCP and/or OCD


The dog is positioned with the affected leg on the surgical table with the medial side of the elbow joint upwards and
placed at the edge of the table. After routine preparation and
draping, the incision line is made starting from the medial
epicondyle with a length of 7 cm in the direction of the first
phalanx. This incision is deepened through subcutis and fascia. The white aponeurosis between pronator teres and flexor carpi radialis (or the more subtle separation between flexor carpi radialis muscle and the humeral head of the deep
digital flexor muscle) is separated by blunt dissection. Using
a curved mosquito, the joint capsule is penetrated while the

distal end of the leg is abducted. With a blade #11, the opening is elongated proximally towards the medial epicondyle
and distally towards the annular ligament, both caudal and
parallel to the medial collateral ligament (MCL). The muscular branches of median nerve are identified and protected.
By opening the joint in this way, the MCL should remain intact. The antebrachium is now endorotated (pronation) by an
assistant, thus exposing the joint space between humerus
and ulna, allowing to inspect the medial coronoid process
caudal to the MCL. Using a curved mosquito the medial
humeral condyle is palpated: roughening is caused by a FCP
(a kissing lesion), cartilage in unattached in case of OCD,
and completely smooth surface makes the presence of FCP
questionable. The cartilage flap is removed when present
and the lesion curetted carefully. When kissing lesions were
present, the coronoid area of the ulna is inspected for fragmentation, abnormal coloring of the cartilage, or small blood
stained fissure/fracture lines indicating a fragmented coronoid process or chondromalacia of the joint cartilage. After
10 minutes of endorotation and abduction of the antebrachium plus retraction of soft tissues, the joint will open sufficiently.2 When the apex of the coronoid process is fractured,
it is removed and the edges smoothened with a small curet.
When the FCP is sandwiched between the ulna and the medial aspect of the radial head, the intact, medial aspect of the
coronoid should be removed allowing the removal of this
type of FCP. Removal of the medial aspect is performed with
a curet or a small (2-5 mm) osteotome, taking great care not
to damage humeral condyle or radius cartilage. When fissures are present in the apex of the coronoid, the apex will
also be removed. The joint is frequently flushed with saline
to improve the surgical view and remove the debris.
In case a partially incised MCL ruptures during enforced
endorotation of radius and ulna, Bunnell sutures using PDS or
non-resorbable suture material and a Robert Jones bandage
for at least 3 weeks, may allow the MCL to heal! However,
usually severe lameness will develop due to elbow instability.
The joint capsule, the muscle bellies, the muscle fascia
and subcutis and the skin are closed in separate layers with
interrupted sutures. An elastic bandage is applied including
the surgery wound but not the olecranon, allowing free
movement and preventing postoperative swelling. Exercise
is restricted during 3 weeks followed by 3 weeks leash restriction. The period during which the lameness disappears
varies between immediately postoperatively and 6 months
after surgery (mean 6 weeks)13. In follow up study, with a
follow-up period ranging from 0.5-8 years (mean 2.7 years)
the success rate was 78% in a group of 64 Retrievers (with
67.8% males) operated at young age. Only 33% of the conservatively treated dogs with a FCP (i.e., low body weight
and controlled activity but no surgery), were not lame13. This
stresses the importance of an early diagnosis and surgical
treatment.

3. INC with or without FCP


Elbow incongruity (INC) due to a short radius is frequently seen in Bernese Mountain Dogs (BMD), but also

205

other breeds (Retrievers, Mastiff Napolitano) may be affected. An ad random study in the Dutch BMD population, revealed that 72% of the dogs had INC. A longitudinal study
by Bienz (1985) demonstrated that this incongruity may normalize spontaneously and is most probably genetical. The
joint surface supporting the humerus is decreased in case of
a short radius. This leads to an increased pressure on the remaining joint surface, e.g., the lateral and medial coronoid
process. This may be the cause of the fragmentation of the
coronoid process. This hypothesis is supported by the finding that INC is seen in 72.6% of the BMD with a fragmented coronoid process (FCP), whereas only 6% had a FCP
without INC. Not in all cases, elbow joint incongruity is
concurrent with FCP; in 12% INC was diagnosed without
evidence of a FCP. Based on a owners survey, we found that
not all Bernese Mountain Dogs with FCP or with INC were
lame, but dogs with LCP and INC were all lame. In dogs
with lameness due to FCP we remove the coronoid, in cases
with lameness due to FCP and severe incongruity, congruity
is restored. In dogs under one year of age this can be performed by a partial (approx. 2 cm) ulnectomy. In animals
over one year of age we perform the restoration of elbow incongruity with the aid of the Ilizarov external ring fixator
(IERF) after partial ulnectomy, since the interosseus is too
rigid to allow for spontaneous correction.

Management of ED affected populations


In some breeds a combination of UAP plus FCP, FCP
plus OCD, or FCP plus INC is seen. The combination UAP
plus FCP may be explained by the smaller diameter of the
joint surfaces of the ulna (i.e., the ulnar trochlear notch) than
of the humeral trochlea, forcing both bony protuberances
from their origin15.
A combination of FCP and OCD has been explained by
Olsson (1993) as a disturbance of endochondral ossification
and as such expressions of the same disease. Osteochondrosis is seen more frequently in certain breeds and sub-populations and can be aggravated by high food intake and excessive calcium intake17. The frequency and severity of the
occurrence of osteochondrosis can thus be prevented by dietary management, including a food with a lowered calcium
to energy ratio and quantitative restriction of food intake.
The radiological findings included in a dendrogram of a
Labrador population revealed that FCP and OCD occurred
in two different groups of closely related dogs although in
one related subgroup both entities were present17. In a dendrogram of the Dutch Berneses Mountain Dog population it
became clear that INC and FCP originate from two different
groups of non-related ancestors but are now seen in 80% of
the Bernese Mountain Dogs with ED. This indicates that
there are different diseases (FCP, OCD, INC) which may occur in the same animal. Since there is strong evidence that
FCP in Retrievers is a recessive autosomal inherited disease,
and therefore dogs which are highly related to an affected
animal can have a normal phenotype, the family history
should be taken into account before including dogs in the
breeding stock18.
In 1989 a group of veterinary radiologists, geneticists

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206

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and clinicians founded the International Elbow Working


Group (IEWG) with annual meetings in the United States of
America and in Europe. The 1998 meeting of the IEWG is
organized in conjunction with the SCIVAC/FECAVA meeting in Bologna and is open for all interested veterinarians.
The IEWG introduced a scoring system for the evaluation of
radiographs, based on the proposal of Audell, (1990) and are
adopted by the Federation Cynologique International, the
World Small Animal Veterinary Association, and different
national kennel clubs. The protocol and additional information is made available on the web site of the IEWG and
through its chairman Dr. M. Flckiger (Veterinrklinik
Zrich, Switserland). Although the scoring of arthrosis according to the guidelines of the IEWG can be performed on
the MLflexed view alone, this underestimates the occurrence
of the primary cause of elbow dysplasia with 12-25%, and
the presence of arthrosis with approximately 12%5,6. However, the protocol can be helpful for breeders to screen the
elbow joints of their stock. Making the results of screening
available to all breeders, a significant improvement in elbow
status can be achieved as has been demonstrated to occur in
Norway and Sweden in Bernese Mountain Dogs, Rottweilers, Labrador Retrievers and German Shepherds3,20. Based
on financial or infra structural limitations and differences in
legislation regarding radiological investigations in different
countries, it is not to be expected that a uniform screening
method in Europe will be introduced by the different national kennel clubs. This may not be a reason to limit either the
quality or the quantity of elbow screening. As a consequence
of the globalization of breeding stock exchange, the differences in level of judging and thus of results warrants a certification which makes clear to breeders and buyers how a
particular dog was screened. It is up to the veterinary community to come to these international appointments.

2.

3.

4.

5.

6.

7.

8.
9.

10.

11.

12.

13.

14.

15.

Key words
16.

Fragmented coronoid process, ununited anconeal


process, osteochondritis dissecans, incongruity of elbow
joint, elbow dysplasia, developmental diseases, dogs, surgical approach radiological investigation, screening program,
hereditary diseases.

17.

18.

References
19.
1.

Swenson L, Audell L, Hedhammar A, (1997), Prevalence and inheritance of, and selection for elbow arthrosis in Bernese Mountain Dogs
and Rottweilers in Sweden and benefit-cost analysis of a screening
and control program. Proceedings International Elbow Working
Group, Birmingham, UK, 1997, pp 16-17 and JAVMA 210, 215-221.

20.

Hazewinkel HAW, Kantor A, Meij BP, Voorhout G, (1988), Fragmented coronoid process and osteochondritis dissecans of the medial
humeral condyle Tijdsch Diergeneeskunde 113, 41s-46s.
Sjstrm L, Kasstrm H, Kllberg M, (1995), Ununited anconeal
process in the dog. Pathogenesis and treatment by osteotomy of the
ulnas. Vet.Comp. Orthop. Traumat. 8:170-176.
Voorhout G, Hazewinkel HAW, (1987), Radiographic evaluation of
the canine elbow joint with special reference to the medial humeral
condyle and the medial coronoid process. Vet. Radiol. 5, 158-165.
Hazewinkel HAW, Meij BP, Nap RC, (1995), Radiographic views for
elbow dysplasia screening in Bernese Mountain Dogs. Annual Meeting
International Elbow Working Group, Constance (Germany) pp 29-32.
Busato A, Lang J, (1997), Comparison of two classification protocols
in the evaluation of elbow dysplasia in the dog. Proceedings International Elbow Working Group, Birmingham (UK), p 11.
Read RA, Armstrong SJ, Black AP, MacPherson CG, Yovich J, Eger
C, (1997), Elbow dysplasia in Rottweilers: correlation between lameness, physical signs and radiographic score in growing dogs. Proceedings International Elbow Working Group, Birmingham (UK) pp 7-8.
Hazewinkel HAW, Kantor A, Meij BP, (1988), Loose anconeal
process Tijdsch Diergeneeskunde 113, 47s-49s.
Roy RG, Wallace LJ, Johnston GR, (1979), A retrospective long-term
evaluation of ununited anconeal process excision on the canine elbow. Vet. Comp. Orthop. Traumat. 7:94-97
Piermattei D, Greely RG, (1979), An atlas of surgical approaches to
the bones of the dog and cat. Philadelphia, USA, WB Saunders
Comp.
Matis U (1992), Treatment of ununited anconeal process. Proceedings 6th annual congress European Society of Veterinary Orthopedics and Traumatology, Roma (Italy), pp 16.
Meyer-Lindenberg A. (1997) Der isolierte Proc. Anconeus: prospektive Untersuchungen zur operativen Behandlung proceedings
Deutsche Veterinrmedizinische Gesellschaft, Hannover August
1997 pp. 105-109.
Meij BP, Geertsen KMK, Hazewinkel HAW, (1995), Results of FCP
treatment in Retrievers; a follow-up study at the Utrecht University
small animal clinic. Annual Meeting International Elbow Working
Group, Constance (Germany), pp 24-26.
Bienz HA. (1985), Klinsche und Radiologische Untersuchungen ber
den Fragmentierten Processus Coronoideus Medialis Im Ellenbogengelenk des Berner Sennenhundes und der andee SennenhundeRassen
Inaug Dissertation Zrich (Switserland).
Wind WP (1986), Elbow incongruity and developmental elbow diseases in the dog: part I. J Am Anim Hosp Assoc 22:711-724.
Olsson SE, (1993), Pathophysiology, morphology, and clinical signs
of osteochondrosis in the dog in: Disease Mechanisms in Small Animal Surgery (M.S. Bojrab ed), Philadelphia (USA) Lea & Febiger, pp
777- 796.
Hazewinkel HAW (1993) Nutrition in orthopedics in: Disease Mechanisms in Small Animal Surgery ed 2. (M.S. Bojrab ed), Philadelphia
(USA) Lea & Febiger, pp 1117-1128.
Ubbink GJ, Hazewinkel HAW, Wolvekamp, (1995), Preliminary results of the genetic analysis of the ED program of the Dutch seeing
eyes dogs. Annual Meeting International Elbow Working Group,
Constance (Germany) pp 43-45.
Audell L (1990), Heredity of elbow dysplasia: can elbow dysplasia be
controlled by judicious breeding? Proceedings Amer. Anim Hosp.
Assoc. meeting 1990, pp. 730-733.
Grondalen J, (1995), Occurrence and genetic aspects of elbow dysplasia. Annual Meeting International Elbow Working Group, Constance (Germany), pp 12-17.

4th European FECAVA SCIVAC Congress

207

Dermatological manifestations
of internal diseases
Dominique Heripret
Med Vet, CES DV, Dipl ECVD
Private Practitioner, Arcueil, Paris - France

Specific problems in dogs


1) Nodular dermatofibrosis
This syndrome has been described first in German Shepherd; the animals present multiple collagenous nevi in association with renal cystadenocarcinoma or renal cystadenoma or
uterine leiomyomas in female dogs. Since then, this syndrome
has been described in other breeds: Golden retriever (Marks
1994), and a cross Labrador (Heripret, unpublished data).
The pathogenesis is uncompletly understood. On the basis of the present knowledge, the hypothesis is that the skin
nodules, renal tumors and uterine tumors develop independently, but closely associated, probably through common genetic mechanisms as the syndrome has been proven to be inherited in an autosomal dominant way in German Shepherd
(Lium 1985, Moe 1992).
In a review of 51 cases (Moe 1997), the authors found no
sexual predisposition. Typical chief complaints are skin nodules or depressed general condition. The skin nodules are often numerous, mostly located on the legs. Some nodules
may become ulcerative and painful leading to lameness.
Fine needle cytology shows no inflammation and often
just few cells.
Histopathology shows epidermal atrophy and collagen
hyperplasia without neoplastic or granulomatous organization, and is diagnostic of collagenous nevi.
At this point, renal examination is mandatory: ultrasonography is the investigation of choice and shows hudge
hypoechogenic bilateral renal cavities.
No effective curative treatment has been found for this
disease: chemotherapy has not been evaluated but paclitaxel
(Taxol, Bristol Meyers) may have an interest (it inhibits the
development of renal cysts in rats that have congenital polycystic kidney disease); there is no report about the dosage
and efficacy of this drug in dogs.
The prognosis is poor: the time from diagnosis to death
is 0,5 year, but the time from the first observation of nodular dermatosis to death is 2,5 years (Moe 1997). It shows the
importance of good early recognition of this disease if we
want to assess a treatment.
2) Superficial necrolytic dermatosis
It is an uncommon necroziting skin disorder of dogs associated with incompletly characterized internal metabolic
disease, mainly severe vacuolar hepatopathy (90%) or
glucagon secreting pancreatic islet neoplasm (10%).
The pathogenesis of cutaneous lesions is not well under-

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The skin may be the reflect of many internal diseases or


problems.
Non specific problems:
- nutritional deficiencies, excesses or imbalances may result in scaling, crusting, alopecia and a dull haircoat. Notable examples are the Zinc responsive dermatosis type I and
vitamin A responsive dermatosis, but these entities may represent genetically related problems rather than true nutritional deficiences. Fatty acids deficiency is uncommon
nowadays because of the good quality of most commercial
foods. Protein deficiency may be seen in dogs suffering from
nephrotic syndrome (hairs are easily epilated, presence of
patchy alopecia).
- Endocrine diseases: spontaneous hyperadrenocorticism
(Cushings disease), iatrogenic secondary hypoadrenocorticism (iatrogenic Cushings disease), hypothyroidism, Sertoli-cell tumor, may induce alopecia and some specific
changes in skin quality (Cushings disease), that are well
known.
- Anagen defluxion: special circumstance (antimitotic
drugs, metabolic disorders) may interfere with anagen, resulting in abnormalities in hair follicle and hair shaft. Hair
loss occurs suddenly, within days of the insult.
- Telogen defluxion: a stressfull circumstance (high
fever, pregnancy, surgery,...) may induce an abrupt cessation
of growth of many anagen follicles and the synchrinzation in
telogen. Within 1 to 3 months after the initial insult, a large
number of telogen hairs are shed.
Specific problems:
some cutaneous lesions may be considered as cutaneous
markers (in some cases specific) of internal diseases. Relationship between cutaneous lesions and internal disease or
often badly understood but it is important to be able to recognize these lesions because they often appear before the
symptoms of the underlying disease.
DOGS - Nodular dermatofibrosis
- Superficial necrolytic dermatitis
- Dermatomyositis
- Calcinosis cutis
- Cutanous amyloidosis
- Xanthoma
CATS - Feline pancreatic paraneoplastic alopecia
- Feline skin fragility syndrome
- Digital metastasis of pulmonary adenocarcinoma
- Exfoliative dermatitis and thymoma
- Pseudo sebaceous adenitis

208

stood: hypoaminoacidemia (epidermal protein depletion and


subsequent keratinocyte necrolysis), low essential fatty acid
and Zinc concentrations, high glucagon concentration (inducing a decrease in amino-acid concentrations) have been
suggested to be involved.
Erosions, ulcerations, exudation, thick and adherent
crusts are seen in the footpads and around mucocutaneous
junctions. Lesions may also be seen on ears, pressure points,
scrotum. Secondary infections (bacteria, Malassezia, dermatophytes) are common. Pain may be severe.
Differential diagnosis include: Leishmaniasis, drug reaction, Pemphigus, Systemic Lupus erythematosus (SLE),
Zinc responsive dermatosis.
Histopathology (choose erythematous plaques with adherent crusts) shows a pink, white and blue coloration. Pink layer: parakeratosis and crusting; pale layer: edema and necrolysis of keratinocytes; blue layer: hyperplastic basal cells.
Biochemical findings include: hypoalbuminemia, hyper
beta and gamma globulinemia, increase ALT and SAP, hypoaminoacidemia (hydroxyproline, proline, glutamine, alanine, arginine, ...); hyperglucagonemia is rarely documented.
Ultrasonography is mandatory (pancreas and liver) and
hepatic liver biopsies are indicated if lesions are seen.
There is no specific treatment except in the case of
glucagon secreting pancreatic islet neoplasm in which removal of the pancreatic tumor may be salvatory (Torres
1997). Non specific treatment includes: essential fatty acids
and Zinc supplementations, addition of eggs, treatment of
infectious complications.
The overall prognosis is bad (1,5 month after diagnosis)
3) Canine dermatomyositis
Canine dermatomyositis is an inflammatory disease of
skin and muscles.
Collies and Shetland collies are predilected breeds; the
disease appears in young animals (< 6 months) with no sex
predilection.
Pathogenesis of the disease is still uncompletly understood: there are some evidence for infectious disease and
others for an immune-mediated disease:
* infectious disease: early age of onset, virus have been
detected, the disease develops in pups housed together, frequency of outcome is increasing after national dog show (in
USA)
* immune-mediated disorder: it looks like systemic lupus erythematosus (SLE) (clinical and histopathologicaly).
Cutaneous clinical signs: it is a waxing and waning dermatitis; at the beginning, skin exhibits vesicules, erythema,
scaling and crusting, then alopecia, hyperpigmentation, scarring. The face, pinnae, tip of tail (frequent) and bony prominences are often involved. Pruritus is mild or absent.
Muscular signs include painful temporal muscle and facial swelling at the beginning, and then, muscle atrophy (usually masticatory muscles); megaoesophagus may be found.
Differential diagnosis includes: SLE, epidermolysis bullosa, pyoderma, demidocosis, dermatophytosis, juvenile
cellulitis.
Skin scrapings may reveal Demodex; CBC and serum
chemistry are usually normal; histopathology shows a mild
mixed interface and superficial perivascular dermatitis, follicular atrophy with prominent fibrous rootsheath, individual

4th European FECAVA SCIVAC Congress

keratinocyte necrosis, subepidermal vesiculation with erythrocytes, ulceration and scarring.


Examination of muscles biopsies shows: myositis, myofiber atrophy, necrosis and regeneration, fibrosis and occasionally vasculitis.
Direct immunofluorescence of skin and muscles biopsies
is negative.
Electromyography is often diagnostic of muscle disease;
motor nerve conduction velocities are normal and repetitive
nerve stimulation shows occaional mild decremental responses.
Treatment: vitamin E, pentoxifylline (10 mg/kg bid or
tid), prednisone at the beginning if inflammation is documented on skin biopsies.
Pronostic depends on the stage of the disease: in mild
cases in young animals, pronostic is good (spontaneous remission); in more severe cases with muscular problems, euthanasia may be required.
4) Calcinosis cutis
Calcinosis cutis is mostly associated with spontaneous or
iatrogenic Cushings disease. Some rare other cases have
been described with severe chronic renal failure with renal
hyperparathyroidism and abnormal equilibrium of calcium
and phosphorus.
Calcinosis is often pruritic and represents a real clinical
problem because there is no treatment except treatment of
the underlying disease; with appropriate treatment, calcinosis may disappear after a few months, especially in iatrogenic Cushings disease. If lesions are generalized, the prognosis may be poor.
Non specific treatment includes frequent shampoo or application of colloidal oatmeal with local anesthesic.
5) Cutaneous amyloidosis
Amyloidosis is not a single entity and amyloid substance
may accumulate as a result of a variety of different pathogenetic mechanisms. Cutaneous amyloidosis have been described in dogs with renal amyloidosis, primary cutaneous
disease and monoclonal gammapathy. In the last case, clinical lesions are nodules involving the tongue and ulcerations
of digits, footpads and bony prominences.
Histopathologic examination shows an amorphous
eosinophilic diffuse or perivascular deposit.
6) Xanthoma
Xanthoma are cutaneous or subcutaneous yellowish lesions resulting from accumulation of lipids in the dermis. In
dogs, it has been associated with diabetes mellitus, hypothyroidism and acute pancreatitis.
Lesions are papules or nodules with no special location.
Histopathological examination shows multinucleated
cells (Touton cells) and spumous histiocytes.
When diagnosing xanthoma, biochemical examination is
mandatory (glycemia, cholesterolemia, lipidemia, lipoprotein electrophoresis, T4 measurement).

Specific problems in cats


1) Feline pancreatic paraneoplastic alopecia (FPPA)
FPPA is characterized by specific cutaneous lesions associated with pancreatic carcinoma or cholangiocarcinoma

(Brooks 1994, Pascal 1996).


Cutaneous lesions: rapidly progressive alopecia, beginning by the face and the ventrum extending to the legs and
flanks. The alopecia is complete and the skin becomes shiny.
Footpads may be involved resulting in pain.
Alopecia appears a few days before or simultaneously
with non specific general signs: anorexia, asthenia. Prognosis is very poor and the cat die in a few days or weeks.
Haematological and biochemical examinations are unremakable or non specificaly altered. Ultrasonography may reveal pancreatic tumor or hepatic metastasis.
Histopathological examination of the skin shows: telogen phase and atrophic hair follicles, slight perivascular inflammation, no stratum corneum, severe adnexiel atrophy.
Immunohistochemical stainings of the pancreatic tumors
have failed to show any endocrine abnormality (insulin,
glucagon, somatostatin, ACTH).
No treatment is available.
The internal disease can be diagnosed on the basis of the
cutaneous lesions.
2) Feline skin fragility syndrome (FSFS)
FSFS is an uncommon disease of cats. The exact pathogenesis of the lesions si unknown. It has been described with
Cushings disease (spontaneous or iatrogenic), diabetes mellitus, hepatic lipidosis (Diquelou, 1991), neoplastic internal
disease (Regnier 1989) and in some cases with no evident
cause.
There is no sexual or breed predilection and the disease
can arise at any age.
Skin defects are often catastrophic: large wounds occuring with a minimum trauma and with cutaneous margins that
are markedly abnormal (cigarette paper aspect). The lesions
are not painful and slightly (or not) hemorragic.
Differential is from feline cutaneous asthenia, a congenital syndrome that may predispose to FSFS.
It is difficult to biopsy the skin of these animals because of
the fragility of the skin. Histopathological examination reveals

209

severe epidermal and dermal atrophy, rare collagen fibers.


There is no specific treatment; surgical closure may be
difficult but must be proposed in case of iatrogenic Cushings disease.
3) Digital metastasis of pulmonary adenocarcinoma
It is a podal dermatosis with uni- or multidigital nodular
to ulcerative painful lesions (Moore 1982, Estrada 1992).
Local osteolysis is a consequence of these lesions.
When facing this kind of lesions, a thoracic radiography
must be proposed: it shows a pulmonary mass (carcinoma).
This pulmonary tumor is generally asymptomatic at the time
of the cutaneous diagnosis.
Cutaneous histopathological examination shows neoplastic infiltration of the digit sometimes with local metaplasia (ciliated epithelioma, mucus cells).
Pathogenesis of cutaneous lesions is not yet understood
but these lesions are specific for a pulmonary carcinoma.
Results of surgical excision of the pulmonary tumor (or
radiotherapy) has not been evaluated for the moment.
4) Exfoliative dermatosis and thymoma
Exfoliative dermatosis has been described in a few cats
in association with thymoma (Scott 1995).
Clinical cutaneous signs begin with erythema and non
pruritic scaling; then scaling becomes more important and
alopecia, crusts and ulcerations appear. Head, ears, neck are
often primarly involved but extension and generalization occure rapidly.
There is no sex or breed predilection.
Cutaneous histopathological examination shows a hydropic interface dermatitis (mainly lymphocytic infiltrate)
with keratinocyte necrosis, similar to erythema multiforme.
Thoracic radiographic reveals a cranial mediastinal
mass; ultrasonographic examination of the thorax shows a
multilobular cystic mass or hyperechogenic mass.
There is one report of resolution of clinical signs after
surgical thymoma resection (Forster van Hufte 1997) but the
histopathological lesions were slightly different in this report.

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211

Diagnostic approach to alopecia


in dogs and cats
Dominique Heripret

Alopecia can be defined as partial or extensive hairloss


linked to a decrease in the total amount of hairs (excess shedding of hair) or shortening of hairs without decreased total
number of hairs. Alopecia may be focal, diffuse, generalized.
Multiple classifications are proposed in the litterature;
however two of them are important: the histopathological
one and the clinical one which is presented here.

A - Clinical classification
1) Congenital and hereditary alopecias
dystrophy or lack of hair follicle:
- alopecia universalis (Sphinx cat)
- hypotrichosis (Siamese breeds, Cocker, Poodle,
Whippet, ...)
follicular dysplasia:
- Color dilution alopecia: seen in blue and other color-diluted dogs (all breeds and mongrels), in association with a color dilution gene. It appears between
4-6 months and 4 years old.
- Black hair follicular dysplasia: alopecia is restricted
to dark-haired areas. This condition is very similar
to color dilution alopecia.
- Canine follicular dysplasia: this is a melting pot
of many unknown conditions gathering congenital
and hereditary alopecias and acquired alopecias. In
Siberian Husky, follicular dysplasia syndrome may
be a castration responsive dermatosis.
- Acquired pattern baldness (Dachshund)
hyperkeratotic diseases of epidermis and secondary
alopecia
- Primary seborrhea (Cocker spaniel, ...)
- Vitamine A responsive dermatosis (Cocker spaniel)
- Canine ear margin seborrhea (Dachsund)
- Ichtyosis
- Zinc responsive dermatitis type I (Siberian Huskies,
Alaskan Malamutes)
2) Acquired traumatic alopecias
Non cicatricial acquired traumatic alopecias:
- secondary to pruritus: all pruritic dermatitis are able
to induce alopecia characterized by cutaneous inflammation and/or primary lesions. Hairs are broken.
Main causes: allergic dermatosis, sarcoptic mange,
feline extensive alopecia (whatever the cause)
- secondary to rubbing: alopecia localized to contact

areas (collar). It has to be distinguished from endocrine alopecia.


Cicatricial acquired traumatic alopecias:
- secondary to physical or chemical traumas: scars,
burns, irritant contact dermatitis
- traction alopecia: described in dogs that have barrettes, rubber bands or other methods to tie up their
hair.
3) Non traumatic acquired alopecias
Non cicatricial, with follicular arrest
- endocrine dermatoses
- telogen effluvium: hair loss occurs up to 2 months
after the insult
- toxic alopecia and anagen defluxion: chemotherapy
- post-clipping alopecia
Non cicatricial with follicular dystrophy: seasonal
flank alopecia, post-clipping alopecia
Non cicatricial, with folliculitis: bacterial, fungal or
parasitic (Demodex); generally, alopecia is multifocal
with a moth eaten appearance.
Non cicatricial, with perifolliculitis:
- Leishmaniasis
- sebaceous adenitis
- alopecia areata
Non cicatricial, neoplastic: mycosis fungoides, metastasis of mammary gland adenocarcinoma
Cicatricial
- infectious diseases: deep pyoderma
- non infectious: dermatomyositis, sclerodermia
4) Miscellaneous
- Canine pinnal alopecia (Dachshund, Yorkshire, ...)
- Excessive shedding syndrome
- Short hair syndrome of silky breeds

B - General diagnostic approach


1) Signalement and history: after the signalement (sex,
breed, age), a thorough history should be obtained. The major objectives of the history are to determine whether:
- pruritus is present or not and, if pruritus is present,
if it is previously to alopecia or not. Determining
pruritus can be difficult in cats
- alopecia is associated with erythema, scaling,
crusts, plaques, nodules
- the alopecia area is enlarging

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- any previous medications or injections that may be


associated with alopecia have been given (glucocorticoids)
- any environmental factors are present that may be
involved in lesion development (contact with irritants, outdoor cats, fleas)
- the response to any previous treatments
- if there is a seasonality of the disease
- if there is any other abnormal symptoms (underlying internal diseases: Cushings syndrome, feline
pancreatic paraneoplastic alopecia, ...)
- if there is possible contagion to other pets or to humans
2) Physical examination
- aspect of alopecia: focal, diffuse or generalized
- localization of lesions
- aspect of hairs: broken or easily epilated
- presence of inflammation
- presence or primary lesions (pustules, papules,
erythema)
- complete physical examination
3) Establishing a differential diagnosis
The list of differential diagnoses should be organised so
that the most likely diagnoses comprise the top two or three
differentials.
4) Diagnostic procedures: in practice, the approach should
include consideration of costs and owners willingness to
countenance diagnostic tests. The diagnostic procedures (or
therapeutic recommendations) will be determined from the
differential diagnosis list.
routine examinations:
- microscopic examination of skin scrapings
- direct examination of hair shafts
- Wood lamp examination (+/- fungal culture)
- cytological evaluation of impression samples
second intention examinations:
- skin biopsies
- haematology, biochemistry (FeLV, FIV for cats)
- endocrine tests

C - Special considerations in cats


1) Focal feline alopecia
Main causes of focal feline alopecia are: dermatophytosis, parasitic diseases, fleas (FAD), post-injection alopecia.
These represent more than 90% of causes of feline focal
alopecia
history: main points
- way of life of the cat (contact with other cats, outdoor environment, stay in cattery, ...)
- contagion
- pruritus
- previous injections or vaccinations (especially
when alopecia is on the neck)
routine examinations:
- direct examination of hair shafts (broken or not),
Wood light
- presence of fleas or flea feces
- microscopic examination of skin scrapings

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- impression smear: eosinophilia, Malassezia, bacteria, acantholytic cells, abnormal cells


- fungal culture
others:
- elimination diet (especially when facial involvment
and pruritus are present)
- skin biopsies
- blood examination
aetiological treatment
2) Feline extensive alopecia (FEA)
First of all, excessive grooming must be proven (history
of self-licking, broken hairs). Main causes of FEA are: FAD,
dermatophytosis and psychogenic (stress and anxiety)
history:
- previous crisis and seasonality
- presence of fleas or possible contact with fleas
- general behaviour of the cat during consultation
(anxiety)
- contagion
look for classical causes
- direct examination of hair shafts (broken or not),
Wood light
- presence of fleas or flea feces
- fungal culture
flea control and short term antipruritic treatment
(prednisone or prednisolone 2 mg/kg/day 3 to 7 days
or chlorpheniramine 10 mg/cat/day 10-15 days)
if recurrency or no benefit (with good flea control):
- behaviour consultation or L-Deprenyl (1
mg/kg/day) or haloperidol (if lesions are lasting for
more than six months)
- or elimination diet (2 months) if possible
if there is no real behavior problem and no benefit of
the elimination diet
- try intradermal skin testing (but atopic dermatits is
not well defined and IDST are not standardized in
cats)
- try maintenance therapy: essential fatty acids supplementation, antihistamines (chlorpheniramine 510 mg/cat, oxatomide 1,5 mg/kg bid, amitriptyline
5 mg/cat bid), high quality diet, flea control. Elizabethan collar are of no use on a long term basis.

D - Canine symmetrical non pruritic


alopecia
Main causes of canine symmetrical non pruritic alopecia
are endocrine skin disorders; but before performing expensive tests, one must be sure of the endocrine origine of the
problem. For exemple, it is no use to perform endocrine tests
in a young blue Doberman Pinscher: microscopic direct examination of hair shafts or skin biopsies are mandatory, before assessing thyroid or adrenal status, because color dilution alopecia is very likely.
1) Diagnostic pathway
The diagnostic pathway of canine symmetrical non pruritic alopecia has to determine whether the skin condition is
associated with endocrine disturbance or not. We must think
about cost effectivness of our examinations.

history:
- breed, age, color of the coat: endocrine disorders
are common in older dogs, congenital or hereditary
problems and demodicosis in younger animals.
- evolution of alopecia, seasonality (recurrent flank
alopecia)
- general symptoms: polyuria, polydipsia, polyphagia,
general examination: pendulous abdomen, amyotrophy, enlarged lymph nodes (Leishmaniasis), enlarged
spleen, abnormal testis, feminization of male dogs, ...
dermatological examination
- aspect of hair shafts (broken or not), epilation, follicular casts (demodecosis, sebaceous adenitis)
- localization of lesions
- scaling, crusts, other lesions
- skin thickness (thin in Cushings disease)
routine examinations: skin scrapings, direct examination of hairs, impression smear
differential diagnosis: at this point one should be able
to decide if alopecia is of endocrine origine or not. If
there is a doubt, skin biopsies are mandatory, before
endocrine testing.
if it is an endocrine alopecia:
- non specific blood examinations: chol, SAP, ALT
(or more complete if possible)
- endocrine measurement is function of differential
diagnosis: ACTH stimulation test if elevated SAP
are present and if clinical aspect is suggestive of
Cushings disease (spontaneous or iatrogenic),
oestradiol measurement in a male dog with abnormal testis or feminization syndrome, basal TT4 or
FT4 (becareful of euthyroid sick syndrome)
- if normal: skin biopsies (if not done previously) to
rule out non endocrine alopecia
- other endocrine procedures: ACTH stimulation test
with measurement of adrenal sexual hormones
(progesterone, androstendione, ...); HCG stimulation test in male dogs; clonidine test with glycemia
measurements
- if everything is normal and the dog too: propose
neutering of a male dog; female dog: wait and see ...
2) Differential diagnosis
non endocrine non pruritic alopecia
- color dilution alopecia
- black hair follicular dysplasia

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- demodicosis
- dermatophytosis
- seasonal flank alopecia
- pattern baldness
- post-clipping alopecia
- sebaceous adenitis
- telogen and anagen effluvium
- superficial pemphigus
- alopecia areata
- leishmaniasis
- epidermotrophic lymphoma
- short hair syndrome of silky breeds
- congenital hypotrichosis
endocrine alopecia
- spontaneous hyperadrenocorticism
- iatrogenic Cushings disease
- hypothyroidism
- testicular neoplasia
- idiopathic feminization syndrome
- castration responsive alopecia of the male dog
- ovarian imbalance (neoplasia, cyst)
- hypogonadism
- primary adrenal sex hormone imbalance
- pituitary dwarfism
- GH responsive dermatosis (?)
3) General considerations about endocrine testing
analysis should be performed by a veterinary laboratory or by a human laboratory used to measure canine
hormones (with canine normal values which is rare)
samples must be collected and stored with caution
the clinician is the only person able to give a good interpretation of a result, based on clinical findings and
suspicion.
no one hormonal test is perfect: a normal ACTH stimulation test does not rule out hyperadrenocorticism,
low stimulation after TRH stimulation test is not diagnostic for hypothyroidism, abnormal UCCR may
be encontered in normal dogs, ...
most hormones interact with each other: main cause
of hypogonadism in adult male dogs is hyperadrenocorticism and hypothyroidism
be aware that many treatments or drugs can alter endocrine measurements: for exemple glucocorticoids
decrease basal FT4 and TT4 and decrease normal testicular response to HCG.

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33
Systemic antipruritic therapy
Dominique Heripret

While prescribing antipruritic therapy we must have in


mind animals health, owners compliance, diagnosis of the
dermatosis, toxicity of the drugs used and price of it, duration of treatment.
We must always privilege a specific treatment because in
most cases, antipruritic treatment will treat the pruritic crisis
but not the underlying cause.
Concepts of summation of itch and pruritic threshold are
important and complications or secondary dermatosis (pyoderma, Malassezia dermatitis, seborrhea, flea) must be
looked for and treated.

Glucocorticoids
They represent the treatment of choice of allergic or irritative pruritic crisis but their prescription must follow some
rules:
- diagnosis or suspicions must be compatible with glucocorticoid therapy.
- Pyoderma and/or Malassezia dermatitis must be treated
before using glucocorticoid.
- If possible, more harmless therapy should have been
tried.
- Use it for a short period of time to relieve animals pain
and owners impatience before other treatment procedure (antihistamines, flea control, immunotherapy,
elimination diet, ...) provides some improvement.
- Use it shortly at minimal effective dosage.
- In chronical prurit dermatosis, corticotherapy is only
palliative and not curative.
- Do not use reposital glucocorticoid (even, if possible,
in cat).
- If long term therapy is mandatory, use alternate day
protocol and add other drugs that may low down corticoid dosage (antihistamines, essential fatty acid,
topics ...) or duration of treatment.
- Secondary effects and contra-indications must be well
known.
The initial dosage (0,5-1 mg/kg/day of prednisolone in
dog and 2 mg/kg in cat) is given to release pruritus and then
is rapidly tappered at half dosage or less on an alternate day
basis if a long term therapy is needed.
In cat, dexamethasone may represent an alternative treatment (0,2-0,4 mg/kg/day).
NB: Megestrol acetate, a progestagen compound, is a

potent anti-inflammatory drug, but has stronger side effects


than glucocorticoids. We do not recommend their use, except, perhaps, for refractory indolent ulcers in cats.

Non steroidal antipruritic drugs


Because of a low rate of secondary effects, these drugs
(antihistamines, essential fatty acids, antidepressant drugs)
can be used in long term management of chronic pruritic
dermatosis especially in atopic dermatitis.
The main indications of these drugs are:
- atopic dermatitis unresponsive to immunotherapy or at
the beginning of immunotherapy.
- Acral lick dermatitis and obsessive-compulsive disorders
- Other behaviour dermatological troubles.
- When corticotherapy is contra-indicated (iatrogenic
hyperglucocorticoidsm, demodicosis, diabetes mellitus, ...).
In cases of flea allergy dermatitis or food allergy / intolerance, eviction of allergen is the treatment of choice.
Antihistamines
Only a few antihistamines have been realy studied in dog
and cat: there is no study on drug absorption and action on
histamine reaction except for ebastine and oxatomide and
there are only few papers with placebo control studies.
Many authors recommend to consider the efficacy of antihistamines on a 7 or 10 days basis: it seems strange because in atopic children, anti-H1 drugs are given for months
before judging the clinical efficacy; moreover, it is thought
that antihistamines have more protecting effects than curative ones. They are most likely to be effective when the skin
is minimally inflamed, so secondary pyoderma and
Malassezia dermatitis should be controled, and pruritus reduced by the use of a short corticotherapy or topical therapy.
For the moment, the use of antihistamines is largely empirical and each author has his preference based on his own
clinical experience.
Drugs more commonly used are:
- clemastine (0,05 mg/kg q12h);
- oxatomide (1,5 mg/kg q12h);
- chlorpheniramine (0,2-0,4 mg/kg q8h in dog, 4 mg/cat
q12h);
- diphenydramine (2 mg/kg q8h);
- hydroxyzine (2 mg/kg q8h);
- trimeprazine (1-2 mg/kg q12h);

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216

- others: terfenadine (5 mg/kg q12h), loratidine (10


mg/animal/day), ketotifen (0,2 mg/kg q24h), cetirizine
(10 mg/animal/day).
According to some authors, trimeprazine, terfenadine,
loratidine seem useless.
Essential Fatty Acid (EFA) supplementation
Metabolisation of EFAs allows formation of polyunsaturated essential fatty acids, eicosanoids (leukotrienes and
prostaglandines) precursors, that may interfer with the inflammatory pathway; they are believed to inhibit leukotriene
B4, a potent pro-inflammatory mediator.
The use of EFAs supplementation has shown his efficacy in reducing pruritus of allergic dogs and cats but many
things remain inconclusive: which fatty acid, whick combination of fatty acids, which ratio of amega-6 to omega-3 and
what dose has to be used?
Large doses of omega-3 fatty acids (7 times those usually given) effectively controlled pruritus in 30 to 60% of the
dogs. Maximal clinical results may only be seen after a long
period of time (6 to 12 weeks).
Just like antihistamines, ideal cases involve dogs with mild
inflammation or pruritus and no infectious complications.
For the moment, we know that the use of EFAs may be
beneficial and is harmless. We recommend to prescribe them
in addition to antihistamines (synergistic effects) and for
their significant steroid sparing effect during glucocorticoid
therapy.
Psychotropics agents as antipruritics
- Amitriptyline (1 mg/kg q12h in the dog, 5 mg/cat q24h)
and doxepine (1 mg/kg q8h) are antihistamines used as
tricyclic antidepressant agents in human. They are contra-indicated in epileptic patients and can induce cardiac arythmias. They are used in atopic dermatitis.
- Clomipramine (0,25 mg/kg q12h) is a tricyclic antidepressant used in obsessive-compulsive disorders in the
dog such as acral lick dermatitis.
- Fluoxetine hydrochloride is a serotonine uptake inhibitor that may be effective in atopic and acral lick
dermatitis (1 mg/kg q24h) without side effetcs.
- Naloxone (1 mg/kg subcutaneously) and naltrexone (2
mg/kg q12h), endorphins blockers, may improve feline
psychogenic alopecia and acral lick dermatitis but is
very expensive.

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- Haloperidol has prooved his efficacy (75%) in chronical feline psychogenic alopecia lasting for more than
six months (0,5 -1,25 mg/kg bid). Side effects may be
important (hallucinatory symptoms, insecure walking, ...) and hospitalisation is recommended at the beginning of therapy.

Adjunctive therapy
- Topical therapy: regular application of cleansing shampoos can reduce the bacterial load and keep the skin hydrated. Adjunction of colloidal oatmeal, which has a
specific anti-inflammatory effect for a few hours or
days, can be beneficial.
- Flea control: by the effect of summation of itch, a flea
infestation can push a patient over his pruritic threshold. A good flea control (fipronil for the dog or the cat,
lufenuron and insect growth regulator or chitin inhibitor for the premises) is mandatory.
- Diet: a nutritionaly balanced diet is recommended for
dogs with chronic pruritus. Omega-3 supplemented diet seems interesting.
- Systemic antibiotics: Staphylococcus intermedius can
induce pyoderma and pruritus, but can act as a superantigen in atopic dermatitis and even dogs with no evidence of secondary pyoderma may benefit from the use
of an effective systemic antibacterial agent.

Conclusion
Appropriate diagnosis is the corner stone of pruritic dermatitis treatment.
In chronical cases (especially atopic dermatitis), glucocorticoid is no longer the sole therapy for pruritus: they have
to be used on short periods of time, to relieve a pruritic crisis. However, the lack of standardisation of antihistamine or
EFAs use, means that treatment of chronical pruritus must be
adapted to each particular case. Combination of products
and good communication between owner and veterinarian
are essential in these cases.

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217

Identification of lesions (localization & diagnostics)


First part: Brain
Richard A. LeCouteur

Summary
This lecture will review the fundamentals of the organization of the nervous system and the relationship of structures within the nervous system to one another. An understanding of these relationships is essential for a clinician
dealing with nervous system disease. The overview of the
components of the nervous system begins at the highest level and descends to the lowest and it is hoped that it will provide a basis for understanding the mechanisms involved in
the production of clinical signs that appear during the
course of a neurological examination. The lecture will also
discuss the general characteristics and clinical signs of nervous system disease and localization of a lesion to the brain
and to areas within the brain. Diagnostic aids (e.g. CSF
analysis) and the various imaging techniques available to
diagnose brain disorders will also be discussed.

A. INTRODUCTION - AN OVERVIEW OF
THE NERVOUS SYSTEM
The fundamental structural units of the nervous system
are its cells (neurons and glia) and the fundamental functional units are the reflex arcs into which the neurons are organized. An understanding of the details of cellular, axonal,
and synaptic physiology is necessary to understand the
mechanisms by which these basic units operate and allow
the nervous system to accomplish its functions. One cannot
hope for true understanding of the function of this or any
other system without understanding the functions of its fundamental parts and their contribution to the function of the
total system.
In grappling with the mass of data and the concepts that
describe the roles of these fundamental units, it is easy to
lose sight of the organization of these units into larger units,
and the relationship of the larger units to one another and to
the system as a whole.
Understanding the organization and relationship of structures is essential for a clinician caring for animals with neurologic diseases because a clinician deals with the entire animal and with the entire nervous system. This requires a
global approach that is based on an appreciation of how the
functions of the various parts contribute to the function of
the whole. Normal functions must be known before abnormal functions can be recognized.

Abnormal functions must be recognized because neurological diseases are manifested clinically almost entirely by
dysfunction. It is uncommon for the clinical signs to include
readily detectable anatomical changes. Therefore, a clinician
must rely on signs of abnormal function to identify structures that are malfunctioning.
The nervous system lends itself readily to subdivision into major parts, each of which in turn is divisible into smaller parts. There are clinically detectable signs of normal and
abnormal function for each of the major parts and their principal subdivisions.
General divisions of the nervous system are: 1) brain, 2)
spinal cord, and 3) peripheral nerves. Note that peripheral
nerves form part of the motor unit (i.e. Iower motor neuron,
muscle fibers it innervates, and intervening neuromuscular
junctions). Each of these constitutes a higher level of function than the one that follows it, and each is divisible into
smaller units that have functional, and therefore clinical,
importance.
The highest functional subdivision of the brain, and
therefore the highest functional level of the nervous system,
is the cerebrum. The cerebrum is the seat of consciousness
and cognitive functions. It receives all sensory signals that
reach consciousness, makes decisions on the most appropriate response, and initiates that response if one is needed.
In most cases the response the cerebrum initiates is a
movement. This is called a voluntary movement. It is done
by muscles innervated by lower motor neurons of the spinal
cord or brain stem. The specific movement that is initiated is
a phasic (on again, off again) event that may consist of nothing more than movement at one joint of an extremity. However, no matter how simple such movements may be, they
require adjustments of other muscles so that opposing muscles relax or so that some joints are fixed while others are
moved, or so that weight bearing on the legs is adjusted to
accommodate shifts in the center of gravity.
The voluntary movement is initiated by the cerebral cortex and may be said to be an event of consciousness. The associated muscle activity is carried out subconsciously by
successively lower levels of the nervous system: basal nuclei, midbrain, pons and medulla, cerebellum, spinal cord
and brain stem, peripheral nerves and cranial nerves, and effector organ. The function of these lower levels is vital and
without them voluntary movements become impossible.
In ourselves, we are conscious of the effects of these subconscious operations but we are not conscious of the com-

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Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

218

plex neuronal transactions that produce them. These activities can be blocked normally only by very powerful cerebral
cortical override and then only incompletely in most cases.
Presumably animals also are not conscious of the functions
of these subcortical systems and presumably they might
have even less success in overriding them if they somehow
chose to do so.
Abnormalities of movement and posture produce the most
common neurological signs in animals. A very large proportion of these signs are caused by diseases that affect the subconscious events that occur in the many structures interposed
between the cerebral cortex and the lower motor neurons. Because of the importance of these functions and the structures
that produce them, recognizing signs of their dysfunction is
an essential feature of that part of the general physical examination that we call the neurological examination.
The following paragraphs attempt to provide an
overview of the nervous system as a basis for the global approach and understanding that is required for dealing with
neurological diseases. The overview simply provides a
sketch of the overall plan to help form a conceptual framework. It does not provide many of the details that are essential to interpreting the results of a neurological examination.

B. COMPONENTS OF THE NERVOUS


SYSTEM
The overview begins at the highest level and descends to
the lowest. It is hoped that this will provide a basis for understanding the mechanisms involved in the production of
the clinical signs that appear during the course of a neurological examination. The neurological examination actually
is conducted in somewhat the reverse order; that is, by beginning with the peripheral nerves and the reflex arcs. This
approach is used simply because the latter structures must be
functioning before one can determine the function of each of
the successively higher suprasegmental levels of organization. The truth of this last statement becomes evident if one
considers attempting a neurological examination on an animal paralyzed by curare.

Cerebrum
The cerebrum receives all forms of sensory signals. The
various types of stimuli can be classed in sensory channels: olfactory, visual, auditory, vestibular, and somatosensory. All of these channels reach consciousness. Olfaction
does so without passing through the thalamus but all of the
other channels reach the cerebrum after signal processing in
the thalamus.
A major function of the cerebral cortex is consciousness.
Consciousness can be defined as awareness of sensory stimulation. It is said that the cerebrum is responsible for the
content of consciousness while the reticular formation sets
the level of consciousness. This is true but it should not diminish the importance of the cerebrum in consciousness.
The cerebrum is the seat of consciousness and there can be
no real consciousness without it. The ascending reticular ac-

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tivating system (ARAS) acts to adjust the level of activity of


cerebral operations of consciousness but the ARAS does not
itself enter into these operations.
The various sensory channels tend to reach specific areas
of the cerebral cortex. The most important areas clinically
are the visual areas in the occipital regions, the auditory areas in the temporal regions, and the somatosensory areas in
the frontoparietal regions. Much of the remaining cortex is
association cortex.
Information arriving in sensory channels is received and
processed by the specific cortical areas and relayed to the association cortex. Cognition and decision making are functions of the association cortex.
If a decision is made to move, the association cortex is
involved in planning the movement and initiating it. It
brings about the movement by signaling the basal nuclei.
The latter then process these signals and in turn signal the
motor cortex (cruciate region) for execution of the movement (corticospinal tract), and the brain stem and cerebellum
for initiation of the necessary associated muscle activity that
shapes the body and limbs into a base for movement.
Clinical signs of cerebral cortical disease can include: a)
disturbances of consciousness, b) paresis of voluntary movement, c) disturbances of all types of sensory function, and d)
seizures.

Basal nuclei
The basal nuclei are intimately related to movements initiated by the cerebral cortex. They are involved in the details
of programming the movement, whereas the cortex as a command center merely plans and initiates the movement. To
complete this activity the basal nuclei receive input from the
association cortex and send signals to motor cortex and brain
stem. The latter structures then signal the lower motor neurons
via the corticospinal tracts and other descending pathways.
Some of the basal nuclei have an inhibitory effect on the
pathways involved in voluntary movement. When these are
affected by disease, involuntary movements can occur during rest and there is a tendency for dystonia (hypo- or hypertonia). These disorders are most severe in muscles that
are most important in voluntary movement and fine manipulation (e.g. the prehensile muscles).
Some basal nuclei disorders produce difficulty in the initiation of voluntary movement. Large unilateral basal nuclei
lesions produce circling.

Midbrain locomotor centers


Areas in the midbrain and subthalamus contain locomotor regions that are important in triggering locomotion, in
setting the rate and strength of locomotor movements, and in
coordinating respiratory movements with locomotor movements. They operate on the flexion and extension mechanisms of the spinal cord through the reticulospinal pathways.
Clinical signs caused by lesions in these structures are not
well described.

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The cerebellum acts to coordinate all of the subsystems


that operate in locomotion and posture. In keeping with
this, it receives afferents from the cerebral cortex, the basal
nuclei, the vestibular system, the spinal cord, and the reticular formation, and it has efferent connections with all of
these systems. It is important to realize that the cerebellum
has no direct connection with the lower motor neurons. Its
powerful influence on posture and locomotion is brought
about indirectly through its effects on the cerebral and brain
stem structures that produce movement. It is important also to remember that the cerebellum does not initiate movements, but instead coordinates movements that are initiated
elsewhere.
The clinical signs of cerebellar disease reflect its coordinating functions. Thus, the dysmetria of a cerebellar ataxia
reflects loss of the cerebellar influence on phasic movements
of the extremities. The disequilibrium reflects the failure of
the cerebellum to coordinate the vestibular system with the
brain stem and spinal cord systems that maintain equilibrium during the continuously shifting needs of voluntary
movement. Note that neither of these signs of cerebellar disease is present at rest when there is no demand for coordination.
The cerebellum also participates in the coordination of
eye positions and eye movements that occur in response to
vestibular stimulation. The tonic deviations of the eyes and
head and the positional nystagmus that occur in cerebellar
disease reflect disturbances of these functions of the cerebellum.

Medulla and pons


Structures in the medulla and pons have major influences
on the tone of antigravity muscles, thus serving to adjust
weight bearing to compensate for shifts in the center of gravity. They receive afferents from the labyrinths and the spinal
cord and they act on lower motor neurons through vestibulo- and reticulospinal tracts.
These structures also have a very major influence on the
maintenance of the visual axis parallel with the horizon and
fixing the eyes on a target during movements of the head.
Lesions affecting these systems cause disturbances of righting, abnormalities of muscle tone in the limbs, head tilt, and
nystagmus.

reflexes. These signs may be indistinguishable from those


caused by lesions of the peripheral nervous system.

C. GENERAL CHARACTERISTICS
OF NEUROLOGIC DISEASES
Neurologic disease can be acute or chronic, progressive
or nonprogressive. Neurologic signs reflect only the location
of the lesion(s), not the cause. Neurologic diseases can
sometimes cause intermittent signs (as in the case of epilepsy); some peripheral nerve or neuromuscular disease and
some myopathies cause signs that fluctuate in severity from
moment to moment or hour to hour or that vary in severity
with exercise. Aside from these exceptions, the signs of neurologic diseases tend to be continuous and fluctuate very little in severity.
The clinical signs of neurologic disease are caused by
dysfunction of the neurons. The neuronal dysfunction can be
caused by direct effects of the disease on the neurons or by
the effects of the disease on the supporting elements (glia) or
blood vessels.
Neurologic diseases may result from causes inside the
nervous system or outside the nervous system. The causes
include any of the things that cause diseases in other organ
systems.

D. CONCEPTS OF BRAIN LOCALIZATION


The neurological examination provides the examiner with
a list of clinical neurological abnormalities. These abnormalities reflect dysfunction of a part (or parts) of the nervous system. The examiner is able to attribute observed abnormalities
to dysfunction of the appropriate part (or parts) of the nervous system because normal function of these areas is
known. When localizing abnormalities to the brain, it is convenient to use the concept of neurological syndromes. The
basis of this concept is that a specific group of clinical signs
is representative of dysfunction of a specific area of the nervous system. Once a group of clinical signs (or a syndrome)
is recognized, and the affected area of the brain identified,
then a list of possible causes may be completed. Braund has
described this approach in detail in a recent textbook.

E. EXAMPLES OF BRAIN LOCALIZATION


Cerebellar syndrome

Spinal cord
The spinal cord contains neuronal mechanisms that can
produce stepping movements (alternating flexion and extension of the joints of the limb). The supraspinal mechanisms
described above end on these mechanisms and shape or
mold them according to the needs of the movement by acting directly on primary afferents, interneurons, gamma efferents, or alpha efferents. Disorders of the descending pathways produce paralysis or paresis, and exaggerated reflexes.
Disorders of the segmental cells produce depression of

Clinical signs that are seen with lesions involving the


cerebellum are as follows:
Hypermetric gait, especially in thoracic limbs, with
normal strength
Truncal ataxia
Intention tremors of the head
Wide-based stance
Exaggerated postural reactions
Ipsilateral menace deficit (with normal vision)
Anisocoria (contralateral pupil dilated)

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Cerebellum

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4th European FECAVA SCIVAC Congress

Decerebellate posture (rare)


Vestibular signs (rare).

Vestibular syndrome
Vestibular syndrome is frequently recognized in clinical
practice. Signs of vestibular dysfunction may reflect either
central (within medulla) or peripheral (vestibular portion of
VIII, or vestibular receptors in petrosal portion of temporal
bone) involvement. Clinical signs of vestibular dysfunction
are as follows:
Loss of balance
Head tilt
Falling/rolling
Nystagmus (horizontal, rotatory, vertical, positional)
Strabismus (ventrolateral)
(Possible) V, VI, or VII deficits
(Possible) Horners syndrome
(Possible) cerebellar signs
(Possible) mental depression
(Possible) hemiparesis with ipsilateral postural reaction
deficits.

Cerebral syndrome
Cerebral syndrome is characterized by the following
clinical abnormalities:
Seizures
Altered mental status
Change in behavior
Abnormal movement and postures (pacing, compulsive walking, circling, head pressing)
Postural reaction deficits in contralateral limbs
Visual impairment with normal pupillary light reflexes
(Possible) papilledema
(Possible) abnormal (irregular) respiration.

Midbrain syndrome
Clinical signs associated with midbrain syndrome are as
follows:
Paresis of all four limbs or the limbs on the side of the
body contralateral to the lesion
Exaggerated segmental reflexes and muscle tone in
limbs on the side contralateral to the lesion, or in all
four limbs (opisthotonos)
Postural reaction deficits in contralateral limbs, or in
all limbs
Obtundation or coma
Ipsilateral deficits of III (ventrolateral strabismus, dilated pupil unresponsive to light with normal vision,
ptosis)
Altered respiration (hyperventilation)
(Possible) bilateral miosis.

Hypothalamic syndrome
This syndrome is most often associated with pituitary tumors of dogs and cats. The hypothalamus regulates much of
the bodys endocrine activity, and is involved in autonomic
visceral body functions. Abnormalities of this area results in
the following signs of dysfunction:
Abnormal mental status
Changes in behavior (hyperexcitability, aggression)
Abnormal postures and movement (trembling, pacing,
wandering, tight circling, head pressing)
Bilateral II deficits (dilated pupils, depressed pupillary
light reflexes, visual impairment)
Abnormal temperature regulation
Abnormal appetite
Endocrine disturbances (diabetes insipidus, diabetes
mellitus, hyperadrenocorticism, acromegaly)
Seizures.

Multifocal syndrome
Pontomedullary syndrome
Clinical signs that are associated with dysfunction of this
area of the brain are as follows:
Paresis of all four limbs (tetraparesis) or of limbs on
the same side of the body (hemiparesis).
Normal to increased muscle tone and segmental reflexes in all limbs.
Postural reaction deficits in the limbs on the same side
as a lesion, or in all limbs.
Cranial nerve deficits:
Depressed palpebral reflex (V, VII)
Decreased facial sensation (V)
Paresis/paralysis of the jaw (V)
Facial paresis/paralysis (VII)
Head tilt, nystagmus, falling, rolling (VIII)
Laryngeal/pharyngeal paresis/paralysis (IX, X)
Tongue paresis/paralysis (XII)
Abnormal respiration
Mental depression.

Occasionally an animal may have clinical signs that reflect two or more different syndromes. This indicates that
more than one lesion site may be present, and is termed a
multifocal syndrome.

F. DIAGNOSTIC AIDS IN BRAIN DISORDERS


Although it is possible to localize a problem to the brain
and sometimes to the approximate location within the brain,
on the basis of signalment, history, and the results of physical and neurologic examinations, it must be remembered
that these signs may be the same regardless of the underlying cause. Brain tumors, infections, congenital disorders,
trauma, vascular disorders, degeneration, immunologic and
metabolic disorders, toxicities, and idiopathic disorders may
result in similar clinical signs. For this reason it is essential
to follow a logical diagnostic plan for a cat or dog with signs
of brain dysfunction.

4th European FECAVA SCIVAC Congress

Cerebrospinal fluid analysis


Analysis of cerebrospinal fluid (CSF) is recommended
as an aid in the diagnosis of a brain tumor. The results of
CSF analysis may help to rule out inflammatory causes of
cerebral dysfunction, and in some cases may support a diagnosis of a brain tumor. CSF bathes the entire CNS, both internally (the ventricles and central canal) and externally (the
subarachnoid space). CSF composition may be affected by
many nervous system diseases and the ease with which this
fluid may be collected has made it an important diagnostic
tool in the diagnosis of CNS disease. Unfortunately, for cells
to be shed into the CSF a disease must involve the ventricular system or the subarachnoid space. Disorders involving
deeper brain structures (e.g. neoplasms) may not shed cells
into the CSF. Frequently these diseases disrupt the bloodbrain barrier (BBB) allowing protein to leak into the CSF
and resulting in an increased protein level. CSF must be
evaluated keeping in mind history and clinical signs. Neoplasms and some other non-inflammatory diseases may result in inflammatory changes in CSF composition. CSF
composition may also change as a disease becomes more
chronic. Also, following various therapies CSF may no
longer accurately reflect an etiology.
Care should be used in the collection of CSF, because
frequently an increased intracranial pressure (ICP) may be
present in association with a brain tumor, and pressure alterations associated with CSF removal may allow brain herniation. Because CSF pressure measurements are of limited
usefulness, it is often desirable to utilize techniques such as
hyperventilation to decrease intracranial pressure prior to
CSF collection.
CSF may be collected at either the cerebellomedullary
cistern or by lumbar puncture. In general the cerebellomedullary cistern is easier to find, allows collection of a
larger volume and generally has less blood contamination.
All patients undergoing CSF collection should be anesthetized appropriately. If it is suspected that intracranial
pressure is elevated the patient should be hyperventilated for
several minutes prior to collection as well as during and after collection in order to decrease arterial CO2 and intracranial pressure. Complications of CSF collection include needle injury to the brain and herniation of the brain, usually
due to high intracranial pressure. Both these complication

may be fatal if appropriate steps to reduce intracranial pressure (hyperventilation and mannitol administration) are not
instituted immediately.

Cerebrospinal fluid collection


For CSF collection from the cerebellomedullary cistern,
a 20- or 22-gauge 1.5 inch (3.5 cm) spinal needle and a sterile container in which to collect fluid are needed. The hair
over the area should be clipped and the skin prepared as for
a sterile procedure. The patient is placed in lateral recumbency with the head parallel to the table and an assistant
must hold the head flexed at 90o to the long axis of the body.
A line drawn down the middle of the patients face and nose
should be parallel to the table. These patients should be intubated to prevent airway obstruction.
The landmarks for cisternal CSF collection are the wings
of C1 and the occipital protuberance. The needle should be
inserted where the line from the occipital protuberance (the
midline) intersects a line drawn between the two wings of
C1. The needle bevel should face cranially and the needle
should be advanced slowly keeping it perpendicular to the
long axis of the spine. A sudden loss of resistance may be
felt as it enters the subarachnoid space and at that time the
stylet should be removed in order for CSF to flow. Care must
always be taken to prevent accidental needle movement and
the needle should be held firmly with the thumb & forefinger each time the stylet is removed or replaced. In very small
animals the fluid volume available may be very small and
may take 30-45 seconds to appear in the hub of the needle.
If no fluid appears the stylet may be replaced and the needle
advanced further. If bone is encountered then the needle tip
should be redirected. Failure to find the space is usually due
to poor patient positioning, (most often insufficient flexing
of the neck or the patients nose sloping downwards towards
the table) or not being on the midline with needle placement.
If the cisternal space can not be found the needle should
be removed and the entire procedure repeated. If CSF flow is
very slow, carefully occluding the jugular veins will increase
CSF pressure and flow. Apnea or changes in respiratory rate
not associated with anesthetic depth usually indicate brain
herniation or damage. The needle should be immediately
withdrawn, anesthesia discontinued and the patient hyperventilated until consciousness and normal respiration return.
If the patient does not respond within 5 to 10 minutes to these
maneuvers then mannitol should be administered.
Once CSF begins to flow it should be allowed to drip
freely into the container and at least one milliliter collected.
If fluid needs to be stored for any length of time prior to cell
analysis then it should be stored in a plastic container and refrigerated to stop cellular degeneration.

Cerebrospinal fluid analysis


Always note from where the CSF was collected. CSF
from the cisternal space has a lower protein than fluid from
the lumbar space. Analysis should include gross visual examination, cytologic analysis, protein measurement and pos-

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Following a complete physical and neurologic examination, a minimum data base for an animal with signs of brain
dysfunction should include a hemogram, serum chemistry
panel, and urinalysis. Survey thoracic and abdominal radiographs help to rule out problems elsewhere. The major objective in doing these tests is to rule out disease elsewhere as
a cause of the signs of cerebral dysfunction.
Plain skull radiographs are useful for detecting problems
of the skull or nasal cavity which have extended to the brain.
Occasionally, lysis or hyperostosis of the skull may accompany a primary brain tumor (e.g. meningioma of cats) or
there may be mineralization of a neoplasm. Skull radiographs are of little value in detecting dysfunction with the
brain.

221

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sibly fluid culture.


Normal CSF should appear clear and colorless. Turbidity may indicate increased white cell numbers and/or protein
elevation. A pink color to the fluid may be due to blood contamination. Persistence of this color change after centrifugation of a small amount of sample may indicate the presence
of free hemoglobin, suggesting previous subarachnoid hemorrhage, rather than sample contamination. Xanthochromia
develops if more than 48 hours have elapsed following hemorrhage.
Cytological preparation should be completed as soon as
possible (within 30 minutes of collection), since CSF cells
undergo degeneration rapidly. WBCs degrade faster than
RBCs in the CSF, making interpretation difficult. Refrigeration does help to slow WBC lysis. The cytologic evaluation
should begin with a total cell count on the unconcentrated
fluid. A slide should then be prepared of concentrated fluid
for evaluation of cell morphology and differential cell
counts. The two most common slide preparation techniques
are cytocentrifugation and sedimentation. The sedimentation
technique is easy and reliable and may preserve cell architecture better than centrifugation methods.
In normal CSF there should be less than 5 WBC/ul. Cell
numbers may increase most commonly with inflammatory
disease but also with tumors, necrosis, trauma, and vascular
injury. The type and number of cells may reflect the cause of
the inflammation. Again CSF is most accurate in acute, untreated illnesses. Correcting the number of WBCs in the CSF
for blood contamination is possible only with very mild contamination. The WBC numbers in the CSF increase approximately 1 WBC/ul for each 500 to 700 RBCs/ul.
A predominance of polymorphonuclear leukocytes in
CSF may indicate a suppurative meningitis probably due to
bacterial infection or to severe viral encephalitis. The presence of multiple cell types in CSF, including macrophages,
lymphocytes, neutrophils and sometimes plasma cells is
generally the result of a granulomatous inflammation, such
as occurs with fungal, protozoal, and some idiopathic diseases. Mixed cell populations may also be seen with inadequately treated chronic bacterial infections and in response
to foreign bodies. A nonsuppurative inflammation is diagnosed if the increased cell numbers are primarily mononuclear cells, especially lymphocytes. It is most characteristic
of viral and rickettsial infections, although it can also be
seen with neoplasms.
CSF should be submitted for both aerobic and anaerobic
bacterial culture and antibiotic sensitivity testing whenever
abnormalities consistent with meningitis are found. Negative cultures are common even when bacterial or fungal organisms can be seen. Culturing the sedimented or centrifuged CSF may increase the likelihood of obtaining positive CSF culture. Causative organisms may also be isolated
form the blood of animals with systemic infections. It is recommended that a large volume of CSF, preferably 2 or 3 ml,
be collected for bacterial and/or fungal culture. Serology
may also be useful in diagnosis of CNS fungal infections.
In normal cerebellomedullary CSF, protein is less than
25 mg/dl and less than 45 mg/dl with lumbar puncture. Since
storage of CSF does not affect protein it can be sent to an
outside laboratory for protein evaluation. CSF protein is el-

4th European FECAVA SCIVAC Congress

evated with many diseases including encephalitis, meningitis, neoplasms, trauma and infarcts. Over 75% of CSF protein should be albumin. With noninflammatory disruption of
the blood-brain-barrier, (e.g. neoplasm and infarcts), most
CSF protein will be albumin, whereas with increased intrathecal production (e.g. encephalitis) it is predominantly
globulin. Where both albumin and globulin are elevated an
inflammatory process affecting both the meninges and the
CNS (e.g. FIP) should be suspected. Corticosteroid-responsive meningitis (aseptic meningitis) occurs in young dogs
and may be the most frequently occurring form of meningitis in dogs. The diagnosis is made on the basis of increased
white cells and protein in the CSF, failure to isolate an infectious agent from CSF and response to therapy with corticosteroids. It may be difficult to distinguish this disease
form GME on the basis of CSF analysis.
In general, increased CSF protein content and a normal
to increased CSF white blood cell count have been considered typical of a brain neoplasm. In one study, only 39.6%
of dogs with a primary brain tumor exhibited typical CSF
alterations. The results of CSF analysis were normal in 10%
of the dogs in this study, while the remaining 50.4% of dogs
had a variety of nonspecific CSF changes. The CSF from
dogs with a meningioma often may have an elevated white
blood cell count (> 50/ul), with more than 50% of these cells
being polymorphonuclear leukocytes. In another study, glial
cell tumors predominated among those that resulted in CNS
inflammation. Neoplastic cells may be present in CSF, particularly when sedimentation techniques are used for analysis. The use of CSF protein electrophoresis, and IgG index
of CSF, may aid in the determination of the presence of a
brain neoplasm. Little information is available regarding
CSF alterations seen in association with feline brain tumors;
however, changes are similar to those described for dogs.

Imaging
Skull radiographs are useful in patients with suspected
bony or cartilaginous changes (e.g. head trauma, bony tumors), but in general plain skull films are of limited value in
patients with brain disease. Angiography and venography
are amongst the techniques used in the past to try to diagnose brain disorders. These techniques have severe limitations and in most instances fail to define the exact extent of
a neoplasm and its precise relationship to surrounding structures. These techniques have now been replaced with computed tomography (CT) and magnetic resonance imaging
(MRI).

CT and MRI
CT and MRI allow imaging of brain tissue rather than
just the surrounding bony skull. Both can distinguish images
which have only slightly different densities than the surrounding tissues and this can be further enhanced by contrast agents allowing the identification of masses and other
abnormal tissues within the brain. Images obtained by
means of MRI may be superior to those of CT especially in

4th European FECAVA SCIVAC Congress

At the present time, biopsy is the sole method available


for the diagnosis of brain tumor type in cats or dogs. Several biopsy methods have been described, including ultrasound-guided biopsy, and CT-guided biopsy. Ideally, an intracranial lesion should be biopsied prior to the institution of
therapy of any type; however, biopsy is not always attempted because of practical considerations, such as cost and
morbidity.

References for clinical syndromes


Braund KG. Clinical Syndromes in Veterinary Neurology. Second edition.
Mosby - Year Book Inc., Philadelphia, 1994.

MAIN PROGRAMME

certain areas such as the brain stem, although CT is usually


better for bony lesions (e.g. middle ear studies). While the
major tumor types are reported to have characteristic CT or
MRI appearances, non-neoplastic lesions may mimic the CT
or MRI appearance of a neoplasm, and occasionally a
metastasis may resemble a primary brain tumor on CT or
MRI images.
Patients for either CT or MRI must be anesthetized, intubated, and hyperventilated whenever an increase in ICP is
even suspected. Proper patient positioning is extremely important. The animals should be placed in sternal recumbency with the head extended. The entire calvaria should be examined in the non contrast series of images. This should be
followed by a post contrast series of images.

223

4th European FECAVA SCIVAC Congress

225

Identification of lesions (localization & diagnostics)


Third part: Neuromuscular
Richard A. LeCouteur

Summary
Some expression of generalized or localized muscular
weakness is the principal clinical sign of neuromuscular
dysfunction. Neuromuscular diseases are disorders of the
motor unit, which is composed of 1) the motoneuron 2) the
neuromuscular junctions, and 3) the myofibers innervated
by the motoneuron. Based on these anatomic motor unit
components, neuromuscular diseases are broadly subdivided into a) neuropathies, b) junctionopathies, c) myopathies,
and d) neuromyopathies. This lecture will discuss dysfunction of the motor unit and the resulting variation in clinical
signs that may occur. Functional manifestations of neuromuscular weakness may include paresis/paralysis, gait abnormalities, exercise related weakness, dysphagia, regurgitation, and dyspnea. Physical manifestations may include
muscle atrophy, hypertrophy, and skeletal deformities. The
localization and diagnosis of lesions in these areas will be
covered in this lecture.

A. INTRODUCTION
Neuromuscular diseases are disorders of the motor unit the basic functional and anatomical organization of neurons
and muscle fibers. The essential components of each motor
unit include: 1) a motor neuron consisting of its cell body
(located within the CNS, either in the cranial nerve nuclei of
the brainstem, or in the ventral horns of grey matter in the
spinal cord) and its peripheral axon, supported by Schwann
cells, 2) neuromuscular junctions, and 3) the myofibers innervated by the motoneuron.
The arrival of impulses at the axon terminal causes a calcium-dependent release of acetylcholine (ACh) from the
presynaptic axon terminals. This liberated ACh diffuses
across the synaptic cleft to become complexed with specific
ACh-receptor sites located on the postsynaptic sarcolemma
(end-plate) of the myofiber. The formation of ACh-receptor
complexes increases the permeability of the end-plate to Na+
and K+ ions and results in a local depolarization of the endplate, which in turn generates muscle action potentials over
the entire sarcolemmal surface of each myofiber to initiate
their contraction.
The action of ACh is reversed by its diffusion away
from ACh-receptor sites and its hydrolysis by acetylcholinesterase (AChE) present in the synaptic cleft. The

contraction of each myofiber involves the interaction (sliding) of the actin and myosin myofilaments coupled with the
hydrolysis of ATP. The interaction of the actin and myosin
myofilaments is modulated by the regulatory proteins troponin and tropomyosin, and the rate of their interaction
(speed of shortening) is catalyzed by the activity of myosin
ATP-ase.
All motor units are not alike and may vary with regard
to: 1) size (the number of myofibers innervated by a single
motoneuron), 2) histochemical properties of the myofibers,
and 3) functional properties related to their speed of contraction and resistance to fatigue. There are at least three and
possibly five basic types of motor units based on their contractile and histochemical properties. The myofiber type
composition of motor units is homogeneous. Each motor
unit is composed of a single histochemical myofiber type,
and not a mixture of myofiber types. Individual muscles are
usually composed of a mixture of motor unit (myofiber)
types, and the relative proportions of each may vary considerably between muscles. Individual myofibers of each motor
unit are uniformly distributed throughout a relatively large
area in a muscle and myofibers of the same motor unit are
rarely contiguous. This scattered distribution results in a mosaic pattern of myofiber types within transversely sectioned
and stained muscles.
For a given muscle within the same species, the myofiber
type composition, and mosaic distribution pattern within a
muscle, appears to be reasonably constant and characteristic
for that muscle.

B. CLASSIFICATION
OF NEUROMUSCULAR DISORDERS
A useful classification scheme of neuromuscular disease
is based on the anatomic motor unit components which are
primarily involved in the pathogenesis of the muscle weakness. Using this classification neuromuscular diseases are
broadly subdivided into:
1. Neuropathies - disorders of the neuron, its cell body,
axon, and/or Schwann cells (myelin)
2. Junctionopathies - disorders of the neuromuscular
junction
3. Myopathies - disorders of the muscle fiber
4. Neuromyopathies - disorders of both the neurons and
muscle fibers.

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VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN


Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

226

C. CLINICAL SIGNS
OF NEUROMUSCULAR DISORDERS
Dysfunction of the motor unit results in lower motor
neuron signs, seen clinically as muscle weakness. The expression of this weakness may vary considerably, and may
include: paresis/paralysis, gait abnormalities, exercise related weakness, dysphagia, regurgitation, dyspnea, and dysphonia. The distribution of involvement may be local, regional, or generalized. In addition there may be gross deformities of muscle mass (i.e., atrophy, hypertrophy, and skeletal deformities). Any patient presented with some form of
clinical weakness, should be viewed as potentially having a
motor unit disorder. Conclusions that the patient is merely
weak because it is sick should not be readily assumed without meticulous evaluations of the motor unit.

D. DIAGNOSIS OF NEUROMUSCULAR
DISORDERS
Establishing a diagnosis requires an informed and coordinated approach to defining a problem list through associations and direct observations (ie. a diagnostic plan). Since
the signs of neuromuscular disease will be the same regardless of the lesion location (i.e. neuropathy, junctionopathy,
or myopathy), additional diagnostic tests are needed to confirm the anatomic location.
1. Signalment, History, Physical and Neurologic Examinations
Signalment: species, breed, age, sex, use
History: congenital/acquired, course of complaint, response to treatment, exposure to toxins, etc.
Findings: presence and distribution of abnormal findings
on physical and neurologic examinations
2. Minimum Data Base
Minimum data base: CBC, biochemistry panel, urinalysis, thoracic radiographs, and abdominal ultrasound.
Measurement of muscle specific serum enzymes such as
creatine kinase (CK,) as well as aspartate aminotransferase
(AST), and lactic dehydrogenase (LDH), are very helpful in
identifying neuromuscular disorders in which myonecrosis
is a principal pathologic feature. Elevated serum enzyme activities help to differentiate myopathies from other neuromuscular disorders. Also immunologic procedures for the
detection of myoglobin are becoming available, and should
be a sensitive means of detecting myolysis as well.
3. Specific Diagnostic Tests
a. Electromyography (EMG) - involves the detection and
characterization of electrical activity (potentials) recorded
from the patients muscles. A systematic study of individual
muscles permits an accurate determination of the distribution of affected muscles. EMG electrodes detect potentials,
which are then amplified and displayed on an oscilloscope
and a printed record. Potentials are also amplified through
an audio amplifier to record sounds, which often have frequencies and amplitudes characteristic of certain disorders.
In animals, EMG examinations usually are conducted
with the muscles at rest, (i.e., not contracting) and usually
under general anesthesia. Under these conditions, resting po-

4th European FECAVA SCIVAC Congress

tentials across muscle fiber membranes are maintained, and


hence, normal muscles are electrically silent.
With depolarization of muscle fiber membranes, potentials are generated that have a wave form usually consisting
of negative and positive phases. The potentials generated are
evaluated for amplitude, duration, number of phases and polarity, frequency and repetition.
i) Insertional activity - brief bursts of electrical activity
(potential charges) are induced by irritation of single muscle
fibers caused by insertion of the EMG needles. After insertion and cessation of needle movement, normal muscles become electrically silent. Increased insertional activity (an increase in amplitude and prolonged duration) may be observed in neuromuscular diseases. Affected muscle fibers
are hyperexcitable, having a lowered threshold due to diminished membrane potentials.
ii) Spontaneous activity - is the spontaneous generation
of potentials that are independent of mechanical stimulation.
Spontaneous activity is an abnormal finding. The potentials
generated include muscle action potentials generated by individual fibers (fibrillation potentials and positive sharp
waves), and motor unit potentials generated by fibers of a
motor unit (fasciculation potentials).
Pronounced and prolonged spontaneous activity may be
encountered in which there are repetitive, high frequency
potentials generated with needle insertion, or other mechanical stimulation of muscle such as percussion. In myotonia,
a condition of delayed relaxation of muscle fibers, there are
phases of increasing amplitudes and frequencies of discharges, followed by decreasing amplitudes and frequencies,
which convey the sound of diving propeller driven airplanes.
These so-called dive bomber potentials, are also referred
to as myotonic potentials.
When the tip of the EMG needle is placed near the endplate region, spontaneous small amplitude (miniature) endplate potentials (mepps) may be detected. These are normal
potentials due to the spontaneous release of individual quanta
of ACh. This activity is also referred to as end-plate noise.
b. Motor Nerve Conduction Velocity - provides information about the integrity of nerve fibers in peripheral nerves.
Recordings are conducted while the patient in anesthetized.
Demyelinating disorders cause slowed conduction in peripheral nerves. Ulnar and sciatic (perineal-tibial) nerves are
most often employed for evaluation.
c. Evoked Potential Recordings - with repetitive nerve
stimulation provides information about the integrity of neuromuscular transmission.
d. Nerve and Muscle Biopsy Examination. These procedures provide an opportunity to evaluate the morphology of
portions of the motor unit and differentiate between neuropathies, junctionopathies, and myopathies, and in some instances, provides a definitive diagnosis. Since general anesthesia is required for EMG examination and nerve conduction
measurements, muscle biopsy procedures should be done at
the same time so that a second anesthetic is not needed.
Selection of Muscle/Nerve Biopsy. EMG examination
aids in identifying affected muscles/nerves for biopsy. Select
involved, but not end-stage muscle for biopsy. Knowledge
of normal muscle fiber type composition for muscles and
species is required for biopsy interpretation.

Biopsy Procedures. Special methods of handling and


processing are required for proper evaluation of muscle and
nerve biopsies. Fresh frozen sections and special staining
techniques are essential for light microscopic studies of both
muscle and nerve. In addition, special fixatives are required
for electron microscopic studies of muscle as well as
teased nerve fiber studies. Use of formalin fixation of
specimens is of limited value. Open biopsy techniques are
preferred in small animals and punch biopsy techniques
are preferred in horses.

E. HISTOPATHOLOGIC FEATURES
OF NEUROPATHIES
1. General Features
a. Angular Atrophy. The histopathologic hallmark of
denervation is a characteristic patterns of myofiber atrophy.
Myonecrosis is an uncommon reaction to denervation. With
minimal denervation in which only a few myofibers are denervated, the denervated myofibers undergo atrophy and
these atrophied myofibers tend to be angular in appearance.
These angular atrophied type 1 and type 2 myofibers (angular atrophy points to denervation) tend to be scattered
throughout the section and they are present in many fasciculi. This sign of denervation takes several weeks to develop after the denervating event.
The angular morphology develops as a consequence of
fiber atrophy occurring between normal or hypertrophied
fibers. With greater involvement and progressive course, the
angular atrophied fibers become more numerous and tend to
occur in small groups (small grouped atrophy). As denervation progresses, healthy muscle fibers undergo compensatory hypertrophy. As a result, biopsies contain a mixture of
very small and very large fibers.
When most or all fibers in a muscle are denervated at
about the same time (e.g., trauma to a muscles nerve, avulsions, acute severe disorders such as coonhound paralysis), all fibers undergo atrophy (panatrophy) and the angular morphology does not develop. Instead the fibers have a
more uniform puckered or scalloped appearance (large
grouped atrophy).
b. Differentiation of Neurogenic Atrophy from Other
Types of Myofiber Atrophy. Atrophy of muscle fibers is a
common, though non-specific, reaction to a variety of disease states and activity levels. As previously described,
when myofiber atrophy is selective, fibers undergoing atrophy may be angular to anguloid in appearance, while in nonselective atrophy involving all/most fibers, myofibers tend
to be more rounded to polygonal in shape.
(i) Cachetic/Disuse Atrophy - tends to affect all fiber
types resulting in a rather uniform decrease in fiber size of
most fibers; however, quantitative data suggest that type 2
fibers are proportionally more affected.
(ii) Fractures/Tenotomy - shortening of a muscles resting length, secondary to trauma results in selective/preferential atrophy of type 1 fibers.
(iii) Type 2 fiber atrophy - selective type 2 fiber atrophy
which may be angular develops secondarily in the presence
of excess glucocorticoids. The condition is frequently re-

227

ferred to as steroid myopathy. This change has been seen in


patients with Cushings Disease and patients receiving longterm steroid medication for other disorders. Grossly, muscle
atrophy may become severe, particularly the muscles of
mastication in the dog, and result in profound weakness.
c. Pyknotic nuclear clumps - represent the end-stage of
denervation and develop if denervated fibers are not reinnervated. These result from a drastic loss of myofibrils with
clumps of myonuclei enclosed within the sarcolemma. A
chronic change which takes some months to develop.
d. Myofiber type grouping - results when previously denervated muscle fibers are reinnervated. If the new axon is of
a different motor unit type than the denervated fiber, the
reinnervated fiber will assume the characteristics of the new
motor unit (e.g., denervated fast-twitch, type 2 fibers reinnervated by axonal sprouts of slow-twitch motoneurons will
convert to the slow-twitch type 1 fibers). These conversions
alter the normal mosaic distribution pattern to groups of like
fiber types, i.e., muscle type grouping.
Collateral sprouting and reinnervation results in the formation of larger than normal motor units. The motor unit potentials generated by these enlarged motor units are referred
to as giant motor unit potentials. Type grouping may be
though of as the morphologic equivalent of these giant potentials. These changes take 6 months or more to develop,
and they are indicative of a chronic disorder. Denervation of
giant motor units results in large grouped atrophy in histologic sections.
2. Special Features
a. Myofiber Type Predominance or Paucity - describes
the predominance of one fiber type over another in a section.
This may be normal or abnormal, depending on the specific
muscle and the species of animal. In the abnormal state, this
may represent an excess or a deficiency of a given fiber type.
There are two instances in which muscles commonly have
fiber type predominance/paucity:
(i) Growing and Developing Muscle - the onset of neuromuscular disease, particularly neuropathies, superimposed
on the early growth and differentiation of developing muscle
frequently results in type 1 fiber predominance/type 2 fiber
paucity.
(ii) Thyroid Function - also affects the proportion of fiber
types in a muscle. Hypothyroid states result in a transformation of type 2 fibers to type 1 fibers, leading to type 1 fiber
predominance. Conversely hyperthyroid states result in the
opposite effect (type 1 fibers transform to type 2) leading to
type 2 fiber predominance. Polyneuropathies in dogs with
hypothyroidism are not uncommon and biopsies from these
patients often have type 1 fiber predominance.
b. Intramuscular Nerve Branches - are available for evaluation in approximately 40% of the muscle biopsies. Staining techniques applicable to sections of peripheral nerve
provide similar opportunities for evaluation of nerve branches in the muscle biopsy.

F. SPECIFIC NEUROPATHIES
1. Motoneuron Disorders
Inherited and acquired motoneuron disorders have been

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4th European FECAVA SCIVAC Congress

228

described in dogs ( e.g. spinal muscular atrophy of Brittany


spaniels, swedish Lapland, English pointer, german shepherd, Rottweiler, Cairn terrier). These are chronic progressive disorders resulting from degeneration of motoneurons
in the grey matter of the spinal cord and nuclei of the brain
stem. Progressive denervation of muscle fibers results in
paresis, paralysis, and severe muscle atrophy.
2. Peripheral Neuropathies
Polyneuropathies represent the single largest group of
neuromuscular disorders. Many are idiopathic (i.e., our diagnostic skills are insufficient to establish etiology). Disorders include: acute and recurrent polyradiculoneuritis, metabolic (diabetes, hypothyroidism, hypoadrenocorticism, hyperinsulinism), toxic, and lysosomal storage disorders (i.e.,
Krabbes globoid cell leukodystrophy, i.e., galacto-cerebrosidase deficiency, and Niemann-Pick disease, i.e., sphingomyelinase deficiency).
a. Acute idiopathic polyradiculoneuritis
An immune-mediated segmental demyelination and degeneration of axons that is found in dogs which usually, but
not always, have been exposed to raccoons (so called coon
hound paralysis). Typically signs of weakness develop in
the pelvic limbs and ascend rapidly, resulting in flaccid
tetraplegia or paresis 7 to 14 days after exposure. Spinal reflexes are severely depressed or absent. Affected dogs become tetraparetic 24 to 48 hours after signs of muscle weakness first develop and may develop respiratory paralysis.
Defecation, urination, and tail mobility are usually normal as
the sacral and caudal nerve roots are relatively spared and
cranial nerve involvement is uncommon. Although voluntary micturition is preserved it is advisable to help express
the bladder in order to get complete emptying. Swallowing,
gag reflex, and esophageal function are normal and affected
dogs usually maintain an appetite and eat and drink with assistance. Paralysis usually peaks within 10 days of the onset
of clinical signs. Although motor deficits are most obvious,
many animals seem to experience discomfort on light palpation of their extremities. With proper supportive care prognosis for recovery is good. The course of the disease is 3 to
6 weeks and recurrences do occur.
The ventral nerve roots and spinal nerves are primarily
affected, resulting in neurogenic muscle atrophy and electrodiagnostic testing usually provides evidence of widespread motor denervation. Fibrillation and positive sharp
waves are seen frequently and myotonic bursts occur occasionally. The disease must be differentiated from tick paralysis and botulism, both of which are disorders of neuromuscular transmission (i.e. junctionopathies).
b. Hypothyroid neuropathy
Cranial and peripheral polyneuropathies have been associated with hypothyroidism in dogs. Laryngeal paralysis,
megaesophagus, and peripheral vestibular dysfunction, often in association with other cranial and peripheral nerve
deficits, are frequently associated with hypothyroidism.
Clinical signs are those of lower motor neuron dysfunction
(muscle weakness, intermittent lameness, cranial nerve dysfunction), and affected animals may not have obvious signs
of hypothyroidism. The diagnosis is based on the levels of
free T4 and TSH. Denervation potentials and nerve conduction velocity delays are seen on EMG examination. Im-

4th European FECAVA SCIVAC Congress

provement in motor function may take several months of


treatment with thyroid supplementation and dogs with severe, generalized denervation may not fully recover.
c. Diabetic neuropathy
Peripheral neuropathy associated with diabetes has been
reported in dogs and cats. Axons are affected primarily with
secondary demyelination and distal axons are especially susceptible. In dogs the neuropathy may range from being subclinical to acute paresis. Clinical signs are more consistent in
cats and include a characteristic plantigrade stance, depressed patellar reflexes, muscle wasting, and proprioceptive deficits. Clinical signs may take 6-12 months to resolve
once the diabetes is controlled.

G. JUNCTIONOPATHIES
Histopathologic changes are usually absent or non-specific in disorders of the neuromuscular junction. Diagnoses
are usually based on electrodiagnostic, biochemical, immunologic, or toxicologic testing.
1. Presynaptic Disorders
a. Reduced ACh Release - weakness induced by inability to activate sufficient numbers of ACh-receptors.
(i) Hypocalcemia - release of ACh from axon terminals
is calcium ion dependent. Hypermagnesemia causes same
effect and stabilizes postsynaptic membrane as well.
Cows - post-parturient paresis (milk fever), flaccid
paralysis. Principal signs referable to effects on neuromuscular transmission.
Dogs - puerperal tetany (eclampsia). Principal signs
referable to hypocalcemic effect on lowering threshold of
resting membrane potential in neurons thereby causing
spontaneous depolarization of neurons and overriding
blockade of ACh release.
(ii) Botulism - (Clostridium botulinum) - toxin irreversibly binds to presynaptic membrane and blocks release
of ACh. Results in functional denervation of all muscle
fibers. Tick paralysis may be similar but is reversible upon
removal of the tick.
(iii) Aminoglycoside Antibiotics - inhibit ACh release.
These antibiotics also decrease ACh sensitivity of postsynaptic membrane and are contraindicated for use in patients
with postsynaptic disorders such as myasthenia gravis.
b. Increased ACh Release - weakness induced by continued depolarization (hyperexcitability) of postsynaptic membrane.
(i) Hypomagnesemia - grass and transport tetany of
sheep and cattle. Hypercalcemia produces similar effect.
(ii) Black Widow Spider Toxin - binds to presynaptic
membrane and stimulates ACh release.
2. Synaptic Cleft Disorders
Cholinesterase Inhibitors - inhibit breakdown of ACh
and thereby prolong action of ACh on postsynaptic membrane. Important pharmacologic agents include edrophonium chloride (ultrashort acting, minutes), pyridostigmine
bromide (short acting, hours), and neostigmine bromine
(Prostigmin; short acting, hours). Organophosphates are
commonly used to control external parasites in dogs and cats
and for insect control. Organophosphate toxicity results in

the clinical signs of overstimulation of the parasympathetic


nervous system - salivation, lacrimation, bradycardia, pupillary constriction and pronounced gastrointestinal sounds. In
dogs clinical signs usually occur within minutes of ingestion
of excessive compound, but in cats a delayed neurotoxicity
may occur, days or weeks after minimal exposure to
organophosphates.
3. Postsynaptic Disorders
a. Myasthenia Gravis (MG)
Basic lesion is a deficiency of ACh-receptors on postsynaptic membrane. Both congenital and acquired forms of
this condition occur in dogs, cats, and humans. To date, studies suggest the pathophysiology of these conditions are similar among these species.
(i) Acquired Myasthenia Gravis.
Etiology and Pathogenesis. Acquired (immune-mediated) myasthenia gravis is due to antibody-mediated destruction of Ach-receptors and is a common neuromuscular disorder in dogs and sporadically reported in cats. While the
immune-mediated destruction of ACh-receptors is well documented, the underlying cause of this immune mediated disorder remains unknown.
History and Clinical Signs. Acquired MG affects numerous breeds of dogs older than 1 year of age. There appears to be an age-related incidence, with peaks at 2-4 years
and 9-13 years. Signs of muscular weakness may be focal
with selective involvement of the esophageal, pharyngeal,
and facial muscles, or diffuse, with signs of generalized
muscle weakness. In one study it was estimated that one
fourth of the canine patients, presented with idiopathic
megaesophagus, had focal MG. Signs of generalized muscle
weakness may vary considerably, ranging from some intolerance to exercise, which improves with rest, to acute
tetraplegia. Patients with focal or generalized signs, and
megaesophagus, often present with pneumonia secondary to
aspiration. Evaluation of the thorax may reveal the presence
of thymomas, which may be implicated in the etiology of
this immune disorder.
Diagnostic Tests.
Pharmacologic Testing - the IV administration of 1-10
mg of edrophonium chloride. A presumptive positive test
results in transient improvement in the clinical weakness.
Sometimes objective criteria for this test are difficult to establish.
Electrodiagnostic Testing - involves recording evoked
muscle action potentials during repetitive nerve stimulation
at 2-10 Hz. A decline in the amplitude of successive potentials (decremental response), provides a presumptive positive test for MG.
Immunologic Testing - screening tests involve: a) incubating the patients biopsy with the immunoreagent SPAHRP (Staphylococcal protein A conjugated to horseradish
peroxidase), to stain for IgG localization at neuromuscular
junctions, and b) incubating the patients sera on sections
from a healthy dog and subsequently incubating the section
with SPA-HRP to detect fixation of circulating IgG to neuromuscular junctions. Specific testing involves the use of an
immunoprecipitation radioimmunoassay for the determination of ACh receptor antibody titers.
Treatment. This involves improving neuromuscular

229

transmission through the use of cholinesterase inhibitors


(pyridostigmine, 0.5-1 mg/kg per os, BID to TID as needed)
and/or suppression of the immune response with steroids,
(Prednisone, 2 mg/kg BID). Monitor treatment with pyridostigmine for signs of excessive cholinergic stimulation
(salivation, defecation, weakness, etc). It is not uncommon
for dogs to spontaneously abort their immune response, and
fully recover without treatment. This disorder in cats appears
to be more difficult to manage.
(ii) Congenital Myasthenia Gravis.
An hereditary disorder resulting in deficiency of ACh receptors on the postsynaptic membrane. It has been reported
in Jack Russell Terriers, Springer spaniels, and Smooth Fox
Terriers. Onset is usually apparent at 6-8 weeks of age, with
signs of generalized muscular weakness associated with exercise. Megaesophagus is not common. Weakness becomes
progressively severe, leading to tetraplegia and death. Diagnostic tests consist of pharmacologic and electrodiagnostic
tests only. Prognosis is very poor. Treatment with pyridostigmine is helpful and some animals have been maintained for 12-24 months. Genetic counselling is important
since the disorder appears to be inherited as an autosomal recessive condition.
b. Neuromuscular Blocking Agents (Muscle Relaxants).
The effects of two classes of neuromuscular blocking
agents commonly used as muscle relaxants during anesthesia should be included here:
(i) Non-depolarizing agents - include d-Tubocurarine,
gallamine, and pancuronium. These agents compete with
Ach for the Ach-receptor. When bound to the receptor, the
ion channel does not open, preventing depolarization of the
membrane.
(ii) Depolarizing agents - included succinylcholine and
decamethonium. These agents compete with ACh for the
ACh-receptor. When bound to the receptor, the ion channel
opens, causing depolarization of the membrane.

H. MYOPATHIES
In small animals, myopathies are relatively uncommon
and encountered less frequently than neuropathies and junctionopathies, while the converse is generally true in large animals. Myopathies may be generally subdivided into non-inflammatory and inflammatory myopathies.
1. Non-Inflammatory Myopathies
The histopathologic changes in non-inflammatory myopathies usually involve the spectrum of myonecrosis,
phagocytosis, and regeneration, in which the degree of cellular infiltration is proportional to the extent of myonecrosis
present, and its distribution is largely limited to necrotic
fibers. Macrophages constitute the principal cell type. Central nuclei are common. In chronic myopathies there may be
a mixture of atrophied and hypertrophied fibers, with their
morphology being more ovoid than angular, and increased
endomysial connective tissue. Occasionally necrotic fibers
may be calcified. All these changes are relatively non-specific and secondary to agents that result in myonecrosis. In
metabolic myopathies the fibers frequently contain storage
products which appear as vacuoles.

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230

a. X-Linked Muscular Dystrophy of Dogs and Cats


Etiology and pathogenesis. This is an hereditary myopathy
in which there is a deficiency of dystrophin, a cytoskeletal protein associated with the inner face of the sarcolemma. The
pathobiology of this disorder appears to be identical to
Duchenne muscular dystrophy, affecting young male children.
History and clinical signs. The disorder is best recognized and characterized in Golden Retrievers. Other species
of dogs include Rottweilers, Samoyeds, and possibly Irish
Terriers. In cats it has been documented in domestic short
hair cats. In dogs the disorder is usually recognized between
8 and 10 weeks of age. Signs may include generalized weakness, a stiff-limbed, short strided, shuffling gait, some reduced mobility of the jaws, and difficulty with chewing and
swallowing associated with excess salivation. The weakness
and signs are progressive, with poorly developed muscle
mass, body stature, and spinal curvature. In advanced stages
some muscle groups may appear grossly hypertrophied. Cardiac muscle may also become involved.
Recognition of this disorder in cats is more recent and
the findings are similar to those in dogs. While the onset is
likely similar to that in the dog, reported cases have been
somewhat later in onset, 5 to 25 months of age; however the
histories suggest earlier clinical signs. Gross hypertrophy of
the tongue and diaphragm have been a common finding.
Diagnostic Tests. Diagnostic tests include serum CK,
which may be elevated to 300 times normal; EMG examination which reveals repetitive, high frequency discharges; and
muscle biopsy examination which reveals multifocal areas
of necrosis, necrosis and phagocytosis, and regeneration. In
the later stages, muscle fiber hypertrophy and fiber splitting
is common along with fibrosis.
Specific information is provided through the use of immunocytochemical staining techniques to detect dystrophin
in sections (or lack thereof) and/or the muscle may be assayed for the presence of dystrophin.
Treatment. Currently there is no cure and lifespan is
shortened due to secondary complications. Future research
advances in this area will have widespread benefits for both
animals and humans.
b. Metabolic Muscle Disorders
These are relatively uncommon disorders of carbohydrate, lipid, and oxygen metabolism that generally induce
muscle weakness by supplying insufficient energy (ATP) to
sustain muscle contraction, and other cellular functions with
a high energy requirement.
(i) Malignant Hyperthermia - is a hypermetabolic and
hypercontractile muscle disorder triggered by inhalant anesthetics (e.g., halothane), depolarizing muscle relaxants (e.g.,
succinylcholine) or other stressors (e.g., exercise). The defect appears to be due to a hypersensitivity of the calcium
ion release channel of the sarcoplasmic reticulum (i.e., the
ryanodine receptor of the terminal cisternae) that facilitates
channel opening and inhibits channel closing. Affected muscle produces excess lactic acid and heat, resulting in myolysis and the release of potassium and proteins (e.g., myoglobin). The elevation in body temperature can cause damage to
other tissues (nervous, renal, hepatic) and death.
The condition affects humans and swine and it has been
reported, but less well studied in other species, such as dogs

4th European FECAVA SCIVAC Congress

and horses. The condition in pigs is called Porcine Stress


Syndrome, and results in pale, soft, and exudative (PSE)
pork at slaughter. Capture myopathy in wild animals appears
to be a similar syndrome of excessive muscular activity in
attempting to escape, however no basic pre-stressor defect is
likely to be involved.
(ii) Myotonias - are disorders in which there is sustained
(tetanic) muscle contraction associated with repetitive depolarization of muscle fibers. In affected individuals, there is
involuntary contraction of a muscle that persists after voluntary movement or stimulation. Congenital myotonias occur
in goats, dogs, (Chow Chow, Cocker spaniel, labrador retriever, Samoyed, Staffordshire terrier, West Highland white
terrier), horses, and humans. The principal defect is an altered chloride conductance causing postexcitement depolarization of the muscle membrane and continued contraction
of the muscle. Clinical signs include abnormal stiff gait, abduction of forelimbs, muscle hypertrophy and a characteristic myotonic dimple which persists for 30-40 seconds after
direct muscle stimulation (tongue or shaved limb). EMG
findings include high-frequency myotonic discharges with
continuous insertional activity and possible decremental response. Nerve conduction velocity is normal and muscle
biopsy variable (hypertrophy, atrophy and degeneration).
There is no treatment for the disease other than avoiding
prolonged exercise and the disease is not progressive.
(iii) Glycogen Storage Disorders - are rare, usually genetically determined (autosomal recessive), degenerative
disorders resulting from a specific enzyme deficiency. As a
result there is accumulation and storage of the substrate(s) in
cells. Glycogen storage disorders are the result of a deficiency of one of the enzymes involved in glycogen synthesis or degradation. This results in inadequate glycogen utilization, and excess glycogen accumulates in skeletal and
cardiac muscle and in the CNS. These are rare disorders in
dogs and cats. Glycogen storage disorders have been reported in Swedish Lapland dogs, English springer spaniel dogs,
German shepherds, Akitas, toy breed dogs, and cats.
(iv) Lipid Storage Myopathies - are sporadically reported in dogs, with lipid storage occurring in type 1 myofibers.
In humans, carnitine deficiency results in lipid storage within type 1 myofibers. Carnitine serves as a carrier molecule
for long-chain fatty acid transport through the inner mitochondrial membrane for subsequent betaoxidation in the mitochondrial matrix. While a similar pattern of glycogen storage exists in dogs, carnitine deficiency has not been established as the cause.
(v) Electrolyte Myopathies - are abnormalities of potassium metabolism involving both hypo- and hyperkalemic
states, and frequently result in accumulation of fluid filled
vacuoles.
Feline Hypokalemic Polymyopathy is a manifestation of
chronic potassium depletion and is thought to be one of the
most common causes of generalized muscle weakness in
cats. The hypokalemia is thought to be a total body depletion
of potassium rather than a redistribution between the intracellular and extracellular compartments. A combination of
low dietary intake of potassium and increased urinary potassium loss over a period of months may lead to a depletion of
body stores. This condition, or a variant of it, has been re-

ported in Burmese cats, which may be more sensitive to the


effects of low potassium. Affected cats present with acute
onset of generalized weakness, reluctance to walk, persistent
ventroflexion of the neck, stiff gait, muscle pain when handled or palpated, muscle atrophy, anorexia and weight loss
and in severe cases respiratory muscle paralysis.
Abnormal serum chemistry results include: low potassium(<3.5 mEq/L), increased creatine kinase (500-10,000
IU/L), increased creatinine (2.5-5 mg/dl), and mild to moderate metabolic acidosis. Urine specific gravity may be low
and fractional urinary excretion of potassium is increased
(normal is 4.7-14.3%). EMG abnormalities are found in
multiple muscle groups and include frequent positive sharp
waves, fibrillation potentials, occasional bizarre high-frequency discharges with normal nerve conduction velocities.
Muscle histopathology is usually normal.
Potassium administration which initially is usually administered intravenously. High concentrations are usually
necessary to start. Oral potassium elixir and potassium gluconate powder may be used for long term supplementation.
2. Inflammatory Myopathies
The inflammatory myopathies possess many of the
changes described for non-inflammatory myopathies. However, in addition, they are characterized by a disproportionate number of infiltrating cells which may include lymphocytes/plasma cells, polymorphonuclear leukocytes and/or
eosinophils in addition to macrophages. In these disorders,
the cellular infiltrates comprise an integral part of the disorders pathogenesis and not merely a secondary response to
cell death. The infiltrating cells often have a perivascular
distribution. Identification and characterization of the infiltrating cell type assists in the definition, and recognition of
these disorders. The use of the term myositis is reserved
for inflammatory myopathies. Inflammatory myopathies
may be due to infectious or immune-mediated agents.
a. Masticatory Muscle Myositis - (formerly called
eosinophilic and/or atrophic myositis) is an inflammatory
muscle disorder limited to the muscles of mastication in
dogs. Muscles of mastication in dogs are composed of 2M
fibers, which differ from the 2A fibers in limb muscles. An
immune response has been identified in which antibodies are
selectively produced against type 2M fibers. The disorder
may be acute or chronic. Acute onset usually presents with
bilateral swelling of the temporalis and masseter muscles,
and possibly exophthalmia, due to swelling of the pterygoid
muscles. It usually affects large-breed dogs, with no age or
gender predilection. Dogs may be febrile with conjunctivitis, enlarged lymph nodes, tonsils, and splenomegaly. Patients exhibit pain, with opening or manipulation of jaws
(trismus). Chronic onset may result front insidious onset, or
as a result of repeated acute bouts. Dogs present with masticatory muscle atrophy, which may be marked, leaving the
patient with a skull-like appearance.
Diagnostic tests include measurement of CK; however, elevations may be modest, due to limited involvement of masticatory muscles. EMG examination helps define distribution
of involvement, but may be difficult to perform in severely atrophied muscles. Muscle biopsies detect lesions and presence
of IgG in type 2M fibers while serologic testing confirms
presence of circulating antibodies against 2M fibers.

231

Treatment is directed towards the suppression of the immune response with steroids. Long-term medication may be
needed to maintain remission.
b. Polymyositis - is a generalized inflammatory myopathy caused by infectious agents (viral, bacterial, and parasitic) and ill-defined immune mediated mechanisms. Elevations in CK are usually marked and muscle biopsies are frequently helpful in detecting parasitic cysts in Toxoplasma,
Neosporum, Trichinella and Sarcocystis myositis.
c. Dermatomyositis - occurs as a familial disorder in Collies, and possibly Shetland sheepdogs. Dermatitis involves
the face, ears, and distal extremities. Muscle lesions have
been described in muscles of mastication and distal limb
muscles.
d. Protozoal polymyositis. Toxoplasma gondii is the
most common cause of infectious myositis. Neospora caninum causes similar signs and may have been called toxoplasmosis in the past. Both organisms tend to cause more severe signs in very young animals and have an increased likelihood of causing signs in immunosuppressed animals. Toxoplasmosis is often associated with canine distemper infection whereas neosporosis is not associated with concurrent
infection. Gait abnormalities are present in affected animals
and include a hopping gait, progressive pelvic limb paresis,
rigid extension of the pelvic limbs, progressive ascending
paralysis is more common with neosporosis, initially severe
muscle pain and atrophy as the disease progresses. Stupor,
seizures, and chorioretinitis may occur with CNS disease.
Creatine kinase is elevated in the active phase of the disease. Histopathological changes in muscle include: pronounced fiber atrophy, severe multifocal necrosis, mononuclear granulomatous inflammation, and severe interstitial fibrosis in chronic cases. The presence of organisms, free or in
cysts is definitive, but these are not always found. Single antibody titers are not diagnostic, but rising titers support the
diagnosis. Serum with antibodies to N. Caninum does not react with T. Gondii organisms, and vice versa. CSF analysis
may reveal mixed pleocytosis, and a high protein content.
Indirect fluorescent antibody testing of serum, CSF, or tissue
may aid in differentiating N. Caninum from T. Gondii.
Clindamycin or trimethoprim/sulfadiazine are the treatment of choice and animals with acute systemic disease may
respond well.
3. Idiopathic Myopathies
a. Fibrotic Myopathy - is a chronic, progressive disorders
that result in severe muscle contracture and fibrosis. In dogs
this condition has been reported in the semitendinosus,
quadriceps, supraspinatus, infraspinatus, rectus femoris, and
gracilis muscles and in the semitendinosus muscle in the cat.
The cause is not known and possible etiologies include a primary neuropathy or myopathy, frequent intramuscular injections, exercise-induce trauma, or chronic trauma with tearing and stretching of muscle fibers, or a congenital disorder.
Muscle is replaced by dense collagenous connective tissue,
resulting in a taut fibrous band and the affected develops a
nonpainful, mechanical lameness, the severity of which depends on the muscle involved and the extent of the fibrosis.
On physical examination a thin fibrous band can be palpated, which replaces the muscle belly. Histopathology of affected muscles reveals dense collagenous connective tissue

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4th European FECAVA SCIVAC Congress

232

replacing muscle fibers and there is minimal inflammation.


No EMG activity is detected form the fibrous band and
bizarre high-frequency discharges may occur with incomplete replacement of muscle fibers.
Surgery is not recommended unless the lameness is disabling. If surgery is undertaken the goal is to release the fibrous band, but prognosis must be guarded because of the
likely recurrence of the fibrous band within 3-8 months.
b. Infraspinatous Muscle Contracture - occurs primarily
in hunting or working breeds in dogs and is usually unilateral. The cause is not known, but it is thought to be a primary
muscle disorder, possibly associated with trauma, causing
incomplete rupture of the muscle, and resulting in progressive fibrosis and contracture over 2-4 weeks. Initially, the
dog has an acute onset of pain in the shoulder during or soon
after exercise. The lameness gradually subsides, but never
resolves. Two to four weeks after the initial injury, a nonpainful mechanical lameness of the foreleg develops and the
gait is characterized by adduction of the elbow and abduction of the foreleg, with outward rotation of the antebrachium and carpus. The limb is laterally circumducted with each
stride, and the foot flips forward.
Palpation of the forelimb reveals that the humerus rotates
outward when the elbow joint is flexed and range of motion
in the shoulder joint is limited. Disuse atrophy of the infraspinatus, supraspinatus, and spinous deltoid muscles is evident from the prominent scapular spine.
Tenotomy of the tendon of insertion of the infraspinatous
muscle should allow the forelimb to be more easily adducted and the shoulder range of motion is improved. Activity
should be limited for 1-2 weeks after surgery and prognosis
for a full recovery is excellent.
c. Myositis Ossificans - is the formation of bone in muscle. There is usually minimal inflammation, and muscle is
not always involved. It is reported in dogs and cats and has
been well described in dobermans, where some authors believe it may be a separate disease entity - von Willebrand
heterotopic osteochondrofibrosis in Doberman pinschers.
Progressive or generalized myositis ossificans is also known
as progressive ossifying fibrodysplasia or progressive or
generalized ossifying myositis. It is characterized by the development of excessive fibrous connective tissue, which results in widespread muscle degeneration and ultimately
leads to dystrophic calcification and ossification. It has been
reported in young to middle-aged cats. The cause is not
known and the localized form may be associated with trauma, infection, ossifying hematoma, and metaplasia of muscle and connective tissue to cartilage and bone.

4th European FECAVA SCIVAC Congress

Localized ossifying myositis results in a palpable, firm


enlargement in affected muscles, with chronic lameness,
pain after exercise and muscle atrophy. Progressive ossifying fibrodysplasia occurs in young to middleaged cats and
results in firm nodules anywhere on the body, but predominantly on the neck and back. Limbs, especially the pelvic
limbs may be stiff which may progress to difficulty walking.
Proximal limb musculature is enlarged and firm, painful,
and has limited range of motion. Affected cats may be disabled within 2 weeks to several months. Soft tissue mineralization occurs within 3-6 weeks of injury and mature bone in
soft tissue after 2-6 months. Radiographs of affected areas
show multiple mineralized densities. There may or may not
be a periosteal reaction. On histopathology there is progressive maturation of bone centrally to peripherally. The central
zone contains undifferentiated cells and fibroblasts and may
resemble a sarcoma, the intermediate zone contains osteoid
and some areas of immature bone and the peripheral zone
contains mature bone. It does not invade the surrounding
soft tissue. Affected muscle has excessive connective tissue
between muscle fibers, mononuclear infiltration and muscle
atrophy and hyaline degeneration.
If clinical signs are minimal no treatment is recommended for localized ossifying myositis, and rest, compressive
bandages, and aspirin may help to relieve the acute pain.
Surgical excision is indicated to alleviate discomfort and restore normal limb function. In humans if surgery is performed within 6 months, i.e. when the lesion is immature
there is a high rate of recurrence. Post operative physical
therapy is important. There is no effective treatment for progressive ossifying fibrodysplasia.
4. Neoplasia
Muscle tumors may be primary, originating from skeletal muscle (rhabdomyoma, rhabdomyosarcoma) secondary,
metastatic spread from tumors originating elsewhere, or local invasion of tumors into muscle form rapidly expanding
cutaneous or bone tumors. Age of onset is variable although
secondary tumor spread usually occurs in middle-aged animals. Clinical signs depend on the muscle group affected
and firm, nonpainful swelling, distortion of the area, and
lameness are common. Diagnosis is confirmed by biopsy
and histopathologic assessment. Staging of the disease with
lymph node biopsy and thoracic radiographs is important.
For primary neoplasia, surgical excision is preferred, but
may be ineffectual if the neoplasm is difficult to reach or invasive. Amputation of the limb may be necessary to attain
adequate surgical margins. Treatment of secondary neoplasia depends on the therapy indicated for the primary tumor.

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Management of spinal trauma


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

A. INTRODUCTION

The successful management of a dog or cat with spinal


cord injury demands aggressive and prompt attention to
both non-neural and neural injuries. Decisions regarding
medical and/or surgical treatments must be based on thorough physical and neurologic examinations and careful interpretation of radiographic findings. Accurate serial examinations of the affected animal are essential in order to determine the response to therapy already instituted and the
need for more aggressive management. Medical management of animals with spinal cord injuries is effective in many
instances, but must be approached rationally with knowledge of drug effects and indications. While medical management alone may be sufficient therapy in some cases, surgical therapy is often required. Surgical decompression of
the spinal cord following injury should not be considered a
last resort, but should be approached in a timely fashion on
the basis of the recommendations outlined above. Neurosurgical procedures require specialized knowledge and equipment, so prompt referral of dogs and cats suffering from
spinal cord injury to qualified surgeons is often indicated.
Finally, the management of animals with central nervous
system trauma requires time, patience, and attention to detail. Owners should be made aware at the outset of treatment
of such factors as prognosis, expense involved, expected
time form treatment to recovery, and most importantly, the
need for prolonged physical therapy.

Management of a dog or cat with spinal injury requires


understanding of basic neuroanatomy and physiology. It also demands knowledge of effects produced by pharmacologic agents and other interventions, such as fluid therapy.
Most importantly, it requires that a veterinarian establish a
list of priorities for management and recognize those situations that are truly life threatening.

Since the vast majority of spinal cord injuries cases are


caused by direct trauma, a complete physical examination
must be obtained first, as many of these patients will have
additional problems (e.g. pneumothorax, diaphragmatic hernia, urogenital injuries, and other orthopedic injuries). Extreme care must be taken at all times to avoid exacerbating
any spinal cord injury, especially once the patient is anesthetized and no longer able to protect the affected area.
Physical examination and patient stabilization, with management of life threatening injuries, is the initial objective.
Radiographic findings must be evaluated in conjunction
with the neurological examination findings.
This lecture will cover the pathophysiology of spinal
cord trauma and the medical and surgical management of
these patients.

B. ETIOLOGY AND PATHOGENESIS


Spinal cord injuries in dogs and cats result must frequently from direct physical trauma, vertebral fracture or luxation, or from intervertebral disc protrusion/extrusion. Following injury, the spinal cord may undergo sustained compression, distraction, or both. The severity of a spinal cord injury, as determined by the eventual quality of recovery, is related to three factors: the velocity with which the compressive force is applied, the degree of compression (transverse
deformation), and the duration of the compression. The relative roles of these factors in determining the severity of an injury to the spinal cord have yet to be determined.
The molecular and electrophysiologic events of failed
neurotransmission following spinal trauma are not currently
understood in detail. Neural tissue may be physically disrupted and fail on a mechanical basis. More commonly,
though, the spinal cord remains physically intact but is functionally deranged. Within 5 minutes of experimental injury,
the postcapillary venules become markedly congested. This
is soon followed by the opening of endothelial gaps here and
at the capillary level, resulting in diapedesis of red cells and
extravasation of fluid proteins and electrolytes through the
leaky microvasculature.
Within 30 minutes of injury, microscopic hemorrhages
appear in the central gray matter and coalesce over the next
several hours. Vacuolization develops within the endothelial
lining, indicating a profound ischemic or hypoxic insult,
which subsequently leads to coagulative necrosis of the neuronal population. The adjacent white matter is relatively less
affected, but retraction balls and periaxonal swelling may be
observed. These events can progress to autodissolution of
the spinal cord within 24 hours, even without ongoing mechanical compression.
Extrapolation from morphologic findings, these phe-

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Summary

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nomena would appear to have an ischemic basis, and considerable effort has been expended in characterizing the associated microcirculatory alterations. Direct measurements
of spinal cord blood flow do not reveal a consistent trend until 2 to 3 hours after injury, when the gray matter flow drops
to less than half of the control values. Tissue oxygen tension
declines over a parallel time course. Vasomotor autoregulation is disrupted within the injured segment of spinal cord,
while the blood flow in the adjacent white matter (which ordinarily approximates 40 percent of gray matter mass corrected flow) is maintained or increased. However, these observations fail to explain why an instantaneous physical impact immediately suspends neurotransmission, or how delayed microcirculatory failure occurs. Several lines of investigation have been intensely pursued. The possible roles of
free catecholamines, lipid peroxides and free radicals, lysosomal enzymes, Na+/K+ ATP-ase, and endorphins, either in
direct tissue injury or in the modulation of microvascular responses, are under active study.

C. CLINICAL FINDINGS
Dogs and cats with spinal cord injury frequently have serious injuries of other organ systems. A major component of
the clinical assessment of an animals condition, therefore,
is the determination of the relative urgency of treatment of
non-neurologic injuries versus the need for early treatment
of spinal cord injury. At the time of presentation, the animal
should be placed in lateral recumbency and should remain
in that position during subsequent clinical and radiographic
examinations. A thorough assessment of the animals general condition must be made, looking for major problems such
as hemorrhage, shock, pneumothorax, diaphragmatic hernia, or limb fractures. Extreme care must be taken at all
times to avoid exacerbating any spinal injury with excessive
movement.
The most common cause of vertebral fractures is automobile trauma, other causes include bite wounds, gunshot
wounds and underlying infectious, metabolic, or neoplastic
disorders resulting in bone demineralization. Vertebral fractures may occur at any age, but are more common in
younger animals.
A complete neurological examination is performed to localize the site of the injury and determine its severity. Careful palpation of the vertebral column may aid in identification of a vertebral fracture or luxation. Administration of
tranquilizers or analgesic should be delayed until completion
of the neurologic examination, as these agents may alter an
animals responses. A neurologic examination should be
done with minimal movement of the animal in order to prevent further injury resulting from vertebral instability.
The extent of a spinal cord injury usually can be assessed
accurately at the time of initial examination, as most spinal
injuries are nonprogressive, and as spinal shock (a phenomenon resulting in loss of physiologic functions caudad to a
spinal cord injury) is usually not of clinical significance in
subprimates.
Several aspects of the neurologic examination are of special importance in assessing a dog or cat with a spinal injury.

4th European FECAVA SCIVAC Congress

Attention given to the animals posture may aid in determination of location and severity of a lesion. For example,
Schiff-Sherrington syndrome, which results from thoracolumbar spinal cord injury, is of great localizing value and
must be differentiated from other postures such as decerebrate rigidity and decerebellate rigidity. Motor function,
muscle tone, and spinal reflexes must be assessed carefully.
These functions are utilized to localize a lesion to one of
four major regions of the spinal cord: cervical (C1-C5),
brachial enlargement (C6-T2), thoracolumbar (T3-L3), and
lumbar enlargement (L4-Cc5).
Pain perception should be assessed by applying a painful
stimulus and observing the animal for a brainmediated response. The stimulus applied to a foot may result in withdrawal of the limb by a spinal reflex mechanism (the flexion
reflex), even though the spinal cord may have been severed.
It is essential to distinguish these spinal reflex movements
from brain-mediated responses (e.g. turning the head, vocalizing, increased respirations or some sign that the painful
stimulus has elicited a response from the brain). Two types
of pain perception are sometimes distinguished in animals.
Superficial pain perception is manifested by a response to
pricking or pinching the skin, and deep pain perception is
manifested by response to pinching the toes or tail with hemostatic forceps.
When multiple spinal fractures occur, the clinical signs
of a more caudal lesion may mask those resulting from a
second lesion located further cranially. For example, the
lower motor neuron signs caused by a lesion at L5-L6 may
mask the hyperreflexia that would be caused by a second injury at L1.

D. DIAGNOSIS
Results of the neurologic examination usually are extremely revealing in determining the site and severity of
spinal cord injury subsequent to trauma. Radiographs of the
vertebral column are essential. Ventrodorsal radiographs are
best done by means of a horizontal beam, in order to avoid
further spinal injury. The entire vertebral column must be radiographed, and proper positioning is required. Twenty per
cent of patients with traumatic spinal injuries will have a
second spinal fracture/luxation at another location. A logical
approach is to anesthetize the animal as soon as possible after completion of the physical and neurologic examinations.
This will, of course, be influenced by the severity of nonneural injuries in many cases. Anesthesia permits precise positioning and allows for the completion of myelography. The
major values of radiographic studies are in precise lesion localization, discovering unsuspected lesions, and in assessing
the need for surgery and the procedure to be used. Extreme
care must be taken at all times to avoid causing further injury to the animal, especially once that animal is anesthetized and no longer able to protect the affected area. In
some instances it may be prudent not to attempt ventrodorsal radiographs if these can not be accomplished without
moving the animal from lateral recumbency.
Many dogs and cats with spinal trauma have resultant
vertebral fractures or luxations that are evident radiographi-

cally. These fractures or luxations often occur adjacent to


area of rigid stability such as the sacroiliac articulation.
Fractures usually occur transversely from the intervertebral
foramen cranioventrally through the vertebral body or
through the vertebral epiphysis in younger dogs. Alternatively, the vertebral body may be compressed (compression
fracture). Luxations occur through the intervertebral disk
space, with the caudal segment or vertebra usually being displaced cranioventrally. Other animals with spinal trauma
and significant neurologic deficits have no radiographic evidence of vertebral fractures or luxations. In some of these
cases, vertebral displacement may have occurred at the time
of trauma, with immediate return to normal alignment. More
commonly, perhaps, these dogs and cats have spinal cord
contusion analogous to that occurring in the brain as a result
of trauma. The associated intramedullary hemorrhage and
edema may cause myelographic evidence of spinal cord
swelling at the site of injury. Radiographic findings must always be evaluated in conjunction with neurological examination findings.

E. TREATMENT
General considerations
Management of animals with spinal trauma should follow a list of priorities, with the focus of the treatment centered on prevention of secondary central nervous system
damage. Immediate treatment of non-neural injuries is limited to those problems that are life threatening, such as shock
and hemorrhage. Splinting of long bone fractures is indicated, but permanent reduction and fixation should be deferred
until initial management of the spinal cord injury is underway. Temperature, pulse, and respiration should be recorded
for future reference.

Medical therapy
Based on experimental findings, a variety of pharmacologic agents have been advocated in treating spinal cord
trauma. Glucocorticoids and osmotic diuretics have been
used most commonly in an attempt to reduce edema. Glucocorticoids are considered beneficial in the treatment of
spinal cord injury by many researchers. However, highdose
steroid therapy may result in complications leading to increased morbidity and mortality (e.g. gastrointestinal
bleeding), and, therefore, low-dose regimens are recommended. Glucocorticoids should be administered during
the first eight hours following the injury. Dexamethasone
may be given at an initial dose of 2 to 4 mg/kg IV and then
a dose of 0.2 mg/kg IV may be repeated at 6- to 8-hour intervals. Recent evidence supports the use of methyl prednisolone sodium succinate (MPSS) during the first eight
hours after injury. Dosage of MPSS is 30 mg/kg IV followed either by a dose of 15 mg/kg every six hours for 24
hours or a continuous infusion at a rate of 5.4 mg/kg/hour
for 24 hours. Osmotic diuretics have been shown to be beneficial in some experimental studies, but probably are not

235

of benefit in severely injured spinal cord tissue and may


even be injurious.
Much attention has been focused recently on the role of
free catecholamines in the pathogenesis of acute spinal cord
injury and the reversal of these effects through their depletion or pharmacologic blockade. However, the role of catecholamines in spinal cord trauma and treatments directed at
reducing their effects have been questioned. Another suggested therapy involves the use of antifibrinolytics to stabilize clots and limit cord hemorrhage. Hyperbaric oxygen and
dextran have been employed to augment a sluggish microcirculation. Barbiturates and hypothermic cord perfusion
have been used to lessen metabolic requirements and attenuate adverse tissue responses at the injury site. Most recently, naloxone has been administered in an attempt to reverse
beta endorphin-induced ischemia. The clinical usefulness of
these approaches remains unclear.

Surgical therapy
A decision regarding surgical treatment must be made as
soon as non-neural injuries have been treated and medical
management instituted. Ideally, this is within 2 hours of the
time of injury. Surgical decompression by laminectomy is
beneficial when there is myelographic evidence of sustained
extradural compression of the spinal cord. In cases where
extradural compression is not present and spinal cord
swelling is the major source of compression, durotomy or
myelotomy may be combined with laminectomy. If done,
durotomy and myelotomy should be accompanied by saline
perfusion of the spinal cord for at least 1 hour. Perfusion
with chilled fluids probably is no more helpful than perfusion with normothermic fluids, although hypothermia without perfusion is beneficial experimentally.
Alignment and stabilization of the vertebral column is
indicated in animals that demonstrate severe displacement or
instability of a fracture or luxation. Most fractures or luxations must be considered unstable, even though all such injuries will not result in sustained spinal cord compression or
distraction. Satisfactory methods of external fixation of
spinal fractures do not exist, so open reduction and fixation
is recommended. Surgical reduction and fixation can be
readily combined with laminectomy for decompression, if
necessary. Surgical management of spinal cord injury in animals must be considered in all cases, as it provides the best
opportunity for rapid and complete recovery in cases of sustained compression or instability and facilitates postinjury
care. However, conservative therapy, including strict confinement and external splinting for 4 to 6 weeks, may be efficacious in animals with minimal neurologic deficits and
little vertebral displacement.
Numerous surgical procedures have been utilized in stabilizing the spine in the dog and cat. The use of Steinmann
pins and methylmethacrylate is particularly effective at all
levels of the vertebral column, especially in large-breed
dogs.
Regardless of the form of internal stabilization used for
vertebral fractures, the stabilizing device may fail if there is
excessive motion during the initial postoperative phase. For

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236

this reason, strict confinement is advisable for a minimum of


two weeks after surgery.

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perforation. Intestinal protectants (kaolin-pectin, 1 to 2


ml/kg, PO, qid) and cimetidine (10 mg/kg, PO, tid) are indicated in these dogs.

F. COMPLICATIONS
G. PROGNOSIS
Potential complications encountered in dogs and cats
with spinal cord trauma and associated paralysis include urinary tract infections, urine scalding, and decubitus. The potential for urinary tract infections resulting from urine retention should be of paramount concern. Evacuation of urine
form the bladder must be accomplished by either manual expression or catheterization at least three times daily. Indwelling catheters are to be avoided, as they further predispose to infection. Decubitus is mainly a complication of
large recumbent dogs and can be partially countered by placing such animals on a padded surface. Presence of urinary
incontinence in these dogs may also necessitate that the surface be fenestrated. Because of the routine use of glucocorticoids in animals with spinal trauma, steroid-related complications also are relatively common. The most deleterious
of these effects is severe gastrointestinal bleeding and even

Prognosis for an animal with spinal cord injury depends


on numerous factors, with results of the neurologic examination being the major determinant. The most important factor
in neurologic prognosis is pain perception. The loss of superficial pain perception occurs with less severe lesions than
those resulting in loss of deep pain perception. In general,
animals in which any degree of pain perception is detected
with certainty can be expected to be restored to locomotion.
The more severe the depression of pain perception, the longer
the recovery period. In severe injuries, where pain perception
has been absent for a brief period, recovery may require
months and residual ataxia and paresis may persist. Most animals in which pain perception has been absent for 24 hours
or more cannot be restored to locomotion, although occasional recoveries have been seen in such cases.

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237

Lumbosacral disorders of dogs


Richard A. LeCouteur

Lumbosacral disease is often caused by stenosis of the


lumbosacral vertebral canal. Stenosis here results in a variety of disorders as a result of compression of the cauda
equina. Lumbosacral vertebral canal stenosis may result
from several or all of the following: type II disk protrusion
(dorsal bulging of the annulus fibrosis), hypertrophy and /or
hyperplasia of the interarcuate ligament, thickening of the
vertebral arches or articular facets, and (infrequently) subluxation/instability of the lumbosacral junction. The lecture
will cover etiology and pathogenesis of the condition, clinical findings, differential diagnosis, diagnostic tools and
treatment options.

A. INTRODUCTION
The term cauda equina syndrome describes a group of
neurologic signs that results from compression, destruction,
or displacement of those nerve roots and spinal nerves that
form the cauda equina. Disorders of the cauda equina that result in cauda equina syndrome are relatively common and
may be either congenital or acquired, or may be a combination of both these categories (Table 1). The nerve roots involved are L7, S1-3, and Cd 1-5.

B. LUMBOSACRAL VERTEBRAL CANAL


STENOSIS
Etiology and pathogenesis
The term lumbosacral vertebral canal stenosis encompasses a spectrum of disorders that cause a narrowing of the

lumbosacral vertebral canal with resulting compression of


the cauda equina. The term lumbosacral vertebral canal
stenosis is used by this author to describe an acquired disorder of large breeds of dog that results from several or all of
the following: type II disk protrusion (dorsal bulging of the
annulus fibrosus), hypertrophy and/or hyperplasia of the interarcuate ligament, thickening of vertebral arches or articular facets, and (infrequently) subluxation/instability of the
lumbosacral junction. It is likely that several separate disorders currently are included within this single syndrome.
Other terms that have been used to describe this disorder
are lumbosacral instability, lumbosacral malformation/
malarticulation, lumbar spinal stenosis, lumbosacral
spondylolisthesis, and cauda equina syndrome. As stated
above, cauda equina syndrome may result from numerous
causes other than lumbosacral vertebral canal stenosis;
therefore, use of this term to describe this condition is inappropriate. In humans, the term spondylolisthesis refers
specifically to a forward (anterior) movement of a lower
lumbar vertebra relative to a lumbar vertebra or sacrum directly below it. This problem rarely occurs in dogs, in which
the most frequently encountered problem is a ventral slippage of the sacrum relative to the body of the L7 vertebra.
The term retrolisthesis has been proposed to describe this
reverse spondylolisthesis of dogs. Lumbar spinal stenosis
is a term that perhaps is best used to describe a congenital
(idiopathic) syndrome reported to occur in young dogs.
Lumbosacral instability is a misleading term, as instability is
not demonstrated consistently in association with lumbosacral vertebral canal stenosis.
Certain similarities between vertebral and soft tissue alterations seen in dogs with lumbosacral vertebral canal
stenosis and Doberman pinscher dogs with caudal cervical

Table 1. Disorders that result in clinical signs of cauda equina dysfunction in dogs.
1. Congenital disorders
a. Vertebral and/or nerve root anomalies (e.g., stenosis of the vertebral canal, spinal dysraphism, transitional vertebra, dysgenesis of lumbosacral vertebrae, and spina bifida
2. Acquired disorders
a. Infections (e.g., diskospondylitis)
b. Neoplasia (e.g., malignant nerve sheath neoplasia)
c. Intervertebral disk disease
d. Iatrogenic stenosis (e.g., post-surgical scarring)
e. Lumbosacral vertebral canal stenosis (with/without retrolisthesis)
f. Fractures and/or luxations
3. Combined disorders
a. Combination of congenital and acquired disorders (e.g., disk degeneration and lumbosacral vertebral canal stenosis)

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VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN


Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

238

spondylomyelopathy have been noted. As the etiology and


pathogenesis for either condition are incompletely understood, such comparisons are of little significance at the present time. An association has been reported between lumbosacral stenosis and transitional vertebrae in German shepherd dogs. In another report, more than 30 per cent of German shepherd dogs with clinical signs of cauda equina compression had radiographic and pathologic abnormalities
compatible with osteochondrosis of the sacral end-plate.

Clinical findings
Acquired degenerative lumbosacral vertebral canal
stenosis occurs most commonly in large breeds of dog.
Males appear to be affected more frequently than females.
German shepherd dogs appear to be affected more often than
dogs of other breeds. Dogs with the congenital (idiopathic) form appear to be of the smaller breeds. Affected dogs
in both categories are between 3 and 7 years of age, although
the problem may occur at any age. Degenerative lumbosacral vertebral canal stenosis rarely is recognized in cats.
Signs of cauda equina compression seen frequently in affected dogs include the following: apparent pain on palpation of the lumbosacral region, on caudal extension of the
pelvic limbs, or on elevation of the tail; difficulty rising;
pelvic limb lameness (often unilateral); pelvic limb muscle
atrophy; paresis of the tail; scuffing of the toes; urinary
and/or fecal incontinence, or inappropriate voiding due to
an inability to assume a voiding posture; self-mutilation of
the perineum, tail, or pelvic limbs; and rarely, paraphimosis.
These signs most often are insidious in onset and progress
gradually over months, and they are easily confused with
those of hip dysplasia or degenerative myelopathy.
Abnormalities detected on neurologic examination include gait deficits related to sciatic nerve paresis (e.g., dragging of toes). In addition, depression or loss of conscious
proprioception, normal or slightly exaggerated patellar reflexes (pseudoexaggeration related to loss of antagonism
to femoral nerve-innervated muscles by sciatic nerve-innervated muscles), depressed or absent flexion reflexes in
pelvic limbs, decreased anal tone and anal sphincter reflexes, atonic bladder, hypesthesia of the perineum and tail, and
muscle atrophy may be seen. These abnormalities relate to
deficits of the sciatic, pudendal, caudal, and pelvic nerves,
whose nerve roots comprise the cauda equina.

Diagnosis
Characteristic clinical findings may be consistent with a
diagnosis of degenerative lumbosacral vertebral canal stenosis. Careful mapping of areas of loss of cutaneous sensation
may assist in determining involved nerve roots. However,
presence of this syndrome must be confirmed by means of
plain radiographs and special radiographic techniques. Diagnosis of this condition requires completion of several specialized radiographic procedures in sequence. Rarely can
this condition be diagnosed on the basis of plain radiographic findings alone.

4th European FECAVA SCIVAC Congress

Electromyography may complement information available from a neurologic examination and from plain spinal radiographs by confirming denervation in muscles innervated
by the nerves of the cauda equina. Motor nerve conduction
velocity determinations in sciatic and tibial nerves and measurement of evoked spinal cord potentials may also provide
indirect evidence of cauda equina dysfunction.
Plain radiographic findings include spondylosis deformans ventral and lateral to the lumbosacral articulation,
sclerosis of vertebral end-plates, wedging or narrowing of
the L7-Sl disk space, and secondary degenerative joint disease in the region of L7-S1 articular facets. Ventral displacement of the sacrum with respect to L7 (retrolisthesis)
and diminished dorsoventral dimensions of the lumbosacral
spinal canal may be seen; however, such findings must be
interpreted with caution, as they may be seen in normal dogs
in association with slight rotation of the vertebral column on
lateral radiographs. Every effort must be made to ensure that
such rotation does not occur during exposures for lateral radiographic projections. General anesthesia is mandatory for
obtaining radiographs of the lumbosacral vertebral column.
A ventrodorsal projection also is recommended.
Stressed or dynamic plain radiographic projections
(flexed and extended views), completed with careful attention to avoid rotation, often assist in determining the presence of instability or retrolisthesis. Several attempts to
separate normal dogs from dogs with lumbosacral vertebral
canal stenosis by means of objective measurements made
from radiographs have not been successful. Appearance on
plain radiographs helps to eliminate other causes of cauda
equina syndrome (e.g., diskospondylitis or vertebral neoplasia). Linear tomography, when available, may provide
specific information regarding the diameter of the lumbosacral vertebral canal that cannot be obtained from plain
radiographs.
Several specialized techniques exist for examination of
the lumbosacral vertebral canal. Use of such techniques is
necessary for demonstration of soft tissue vertebral canal
stenosis.
1. Myelography. Myelography is useful in the diagnosis
of lumbosacral problems. Although it has been reported that
the terminal portion of the subarachnoid space of dogs fills
unreliably with contrast material at this level, resulting in
misinterpretation of findings, myelography may be reliable
when an animal is tilted for sufficient time (up to 15 minutes) to ensure adequate filling of the caudal subarachnoid
space. The use of stressed radiographs (flexion and extension projections) may be combined with myelography.
Myelography also provides a means to screen the entire
spinal cord for abnormalities, particularly the lumbar enlargement, where a lesion may result in signs of cauda
equina dysfunction. Placement of a needle for completion of
myelography also provides the opportunity for collection of
cerebrospinal fluid.
2. Diskography. A technique that is useful for confirmation of lumbosacral soft tissue stenosis is diskography.
Diskography consists of radiography completed following
the injection of contrast material into the nucleus pulposus
of an intervertebral disk. This technique has special application to the lumbosacral disk space.

3. Epidurography.
4. Computed tomography (CT). Computed tomography
is best completed prior to any of the contrast procedures discussed above, as interpretation of CT images is difficult in
the presence of epidural contrast.
5. Magnetic Resonance Imaging (MRI). Magnetic resonance imaging may provide further information regarding
soft tissue stenosis of the lumbosacral vertebral canal. These
images may be generated after contrast procedures have
been completed, as the presence of epidural contrast will not
affect the images.
6. Surgical exploration. Surgical exploration may be indicated in dogs (with appropriate history and clinical signs)
in which results of ancillary diagnostic tests do not provide
a definite diagnosis of soft tissue stenosis.

Treatment
Some affected dogs in which clinical signs are mild or in
which apparent lumbosacral pain is the sole problem improve temporarily after strict confinement and restricted
leash exercise for a period of 4 to 6 weeks. Use of analgesic
drugs or corticosteroids has been recommended; however,
their use must be accompanied by strict confinement.
Clinical signs commonly reoccur in affected dogs treated only by means of medical therapy. Dogs with reoccurrence of signs, or dogs that are moderately to severely affected at the time of initial presentation (especially those

239

with urinary/fecal incontinence), should be considered candidates for surgical therapy. Dorsal decompressive laminectomy of L7 and S1 vertebrae is recommended. This procedure may be combined with foraminotomy or facetectomy in
dogs in which compression of spinal nerves at the level of
the intervertebral foramina is suspected. In animals with radiographically confirmed instability or significant retrolisthesis, fusion of the lumbosacral articulation may be necessary. A dorsal approach for fusion has been recommended,
and successful ventral lumbosacral fusion by means of a lag
screw fixation has been reported.
Dogs should be strictly confined for 4 to 6 weeks postoperatively. Postoperative complications include seroma
formation at the surgical site and formation of a laminectomy scar at the site of the laminectomy. Both may be avoided by use of appropriate surgical technique and postoperative patient management.
Attention to bladder emptying may be necessary in
dogs with bladder atony prior to surgery. The bladder
should be manually expressed three times daily in such
dogs. Urine should be submitted for culture and sensitivity
testing prior to and 2 weeks after completion of surgery,
and appropriate antibiotic therapy instituted as indicated by
results.
Prognosis for affected dogs is dependent on the severity
of signs prior to surgery. Return to normal function may be
expected in dogs that are mildly affected prior to surgery.
Dogs with bladder atony or a flaccid anal sphincter prior to
surgery have the poorest prognosis.

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241

Neoplasia of the central nervous system


Richard A. LeCouteur

Summary
The widespread availability of computed tomography
(CT) and magnetic resonance imaging (MRI) during the past
decade, have allowed veterinarians to conclusively diagnose
brain tumors with far greater frequency than was previously
possible. The development of advanced neurosurgical and
anesthetic techniques, have also made complete or partial
surgical removal of brain tumors a more frequent treatment
option. In addition to providing a definitive diagnosis of tumor type, even partial removal of a brain neoplasm may also help to relieve some of the signs of cerebral dysfunction,
and may make the animal a better candidate for other forms
of treatment, such as radiation therapy. Dogs with spontaneous brain tumors provide a unique model for brain tumor
research, as they are immunocompetent, have tumor types
with cell kinetics identical to those of people, and they are a
large animal with a brain size similar to that of people. Current research focuses on whether new approaches which selectively target brain tumor cells may provide a way to treat
brain tumors without damaging normal tissue.

INTRACRANIAL NEOPLASIA

carcinoma. Skull tumors that affect the brain by local extension include osteosarcoma, chondrosarcoma, and multilobular osteochondrosarcoma.
Although brain tumors occur in dogs of all breeds, either
sex and any age the incidence increases over 5 years of age
and a median age of 9 years was reported in one study of 86
affected dogs. Certain breeds have a higher incidence of
some tumor types. Glial cell tumors and pituitary tumors occur commonly in brachycephalic breeds, whereas meningiomas occur most frequently in dolichocephalic breeds. Canine breeds that are over-represented include the boxer,
golden retriever, Doberman pinscher, Scottish terrier, and
Old English sheepdog.
Meningioma is the most commonly reported primary
brain tumor of cats. Older male cats appear to be most susceptible and meningiomas in cats may occur without clinical
signs. Meningiomas involving multiple intracranial sites occur relatively commonly in cats. Primary brain tumors other
than meningiomas rarely occur in cats.
Secondary tumors that have been reported to occur in the
brain of cats include pituitary macroadenomas and macrocarcinomas, and metastatic carcinomas. Local extension
may occur either from squamous cell carcinoma of the middle ear cavity or from nasal adenocarcinoma.

A. INTRODUCTION
B. PATHOLOGY
The occurrence of intracranial neoplasia appears to be
more common in dogs than in other domestic species, but
few studies of the incidence of CNS tumors in dogs and cats
have been undertaken. In one study the incidence of CNS
neoplasia in dogs was reported as 14.5 per 100,000 of the
population and as 1-3% of all canine necropsies in another
study. The incidence in cats has been reported as 3.5 per
100,000 population. A broad spectrum of tumor types occurs
in dogs with gliomas (e.g., astrocytomas and oligodendrogliomas) and meningiomas appearing to be the most frequently occurring primary brain tumors of dogs. Although
most primary brain tumors are solitary, multiple primary
brain tumors and multiple tumors of different histologic
types have been reported. Meningiomas and lymphomas account for the majority of brain tumors in cats.
Secondary tumor spread may occur from local extension,
most commonly of nasal adenocarcinoma and metastases
from mammary, prostatic, or pulmonary adenocarcinoma,
hemangiosarcoma, and extension of pituitary adenoma or

The intracranial neoplasms of cats or dogs may be classified as either primary or secondary, depending on their cell
of origin. Primary brain tumors originate from cells normally found within the brain and meninges, while secondary tumors are those that have reached the brain by hematogenous
metastasis from a primary tumor located outside the nervous
system, or by local invasion, or extension, from adjacent
non-neural tissues such as bone. Pituitary gland neoplasms
(adenomas or carcinomas) and tumors arising from cranial
nerves (e.g., nerve sheath tumor of the oculomotor or
vestibulocochlear nerves) are considered secondary brain tumors, as they affect the brain by means of local extension.
Care must be exercised in the application of the terms benign and malignant to a brain neoplasm. In assessing the malignant potential of a brain tumor, the difference between cytologic and biologic malignancy should be emphasized. Cytologic malignancy is a morphologic assessment of anaplasia, while biologic malignancy is the likelihood that a tumor

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Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

242

will kill the animal. Most cytologically malignant brain tumors are also biologically malignant, despite the treatments
presently available. Cytologically benign tumors of the brain
may also be biologically malignant because of various secondary effects such as increased intracranial pressure (ICP).
Particular care must be exercised in the use of the term benign when discussing the meningiomas of dogs and cats. Although a canine meningiomas may be classified as benign, it
may be locally invasive and have poor demarcation from
normal brain tissue. Meningiomas in cats are almost always
well defined with a clear demarcation between normal and
affected brain tissue. Feline meningiomas appear to grow
more slowly than canine meningiomas.
Brain tumors cause cerebral dysfunction through primary effects such as infiltration of normal brain tissue, compression of adjacent structures, disruption of cerebral circulation and local necrosis. Secondary effects include hydrocephalus, increased intracranial pressure (ICP), cerebral edema and brain herniation. Primary brain tumors often are
slow growing and because the brain is contained within the
confines of the calvaria, gradual compression permits surrounding structures to adapt to increasing pressure. This occurs through a process termed compensation. During the
time the brain is able to compensate, there may be a prolonged history of vague signs (e.g., subtle behavior alterations). However, even with a very slowly progressive tumor, clinical signs may progress rapidly when compensatory mechanisms have been exhausted. Rapidly growing tumors do not permit compensation to occur to the same degree and in such cases a sudden onset of severe neurologic
dysfunction may occur in the absence of premonitory signs.
Should a neoplasm erode or obstruct a major blood vessel,
causing hemorrhage or infarction, an acute onset of neurologic deficits may ensue.
The patterns of spread of brain tumors are different from
those of other tumors because of several factors, including
lack of a well-developed lymphatic system within the brain.
Spread often involves local invasion and CSF seeding.
Brain tumors, particularly astrocytomas, have cells that are
capable of invading the normal brain. The biology of brain
tumors and the role of the immune system is an area of very
active investigation. It is well known that human brain tumor patients, especially those with high grade malignancies, have impairments of their immune systems, such as
defects of T-cell function, reduced levels of circulating Thelper/inducer cells, and T-cell suppressor factors. Glioma
cell lines in vitro can produce a protective mucopolysaccharide coating that impairs the generation of specific cytotoxic lymphocytes.

C. HISTORY AND CLINICAL SIGNS


History and neurologic examination are the first steps to
a definitive diagnosis in the evaluation of a dog or cat suspected of having a brain tumor. The neurologic signs resulting from a brain tumor depend primarily on the location, size
and rate of growth of the mass. Many dogs or cats will have
a long history of vague signs that are overlooked, such as
not wishing to be handled, hiding during the day, decreased

4th European FECAVA SCIVAC Congress

frequency of purring or diminished activity levels. One of


the most frequently recognized clinical signs associated with
a brain neoplasm of a dog or cat is seizures. This may take
the form of a generalized seizure, or it may be a focal
seizure. Focal seizures may aid in localizing a neoplasm.
Should a neoplasm involve the brain stem, cranial nerve
deficits in vision, hearing, or smell, may occur. Visual
deficits involve the visual pathways from the occipital lobe
of the cerebrum to the optic nerve. Hearing loss involves the
cerebellomedullary region, the brain stem, or temporal lobes
of the cerebrum. Problems with the ability to smell are seen
in association with lesions of the cribriform plate, olfactory
or temporal lobes of the cerebrum, or other rhinencephalic
connections. Difficulties with balance or gait suggest cerebellar or vestibular involvement.
The secondary effects of brain tumors, such as increased
ICP, represent further advancement of tumor growth. By the
time these effects occur, either a large tumor or significant
cerebral edema is present. The signs include alterations in
behavior (e.g., lethargy, irritability), circling, head pressing,
compulsive walking, altered states of consciousness, or associated locomotor disturbances. Unfortunately the majority
of cats or dogs with a brain tumor will be presented to a veterinarian with problems that relate to the secondary effects
of a tumor suggesting that brain tumors of cats and dogs usually have reached a large size by the time an owner seeks
veterinary attention. This is especially true with frontal lobe
neoplasms of dogs, which may reach a very large size before
causing clinical signs.
As in humans meningiomas in dogs are more common in
females and again as in humans meningiomas in dogs and
cats have receptors for estrogen, progesterone, and androgen, which may influence the growth and behavior of these
tumors. In contrast oligodendrogliomas occur twice as often
in males as in females.

D. DIAGNOSTIC TECHNIQUES
AND WORK-UP
On the basis of signalment, history, and the results of
complete physical and neurologic examinations, it is possible to localize a problem to the brain and, in some cases, to
determine the approximate location. However, it must be remembered that the signs that result from a disease in a given location in the nervous system will be similar, regardless
of the precise cause. The categories of disease that may result in clinical signs similar to those of a brain tumor include
congenital disorders, infections, immunologic and metabolic disorders, toxicities, nutritional disorders, trauma, vascular disorders, degeneration, and idiopathic disorders. These
other categories of disease must be eliminated before a diagnosis of brain tumor may be made. For this reason it is essential to follow a logical diagnostic plan for a dog or cat
that has signs of brain dysfunction.
A minimum data base for a dog or cat with signs of a
brain lesion should include a hemogram, serum chemistry
panel, and urinalysis. Survey radiographs of the thorax and
abdomen help to rule out a primary malignancy elsewhere in
the body. The major objective in the completion of these

tests is to eliminate extracranial causes for the signs of cerebral dysfunction.


Plain skull radiographs are of limited value in the diagnosis of a primary brain tumor; however, they may be helpful in the detection of neoplasms of the skull or nasal cavity
that have involved the brain by local extension. Occasionally, lysis or hyperostosis of the skull may accompany a primary brain tumor (e.g., meningioma of cats), or there may
be radiographically visible mineralization within a neoplasm. General anesthesia is necessary for precise positioning of the skull for radiographs.
Analysis of CSF is recommended as an aid in the diagnosis of a brain tumor. The results of CSF analysis may help
to rule out inflammatory causes of cerebral dysfunction, and
in some cases may support a diagnosis of a brain tumor. Care
should be used in the collection of CSF, because frequently
an increased ICP may be present and pressure alterations associated with CSF drainage may lead to brain herniation. It
is often desirable to hyperventilate the animal to decrease intracranial pressure prior to CSF collection.
In general, increased CSF protein content and a normal
to increased CSF white blood cell count are considered typical of a brain neoplasm although often CSF may be normal. Neoplastic cells may be present in CSF, particularly
when sedimentation techniques are used for analysis. Little
information is available regarding CSF alterations seen in
association with feline brain tumors; however, changes are
similar to those described for dogs.
Computed tomography (CT), provides accurate determination of the presence, location, size, and anatomic relationships of intracranial neoplasms. More recently, magnetic
resonance imaging (MRI) has allowed these principles to be
advanced even further. Images obtained by means of MRI
are superior to those of CT in certain brain regions (e.g. the
brainstem), and the diagnostic specificity of MRI may eventually render the biopsy of tumors prior to treatment unnecessary. While the major tumor types in dogs are reported to
have characteristic CT or MRI features, it must be remembered that non-neoplastic space-occupying lesions may
mimic the CT or MRI appearance of a neoplasm and that occasionally a metastasis may resemble a primary brain tumor
on CT or MRI. At the present time, biopsy and/or surgical
excision is the sole method available for the diagnosis of
brain tumor type in cats or dogs. The development of a
stereotactic frame that positions the head of a dog or cats so
that, using CT imaging, a precise fine-needle biopsy of the
animals brain tumor can be taken, has made the biopsy of a
brain tumor more routine in our hospital.

E. THERAPY
The major goals of therapy for a brain tumor are to control secondary effects, such as increased ICP or cerebral edema, and to eradicate the tumor or reduce its size. Palliative
therapy for dogs or cats with a brain tumor consists of glucocorticoids for edema reduction and, in some cases (e.g.,
lymphoma), for retardation of tumor growth. Some animals
with a brain tumor will demonstrate dramatic improvement
in clinical signs for weeks or months with sustained gluco-

243

corticoid therapy. Should seizure therapy be needed, phenobarbital is the drug best suited for the control of generalized
seizures.
Four methods of therapy for a brain tumor are available
at this time for use in dogs and cats: surgery, irradiation,
chemotherapy, and immunotherapy (or biologic response
modification). Surgery has become more frequent during the
past few years with the availability of CT and MRI, and the
development of advanced anesthetic techniques. Neurosurgical intervention is now an essential consideration in the management of intracranial neoplasms of cats or dogs, whether
for complete excision, partial removal, or biopsy. The precise
location, size, and extent of a neoplasm, determine the extent
of removal. The possibility of complete excision is also affected by tumor type. Meningiomas, particularly those located over the frontal lobes of the cerebrum, often may be completely removed, especially in cats. In contrast, there is a significant morbidity and mortality associated with the surgical
removal of neoplasms located in the caudal fossa and brainstem of cats and dogs. In addition to providing a tissue diagnosis of tumor type, partial removal of a brain neoplasm may
relieve signs of cerebral dysfunction and, may render an animal a better candidate for other forms of therapy, such as radiation therapy. Surgical biopsy of a tumor must be approached with care, as seeding of a tumor to previously uninvolved tissue may result in some cases.
The use of radiation therapy for the treatment of primary
brain tumors of dogs and cats is well established and it may
be used either alone or in combination with other treatments.
The objective of radiation therapy is to destroy a neoplasm,
while at the same time minimizing damage to any normal
tissue that must be included in the irradiated volume. External beam, megavoltage irradiation currently is recommended for the therapy of brain tumors in dogs or cats. Orthovoltage radiation has been used for the treatment of canine
brain tumors, but it should be stressed that orthovoltage radiation is not optimal because of poor beam penetration,
profile, and limited field configuration. Careful treatment
planning by a qualified and experienced radiation therapist
is essential to the success of radiation therapy. The selection
of a radiation dose is based partly on considerations such as
tumor type and location, and partly on tolerance of the tissues that surround the tumor and that have not been invaded
by the tumor.
Surgical removal of a solitary meningioma in cats results
in excellent long- term survival. At this time there are few
published reports concerning surgery or radiation therapy of
dogs and cats for the treatment of tumor types other than
meningioma. Radiation therapy alone has been used for the
treatment of caudal fossa neoplasms of dogs, granulomatous
meningoencephalomyelitis of dogs, and ACTH-secreting pituitary neoplasms of dogs. The preliminary results of these
groups of animals confirm that the prognosis for these animals is greatly improved following radiation therapy.
Because current treatments for brain tumors have proven
to be of limited effectiveness, the outcome for human and
veterinary patients with brain tumors has not improved over
the last three decades. New approaches that selectively target brain tumor cells may provide a way to treat brain tumors in the future without damaging normal tissue. These

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4th European FECAVA SCIVAC Congress

244

new treatment are based on the transfer of DNA to brain tumor cells which, unlike normal adult brain cells, are growing and multiplying. Work is underway at our institution to
determine whether genetically engineered viruses are capable of transferring new genes to canine brain tumor cells.
After being genetically modified with the viral DNA, the tumor cells may then be killed by drugs that have no harmful
effects on normal brain cells. Although experimentally brain
tumors may be induced in rats and dogs using nitrosourea
and avian sarcoma virus, dogs with spontaneous brain tumors provide a unique model for brain tumor research as
they are immunocompetent, have tumor types with cell kinetics similar to those of people, and they are a large animal
with a brain size similar to that of people. In the first phase
of this research we are studying whether brain tumor cells
will incorporate injected DNA. The client-owned dogs in
the project first undergo a stereotactically-guided, fine needle biopsy of their brain tumor. Once the presence of the appropriate tumor type has been confirmed, the same fine needle can be used to inject the engineered genes. Each patients tumor is removed surgically 48 to 72 hours later. The
tumor cells are then examined to see if the new genetic material is present.

SPINAL CORD NEOPLASIA


A. INTRODUCTION
Primary spinal cord neoplasms occur infrequently in
dogs. Tumors affecting the spinal cord may be considered as
extradural, intradural-extramedullary, and intramedullary.
Extradural neoplasms comprise approximately 50% of all
spinal neoplasms, while intradural-extramedullary tumors
and intramedullary tumors comprise 30% and 15%, respectively. Meningiomas appear to be the most frequently diagnosed primary spinal neoplasm of dogs and have a high incidence in the cervical spinal cord.
Primary spinal cord neoplasia, with the exception of
lymphoma, is relatively rare in cats. Most cats with spinal
lymphoma are young (median age 24 months). In cats, feline
leukemia virus (FeLV) is frequently associated with lymphoma and therefore must be considered a risk factor in the
development of spinal lymphoma. However, a cat with
spinal lymphoma may test negative for FeLV. Spinal lymphoma has also been identified in association with feline immunodeficiency virus infection.

B. PATHOLOGY
In dogs the most frequently reported extradural tumors
are primary malignant bone tumors and tumors metastatic to
bone and soft tissue. Meningiomas and peripheral nerve
sheath tumors are the most frequently occurring intraduralextramedullary neoplasms of dogs. These tumors are reported to occur most frequently in older dogs.
Intramedullary spinal tumors of dogs occur infrequently.
They are predominantly of glial cell origin. Granulomatous
meningoencephalomyelitis may also occur as a primary

4th European FECAVA SCIVAC Congress

spinal cord neoplasm. Intramedullary spinal cord metastases


may occur in dogs with systemic malignancy. It appears that
hemangiosarcoma and lymphoma have a propensity for intramedullary spinal cord involvement.
Extradural lymphoma, either primary or secondary, occurs frequently in cats. Of feline extradural tumors, osteosarcoma is the most common primary vertebral neoplasm.

C. HISTORY AND CLINICAL SIGNS


Extramedullary spinal cord neoplasms typically are slow
growing and result in gradual spinal cord compression. The
signs of spinal cord dysfunction usually worsen over weeks
or months. Occasionally, an acute onset of signs may accompany hemorrhage or ischemia associated with a neoplasm. Intramedullary tumors, which may grow more rapidly, are characterized by a higher incidence of ischemia,
necrosis, and hemorrhage.
The clinical signs seen in association with a spinal cord
tumor usually reflect the location of the neoplasm and often
are indistinguishable from the signs caused by other transverse myelopathies at the same location. The presence of
certain signs should cause suspicion of a spinal cord neoplasm. Extradural tumors may involve the meninges, spinal
nerves, or nerve roots, resulting in discomfort that may
progress to extreme spinal hyperesthesia. Neurologic
deficits (e.g., paresis) may not be seen initially and, when
present, may be intermittent (i.e., worsen with exercise).
There is usually a progressive worsening of neurologic function caudal to the lesion. Intraduralextramedullary tumors
may also result in a prolonged, intermittent expression of
clinical signs and hyperesthesia; however, the signs may be
alleviated by exercise. Brachial or lumbar intumescence involvement may be evidenced by lameness, holding up of a
limb, neurogenic muscular atrophy, and depressed spinal reflexes. Rarely, unilateral spinal cord compression may cause
deficits in the contralateral limb. In contrast, intramedullary
spinal cord tumors usually cause rapid progression of neurologic dysfunction. Hyperesthesia rarely is associated with
such tumors.

D. DIAGNOSTIC TECHNIQUES
AND WORK-UP
The diagnosis of a neoplasm affecting the spinal cord requires a systematic approach. The procedure is based on the
collection and interpretation of a minimum data base that includes appropriate serologic tests (hemogram, biochemical
profile), and thoracic radiographs for primary or metastatic
neoplasia. Following this, survey radiographs of the vertebral column, CSF collection and analysis, and myelography
may be completed during a single period of anesthesia.
General anesthesia permits accurate positioning of a dog
or cat for survey radiographs of the vertebral column and allows stressed or oblique projections to be done. Primary or
secondary vertebral tumors may produce bone lysis or new
bone production, or both. The vertebral body and arch are
more frequently affected by a neoplasm than the dorsal spin-

4th European FECAVA SCIVAC Congress

E. TREATMENT
A limited number of therapeutic options exist for a dog
or cat with a spinal cord neoplasm. Appropriate therapy de-

pends on tumor location, extent, and histologic type. An immediate goal of therapy is to relieve the deleterious effects
of sustained spinal cord compression. This may be achieved
medically (e.g., glucocorticoids) or surgically. Surgery may
permit the complete removal or reduction and biopsy of a
neoplasm. In cases in which complete removal is not possible, recurrence is to be expected, and adjunctive therapy
such as irradiation is recommended. The development of advanced neurosurgical techniques and the introduction of
new biopsy methods has improved the outcome in many
cases.
Accurate biopsy diagnosis of lymphoma is essential, because lymphoma of the spinal cord may be successfully
treated with chemotherapy or irradiation alone, or in combination.

F. PROGNOSIS
There are few reports in the veterinary literature concerning the long-term follow- up of dogs and cats with
spinal neoplasia. The prognosis depends on the resectability,
histologic type, location, and severity of clinical signs. Generally, dogs or cats with an extradural metastatic neoplasm
or vertebral neoplasm have a poor prognosis, and palliative
therapy only is attempted. Removal of an affected vertebra
(spondylectomy), particularly in the cranial lumbar region,
may be attempted in selected cases. Occasionally, intradural- extramedullary tumors may be completely resected, and
in such cases the prognosis must be considered good.

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ous processes or transverse processes. Plain radiographic


abnormalities are uncommon with primary nervous system
neoplasms. Expansion of a spinal tumor may result in the enlargement of an intervertebral foremen, widening of the vertebral canal, or thinning of surrounding bone.
Cerebrospinal fluid collection and analysis are always
indicated especially since plain radiographs may not provide
a complete diagnosis. A lumbar puncture is recommended
for CSF collection, and the needle may be left in place for
myelography, pending the results of the cytologic examination of CSF. The alterations in CSF caused by spinal tumors
should be interpreted according to the same criteria discussed for brain tumor diagnosis; however, it must be remembered that the protein content of CSF collected from a
lumbar location is normally higher than that of CSF collected from the cerebellomedullary cistern. Lymphoma affecting the spinal cord often results in an elevated white cell
count, predominantly abnormal lymphocytes.
Myelography is essential for the accurate determination
of the location and extent of a spinal cord neoplasm. On the
basis of myelography, the tumors may be classified as extradural, intradural- extramedullary, or intramedullary, although this distinction cannot always be made. CT or MRI
may provide more exact localizing information.

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247

Extrasystoles on the ECG: the rational approach


Christophe W. Lombard

Summary
VPCs are recognized by a widened and bizarre shaped
QRS-complex that occured prematurely among normal sinus
beats. The recognition of prematurity is essential to avoid
confusion or false diagnosis of the rare ventricular escape
complexes occuring with sinus pauses or exit blocks. An important differential diagnosis for very widened, bizarreshaped complexes is bundle branch block; these complexes
have however preceeding P-waves and normal PR-Intervals,
and are much wider than VPCs.
Once diagnosed to be indeed premature ventricular activity, the determination of the hemodynamic importance
and electrophysiologic danger should be made. The latter
is speculative and stands for the risks of evolving into a severe tachyarrhythmia, leading to possible hemodynamic collapse and so-called sudden cardiac death.
The hemodynamic consequences of ventricular tachyarrhythmias can be determined by the severity of the pulse
deficit, abnormality of the capillary refill time, reduction of
blood pressure, and reduced pulse oxymetry measurements.
The determination of the need for therapy, based on
these abnormalities, is very empiric; implementation of
treatment varies highly among clinicians. I prefer to have
additional clinical data such as electrolyte and acid base
status of the patient, as well as some data (mostly echocardiographic) about heart size and contractility, before deciding about the need for treatment. As a general rule, ventricular tachyarrhythmias without underlying primary heart
disease need not be treated very aggressively, because they
very rarely lead to fatalities and have little reduction of
blood pressure and cardiac output. Rather, the probable etiologic abnormality leading to hypoxia and/or acid-base and
electrolyte abnormality should be treated. When signs of primary myocardial disease (dilated chambers, reduction of
fractional shortening, evidence of dyskinesis etc) are present, antiarrhythmic therapy is more likely indicated to improve and normalize the hemodynamic situation.
In most clinical situations associated with ventricular
tachyarrhythmias, oxygen support can only be beneficial
and frequently palliates the irregular rhythm. Then, I like to
initiate antiarrhythmic therapy with mexiletine, and lidocaine as my second choice. Mexiletine is preferred because
of its high efficacy and availability both as injectable and
oral preparations, facilitating a later switch to longterm
treatment when necessary. In cases with suspected influence

of high endogenous catecholamine release (stress, anxiety),


the drug sotalol with its class II and III antiarrhythmic effects (Vaughn-Williams classification) is a reasonable
choice. Severe chronic ventricular arrhythmias, most often
associated with some degree of myocardial impairment, can
be treated with amiodarone. This drug has a very powerful
antiarrhythmic efficacy, but large scale studies of suppression rates and side effects are lacking in veterinary patients.

1. Recognition and differentiation


of extrasystoles
Extrasystoles are recognized as prematurely occuring
heart beats with a different morphology than normally conducted beats originating from the sinus node. In this presentation, we will limit the discussion to ventricular extrasystoles; they do have an broadened, bizarre shaped QRS-T
complex, always a discordant T-wave and no relationship to
an eventually preceeding p-wave. Ventricular extrasystoles
(VES, or better termed ventricular premature contractions,
VPC) may occur as isolated events, coupled 1:1 with sinus
beats (ventricular bigeminy), in pairs of two (couplets), three
(triplets) or as runs of four or more VPCs; this is called
paroxysmal ventricular tachycardia (pVT).
Paroxysmal ventricular tachycardia can be further divided into nonsustained tachycardia (runs of less than 20-30 sec)
and sustained tachycardia (runs lasting longer than 30 sec),
Muir 1991. Uniform or unifocal VPCs are differentiated
from multiform or multifocal VPCs, where several morphologically different QRS-T-types occur and may suggest that
they originate from different foci within the ventricles. This
concept is most often correct, but neglects the explanation
that unifocal VPCs may look different from each other if
some beats have so-called aberrant conduction. Based on
morphology, the origin of the VPC may also be guessed; left
ventricular origin VPCs usually have a more abnormal morphology (inverted QRS-complexes in leads I, II, III and aVF)
and greater QRS-duration than sinus beats, while right ventricular or septal origin VPCs have reasonably normal configuration (upright in leads I, II, III and aVF) together with
broadening of the QRS-complex. Ventricular premature complexes must be differentiated from ventricular escape beats
that have similar morphological features (broadened and
bizarre QRS-T-complex), but occur late, with a greater that
usual RR-interval; escape beats or escape rhythms occur with

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DVM, Dipl ACVIM, Dipl ECVIM


Klinik fr kleine Haustiere - Universitt Bern - Berne - Switzerland

248

extreme bradycardias or because of failure of the primary


pacemaker (sinus node) to maintain a sufficiently high rate.
They must not be confused with VES. Their therapeutic approach, if necessary, is totally different.

2. Determination of the severity


and its hemodynamic consequences
While the detection and the classification of arrhythmias
is relatively easy, finding rational reasons to justify treatment is much harder to accomplish. Most often the decision
is made based on some arbitrary values indicating the severity or frequency of VES, some impression of hemodynamic
compromise of the patient because of the arrhythmia, and
some feeling about the danger that the arrhythmia might deteriorate into more life threatening forms such as very fast
ventricular tachycardia, torsade des pointes (TDP) and ventricular fibrillation. These extremely dangerous forms of arrhythmias result in a very rapid deterioration of cardiac output and perfusion, peripheral as well as coronary, and to collapse of the patient. Another descriptive term for these
events is sudden cardiac death (SCD). If not resuscitated immediately, the patient will die from the lack of perfusion of
the essential vital organs (brain, lungs and the heart).
It is therefore necessary to determine danger and hemodynamic deterioration of arrhythmias in order to make rational decisions regarding management and therapy. This simply because antiarrhythmic therapy is not without certain
hazards itself. Most available antiarrhythmic drugs unfortunately cause either some lowering of the blood pressure or
have negative inotropic side effects on the myocardium, or
both. Unfortunately, most antiarrhythmic drugs have also
been shown to have a low incidence of proarrhythmic side
effects under specific circumstances, potentially worsening
the cardiac rhythm and jeopardizing the patient. Particularly
class 1A and some class 1C drugs may prolong the QT-interval and set up the stage for arrhythmias caused by early
afterdepolarisations. The need for any antiarrhythmic therapy, however difficult it may be to establish this parameter,
should clearly be shown; the benefits must outweigh the potential risks, and close initial monitoring is essential to recognize any worsening with antiarrhythmic therapy.
The parameters that should be considered in evaluating
the severity of any cardiac arrhythmia are the following:
heart rate changes,
frequency and complexity of VES,
electrophysiologic danger of the VES,
resulting reduction of the stroke volume or cardiac output,
resulting reduction of blood pressure,
resulting reduction in peripheral tissue oxygenation.

2.a. Heart rate changes


Any arrhythmia leading to an excessively elevated (our
limit 160-180/min) or lowered (our limit 50-60/min) heart
rate may cause a reduced cardiac output (CO). This important functional parameter is determined by multiplying
stroke volume (SV) with heart rate (HR). Severe bradycar-

4th European FECAVA SCIVAC Congress

dias simply lack enough heart beats to keep up a sufficient


CO, while severe tachycardias cause such a short diastolic
filling time resulting in a reduction of the SV that isnt compensated by the elevated heart rate. It isnt very practical to
measure stroke volume in clinical cases with arrhythmias.
With Doppler-echocardiography however, the reduction of
the velocity-time-integral of the aortic flow signal (VTI, aequivalent to stroke volume) of a VES in comparison with a
normal sinus beat can clearly be documented. It results
mostly from a shortened diastolic filling time and additionally from an abnormal sequence of the ventricular depolarisation and therefore diminished systolic emptying of the
ventricle with a VES. Recognizing this reduced stroke volume of a VES, It makes sense to consider the frequency of
VES as a reliable indicator of the hemodynamic compromise, i.e. the reduction of cardiac output.

2.b. Frequency, complexity,


and electrophysiologic danger of VES
Holter-electrocardiography (ambulatory longtime
recording onto a specialized cassette recorder and afterwards
analysis with specialized computer software) is the method
of choice for an accurate count of VES per hour or during a
24 hr period. This technique unfortunately is quite time consuming and somewhat expensive; the method is usually
found at university hospitals and reserved for research work
or special investigations about drug efficacy. In the set-up of
private practice, the frequency of VES is simply calculated
as a percentage of the sinus beats or as an absolute number
per minute, counted from a short ECG-rhythmstrip recorded
over 30 to 60 seconds. Obviously, this method is very inaccurate and not very reliable, particularly in patients with intermittent arrhythmias. It is however the only practical
method to determine the frequency of VES and the need for
antiarrhythmic therapy. Auscultation of the heart and recording the incidence of VES by counting is not practical. In the
literature, numbers indicating the severity of an arrhythmia
and the need for intervention appear quite arbitrary. Single
VES occuring less than 20 to 30 times per minute may be
considered not worthy of therapy and could be totally innocuous (Muir 1991). This number is equivalent to approximately 25% of heart beats being of ectopic origin. Personnally, I prefer a lower limit and start therapy with VES-frequencies over 10-15% of the sinus beats (< 20 VES/min). In
the Doberman breed however, single VES occuring at very
low frequencies (< 1000/24hr) are a reliable early indicator
of the impending particular cardiomyopathy of that breed
(Calvert 1995). With frequencies between 30 and 75% of ectopic beats (30-100 VES per minute), veterinary cardiologists usually agree that this represents a moderate severity
and deserves to be treated. Higher frequencies of VES result
in elevated heart rates, are considered severe arrhythmias
and should be managed with rather aggressive therapy. Short
bouts of fast ventricular tachycardias (heart rates over 180200/min during the episodes) or displaying the feature of sinusoidal twisting of the QRS-axis around the isoelectric
point = torsades des pointes (TDP) are equally considered to
be severe and treated aggressively).

The occurance of multiple forms of VES (multifocal


VES) is generally considered as a worse arrhythmia, with
more electrical instability and more potential for electrical
deterioration into fatal ventricular fibrillation. Multifocal
VES likely indicate more widespread foci of increased automaticity and/or reentry circuits in a heart that is suspected to
be suffering from some ischemia or cellular damage.
The amount of prematurity, i.e. closeness of the VES to
the T-wave of the preceeding normal sinus beat, is important
for the determination of electrophysiologic danger; the
phase of increased or supranormal excitability of the ventricular myocardial cells occurs during the T-wave of the
body surface ECG. VES occuring at that particular time, displaying the so-called R-on-T phenomenon, have great potential for inducing ventricular tachycardia and fibrillation
(Muir 1991).

2.c. Resulting hemodynamic alterations


It is very important to know if the patient with an arrythmia is suffering from heart failure or not. Heart failure, especially insufficient perfusion of peripheral tissues, will be
recognized by abnormal clinical signs such as generalized
fatigue and weakness, weak arterial pulses, prolonged capillary refill time and an elevated heart rate. Pulmonary congestion is indicated by dyspnea and/or tachypnea, the presence of crackles and usually cough; right sided congestive
heart failure is indicated by venous congestion, ascites and
sometimes pericardial and pleural effusion. In such cases,
radiographs should be obtained as soon as possible and the
signs of pulmonary edema and the effusions confirmed. At
the same time, the size of the heart is evaluated, and any
signs of cardiomegaly interpreted as preexisting underlying
cardiac disease that may even be the cause of the arrhythmia. Determination of the hemodynamic consequences of
an arrhythmia serves primarily to derive indications and justification for treatment, and to indicate how aggressive the
therapy should be. In cases with suspected preexisting cardiac disease and hemodynamic compromise, arrhythmias
are likely to compound the poor perfusion and congestion
even more. In such cases, a more aggresive approach appears justified. It may not always be possible or practical to
measure the hemodynamic depression very accurately, but it
should be attempted. The available methods are the measurement of peripheral arterial blood pressure and tissue
oxygenation with pulse oxymetry. They are now easily accomplished with simple devices. Especially with intermittant tachyarrhythmias, diminished perfusion and lowered
oxygen saturation can sometimes directly be correllated
with runs of tachycardia. With echocardiography, diminished ventricular excursions may be demonstrated during
runs of tachycardia. Multifocal tachyarrhythmias are usually associated with poorer ventricular function. Diminished
aortic flow of VES or tachycardic episodes can be documented with Doppler recordings, particularly the VTI
(equivalent to the cardiac stroke volume). During tachycardic episodes, the pulse deficit may be severe. While documentation of peripheral hemodynamic depression may be
feasible with pulse oxymetry, one can only speculate on the

249

arrhythmias effect onto coronary perfusion. Herein lies the


danger of many severe tachyarrhythmias; they cause coronary ischemia and hypoxemia of already damaged myocardial cells. If a critical threshold of hypoxemia is reached in
areas of electrical instability, new and potentially fatal arrhythmias are facilitated.

3. Evaluation of underlying heart disease


Results from a very thorough evaluation of the history
and an in depth physical examination should enable the clinician to determine if the patient has preexisting primary
heart disease, or if the arrhythmia is more likely caused by
extracardiac or systemic problems that affect the heart secondarily. Systemic problems super-imposed on primary cardiac disease may occur and usually result in worse clinical
signs and arrhythmias that are more challenging and more
resistant to therapy. The prognosis appears to be worse as
well. As an example, VES in dogs with vegetative endocarditis, fever and poor general condition appear to cause a
high incidence of SCD. Features such as age, breed and particularly the presence of either heart murmurs or additional
heart sounds or gallop-rhythms are valuable indicators of
preexisting heart disease. If primary underlying heart disease is suspected, a complete cardiovascular data base including a full ECG, thoracic radiographs, blood pressure
measurement, blood gases and echocardiography should be
established as soon as possible. The ECG should be carefully analysed, the usual intervals measured and dangerous features such as long QT-intervals, evidence of afterdepolarisations, torsades des pointes (TDP) and ST-deviations (signs
of ischemia) recognized. Depending on the severity of clinical signs, the data base for critically ill patients should be
collected and analysed as the highest priority. This should
include a blood count, a complete serum chemistry (especially the electro-lytes potassium, calcium, and magnesium),
and the blood gas/acid-base status.
In patients without suggestions or evidence of primary
cardiac disease, the clinician should concentrate on collecting a complete data base for that particular organ system
with dominating signs and obtain cardiac images at a later
time. The following diseases are all known conditions associated with cardiac arrhythmias, particularly when cardiac
damage is severe and signs of decompensation or failure begin to appear.
Primary heart diseases (adapted from Sisson 1988)
congenital defects: subaortic stenosis PDA, VSD with
signs of CHF, advanced mitral and
tricuspid dysplasia
tetralogy of Fallot, pulmonic stenosis inherited SCD in German Shepherds (Moise 1992)
AV-bundle stenosis in Pugs
acquired diseases:
special forms of cardiomyopathy:
Dobermann (Calvert 1995)
Boxer (Harpster 19xx)
vegetative endocarditis regular
cardiomyopathy (esp. hypertrophic,

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4th European FECAVA SCIVAC Congress

250

specific infections:

neoplasias

4th European FECAVA SCIVAC Congress

restrictive, dilated) advanced degenerative valvular disease, especially


with arteriosclerosis, ischemia and
MIMI
myocardial failure and hypoxia
pericarditis
ventricular preexcitation syndromes
(Atkins 1995)
sick sinus syndromes (Miniature
Schnauzers, others)
Chagas disease (T. cruzei, granulomatous myocarditis)
Rocky Mountain Spotted Fever
(Rickettsia rickettsii)
Lime carditis (Borrellia burgdorferi)
primary right atrial HSA, chemodectoma, lymphoma

Extracardiac causes of arrhythmias (adapted from Sisson


1988)
hypoxia
severe anemia, hypotension, shock,
pulmonary parenchymal disease,
pleural disease, airway obstruction,
thromboemboli.
electrolyte and
hyperkalemia, hypercalcemia, any
metabolic acidosis
acid-base disorders hypomagnesiemia, hypokalemia
trauma
traumatic myocarditis (Abbott 1995)
any trauma leading to shock, hypoxia and excessive sympathetic stimulation
metabolic and
gastric torsion and volvulus, sepsis,
pancreatitis, uremia,
endocrine problems peritonitis, hyperthyroidism, diabetes mellitus, Cushings syndrome,
hyperviscosity syndromes, hyperthermia, heat stroke
systemic infections infectious myocarditis (all causes, Liu
et al 1995): viral, rickettsial, protozoan, spirochaetal, fungal, algae-like
drugs/toxins
halothane, xylazine, thiobarbiturates,
doxorubicin, digitalis glycosides,
dobamine/dobutamine, other catecholamines, toad poison (Bufo marinus), oleander, thallium, lead, ethylene glycol, cobalt
neoplasias
phaeochromocytoma, LSA, other
metastatic tumors
CNS-disease,
increased intracranial pressure, CNS
disorders
neoplasia, encephalitis, spinal cord
of the autonomic NS trauma, autonomic imbalance.

4. Possible mechanisms leading


to arrhythmias
The two principal mechanisms leading to cardiac arrhythmias are either increased automaticity of a group of diseased cells that is normally not having pacemaking function,
or the developement of reentry circuits (abnormal conduc-

tion, i.e. unidirectional block, through diseased cell groups)


that can lead to circus or reentrant tachycardias. For practical
purposes, differentiation of the two mechanisms is of minor
importance. Any damage to the cardiac cell membrane (ischemia, hypoxia, reperfusion injury, acidosis, electrolyte imbalance, excessive sympathetic stimulation, stretch, necrosis) can alter its ionic permeability and stability to an extent
where spontaneous depolarisation occurs, or where conduction is altered, Russel and Rush 1995. These predisposing
factors or causes of arrhythmias have primarily been recognized in cardiac muscle fiber preparations investigated in organ bath solutions, and the knowledge gained from these experiments was extrapolated to the entire heart. Nervertheless,
these basic metabolic derangements are recognized with
many systemic diseases, and it appears permissible and logic to speculate that the measured electrolyte and acid base
abnormalities of the serum reflect ionic changes occurring at
the cardiac cellular level. Recent interest has focussed onto
excessive sympathetic stimulation in conditions with fever,
hypotension, hypovolemia, shock, neurological and spinal
cord disease. Catecholamines are known to increase automaticity of pacemaker cells by increasing the slope of phase
4 cellular depolarization, by increasing conduction through
the sodium and calcium channnels. A similar increase in automaticity probably takes place in diseased, partially depolarized Purkinje cells. Catecholamines also increase the amplitudes of afterpotentials, thereby favorizing so-called triggered automaticity. Catecholamines also alter conduction
velocity through diseased myocardium present in reentry
loops, thereby favorizing reentrant arrhythmias. Additionally, excessive alpha-adrenergic stimulation may lead to coronary vasoconstriction and ischemia.
Another area of new interest is reperfusion injury to myocardial cells, known to occur after conditions such as the
GDV-complex, and severe trauma with shock and hypotension, Russel and Rush 1995. The superoxide radicals generated during reperfusion are very damaging to myocardial
cells and destabilize the normal ionic balance responsible for
maintaining normal automaticity and conduction. Myocardial necrosis and subendocardial hemorrhage, facilitating
dysfunction and arrhythmias of damaged myocardial cells,
have also been seen in trauma (general and spinal cord, Abbott 1995), GDV, and splenic masses.
The mechanism of arrhythmogenesis with neurologic
disease or injury seems to be mediated through excessive
activation of the sympathetic nervous system, Russel and
Rush 1995.
The importance of an altered electrolyte status for arrhythmiagenesis and maintenance of irregular rhythms
should be emphasized. Many of the commonly used class
1A and 1C- antiarrhythmic drugs (Quinidine, Procainamide,
and Lidocaine) can not develop their antiarrhythmic efficiency during hypokalemia, occuring with many systemic
diseases and prolonged anorexia, Russel and Rush 1995.
Hypercalcemia as a cause of cardiac arrhythmias appears to
be rare; the arrhythmogenic effect of too rapid calcium-infusions in patients with hypocalcemia however is well known.
The influence of magnesium on arrhythmias has gained interest in veterinary medicine; it appears well established in
human medicine. It is unfortunate that serum levels do not

4th European FECAVA SCIVAC Congress

5. Therapy of ventricular
tachyarrhythmias

etc.) with buprenorphine at a dose of 0.01-0.02 mg/kg im.


During the time of these corrections, the ECG should be
monitored frequently and the patient prepared for continuous ECG-monitoring with stick-on electrodes (modified
bipolar leads, e.g. base-apex) and an oscilloscope with a
strip chart recorder having slow recording speeds (i.e. 5 or
12.5 mm/sec), if this equipment is available.

5.b. Selection of a drug


Many protocols about the use of lidocaine, quinidine and
procainamide, both as boli and constant rate infusions for
VES and ventricular tachycardia, have been published in the
specialized veterinary literature, Muir 1991. We have focussed our interest on newer drugs like mexiletine that are
supposedly safer with less side effects; Lunney and Ettinger
1991, Gonin and Lombard 1997. Reports in the veterinary
literature about these newer drugs are unfortunately sparse.
One of the advantages of using mexiletine is that this drug
does nor interfere with serum digoxin levels; it may be combined with other antiarrhythmics, and together with quinidine has more than additive antiarrhythmic effects.

5.a. Supportive measures


From the discussion above, it is evident that elimination
of any predisposing factors leading to ventricular tachyarrhythmias may often abolish abnormal rhythms and already solve the problem. As many of the mentioned metabolic derangements can be corrected relatively easily in an
intensive care setup, they should be initiated as soon as they
are recognized, before selecting an antiarrhythmic drug. We
propose to take the following steps:
1. Oxygen support (nasal catheter etc.) if peripheral pulse
oxymetry falls below 95%, or if the patient is tachypneic
and/or cyanotic. Transfusion of RBCs if the packed cell
volume is below 20-25%.
2. Rehydration of an exsiccotic patient over a 4-6 hr period;
mandatory monitoring of the central venous pressure to
avoid iatrogenic pulmonary edema if primary cardiac disease is present.
3. Monitoring of arterial blood pressure with noninvasive
devices, if available.
4. Correction of any metabolic acidosis with pH-values below 7.15 or plasma bicarbonate values below 12-15
mEq/l. Standard guidelines about the amount of sodium
bicarbonate to be infused should be followed.
5. Correction of an eventual hypokalemia (our normal range
4.0-5.5 mEq/l) through the supplementation of 1-2
mEq/kg/24hr period. With severe hypokalemia, a more
rapid supplementation of 1-2 mEq/kg over 6 hrs while
monitoring cardiac rhythm and repeating K- measurements frequently is advocated.
6. Correction of an eventual hypomagnesemia (normal
range 1.7-2.4 mEq/l) through the infusion of 0.75-1.0
mEq/kg/24hr period. With severe hypo- magnesemia,
rapid iv-substitution of 0.1-0.3 mEq/kg in D5W or saline
over a 15min period can be attempted (Dhupa 1995).
7. Analgesia in cases with known painful conditions (posttrauma, fractures, peritonitis, postoperative situations

5.b.1.Guidelines for using mexiletine


We start with a bolus of 2.5 mg/kg intravenously, diluted
in saline, D5W or lactated Ringers solution and given over
2-3 minutes. It can be repeated safely once or twice after 105 minutes respectively, and primarily serves to document the
efficacy of mexiletine for the suppression of VES.
In the meantime, a constant rate infusion (CRI) with a
concentration of 250 or 500 mcg/ml (= 0.025% or 0.05%,
depending of the hydration status of the patient) in any fluid
is prepared, and applied at a loading dose of 30 mcg/kg/min
for 3 to 5 hrs. The following formula has proven very simple for the calculation of the drip speed with a suitable infusion pump:
mexiletine dose (30 mcg) x body weight
(in kg) x 60 min
= volume (in ml/hr)
drip concentration (500 or 1000 mcg/ml)
The original concentration of mexiletine is 25 mg/ml in
10 ml glass vials, so 20 ml (2 full vials) or 40 ml (4 full
vials) are placed into 1000 ml of infusion to obtain the desired concentration of 500 (0.05%) resp. 1000 mcg/ml
(0.1%).
After 3-5 hrs of infusion at the 30 mcg/kg/min rate, the
patient is reevaluated and the drip speed reduced to a maintenance dose rate of 5-8 mcg/kg/min, using the above mentioned formula again.
With persistance of the VES, the high dose of 30
mcg/kg/min can be kept safely for up to 10 hrs, provided that
the patient is intensely monitored. If VES reappear during
the maintenance dose of 5-8 mcg/kg/min, the drip can also
safely be re-increased to 30 mcg/kg/min for one or several
more hours.

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reflect intracellular (cardiac and other body cells) stores accurately. Hypomagnesemia is present in many critically ill
human patients in an emergency room setting (Sachter
1992), and magnesium levels likely follow abnormalities of
potassium. Magnesium is important for the normal function
of the Na+/K+ ATPase pump, which maintains normal intracellular potassium levels. Hypomagnesemia therefore may
favorize reduced intracellular potassium levels, leading to
partial depolarisation and electrical instability of myocardial
cells, particularly if additional digitalis therapy has already
reduced the function of the ATPase-pump. Dogs and cats
with heart failure receiving vigorous diuretic therapy may
have a depletion of both potassium and magnesium. There is
circumstancial evidence that magnesium administration may
help to abolish supraventricular arrhythmias (PAT, atrial fibrillation) as well as refractory ventricular arrhythmias, especially those associated with myocardial infarction and digitalis intoxication, Russel and Rush 1995.

251

252

Side effects with this protocol are rare. Signs of toxicity


may include nausea, vomiting, muscle fasciculations and
possibly seizures. They should be managed with diazepam
to effect (2.5-5 mg boli iv). We have archieved good control
of VES with different etiologies (mostly secondary conditions such as GDV affecting the heart) with this protocol in
many patients, Gonin and Lombard 1997.
In situations with less severe arrhythmias or less urgent
need for suppression, mexiletine can be given as intramuscular injections or at an oral maintenance dose of 3-8 mg/kg
2-3 times daily. Higher doses should only be given with
close monitoring of the ECG (prolongation of the QRS-duration and the QT-interval over 30% of initial values may be
warning signs of impending toxicity). In our experience,
mexiletine has also shown good success in suppressing VES
with primary cardiomyopathies, in various breeds as well as
in Boxers and Dobermans.

5.b.2. Combination of antiarrhythmic drugs


with Beta-blockers
In Dobermans, resistance to antiarrhythmic monotherapy
has been observed, Calvert 1995. Combinations of class I
antiarrhythmic drugs with B-blockers may be necessary for
a reasonably high, though sometimes still incomplete suppression of VES. The therapeutic goal in such cases may
have to be modified and include only the suppression of dangerous forms of multifocal VES and ventricular tachycardia,
thereby hopefully eliminating the danger of sudden cardiac
death, rather than intoxicating the patient with dangerously
high drug dosages.
Such blockage of excessive sympathethic tone may obviously also be tried in other breeds with cardiomyopathy
and resistent VES, as well as in cases without primary cardiac disease where the clinician feels that high catecholamine levels may contribute to arrhythmiagenesis. The
negative inotropic side effect of the beta-blocker should
carefully be considered, and the patient monitored intensively (blood pressure, echocardiography, auscultation of the
lungs) when such potentially dangerous drug combinations
are applied. The ultrashort acting betablocker esmolol may
be tried to test the effect of beta blockade with repeated intravenous boli of 0.1 mg/kg or with infusions (CRI) of 50200 mcg/kg/min. Longacting betablockers used for that purpose in dogs are:
metoprolol 0.2-1 mg/kg 3xdaily
atenolol 0.5 mg/kg 2xdaily

5.b.3. Propafenone, sotalol and amiodarone


Propafenone is a class 1 antiarrhythmic drug and has
supposedly very weak additional class 2 (betablocking) and
class 4 (calcium channel blocking) effects, Gabriel and Kersten 1993. It was used in a series of dogs with primary and
secondary cardiac disease by these authors. Suppression of
VES and ventricular tachycardia was good in the majority of
cases at oral doses of 3 mg/kg TID, with the effect only developing after a few days because of a relatively long time

4th European FECAVA SCIVAC Congress

needed for tissue saturation. Using slow intravenous boli of


1 mg/kg or CRI at 0.008 mcg/kg/min showed complete suppression of VES in a few dogs.
Sotalol has combined betablocking (class 2) and action
potential-prolonging (class 3) antiarrhythmic effects. This
may represent certain advantages in patients with suspected
high sympathetic drive. We have used the drug in selected
cases where mexiletine resulted in only partial suppression
of VES, with quasi equal or slightly better results of arrhythmia suppression. There arent any published reports
about veterinary use of the drug.
Amiodarone is an extremely powerful antiarrhythmic
drug (class 3) that is reserved for the suppression of
lifethreating tachyarrhythmias not controlled by other drugs
in man because of ist severe and frequent, dose dependant
gastrointestinal, neurologic and thyroid side effects. Only
anecdotal reports abouts its use in dogs are available. Its indication may be severe arrhythmias resistant to other drug
combinations, in primary cardiomyopathies of Dobermans
or in the inherited SCD-syndrome of young German Shepherds. The potential benefits must clearly outway the risks in
such adrug with unproven safety.

5.b.4. Antiarrhythmic therapy in cats


The antiarrhythmic drugs of choice for suppressing VES
in cats are either beta-blockers or procainamide.Very little is
published about the efficacy, mostly recommendations for
therapy. Generally doses should start low and be increased
according to tolerance and antiarrhythmic effect.
Propranolol
2.5 - 5.0 mg TID po.
Atenolol
6.25 - 12.5 mg/24 hr period.
Procainamide
3-8 mg/kg po q 6-8hrs.

6. Monitoring
With arrhythmias caused by secondary, extracardiac disease, the patient usually improves rapidly with therapy directed at the specific organ dysfunction, and the antiarrhythmic therapy can frequently be switched to oral preparations
after 48 hr of intravenous therapy or even discontinued completely. Initially, frequent controls of the electrolyte and
acid-base status serves to document such improvement,
while the cardiac monitoring should include blood pressure
control and frequent ECG-recordings (with measurement of
the important intervals).
Repeated echocardiography and holter-ECGs are particularly suited for the longterm monitoring of arrhythmic dogs
(particularly Dobermans) with underlying primary cardiomyopathy, Calvert 1995. Once the shortening fraction
falls under 20%, progressive left ventricular dysfunction
seems to accelerate and is best monitored by measuring the
indexed left ventricular endsystolic volume (ESVI). The
ventricular tachyarrhythmias tend to progress to worse
forms despite chronic antiarrhythmic therapy in severely affected Dobermans, and fatal episodes of SCD have been
shown to occur in approximately 25% of these dogs, Calvert
1995.

4th European FECAVA SCIVAC Congress

253

Dosages of commonly used ventricular antiarrhythmic drugs


Class (VW)

iv. Bolus

Constant rate infusion (CRI)

Lidocaine

1b

2 - 4 mg/kg
repeat 1-2 x

40 - 80 mcg/kg/min

Procainamide

1a

2 mg/kg q. 5min
max 20 mg/kg

20 - 50 mcg/kg/min

Quinidine

1a

Mexiletine

1b

2.5 mg/kg
repeat 1-2 x

loading: 30 mcg/kg/min
maint.: 5 - 8 mcg/kg/min

3 - 8 mg/kg TID, im. or po.

1c
(2 and 4)

1 mg/kg
repeat 1-2x

maint. 8 mcg/kg/min

3 mg/kg TID po.

5-10 mcg/kg/min

3-10 mg/kg/ 24hrs

Propafenone

Sotalol
Amiodarone

Maintenance

6 - 20 mg/kg TID, im. or po.

5 - 15 mg/kg q 6-8hrs im. or po.

2 and 3
3

References
Abbott JA (1995): Traumatic myocarditis. In Bonagura JD Ed: Kirks Current Veterinary Therapy XII Ed., WB Saunders Philadelphia, pp 846849.
Atkins CE, Wright KN (1995): Supraventricular tachycardia associated
with accessory atrioventricular pathways in dogs. In Bonagura JD
Ed: Kirks Current Veterinary Therapy XII Ed., WB Saunders
Philadelphia, pp 807-813.
Calvert CA (1995): Diagnosis and management of ventricular tachyarrhythmias in Doberman Pinschers with cardiomyopathy. In
Bonagura JD Ed: Kirks Current Veterinary Therapy XII Ed., WB
Saunders Philadelphia, pp 799-806.
Dhupa N (1995): Magnesium therapy. In Bonagura JD Ed: Kirks Current
Veterinary Therapy XII Ed., WB Saunders Philadelphia, pp 132-133.
Gabriel A, Kersten U (1993): Therapy of cardiac rhythm disturbances with
propafenone (in German). Kleintierpraxis 38: 485-495.
Gonin-Jmaa D, Lombard CW (1997): Therypy of ventricular arrhythmias
with mexiletine in 16 dogs (In german). Tierrztl Praxis 25: 506-511.
Harpster NK (19xx): Boxer cardiomyopathy, a review of the longterm ben-

10 - 15 mg/kg BID, then


5 - 7.5 mg/kg BID, then
7.5 mg/kg SID po.

efits of antiarrhythmic therapy. Vet Clin North America 21, Nr. 5:


989-1004.
Liu SK, Keene BW, Fox PR (1995): Myocarditis in the dog and cat. In
Bonagura JD Ed: Kirks Current Veterinary Therapy XII Ed., WB
Saunders Philadelphia, pp 842-845.
Lunney J, Ettinger SJ (1991): Mexiletine administration for management of
ventricular arrhythmia in 22 dogs. JAAHA 27: 597-600.
Moise NS, Gilmour RF (1992): Inherited sudden cardiac death in German
Shepherds. In Kirk RW and Bonagura JD Eds: Current Veterinary
Therapy XI Ed., WB Saunders Philadelphia, pp 749-751.
Muir WW (1991): Antiarrhythmic drugs: treatment of cardiac arrhythmias.
Vet Clin North America 21, Nr. 5: 957-988.
Russel LC, Rush JE (1995): Cardiac arrhythmias in systemic diseases. In
Bonagura JD Ed: Kirks Current Veterinary Therapy XII Ed., WB
Saunders Philadelphia, pp 161-166.
Sachter JJ (1992): Magnesium in the 1990s: Implications for acute care.
Top Emerg Med 14: 23.
Sisson DD (1988): The clinical management of cardiac arrhythmias in the
dog and cat. In: Fox PR Ed : Canine and feline cardiology, Churchill
Livingstone, New York, pp 289-308.

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Substance name

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255

Cardiomegaly in the cat: what do I do next?


Christophe W. Lombard

Summary
Prerequisites for a correct diagnosis of cardiomegaly are
techniqually adequate radiographs, with proper positioning
of the patient, taken in full inspiration. Rotation on the VD
or DV-views should only be tolerated to an extent where the
spinous processes lie within the borders of the vertebral
bodies. Artefacts or conditions leading to a false diagnosis
of cardiomegaly may be caused by the following: obesity,
masses within the cranial mediastinum (thymus in juvenile
patients, thymoma or LSA), malformations of the last few
sternebrae, poor inspiration, and fat depositions (primarily
at the cardiac apex and along the phrenic nerves).
While severe cardiomegaly is easily recognised, borderline cardiac enlargement is more difficult to diagnose. Measurement techniques have been proposed. The vertebral
heart score (VHS, using VD and Lateral radiographs,
Buchanan 1991), measures the width and length of the heart
in number of vertebral bodies, and is an easy procedure to
perform. The range for normal hearts varies from 3.5 to 3.8
for the cardiac width and the combined width and length
should measure less than 8 vertebrae.
I consider it appropriate to use any information from the
clinical examination (symptoms, presence of a heart murmur, abnormal gallop rhythms etc) while evaluating radiographic changes of the heart size. In most cases, any tentative diagnosis will have to be confirmed by either angiography or echocardiography and Doppler investigations
anyhow.
Severe cardiomegaly without any apparent clinical
signs is suspicous for a peritoneo-pericardial diaphragmatic hernia (PPDH). Nonspecific signs such a lethargy, inappetence and difficulties with breathing, together with generalized cardiomegaly, may be due to pericardial effusions
or dilated cardiopathy. The presence of a loud heart murmur and cardiomegaly in young to middle aged cats redirects the diagnosis towards congenital malformations with
shunts or valvular malformations. Differential diagnoses
include PDA, mitral and tricuspid dysplasias, subaortic
and pulmonic stenoses, atrial and ventricular septal defects, endocardial fibroelastosis and sometimes combined
multiple lesions.
In middle aged to old cats, nonspecific abnormalities of
the history and physical examination may occur together
with heart murmurs and/or gallop rhythms. In these cases,
the cardiac enlargement is most often caused by one of the

cardiomyopathies, their subtypes being idiopathic hypertrophic, restrictive, hyperthyroid, hypertensive and sometimes non-classifiable. A definitive diagnosis of the pathology and possibly the etiology is only possible with echocardiography/Doppler and additional laboratory examinations.

A. Technical requirements for radiography


and patient related, non-cardiac effects
Properly exposed radiographs without motion artefacts
(rare in cats) are an essential prerequisite for any correct diagnoses of thoracic abnormalities. In addition, the cat must
be properly positioned for two views. Rotation of the VD or
DV-view is only acceptable to the extent that the spinous
processes still lie within the limits of the lateral borders of
the vertebral bodies. The DV-position provides less possibility for the cardiac apex to shift to either side, and less variation in the shape of the heart and better vascular detail (Farrow 1994). The VD-position provided however a more constant appearing heart size in normal cats (Farrow 1994). The
feline thorax is also very pliable, and fewer compression
artefacts of the ribcage can be expected from the VD-view,
preferred by some cardiologists for the evaluation of the cardiac silhouette (Buchanan 1991). This view is also less sensitive to obscuring of the cardiac silhouette by small pleural
effusions. In a lateral position, the front legs must be pulled
forward, and a superimposition of the humeri or elbows over
thoracic structures is not acceptable. The images must be
generated with a fully inflated lung, as a reduced inspiration
leads to a greater cardiac/thoracic ratio and facilitates an incorrect diagnosis of cardiomegaly.
The full outline of the cardiac silhoutte must be visible
for a proper evaluation. Obviously, any considerable amount
of pleural effusion renders a correct evaluation of heart size
very difficult and imprecise; the cat should be reradiographed after as complete a drainage of any effusion as
possible.
Lack of a distinct cranial borderline may be caused by
remnants of the thymus in young animals, or by cranial mediastinal masses such as thymic lymphosarcoma or thymomas in adult cats. These conditions cause also a widening of
the cranial mediastinum on the VD or DV-view. Malformations of the distal parts of the sternum (pectus excavatus or
carinatus) as well as fat deposits at the cardiac apex may be
responsible for an obscured view of the tip of the heart. This

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DVM, Dipl ACVIM, Dipl ECVIM


Klinik fr kleine Haustiere - Universitt Bern - Berne - Switzerland

256

may cause difficulties for the precise evaluation of the


length (apico-basal dimension) of the heart. Obesity in general may be responsible for a false diagnosis of cardiomegaly, as it may cause incomplete inspiration; and the
fat deposits occur at preferred sites such as the cardiac apex
and along the phrenic nerves, causing widening of the
cranio-caudal width of the heart. Aged cats tend to have a
cardiac long axis more parallel to the sternum, with a resulting wider curving arch of the aorta.
Most radiologists like to read radiographs initially without any bias from the history and physical examination.
Though this may warrant a more objective analysis of the radiographs, it does not at all reflect the usual procedure in
daily practice, where radiographs are taken once the examining clinician has finished performing the physical examination. He or she will also be the one interpreting them as
soon as they have been taken. We will therefore, after an initial discussion about radiographic diagnosis of cardiac enlargement, proceed with the knowledge and due consideration of the history and the abnormal findings from the physical examination.

B. Indicators of cardiomegaly
B.1. Lateral view: Enlarged hearts are recognized by an
increased length of the apico-basal dimension, leading to an
elevation of the tracheal bifurcation (carina) and a reduction
of the angle formed between the thoracic spine and the trachea. Supporting evidence of cardiomegaly may be gained
by an uphill course of the caudal vena cava in selected
cases. Another indicator, but somewhat more difficult to
recognize, is the increase of the maximal width (cranio-caudal dimension, measured at a right angle with the apicobasal dimension).
B.2. VD or DV-view: An increase of the length and especially of the maximal width of the cardiac silhouette is
supposedly a very reliable indicator of cardiomegaly. This
dimension has been compared to the number of thoracic vertebrae in the vertebral heart score concept (VHS,
Buchanan 1991). Normal cats were shown to have average
widths between 3.5 and 3.8 vertebral bodies. When width
and length of the heart were combined (as in the canine
VHS, in which always both dimensions are used), the number for cats should be less than 8 vertebral bodies.
The increase of the width of the heart in this projection
is often caused primarily by biatrial cardiac enlargement, i.e.
the protrusion of both atria or especially their atrial appendages over the normal silhouette. The cardiac apex usually lies slightly to the left or on the midline of the thorax in
this projection. A normal size of the ventricles causes the
apex to appear pointed, while a more rounded apex indicates
enlargement of the ventricles. Enlargement of all 4 cardiac
chambers can therefore be deducted from a widened and
elongated silhouette with a rounded apex.
B.3. Supportive evidence from vascular structures
Enlarged vascular markings (both arteries and veins) indicate overcirculation of the lungs and may give supportive
evidence to the diagnosed cardiomegaly in cats with suspected malformations with shunts (VSD or PDA). If only

4th European FECAVA SCIVAC Congress

pulmonary veins appear large and congested, restriction to


left atrial filling as an early sign of congestive heart failure
is present. As the left atrium is pliable and easily distended,
signs of left atrial enlargement should be searched for on
both views.
B.4. Differentiation of right sided vs left sided cardiomegaly: Echocardiography will always be superior to radiography for making this differentiation, because the position of the interventricular septum can clearly be identified
with the former technique. Nevertheless, radiographs may
give some indications about the side of the heart that appears
preferentially enlarged.
On the lateral view, right sided cardiac structures lie cranially to the line drawn from the carina to the apex of the
heart and form a more convex border than the caudal one.
The right atrium and right ventricle lie adjacent to each other, and it is nearly impossible to differentiate their respective
limits. The caudal border of the heart is more straight and is
generated by the left ventricle and the left atrium. The dividing point between them is usually located at the site
where the posterior vena cava crosses the posterior cardiac
border.
Right sided cardiac enlargement can therefore be expected from an exaggerated rounding (increased convexity)
of the cranial borderline, leading to an increased sternal contact, and some increase of the cardiac length. In severe cases, the enlarged right heart causes the apex to be lifted up
from the sternum and displaced caudodorsally towards the
left side. Elevation of the trachea caused by the more cranial
parts of the heart base is also supportive evidence of right
heart enlargement.
Left heart enlargement can be recognized by an increase of the long axis and an elevation of the trachea, resulting in a decreased angle between the trachea and the
thoracic spine. The increased length cannot differentiate
between left atrial and left ventrical enlargement. Those
are indicated by increased convexities of their respective
borderlines.
On the ventrodorsal view, an elongation of the heart is
more common to left heart enlargement; often the apex is
shifted towards the midline or even to the right side of the
dividing long axis. With right heart enlargement, its borderline becomes more convex, and the apex may be severely shifted towards the left side. As already mentioned, a
more pronounced atrial enlargement may be recognized by a
more dominant widening of the cardiac silhouette, while the
ventricular enlargement is indicated by a more important
lengthening of the heart and a simultaneous rounding and
widening of the apex.

C. Information and/or bias


from the signalment, history and physical
examination
Most complaints and details from the history (listlessness, inappetence, lethargy, difficulty with breathing, vomiting etc.), are usually not specific enough to firmly point towards cardiac disease. An exception may be the sudden onset of hindleg paralysis, where thromboembolization of the

4th European FECAVA SCIVAC Congress

rarer Eisenmenger syndrome. In these cases, a hematocrit


should be checked immediately for polycythemia (as a sign
of chronic hypoxia associated with the chronic R>L-shunt.
Based on additional bias from the patients age (under or over
2 years) and certain breed predilections for certain diseases,
I tend to assign my patients provisionally to one of the three
following groups for further investigation:
(primary heart disease)

(sec. heart disease)

- congen. heart disease


- cardiomyopathy
- acquired valvular disease
- neoplasia

- hyperthyroidism
- hypertension
- metastat. neoplasia
- pericardial disease
- other

Each of these groups has a slightly different data base or


at least a different sequence of the further diagnostic investigations. In the ideal situation, all of the following examination procedures are performed in each feline patient. But
the goal should be to obtain the correct diagnosis with the
minimum of examinations, in order to keep the clients bill
from rising unnecessarily!

Establishing a Data-Base for the suspected condition and proposed sequence:


congenital heart disease

primary heart disease:


cardiomyopathy
or acquired valvular disease

second. heart disease:


hyperthyroidism,
hypertension, other

thoracic radiographs

thoracic radiographs

hemogram, chemistry panel plus T4,


urinanalysis, heartworm serology

ECG

ECG

BP-measurement

Echocardiogram ECG

Echocardiogram

thoracic radiographs

hematocrit or hemogram,
evt. chemistry profile

Hemogram, chemistry profile,


evt. T4, evt. growth hormone

ECG

evt. BP-measurement

evt. BP-measurement

echocardiogram

evt angiogram

Rarely angiogram

evt. szintigram

D. Electrocardiography
The ECG is quite useful for differentiating tachyarrhythmias in cats with suspected cardiac disease. The usual abnormalities are: sinus tachycardia, ventricular premature
contractions and paroxysmal tachycardias. The ECG however is not very useful for an etiological determination of a
cardiomegaly. There are only weak correlations between radiographic and electrocardiographic signs of cardiac en-

largement, the latter preferentially providing supportive evidence of hypertrophy.


I concentrate on the search for enlargement patterns (left
ventricular hypertrophy LVH, right ventricular hypertrophy
RVH, p-mitrale and p-pulmonale) or conduction abnormalities such as partial left bundle branch blocs (left fascicular
bloc or anterior hemibloc), Presence of one of these 3 major
ECG-abnormalities provides strong supportive evidence of
primary or secondary cardiac disease in the feline.

MAIN PROGRAMME

aorto-iliac trifurcation (secondary to cardiac disease: hypertrophic CMP, endocarditis) has to be very high on the list of
differential diagnoses. Additionally, in areas endemic for feline heartworm disease, coughing and vomiting in an unprotected cat (not on heartworm prevention) rises the suspicion
for dirofilariosis.
After the physical examination of most cats with heart
disease however, one or more of the following will almost
certainly have been recognized:
-Tachycardia over 180/min,
- some abnormality of the auscultatory rhythm or arterial pulses (caused by either a gallop rhythm or a primary
cardiac arrhythmia), or
- some heart murmur (mostly systolic, indicating a shunt, a
semilunar valvular stenosis, or AV-valvular regurgitation).
Diastolic murmurs are extremely rare in cats and very
difficult to recognize because of the usually elevated heart
rate, making the diastolic time period quite short. Recognition of a machinery murmur already confirms the diagnosis
of a PDA, though this defect is very rare in cats. Cyanosis,
exacerbating with excitement or exercise, is also very rare in
cats and points towards a congenital malformation with a
right to left shunt such as Tetralogy of Fallot, or the much

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4th European FECAVA SCIVAC Congress

ECG-criteria of these major abnormalities:


LVH

RVH

Left fascicular bloc

R-wave (lead II) > 0.9 mV


positive lead I (qR-type)
MEA normal or to the left
QRS slightly widened
evt. p-mitrale

rS-type QRS in II, III, aVF


Negative lead I (QS-type)
MEA to the right
QRS slightly widened
evt. p-pulmonale

rS-type QRS in II, II, aVF


positive lead I (qR-type)
MEA to the left and cranial
QRS-duration +/- normal
normal p-wave

LVH

RVH

Left fascicular bloc

- hypertrophic CMP

- specif. congen. malformations


Tetralogy, PS, TV-dysplasia
- dirofilariosis (very rare)

- hypertrophic CMP

Occurrance of these patterns:

- restrictive CMP
- hyperthyroidism
- dilated CMP (rare)

Differentiating right from left sided hypertrophy is particularly useful for differentiating congenital malformations.
Tetralogy of Fallot and pulmonic stenosis almost always
have RVH-patterns, while the presence of LVH supports a
diagnosis of either subaortic stenosis (SAS), ventricular septal defect (VSD), mitral valve dysplasia or PDA.
It must be emphasized that the information gained from
the ECG about cardiac enlargement or hypertrophy complements the radiographic information quite often, but a disagreement is not necessarily an error or an incompatibility.
Echocardio-graphy will be the deciding judge in these cases.

E. Echocardiography for the


differentiation of radiographic
cardiomegaly
This technique has established itself very well in feline
cardiology. It has tremendously facilitated the differentiation
of the various forms of cardiomyopathy and acquired valvular disease, and has become an essential part of the work-up
of the feline with suspected heart disease. In some diseases,
echocardiography provides an instantaneous diagnosis without any cardiac measurements or necessary great skills at sophisticated imaging.

E.1. Severe radiographic cardiomegaly,


rather rounded cardiac silhouette
Differential diagnoses should include:
- peritoneo-pericardial diaphragmatic hernia (PPDH)
- other severe congenital cardiac malformations
- severe dilated cardiomyopathy
- pericardial effusion.
In many cases of suspected PPDH, the radiographic diagnosis can be supported by gas shadows (bowel loops or
stomach parts) superimposed onto the cardiac silhouette;

- restrictive CMP
- dilated CMP (rare)
- hyperthyroidism (rare)

other criteria are an incomplete outline of the diaphragm, a


suspicously empty abdomen with diffulties in recognizing
liver and stomach, or the recognition of a dorsal peritoneopericardial mesothelial remnant (DPMR), (Berry et al
1990.) PPDH can be an incidental finding in otherwise
asymptomatic felines of a wide age range. In a retrospective
comparative study of PPDH, 11% were asymptomatic; the
other cats showed non-specific signs varying from dyspnea
(32%), inappetence, vomiting (15%), lethargy (12%),
weightloss or stunted growth (9%), (Skrodzki 1997). The
echocardiographic examination allows an immediate recognition of the foreign material (bowel loops with gas-shadows, omentum, liver lobes etc. immediately adjacent to the
heart, and in most cases the lack of a continuous diaphragm,
separating the thoracic structures from the abdomen. The
recommended therapy for PPDH is surgical correction (Wallace et al, 1992).
In cats presented with generalized congestive heart failure, the now very rarely recognized dilated cardiomyopathy may be another cause of the radiographic cardiomegaly.
The silhouette of the heart may become quite rounded. The
echocardiographic signs of severe dilatation of all 4 chambers with additional hypokinesis of both ventricles are very
easily recognized and not difficult to diagnose.
Therapy of dilated cardiomyopathy consists of diuretics,
positive inotropes (digoxin), ACE-inhibitors and dietary
modification (switch to a well-known brand name catfood)
as well as taurine substitution. The latter is usually done as
a therapeutic trial for several weeks without even measuring
plasma levels of taurine, which can only be done by specialized laboratories.
Pericardial effusions are very easily diagnosed on
echocardiograms by recognizing an echofree (fluid-dense)
space surrounding the entire heart. In contrast to the canine,
the effusions in cats are usually less voluminous and only in
very isolated cases so severe to result in tamponade, with the
patient having severe jugular distension, hepatosplenomegaly
and ascites (Rush et al, 1990). The more common clinical

4th European FECAVA SCIVAC Congress

ious forms of cardiomyopathy or neoplasia (primary vs


metastatic, lymphosarcoma was the most frequent type). Pericardiocentesis needs to be performed with large effusions only; the technique is the same as in the dog. Any effusion
should be differentiated into pure transsudate, modified
transsudate and exsudate for diagnostic reasons. The treatment is directed against the underlying primary cause; many
not too large effusions disappear with diuretics. Inflammatory or septic pericardial effusions should be treated with
drainage, lavage, antiinflammatory and where needed antibiotic therapy (Bonagura 1989).
The following table provides a simplified echocardiographic differentiation of the 3 conditions:

PPDH

Pericardial effusion

Dilated cardiomyopathy

pericardium not visualized

pericardium very well visualized,


separated from the epicardium

pericardium normal

normal chambers, possible


abnormal anatomical
position of entire heart

echo-free fluid space of varying


size surrounding the heart

severe dilatation of all 4


cardiac chambers

foreign structures
(liver, gas-filled bowel loops etc.)
next to the heart

a. chambers normal to small, possible


RA- and RV-tamponade (collapse)
or
b. chambers abnormal according
to an underlying cardiomyopathy
or
c. masses (tumors) with
abnormal echodensity

severe hypokinesis
of both ventricles

E.2. Moderate cardiomegaly


As mentioned earlier, differential diagnoses for these patients include:
primary heart disease: cardiac malformations (young animals) cardiomyopathy chronic
degen. valvular disease, rare in
cats primary neoplasia (very rare)
or
secondary heart disease: hyperthyroidism, hypertension,
chronic renal failure, dirofilariosis, toxoplasmosis, other (infiltrative, neoplasia, etc.).
The echocardiogram, together with levels of T4, results
of arterial blood pressure measurement, heartworm serology,
and evt. growth hormone determination helps to differentiate these conditions. In contrast to the three previous diagnoses of PPDH, pericardial effusion or DCMP, established
with very little echocardiographic skills, a systematic and
precise, step-by-step echocardiographic approach with detailed measurements of the cardiac structures will be necessary here for differentiating these underlying conditions.
Echocardiographic technique: I like to start the echocardiographic examination with an overview or screening of the

heart in both the right parasternal long axis and short axis
projections, to get an image of the entire heart and recognize
any abnormalities to be primarily right sided or left sided. It
is also helpful to have a somewhat systematic approach
and organized search for abnormalities, trying to recognize:
structural abnormalities: - septal defects
- thickening or abnormal anatomy
of valves
- abnormal papillary muscles and
moderator bands
- altered echodensity of the myocardium and/or endocardial and
subendocardial structures
functional changes:

- hypokinesis, hyperkinesis
- diminished or excessive fractional thickening of the septum
and/or LV-wall

dimensional changes:

- cavities (dilatation, reduction in


size)
- walls (global or regional hypertrophy, thinning quite rare)

MAIN PROGRAMME

presentation is nonspecific, and their radiographs also lack


the very large and rounded pumpkin-shaped silhouette so typical for canines with pericardial effusion. In my own experience, most incidences of finding considerable amounts of
free pericardial fluid on echocardiographic examinations of
cats with radiographic cardiomegaly come as a surprise. Pericardial effusions are often associated with simultaneous
pleural effusions (53%) and ascites (30%), (Rush et al 1990).
Feline infectious peritonitis (FIP) was a common cause of
pericardial pathology in that retrospective study, however
without any indication of the amounts or seriousness of the
effusion. Near 30% of cats had some form of structural cardiac disease; it can be expected that these underlying signs
dominate and will lead to a proper diagnosis of any of the var-

259

260

Measurements can be generated throughout the


echocardiographic examination or en bloc at the end, after a
good overview of the heart. Accepted standards for measurement technique and normal values have been published
elsewhere, Moise 1988.
I consider it essential to compare and verify any cardiac
measurements generated from long axis views with those
obtained from right parasternal short axis projections. In this
plane, a more symmetrical view of the left ventricle is obtained, with an easier placement of the M-mode cursor between the papillary muscle heads for measuring cavity dimensions and septal and free wall thickness. This view has
additional advantages for a more precise evaluation of LAsize. The LA/Ao-ratio reflects a section through the atrial
appendage only. True left atrial size would probably best be
compared to the aortic root by planimetry or at least by an
oblique dimension of its greatest width, as was proposed by
Hanson et al 1993 for the dog.
Structural abnormalities: The long axis imaging plane
permits the screening of both the interventricular (membraneous) and atrial septum for defects, and with Doppler investigation (if available) the confirmation of any suspected
shunts. Isolated VSD and ASD seem to be very rare in cats.
They are frequently associated with other structural abnormalities (e.g. dysplastic or cleft atrioventricular valves) as
part of complex cardiac malformations. I find it quite difficult to recognize definite structural valvular abnormalities
on feline echocardiograms, because of the small size of the
visible valve leaflets and the elevated heart rate, causing
very rapid motion patterns. Neither pulmonic nor aortic or
subaortic stenosis can be well visualized. Those diagnoses
are usually established by Doppler evidence of increased
and turbulent outflow velocities and 2D-evidence of secondary ventricular hypertrophy. Most often, a dysplasia of
an atrioventricular valve is recognized by simultaneous severe atrial and moderate ventricular dilatation, and additional evidence of severe regurgitation (loud heart murmur,
Doppler confirmation). Additional abnormal shapes or positions of papillary muscles may provide supportive evidence
for congenital valvular dysplasia.
Otherwise, malformed papillary muscles with abnormally echodense moderator bands and chordal network in generally relatively normal sized ventricles, but with areas of
hypertrophy and others of thinning and/or dyskinesis, are
suggestive of restrictive cardiomyopathy. A clear differentiation between restrictive and other forms of cardiomyopathy is not always possible. Altered echodensity of the myocardium is most often found in areas of hypertrophy, suggesting fibrous invasion of that area.
Isolated septal hypertrophy in the region of the f LV-outflow tract may be responsible for a dynamic outfow obstruction, with or without systolic anterior motion (SAM) of
the mitral valve. This could also be associated with dyskinetic septal motion, and the generated pressure gradient between the left ventricle and the aorta can be documented
with Doppler. CFDoppler shows turbulence in the LV-outflow tract in such cases.
Degenerative valvular lesions, secondary to endocardiosis, are also very difficult to recognize; they occur mostly
left-sided in aged cats. In general, moderate to severe left

4th European FECAVA SCIVAC Congress

atrial dilatation with moderate left ventricular dilatation and


some hypertrophy is recognized, together with (Doppler
proven) mitral regurgitation.
Functional changes: It is simple to recognize diminished
excursions of the septum and free LV-wall as signs of hypokinesis and (dilated) cardiomyopathy. A normal to elevated shortening fraction (various degrees of hyperkinesis) are
found with all other forms of cardio-myopathies; hyperkinesis should always be evaluated together with any dimensional changes of the cavities.
Dimensional changes: Right side. Isolated right sided
cardiac enlargement is quite rare in the cat, and may be the
endstage of a restrictive (or unclassified) CMP. Possibilities
include tricuspid valve dysplasia or pulmonic stenosis,
heartworm disease causing only mild right cardiomegaly. If
severe right atrial and moderate right ventricular dilatation
dominate the image and indicate severe volume overload,
tricuspid valve dysplasia or acquired tricuspid insufficiency
secondary to degenerative valvular disease (old cats, very
rare) should be suspected and confirmed with Doppler. If
right ventricular hypertrophy dominates the image, pressure
overload of the RV and therefore an outflow obstruction
(pulmonic stenosis) should be suspected.
Left atrium. I like to switch back and forth between the
long axis imaging planes showing the entire left atrium and
planes showing the left ventricular outflow tract and aortic
root. This allows the recognition of left atrial dilatation,
based on a subjective impression of LA-size in comparison
to the left ventricle and in relation to the aortic diameter. It
should be measured with M-mode as an LA/AO-ratio in this
projection and later verified in the short axis projection.
LA/AO-ratios should not exceed 1.3-1.5 in normal cats
(Moise 1988). The left atrium, and especially its atrial appendage, should also be checked carefully for echocardiographic smoke (clouding, or spontaneous contrast effects,
indicating the danger of thromboembolization) or echodense
masses suggesting the presence of a thrombus.
Left ventricle. The long axis view also permits the
recognition of increased thickness of the septum and LV-free
wall, and especially the distribution of any hypertrophy
(symmetric, asymmetric, septum only, overall), for a preliminary diagnosis of hypertrophic cardiomyopathy. Moise in
1993 illustrated the various distribution patterns of LV-hypertrophy with this disease. We use 5-6 mm thickness of the
septum and LV-free wall as an upper limit of normal, and dimensions greater than 7 mm as definite signs of hypertrophy,
irrespective of body size of the patient (Kittleson 1995). The
significance of regional versus global LV-hypertrophy remains unclear and its etiology is somewhat mysterious. I am
unaware of any difference in treating the various forms of
hypertrophy.
The fractional thickening of both the septum and LV-free
wall (percentage increase between diastolic and systolic
thickness, usual range 30 to 50%) should also be evaluated.
An excessive thickening points towards hypertrophic cardiomyopathy, whereas diminished thickening is associated
with dilated cardiomyopathy. The fractional thickening
should however always be interpreted together with the left
ventricular dimension. Hypertrophy of the LV-walls, a diminished systolic dimension (under 08 mm) together with an el-

4th European FECAVA SCIVAC Congress

A variety of abnormal structures (dysplastic valves, additional septal defects) with various degrees of ventricular
hypertrophy and atrial dilatation are found with complex
cardiac malformations. A careful investigation of each inflow- and outflow-tract with Doppler is needed for a correct
diagnosis, which may not be completely possible ante
mortem in each case.
The following table 1 uses a rather simplified approach,
using generalizing statements, for the differentiation of the
various etiological forms of left heart enlargement/ hypertrophy in the cat.

F. Therapeutic guidelines
Obviously, the underlying problem leading to secondary
cardiomyopathy should be eliminated if possible. For example, hyperthyroidism can be treated with either methimazole,
surgery or radiation therapy, Salisbury 1991. In feline hypertension, the calcium-channel antagonist amlodipine at a
dosage of 0.625 mg, per cat once daily, has been shown to
be efficacious, Henik et al 1994.

Table 1. Simplified echocardiographic differentiation of feline myocardial hypertrophy


classic HCMP

restrictive CMP

acquired myocardial hypertrophy

Etiology: unknown, idiopathic


(poss. growth hormone excess)

unknown, idiopathic
(possible previous myocarditis)

hyperthyroidism,
systemic arterial hypertension (CRF)
aortic stenosis, mitral regurgitation
(chron. valvular degeneration)
neoplastic infiltration, acromegaly

LV-Hypertrophy: moderate to severe,


concentric, including papillary muscles,
varies from global to regional, occasional
hyperechogenicity of the myocardium, esp.
papillary muscles, in some cases (SAM)

mild to moderate only, more often regional,


sometimes involving papillary muscles.
Frequent patchy endocardial and
endomyocardial hyperechogenicities, esp.
with apical hypertrophy

mild to moderate, rarely severe, global,


concentric with AS
normal echogenicity of the myocardium

LV-cavity: small

normal to small, abnormal chordae


and/or moderator bands

normal to slightly large


small with AS

Shortening fraction: normal to high

normal to low, possible regional


LVW-dyskinesis

normal to high

LA-size: mild to severe increase, somewhat proportionate to the LV-hypertrophy

severe increase, disproportionate to the


degree of LV-hypertrophy

normal to moderate increase

Doppler, LV-outflow: dynamic subaortic


stenosis

mostly normal (??)

mostly normal,
moderate to severe turbulence with AS

Doppler, Mitral valve: mitral regurgitation


proportionate to LA-size

mild to moderate mitral regurgitation,


restrictive inflow patterns difficult to obtain

mild to moderate mitral regurgitation, in


selected cases only (?)

Developement of CHF: moderately


frequent, dependant upon the severity of
LV-hypertrophy and LA-size

very common and severe

uncommon, mild to moderate only (?)

Thromboembolization: yes

common to very frequent

rare

MAIN PROGRAMME

evated shortening fraction (over 55%, both subjective judgements), allows a classification of concentric hypertrophy of
the left ventricle, which is an essential basis for the diagnosis
of the classic idiopathic hypertrophic cardiomyopathy, Kittleson 1995. It must be emphasized that other forms, with
normal or nearly normal dimensions of the cavities and only
some form of septal and free wall hypertrophy, occur frequently in cats and make the diagnosis less clear-cut. Hyperthyroidism for example often presents with mild to moderate
hypertrophy (symmetric for the septum and the LV-wall) but
normal to slightly large dimensions of the cavities and normo- to hyperkinesis (Bond et al 1988, Moise et al 1986).
In some patients, relatively normally sized left ventricles
are recognized with very large left atria. The ventricles however show very abnormal echodensities in the endocardium
and myocardium and/or unusal trabecular and chordal network. These abnormalities allow a classification of restrictive cardiomyopathy. The term is based primarily on the
dominant hemodynamic abnormality (abnormal diastolic
filling patterns, illustrated with Doppler echocardiography),
and not so much upon definite pathologic-anatomical features. This diagnostic group is quite inhomogenous.

261

262

A good number of cats will present with signs of respiratory distress due to congestive heart failure secondary to
the severe hypertrophy of the heart. Initially, diuretics at a
dose of 1-2 mg/kg 2-3 times daily (intravenously or intramuscularly) are given, Kittleson 1995. These doses should
be reduced as soon as the distress abates, in order to avoid
dehydration and electrolyte disturbances. We believe that
ACE-inhibitors are also beneficial in acute CHF of cats,
though experimental evidence is still lacking. Dose rates are
0.25-0.5 mg/kg enalapril twice daily and 0.5 mg/kg benazepril once daily.
Recommendations for longterm therapy are still somewhat controversial, Kittleson 1995. Both betablocking drugs
and the calcium antagonist diltiazem can be used with good
justification, Fox 1991. Both drugs produce symptomatic relief. Diltiazem has shown to reduce pulmonary edema and
reduce the need for diuretics, Bright et al 1991. It is thought
to improve diastolic relaxation and improve the ventricular
compliance; there was also evidence that the ventricular hypertrophy regressed in some cases. Propranolol on the other
hand probably reduces the amount of SAM of the mitral
valve and the degree of mitral regurgitation, Kittleson 1995.
Clinical experience with betablockers is widespread and
anecdotally reported to be good. More recent interest has focussed on the use of ACE-inhibitors, not so much because of
the plasmatic effect reducing aldosterone levels and volumeoverload, but more because of the tissular blockage of ATII
formation and prevention of angiotensin-mediated cardiac
remodelling, i.e. induction of cardiac hypertrophy. Preliminary results with enalapril (Rush et al 1998) and Bbenazepril
(unpublished own data, 1998) are promising. ACE-inhibitors may also be indicated and a good choice in cats with
early restrictive cardiomyopathy without severe signs of
failure, Bonagura and Fox 1995.
For asymptomatic cats with hypertrophy, either drug
may be tried, and their effects should be studied by followup echocardiography, in order to justify longtern administration. With respect to prevention of thromboembolisms, the
specific literature should be consulted, Harpster and Baty
1995.

4th European FECAVA SCIVAC Congress

References
Berry CR, Koblik PD, Ticer JW (1990): Dorsal peritoneopericardial
mesothelial remnant as an aid to the diagnosis of feline peritoneopericardial diaphragmatic hernia. Vet Radiol 31: 239-245.
Bonagura JD (1994): Cardiovascular diseases. In Sherding RG (Ed): The
Cat: Diseases and Clinical Management II Ed., Churchill Livingstone, New York, 819-978.
Bonagura JD, Fox PR (1995): Restrictive cardiomyopathy. In: Bonagura JD
(Ed), Current Veterinary Therapy XII, small animal practice, WB
Saunders, Philadelphia, 863-867.
Bond BR, Fox PR, Peterson ME, Skavaril RV (1988): Echocardiographic
findings in 103 cats with hyperthyroidism. JAVMA 192: 1546-1549.
Buchanan JW, Bucheler J (1991): Vertebral scale system to measure heart
size. Proc 9th ACVIM Forum, New Orleans, pp. 689-670.
Farrow CS, Green R, Shively M (1994): Radiology of the cat Mosby Year
Book, Inc. St. Louis, 45-131.
Hanson K: Assessment of left atrial enlargement, comparison between thoracic radiography, B-mode and M-mode echocardiography. Proc XII.
ESVC- meeting 1993, Berlin, 2-3.
Harpster NK, Baty CJ (1995): Warfarin therapy of the cat at risk of thromboembolism. In: Bonagura JD (Ed), Current Veterinary Therapy XII,
small animal practice, WB Saunders, Philadelphia, 868-873.
Henik RA, Snyder PS, Volk LM (1994): Amlodipine besylate therapy in
cats with systemic arterial hypertension secondary to chronic renal
disease. Proc. 12th ACVIM-Forum, San Francisco, 976.
Kittleson MD (1995): CVT update: Feline Hypertrophic Cardiomyopathy.
In Bonagura JD (Ed), Current Veterinary Therapy XII, small animal
practice, WB Saunders, Philadelphia, 854-862.
Moise NS, Dietze AE, Mezza LE, Strickland D, Erb, HN, Edwards NJ
(1986): Echocardiography, electrocardiography, and radiography of
cats with dilatation cardiomyopathy, hypertrophic cardiomyopathy
and hyperthyroidism. Am J Vet Res 47: 1476-1486.
Moise NS (1988): Echocardiography. In: Fox PR (Ed), Canine and Feline
Cardiology, Churchill Livingstone, New York, 113-156.
Moise NS (1993): Echocardiography of cats with cardiomyopathy. Proc
2nd International Symposium of Veterinary Echography, AcropolisNice/France, 72-76.
Rush JE, Keene BW, Fox PR (1990): Pericardial disease in the cat: a retrospective evaluation of 66 cases. JAAHA 26: 39-46.
Salisbury SK (1991): Hyperthyroidism in cats. Comp Cont Ed 13: 13991409.
Skrodszki M, Allgoewer I, Grevel V (1997): Congenital peritoneopericardial hernias in 16 cats. Part 1: Literature review and cases (in German). Kleintierpraxis 42: 973-996.
Wallace J, Mullen HS, Lesser MB: A technique for surgical correction of
peritoneo-pericardial diaphragmatic hernia in dogs and cats. JAAHA
(1992) 28: 503-510.

4th European FECAVA SCIVAC Congress

263

Anaemia in the young dog


George Lubas
Med Vet
Department of Veterinary Clinic - University of Pisa - Italy

Summary
RBC indexes in young Beagle dogs
100
80
60
40
MCV (fL)

20

MCH (pg)
0
birth

MCHC (%)
1st

2nd

3rd

4th

6th

8th

12th 16th 20th 24th

Weeks of age

Figure 1 - Behaviour of the RBC indexes (MCV, MCH, and MCHC) in


young Beagle dogs1,7,11

Introduction
Before developing an algorithm to reach a diagnosis for
anemia, it is important to consider the evolution of the hemopoietic pool in the dog from birth to one year of age; it is
only after the age of one year that several hematic parameters are fixed in the adult reference interval. Unfortunately
data on the this topic are rather outdated and usually only refer to the Beagle, a purpose-bred dog often used in research
where environmental influences are minimal, and studies are
often restricted to nutritional or pathological effects. Data so
generated, however, potentially could be extrapolated to other canine breeds as long as changes are not over interpreted.
In this review, the diagnostic approach to anemia is similar
to that already reported in the previous speeches, and is derived from current knowledge in this field. The emphasis
here will be on epidemiology and the resulting specific hemopoietic effects in the young dog.

Erythroid and myeloid pool in the young dog


At birth the red blood cells (RBCs) of foetal origin are
quite large (Mean Cell Volume; MCV; 95-100 fL). As foetal
RBCs are replaced, the MCV progressively decreases, so
that by 2-3 months of age, the RBC size is similar to that of
the normal adult dog. Similarly the Mean Cell Hemoglobin
(MCH) is about 33 pg at birth and decreases to approximately 22 pg by 2 months of age. Mean Corpuscular Hemoglobin Concentration (MCHC) differs only slightly with
age, being almost 35% at birth and decreasing to 33% at 2
months of age and remains quite constant at approximately
32% despite the fluctuations of hematocrit (Hct; figure 1).
This particular index may fluctuate within a normal range by
3-5% due to physiological and technical variations1,3,7,9,11.

As a consequence of the behaviour of the RBC indexes,


the values of hemoglobin (Hgb) and Hct are quite high at
birth, but fall rapidly as the pup begins to nurse. The decrease in the above parameters continues during the first
month of life (see figure 2). Circulating RBC mass is significantly reduced, due to an increased destruction of foetal
RBCs as well as to the rapid growth of the puppy (generally
it reaches from 3 to 4 times the birth weight by one month
of age). Therefore a relative anemic state often exists in the
young representing physiologic adaptation to extra uterine
environment. At the beginning of the second month of life
there is a gradual and steady increase of RBC count as well
as in Hgb and Hct values which ends at approximately 1
year of age when adult values are attained. Other influences
on these changes include stress and inherent breed differences. The spleen acts as an a RBC reservoir, releasing
RBCs into circulation in response to apprehension due often
to difficulties in collecting adequate blood for examination,
particularly in small or toy breeds2,3,4,6,9,10,14.

RBC values in young Beagle dogs


50
40
30
Hct (%)

20

Hgb (g/dL)

10
0
birth

1st

2nd

3rd

4th
6th
8th
Weeks of age

12th

16th

20th

RBC
(M/mcL)

Figure 2 - Behaviour of RBC values (Hct, Hgb, and RBC count) in young
Beagle dogs2,4,6,10,14.

MAIN PROGRAMME

Anemia is considered a frequent clinical finding in the


young dog. This sign should be thoroughly examined in order to determine 1) if red cell regeneration is occurring and
then 2) assessing, as far as possible the etiology. The hematological reference intervals in the young dog are different
than adult canine reference intervals, particularly in the first
months of age. This review considers the most important
clinical disorders manifesting with anemia, from an epidemiological perspective, in the first months of canine life.

264

4th European FECAVA SCIVAC Congress

The rapid replacement of foetal RBCs and physiologic


compensation due to rapid body growth result in increased
erythropoietic activity manifest by increased circulating
reticulocytes. Indeed in puppies up to one month of age the
reticulocyte count may be close to 7% as compared to normal adult values of 1-2%. The same observation is noted
with nucleated red blood cells (NRBCs), with a peak of
about 4 NRBCs per 100 White Blood Cells (WBCs) occurring after 1 week of age. The NRBCs disappear around two
months of age. Similarly, during the same period the reticulocyte count falls to about 4% (figure 3). It also reported that
young female dogs under 16 months of age have a reticulocyte count lower than males3,5,6,9,11.

RBC regenerative signs in young Beagle dogs


7
6
5
4
3
2

NRBC/100 WBC

Rets (%)

0
birth

1st

2nd

3rd

4th

6th

Very little information are available on the immature canine platelet (Plt) pool; lower thrombocyte count have been
reported in young dogs in contrast to adults, while other studies report no association between platelet count and age3,9.

Classification of anemia in the young dog


Anemia is defined, even in a young animal, as a decrease
in the number of circulating RBCs together with a decrease
in Hgb concentration or Hct percentage. The characteristic
signs are related to reduced oxygen transport. Anemia can be
classified as either regenerative or nonregenerative based on
the reticulocyte response observed in peripheral blood3,9,12.
Age is always an important consideration because of erythroid physiological behaviour. This review will discuss only the remarkable differences reported in young dogs, focusing on the causative agents and the hereditary component for
some hemolytic anemias, as well as the main causes of nonregenerative anemias in this age group. The blood loss anemias (included in the regenerative classification of anemias)
dont show any special figures for young dogs, although at
this age inherited coagulation disorders should be considered as possible causes of severe blood loss.

8th

Weeks of age

REGENERATIVE ANEMIA
Figure 3 - Reticulocyte count and NRBCs in young Beagle dogs5,6,11.

The normal wide ranges reported for canine WBC counts


(6,000-17,000/mcL) reflect the effects of age and normal activity. The WBC count is highest in young dogs. As an example, a WBC count of 7,000/mcL is normal in an old dog
while it can be suggestive of leukopenia in a dog less than
18 months of age. The gradual decrease of WBC count with
age is primarily due to both changes in lymphocyte and neutrophil numbers. In a study on Beagles focused on WBC
count modification as well as on the number of leukocyte
types from birth up to 24 weeks of age, a neutrophilia was
observed at birth (due perhaps to the stress of birth) which
disappeared within a week. Neutrophil and lymphocyte
counts were similar at the 3rd week of age (caused by weaning, change in feeding, and new antigen exposure), after
which neutrophil numbers steadily increased relative to
lymphocyte numbers (see figure 4)3,4,9,11.

WBC values in young Beagle dogs (K/mcL)


18
16
14
12
10
total WBC

Neu Band

Puppies of 4 months of age or younger are quite susceptible to Babesia spp. (B. canis, B. gibsoni, and B. vogeli) and
frequently have more severe infection than do adult dogs.
Mild strains of B. canis may cause apparent disease only in
puppies and B. gibsoni has been identified in the blood
smear of a bitch and her 3-day old puppies, suggesting that
transplacental transmission occurred. These diseases are
tick-borne (Rhipicephalus sanguineous, Dermacentor spp.
and Hyalomma spp.). The hemolysis induced by these parasites is both intravascular and extravascular with signs of
bone marrow regeneration (reticulocytes and, secondarily,
NRBCs). Other laboratory findings may include thrombocytopenia, hyperbilirubinemia, bilirubinuria, hemoglobinuria,
and azotemia. Metabolic acidosis and disseminated intravascular coagulation (DIC) may develop as a complication. Definitive diagnosis requires a careful examination for Babesia
spp. in RBCs. An indirect immunofluorescence (IFA) test
may be used in chronic disease because the titers will be detectable 2.5 weeks after onset of infection3,9.
Infections by Haemobartonella canis are reported as frequent in dogs of all ages with severe hemolytic anemia occurring in especially young animals3,9.

Neu Seg

Lymp

Mono

0
birth

Hemolytic anemia caused by infectious


agents

Eosi
1st

2nd

3rd

4th

6th

8th

12th

16th

20th

24th

Baso

Immune mediated hemolytic anemia (IMHA)

Weeks of age

Note: Neu = neutrophil; Seg = segmented; Lymp = lymphocyte; Mono = monocyte;


Eosi = eosinophil; Baso = basophil

Figure 4 - Total and differential WBC values in young Beagle dogs4,11.

IMHA occurs rarely in dogs younger than 6 months of


age, and may be induced by many processes including
drugs, alloantibody formation, infectious processes, vac-

4th European FECAVA SCIVAC Congress

Heinz body hemolytic anemia


This type of anemia occurs when there is excessive accumulation of oxidised RBC Hgb often as the result of ingested oxidants. This situation may occur in young dogs
from ingesting oxidative drugs (methylene blue, topical benzocaine, acetaminophen, vitamin K3 or menadione, and
phenylhydrazine) or chemicals (zinc or onions). In addition
to Heinz bodies, RBC membrane damage including poikilocytosis and schistocytosis and signs of RBC regeneration
may occur3,8,9,12.
The RBCs of the Japanese Akita and Shiba have reduced
glutathione activity and increased intracellular potassium
concentrations that result in an increased sensitivity to
onion-induced Heinz body formation and hemolysis occur3,8,9,12.
Anemia associated with Heinz body formation will appear nonregenerative if observed within the first 2 to 3 days
after the onset, before the bone marrow erythropoietic response. However this disease does not require specific therapy other than removing access to or discontinuing administration of the offending oxidative agent. As an alternative NAcetylcysteine could be used within hours of ingestion of
the offending substance at a dosage of 140 mg/kg per os
(PO) followed by 70 mg/kg PO every 6 hours for seven
treatments. In severe, life-threatening anemia, blood transfusion is indicated occur3,8,9,12.

Hemolytic anemia on inherited basis


This type of anemia should be suspected when the animals exhibit persistent reticulocytosis and hemolytic anemia, have negative direct antiglobulin tests (DAT; Coombs
test), negative examinations for Babesia spp. infection, and
a negative history of toxin exposure causing production of
Heinz bodies8.
Deficiency of Pyruvate Kinase (PK)
This deficiency causes a nonspherocytic hemolytic anemia in Basenji dogs as a congenital disorder and in Beagles,
West Highland White and Cairn Terriers as isolated occurrences. The mode of inheritance is a simple autosomal recessive trait; matings between carriers of the defect produce
normal or anemic or carrier puppies, whereas the offspring
of affected anemic parents are always affected. Carrier dogs
are not anemic, but can be identified by their notable reduction of RBC pyruvate kinase activity. This deficiency is not
often observed until puppies are 4 months to 1 year of age.
Premature RBC destruction, with moderate to severe anemia (Hct from 12 to 26%), and evidence of RBC regeneration (polychromasia/reticulocytosis, anisocytosis, increased
NRBCs) could be observed. As the dog ages, the early intense erythropoietic response declines until the bone marrow aspiration may be unsuccessful as the hematopoietic
compartment is replaced with fibrous tissue (myelofibrosis).
This occurs from 2 to 5 years of age as impaired RBC production leads to death from nonregenerative anemia and hepatic failure. There is no effective long term treatment for
this type of hemolytic anemia, which could only be corrected by a bone marrow transplantation from normal littermates occur3,8,9,12.
Deficiency of Phosphofructokinase (PFK)
This deficiency is recognised in the English Springer
Spaniel as well as in the American Cocker Spaniel (presumably because of intercrossing between this two breeds), and
is inherited as a simple autosomal recessive gene. It is characterised by chronic hemolysis with recurrent hemolytic crisis and mild myopathy. Crises may be precipitated by
episodes of hyperventilation induced by extensive exercise,
excessive barking, and/or elevated environmental temperature. During the crises, dogs may become severely anemic or
icteric with a transient hemoglobinemia, hemoglobinuria,
and bilirubinuria that usually resolves with therapy for
IMHA. Spontaneous resolution does occur. The activity of
PFK is, respectively, about 20% and 5% of the normal concentration of RBCs and muscle. The PFK deficiency results
in an early blockage of glycolysis induced by marked reduction 2,3-diphosphoglycerate (2,3 DPG) RBC concentration.
This in turn provokes increased Hgb oxygen affinity, increased intraerythrocytic pH and increased RBC fragility as
the result of intraerythrocytic alkalosis occur3,8,9,12.
Inherited Stomatocytosis of Alaskan Malamute
This RBC shape alteration results in reduced RBC life
span and is also related to autosomal recessive-transmitted
chondrodysplasia (short-limbed dwarfism) in the Alaskan
Malamute. The other hematological findings include an appropriate PCV with reduced hemoglobin content; the RBC
indices include increased MCV, decreased MCHC, and normal MCH. Despite this macrocytosis few RBCs are reticu-

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cines, or may be ill-defined true autoimmunity3,9,12,13.


Neonatal isoerythrolysis results from previous sensitisation of the bitch (exposure to red cell antigens of puppies
having the fathers blood type; previous blood transfusions).
Indeed alloantibodies against dog erythrocyte antigen
(DEA) 1.1 are produced when DEA 1.1 positive blood is
transfused into a DEA 1.1 negative bitch and the bitch subsequently is mated to a DEA 1.1 positive dog. Her puppies
may experience hemolytic anemia, nursing during the first
48 hours of life as they receive the mothers colostral antiDEA 1.1 alloantibodies. Puppies with the DEA 1.2 blood
group could be also mild affected, while alloantibodies toward other blood group types have not been implicated in
causing anemic problems in newborn puppies3,9,12.
Neonates that experience isoerythrolysis are generally
healthy and normally sized at birth but develop hemolysis
within several hours or days after ingestion of colostrum.
They exhibit progressive weakness, pale mucous membranes, hemoglobinemia, hemoglobinuria, and icterus. The
severity of the hemolytic anemia is variable, depending
somewhat on the quantity of colostral alloantibodies absorbed and the nature of the antigen-antibody reaction (direct
or indirect agglutination and hemolysis). Severely affected
puppies often die within 24 hours from respiratory distress or
within 2 to 6 days owing to complications due to DIC or from
acute renal failure. The puppies should be separated from
their mother for the first 48 to 72 hours and given milk replacer or allowed to nurse from a foster mother with the same
blood type as the puppy and not producing colostral alloantibodies. Withholding colostrum from subsequent litters of
dams proven or suspected to be sensitised is advisable3,9,12.

265

266

locytes and about 4 percent of the RBCs are stomatocytes.


Treatment is generally not necessary as the disease is not
life-threatening. Efforts should be made toward to control
and eliminate of heterozygous carrier dogs from the breeding population occur3,8,9,12.
Nonspherocytic Hemolytic Anemia of the Poodle and
Beagle
A severe (Hct from 10% to 26%) nonspherocytic hemolytic anemia characterised by a markedly regenerative
RBC response, hepatosplenomegaly, bone marrow myelofibrosis and osteosclerosis, with a fatal course has been described in related black miniature Poodles. A similar disease
but less severe and without significant fatalities has been reported in Beagles. In these breeds an autosomal recessive
mode of inheritance has been postulated altering the RBC
membrane and the calcium-adenosine triphosphatase (CaATPase) enzyme, but the cause remains undetermined. In
Poodles the unremitting anemia with macrocytosis is most
evident by one year of age and often fatal by 3 years of age.
In this breed there is no effective, long term treatment for the
severe anemia; however, correction by bone marrow transplantation from hematologically normal littermates may be
effective occur3,8,9,12.

NON REGENERATIVE ANEMIA


Nonregenerative anemia is defined as an anemia longer
than 5 days duration with inappropriately low corrected
reticulocyte counts. Based on complete blood count, nonregenerative anemia may also be identified as being a refractory anemia or a component of pancytopenia. In refractory
anemia, the WBC and Plt counts are normal or increased,
while in pancytopenia the disorder involves these two cell
lines as well. Based on the RBC indexes, refractory anemia
may be further subdivided in normocytic, normochromic
(the most frequent); macrocytic, normochromic; and microcytic, hypochromic. Bone marrow examination and iron
studies should be evaluated to delineate the cause of the refractory anemia occur9,12,13.

Refractory anemia
Failure of appropriate RBC production
Pure red cell aplasia (PRCA) resulting in selective and
severe erythroid bone marrow hypoplasia has not been reported in dogs younger than 6 months of age. However, secondary marrow failure as a result of long-standing disease
(e.g., advanced renal or hepatic disease, inflammatory disease, malnutrition, Ehrlichiosis) frequently causes refractory
anemia (normocytic and normochromic). In particular, the
anemia of inflammatory disease is characterised by mild to
moderate, poorly regenerative anemia and altered iron metabolism. Low serum iron and total iron binding capacity, as
well as increased sequestration of iron in marrow
macrophages are described3,9,12,13.
Nuclear maturation defects
These anemias, characterised by macrocytic and normochromic RBCs, result from defective marrow DNA syn-

4th European FECAVA SCIVAC Congress

thesis in erythroid precursor cells causing decreased RBC


division and the appearance of large NRBCs and macrocytes
in peripheral blood. In addition, the disturbance may cause
mild reduction in WBC and Plt numbers. This type of anemia is uncommon in young dogs and is associated with vitamin B12 and/or folate deficiency3,9,12,13.
A selective cobalamin (vitamin B12) malabsorption in
Giant Schnauzers is related to an autosomal recessive mode
of inheritance. The disease is characterised by cachexia, dementia, and nonregenerative anemia. Cobalamin is required
for purine and pyrimidine synthesis, both precursors of
DNA. Nuclear maturation is impaired and results in reduced
mitotic division and large NRBCs (megaloblasts) that have
asynchronous maturation of nucleus and cytoplasm. Other
cell lineages can also be affected. The clinical signs initially appear at 3 months of age and are characterised by lethargy, anorexia, and cachexia. The hematological data include
mild to moderate anemia, anisocytosis without reticulocytosis or other evidence of regeneration, poikilocytosis with
some macrocytes, neutropenia and hypersegmented neutrophils. The serum cobalamin concentrations are low and
an increase of urinary methylmalonic acid is observed.
Treatment with cobalamin, 0.25-1.00 mg subcutaneously
(SQ) once daily (SID) for one week then once monthly often resolves the defect3,9,12,13.
Folate deficiency is more likely to occur due to the administration of drugs which inhibit bacterial folate synthesis
(pyrimethamine, and trimethoprim) through a competitive
inhibition of tetrahydrofolate reductase, thus inhibiting the
reduction of folate to its active form, dihydrofolate and
tetrahydrofolate. Generally the drug-induced anemia appears well before any overt signs of illness are noted3,9,12,13.
A congenital macrocytosis has been reported in Miniature and Toy Poodles. The affected dogs have normal Hct
and Hgb concentrations because of macrocytosis, but they
have a slightly reduced RBC numbers. Hypersegmentation
of neutrophils in peripheral blood and megaloblastic RBCs
in bone marrow may be observed3,9,12,13.
Hemoglobin synthesis defects
The result of altered hemoglobin synthesis is RBC microcytosis which is initially normochromic and becomes a
frankly hypochromic, and then refractory anemia. This commonly occurs secondary to iron deficiency in young malnourished or heavily parasitized dogs (by bloodsucking internal or external parasites). Iron deficiency occurs when
iron loss or utilisation exceeds iron absorption from the intestine and rapidly develops in newborn and young animals
who have limited iron stores and require a steady increase in
their total RBC mass for growth needs. The nonparasitic
causes of external blood-loss induced iron deficiency in
dogs may include bleeding disorders, infectious enteropathies, and gastrointestinal ulcerations. Other potential
but rare causes of microcytic, hypochromic refractory anemia include copper or vitamin B6 deficiency, or iron deficiency as the result of lymphocytic-plasmacytic intramural
intestinal disease3,9,12,13.
Dyserythropoiesis of English Springer Spaniel
A nonregenerative anemia associated with a polysystemic disorder (polymyopathy with megaesophagus and
varying degrees of cardiomyopathy) has been reported in a

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Pancytopenia
Aplastic Anemia
Aplastic anemia is a collective term describing a condition characterised by anemia, thrombocytopenia, and granulocytopenia with an acellular or markedly hypocellular bone
marrow. The failure of the hemopoietic activity may be due
to marrow necrosis and/or inflammation, a defect in the proliferative capacity of the pluripotential stem cell in the marrow, or a defect in the hemopoietic-inductive bone marrow
microenvironment. This disorder could be associated with
estrogen or trimethoprin therapy, phenylbutazone toxicity,
use of chemicals such as benzene compounds, and infections
by several agents including canine distemper virus, canine
parvovirus and Ehrlichia canis3,9,12,13.
Myelophthistic Disorders
Myelophthistic disorders are extremely rare in young
dogs but may result from bone marrow infiltration by primary hematopoietic tumors or fibrous tissue (myelofibrosis)
or from congenital failure to develop normal bone marrow
cavities as occurs in inherited osteopetrosis3,9,12,13.
Lead Toxicosis
This toxicity is well recognised, affecting dogs from 2 to
8 months of age. At that age dogs often have a curious nature and chewing habits often result in ingestion of strange
substances. Moreover lead tends to accumulated more in
younger animals. Lead toxicosis induces a nonregenerative
anemia that could be misinterpreted as regenerative. Indeed,
a large number of NRBCs (from 15 to 40/100 WBCs) may
be found in peripheral blood along with a mild normocytic
normochromic anemia (Hct around 30%). Other RBC abnormalities include basophilic stippling, poikilocytosis and,
sometimes hypochromasia. Lead causes profound alterations in hemoglobin synthesis with an inadequate formation
as well as a shortened RBC survival time. The RBC modifications occur very early in lead toxicosis, even before other
clinical signs3,9,12.
A definitive diagnosis is established by performing a
lead analysis, collecting oxalate or heparin whole blood
sample in a clean, lead free glass vials. Baseline concentrations for lead generally range between 5 to 25 mcg/dL (0.050.25 ppm); suspicious values range from 30 to 50 mcg/dL
(0.3-0.5 ppm) and indicate lead poisoning if associated with
typical gastroenteric and neurologic signs and hematologic
findings. The findings of concentrations over 60 mcg/dL
(0.6 ppm) are diagnostic for lead poisoning. Therapy is
based on chelation which effectively removes lead by combining to form nontoxic complexes rapidly excreted via bile
or urine. The chelating agent of choice in young dogs is cal-

cium disodium edetate and/or succimer. As soon as chelation


therapy is initiated, RBC abnormalities quickly disappear3,9,12.

Conclusions
As will be evident from this review, there are many gaps
in our knowledge about the evolution of the hemopoietic
system in the young dog. Detailed studies are needed in this
area, and should include the use of representative breed of
the various dogs sizes. It is well known that differences in
the hematological reference intervals between breeds such
as the Yorkshire terrier and the Great Dane are perhaps even
more apparent at a young age. Improved instrumentations in
veterinary hematology should improve the accuracy of these
determinations.
Secondly, there is a need to develop a reporting system
for inherited erythrocytic disorders, which at the moment
are only reported in certain breeds primarily in USA. It is
possible that these defects are present in other breeds and
that they are geographically more diverse. In the near future
the diagnosis of these diseases should be by specific referral
laboratories using genetic biotechnologies. Indeed they
should not be considered as exclusive of some kennel clubs
or some countries, but are world-wide problems especially
considering the constant animal movement possible in the
world today.
Finally, data on anemic processes in the young animal
are not, as yet, widely recognised. Hopefully this review
may help. Many of the diseases described herein have been
determined relatively recently and are now being recognised
by private veterinary clinicians as routine hematologic examination becomes an integral part of clinical practice. It is
essential for correct evaluation of a pediatric patient that the
proper collection of an adequate sample for analysis be accomplished in order to reach definitive diagnoses.

References
(For shortness the books consulted and some publications are only here reported; the extended reference version could be requested directly to the
author).
1. Andersen AC & Schalm OW (1970), The beagle as an experimental
dog, In: Hematology, Andersen AC, ed. Iowa SU press, Ames.
2. Andersen AC & Gee W (1958), Normal blood values in the Beagle,
Vet Med, 53:135.
3. Bounous DI (1995), Hematology of normal dogs and cats and response to disease In: Hoskins JD (ed), In: Veterinary pediatrics: dogs
and cats from birth to six months, 2nd edit, WB Saunders, Philadelphia, 337-353.
4. Bulgin MS et al (1970), Hematological changes to four and one-half
years of age in clinically normal beagles, JAVMA 175: 1064.
5. Brunk R & Becker-Berger S (1980), Statistiche untersuchungen auf
alters- und geschlechsspezifische unterschiede von blutparametern an
englischen beagle-hunden, Berl Munch Tierarztl Wochenschr,
93:128.
6. Earl FL et al (1973), The hemogram and bone marrow profile of normal neonatal and weanling beagle dogs, Lab Anim Sci, 23: 690.
7. Ederstrom HE & DeBoer B (1946), Changes in the blood of the dog
with age, Anat Rec, 94: 663.
8. Giger U (1989) Hereditary disorders of canine erythrocytes, In: Current Veterinary Therapy X. Small Animal Practice, Kirk RW (ed),

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limited number of this type of dog aged from 3.5 months to


2 years old. The dyserythropoiesis is characterised by abnormal erythroid cells with arrested or abnormal mitosis in
the bone marrow and many NRBCs in the peripheral blood
without appropriate reticulocytosis. Other RBC abnormalities such as microcytosis, spherocytosis, schistocytosis, and
poikilocytosis may occur. Until now the prevalence, underlying mechanism, and mode of inheritance are unknown3,8,9,12.

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9.
10.
11.

4th European FECAVA SCIVAC Congress


WB Saunders, Philadelphia, 429.
Jain NC (1986), Schalms Veterinary Hematology, Philadelphia, Lea
& Febiger, 103.
Lee P. et al (1976), Blood volume changes and production and destruction of erythrocytes in newborn dogs, Am J Vet Res, 37: 561.
Shifrine M et al (1973), Hematologic changes to 60 days of age in
clinically normal beagles, Lab Anim Sci, 23:894.

12.

13.
14.

Tvedten H (1994), Erythrocyte disorders, In: Willard MD, Tvedten


H, Turnwald GH (eds), Small animal clinical diagnosis by laboratory
methods, 2nd edit, WB Saunders, Philadelphia, 31.
Tyler RD & Cowell RL (1996), Classification and diagnosis of anemia, Comp Haem Intl, 6: 1.
Weisse I et al (1971), Das blutbildder englischen beagle-hund in abhangigkeit von alter und geschlecht, Arzneim Forsch, 21: 1703.

4th European FECAVA SCIVAC Congress

269

Contemporary application and interpretation


of hepatic tests
Denny Meyer

For the study of medical diseases of the liver, it is essential that the pathologist be apprised of the clinical findings and the results of laboratory tests and radiographic studies. The correct diagnosis is most likely to be reached by the
pathologist and clinician working as a team. Kamal Ishak,
MD; pathologist.
The serum hepatic enzyme tests are grouped into those
that indicate hepatocellular injury/repair and those that reflect increased enzyme production stimulated by retained
bile or drug induction. The magnitude and duration of increase in plasma enzyme activity is dependent on 1) its innate tissue activity, 2) its cellular location, 3) its rate of removal from the plasma, and 4) the type, severity and duration of the injury/stimulus. The rate of removal seems to
have molecule-specific and species-specific properties; neither well-characterized in veterinary medicine. Table 1 lists
examples for the dog and cat.
Leakage Enzymes.
Alanine aminotransferase (ALT); Aspartate aminotransferase (AST). There is a high activity of alanine aminotransferase (ALT) in hepatocellular cytoplasm of the dog, cat, and
primate; the equine, bovine, birds, and marmoset are notable
exceptions. One can think of each hepatocyte like a little balloon filled with ALT. Altered permeability of the hepatocellular membrane caused by injury or a metabolic disturbance
results in a release of this soluble enzyme. Subsequent to an
acute, diffuse injury, the magnitude of increase in the plasma crudely reflects the number of affected hepatocytes. A
variety of tissues, notably skeletal muscle and liver, contain
high aspartate aminotransferase activity (AST). Skeletal
muscle injury is best defined biochemically by the measureTable 1. Approximate plasma half-life of hepatic
enzymes in the dog and cat
Enzyme
ALT
AST
GLDH
ALP
-hepatobiliary isoenzyme
-corticosteroid isoenzyme
-intestinal isoenzyme

Dog

Cat

61 (or 40) h*
12 h
18h

3.5 h
1.5 h
-

66 h
74 h
6m

6h
2m

*references differ; h = hours, m = minutes.

ment of the serum creatine kinase (CK, CPK) activity, a specific skeletal muscle enzyme.
Our experience suggests that there is value in the interpretation of the serum activities of ALT and AST for liver
disease in the dog and cat. Following an acute injury resulting in a moderate to marked increase in the serum ALT and
AST activities, the serum AST activity will return to normal
more rapidly (hours to days) than the serum ALT activity
(days) due to their difference in plasma half-lives and cellular location. By determining these values every 2 to 5 days
for the dog following an acute insult, a sequential "biochemical picture" indicative of resolution is obtained. Persistent mild to moderate increases of the serum ALT and
AST activities (documented multiple times over months)
suggest a smoldering inflammatory process, chronic hepatitis. The persistent increase in the aminotransferase activities is probably a consequence of increased release subsequent to both cell injury and on-going hepatocelluar reparation (regeneration).
Novel Concept-1. Clinically, the decrease in the serum
ALT and AST activities is often slower than their plasma
half-lives would predict following a one-time release phenomenon subsequent to cellular injury. This is probably due
in some cases to the temporary persistence of the insulting
agent and the ensuing inflammatory reaction. An explanation that can be more generically applied to explain this discrepancy focuses on the relatively unique regenerative ability of the hepatocyte. Studies in the rat indicate that 24 hours
following carbon tetrachloride-induced hepatocellular injury, the expected increase in the plasma ALT and AST activities occurs. If the increase in the plasma was due solely
to a one-time release from the damaged tissue, the corresponding hepatic tissue activity would be expected to be decreased. Recent studies demonstrate that the hepatic tissue
activities for both aminotransferases are actually moderately
increased at 24 hours. The finding suggests that the remaining viable hepatocellular tissue has increased its synthesis of
the aminotransferases as a consequence of, and/or in support
of, the reparative/regenerative process. This concept is supported by repeating the carbon tetrachloride study and coadministering cyclohexamide, a nonspecific inhibitor of protein synthesis. Following the administration of this cocktail to rats, the rise in the plasma aminotransferase activities
is blunted by approximately 60% compared to the group that
received only carbon tetrachloride. Clinically, a precipitous
decrease in the serum ALT and AST activities following

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DVM, Dipl ACVIM, Dipl ACVP


NeXstar Pharmaceuticals, Boulder, Colorado - USA

270

their moderate increase may be suggestive of insufficient hepatic mass to support repair and a harbinger of fulminant hepatic failure.
Novel Concept-2. Hepatic AST appears to be released
later and as a consequence of more severe injury than ALT.
Perhaps this explains the finding in one study that an increase in the serum AST activity has high specificity (but
low sensitivity) for hepatic disease in the dog. The subcellular location of AST activity is divided between a soluble cytosolic form (c-AST) and a mitochondrial form (m-AST).
The c-AST is the predominant form. Experimental studies
and clinical observations suggest that 1) the magnitude of increase is greater for serum ALT activity than for AST and 2)
an increase in serum ALT activity precedes AST. Mitochondrial injury is necessary for m-AST to contribute to the
serum AST activity. Since its release is consequent to necrobiosis, measurement by electrophoresis or immunochemistry is being investigated in human patients as an index of
severity.
Markers of Cholestasis and Drug - Induction.
Alkaline phosphatase (ALP) and Gamma glutamyltransferase (GGT). Alkaline phosphatase and gamma glutamyltransferase (gamma glutamyltranspeptidase, GGTP) show
minimal activity in normal hepatic tissue but can become
markedly increased in the serum subsequent to increased enzyme production stimulated by either impaired bile flow or
drugs. The increased synthesis begins within hours with subsequent appearance in the plasma by release mechanisms
that are not clearly defined. These enzymes have a membrane location; ALP associated with the canalicular membrane and GGT associated with epithelial cells comprising
the bile ductular system. Alkaline phosphatase is a enzyme
located on the membrane of a variety of tissues but only two
are diagnostically important; hepatobiliary and bone. Each
tissue has an ALP isoenzyme that can be separated by electrophoresis. With the exception of the growing animal or the
patient with bone disease, an increased serum ALP activity
is of hepatobiliary origin. There is considerable species variation for the diagnostic application of ALP. The reference
range is wide for horses and ruminants limiting its diagnostic sensitivity. The hepatobiliary tissue of the cat has a limited capacity for accelerated ALP production. The diagnostic
sensitivity and magnitude of increase in the cat is further attenuated by a plasma half-life of 6 hours. In contrast, the dog
liver has a robust ability to increase ALP production and a
relatively long plasma half-life of 66 hours.
There is minimal increase in the plasma following an
acute, severe insult (in contrast to ALT and AST). Any initial rise is probably a reflection of enzyme activity on cell
membrane fragments released to the plasma as a consequence of the damage. Disruption of the hepatobiliary architecture causes local impairment to bile flow which stimulates increased ALP production within hours. During hepatic reparation following an injury, the serum aminotransferase activity slowly decreases while the serum ALP activity often increases until the local cholestasis has resolved.
Consequently, the serum ALP activity is usually the last
serum hepatic enzyme test to return to normal in the dog following resolution of an acute insult.
A primary event that obstructs the flow of bile, whether

4th European FECAVA SCIVAC Congress

intrahepatic or extrahepatic, is initially associated with an


increase in the serum ALP activity. The retention of bile
acids is linked to initiation of alkaline phosphatase synthesis
by an ill-defined mechanism. If the insult is protracted and
severe, increased serum total bile acid concentration, bilirubinuria (notably dog), and finally hyperbilirubinemia resulting in jaundice. The magnitude of increase in the serum ALP
activity is not a reliable index for differentiating extrahepatic and intrahepatic cholestatic disorders. Lesser increases in
the serum aminotransferase activities often develop either as
a consequence of the primary pathologic event and/or the
detergent effects of the retained hydrophobic bile acids altering membrane permeability.
An increase in the serum ALP activity is associated with
the use of glucocorticoids and anticonvulsant medications.
There is remarkable individual variation in the magnitude of
these increases and there is no concomitant hyperbilirubinemia. In the dog, the increased serum ALP activity associated
with corticosteroids has been attributed to a an induction of
the synthesis of a novel ALP (CIALP) isoenzyme that can be
distinguished from the cholestatically-induced liver ALP
(LALP) isoenzyme by several procedures.
More recently this variable, unique increase of ALP in
dogs associated with corticosteroids may be related to a novel concept pertaining to the formation of the CIALP isoenzyme. The CIALP isoenzyme has been diagnostically used
for hyperadrenocorticism. Unfortunately, an increase in this
isoenzyme can be associated with hepatobiliary disease, diabetes mellitus, hypothyroidism, acute pancreatitis, and phenobarbital treatment. Its judicial use in the context of the patients history and other biochemical findings may have supportive differential diagnostic value for hyperadrenocorticism. A moderate to marked increase in serum ALP activity
without concurrent hyperbilirubinemia and minimal increase in the aminotransferases is most compatible with a
corticosteroid effect and warrants a review of the patient's
history (topical or systemic corticosteroids) or evaluation of
adrenal function.
Occasionally this biochemical pattern mimics primary
hepatic disease, especially early cholangiohepatitis, and a
hepatic biopsy is required for the differentiation.
Anticonvulsant medications (phenobarbital, phenytoin,
and primidone) can increase the serum ALP activity in the
dog. The aminotransferase activities may be increased to a
lesser magnitude and there is no hyperbilirubinemia. This is
important to realize because these medications can occasionally cause chronic hepatitis. A prominence of the serum
ALT activity in these patients during treatment, especially if
accompanied by an increased serum GGT activity, warrants
further investigation, e.g., measurement of the serum total
bile acid concentration or biopsy.
Novel Concept. The variable, unique increase of ALP in
dogs associated with corticosteroids may be related to a
novel concept pertaining to the formation of the CIALP
isoenzyme. Experimental findings in the dog clearly demonstrate that the hepatic ALP isoenzyme is the one that initially increases subsequent to the administration of corticosteroids. It is the predominant component of the total serum
ALP activity for at least 30 days with a smaller contribution
by the CIALP isoenzyme after about one week. A fascinat-

ing study measured the rate of clearance for the intestinal


ALP isoenzyme by the asialoglycoprotein receptor pathway
both in vivo and in vitro using isolated hepatocytes from
dogs treated with corticosteroids. The findings indicate that
the structurally-related intestinal and CIALP isoenzymes
may be metabolically related through the asialoglycoprotein
receptor endocytosis pathway. A portion of the intestinal
ALP isoenzyme normally endocytosed through this pathway
in corticosteroid-treated dogs may be recycled and hyperglycosylated to form the isoenzyme measured as the CIALP
rather than being degraded by the hepatocyte. This abnormal isoenzyme is not cleared as rapidly as the intestinal
isoenzyme (plasma 1/2 life of 74 hours and 6 minutes, respectively) and accumulates in the plasma. The electrophoretically isolated CIALP isoenzyme has been shown
to be a product of the same gene as the intestinal ALP isoenzyme with only a slight difference in their carbohydrate
moiety.
This concept is not new in medicine and has been documented in humans, both juvenile and adult, with viral infections, hepatic cirrhosis, diabetes mellitus, chronic renal failure, and undergoing hemodialysis. The increase of the
serum activities of ALP (or GGT) in these conditions has
been shown to be due to a decreased clearance. An alteration
of the terminal carbohydrate moiety (increased sialic acid
content) has been suggested to affect receptor recognition
which impairs its clearance. Following a viral infection, for
example, the temporary increase of serum ALP activity may
last weeks or months. Altered clearance has been shown to
occur for the macroenzymes resulting in measurement as increased activity. It is possible that the relatively high serum
ALP values in cats with hepatic lipidosis, an intrahepatic
disorder, also may be due to delayed clearance. Certainly
more studies are indicated. The added message is that increased plasma enzyme activity can be a consequence of
predominantly increased release, predominantly formation
and release (the traditional concepts), or predominantly decreased removal.
Benign familial hyperphosphatasemia refers to an inherited condition in human beings in which a markedly raised
serum ALP activity is serendipitously identified in childhood and persists into adulthood. The cause of the increased
enzyme activity is not known but it is not associated with
underlying pathology, hence the term benign. It is a biochemical curiosity with no adverse effect other than potentially causing an unnecessary evaluation for bone or hepatic
disease. A biochemically similar condition has been described in Siberian husky pups.
Gamma glutamyltransferase (GGT) is enzyme that is located on the membrane of a variety of tissues. Increased
serum GGT activity is associated with impaired bile flow
and glucocorticoid administration in the dog. Anticonvulsant
medications cause minimal to no increase in the serum GGT
activity in the dog which is in contrast to humans and their
effect on ALP. The serum GGT activity is a useful marker of
biliary tract disease in the horse and ruminant. It may also be
more diagnostically sensitive than ALP in the cat. Acute, severe hepatic injury can cause a mild increase in the serum
GGT activity in the horse and ruminant because of the relatively high activity associated with the biliary tissue. This in-

271

creased serum activity may be a consequence of these enzyme-rich membrane fragments from the damaged tissue
reaching the peripheral circulation. The magnitude of this increase is much less than that associated with predominantly
cholestatic disease in these species. Bone does not contain
GGT, therefore growth and bone disease are not associated
with increased serum GGT activity. Colostrum and milk
have high GGT activity and nursing animals develop increased serum GGT activity. The renal tubular epithelial
cells have a relatively high GGT tissue activity. Acute tubular injury results in a rapid increase in the activity of GGT in
the urine (but not the serum). The measurement of urine
GGT activity is a useful indicator of early nephrotoxicity
secondary to the use of aminoglycoside antibiotics in all
species.
Macroenzymes. In human patients, unexplained persistent increases in serum enzyme activity has been demonstrated with increasing frequency to be the result of
macroenzymes. The hepatic enzymes reported include ALT,
AST, ALP, GGT, CK, LD, lipase, and amylase. These highmolecular-mass enzyme forms can be immunoglobulinbound or nonimmunoglobulin-bound. In either case the enzyme clearance is reduced. In dogs with proteinuria, an immunoglobulin-amylase complex (macroamylase) resulting
in an increased serum amylase activity without clinical
signs of pancreatitis has been reported recently. A raised
serum enzyme activity without clinical and/or histomorphologic abnormalities should prompt consideration of a
macroenzyme.
Function Tests
Bilirubin. Bilirubin is a pigmented compound produced
largely from the degradation of the heme by the macrophage
system (forming unconjugated bilirubin) from aged erythrocytes and excreted by the hepatobiliary system following its
conjugation. The uptake site for bilirubin is also shared by
other organic anions such as sulfobromophthalein (BSP) but
not bile acids. Species variation in the metabolism of bilirubin compared to humans precludes the reliable diagnostic
use of the unconjugated:conjugated bilirubin ratio or the
magnitude of rise in defining the causation of hyperbilirubinemia. Linking jaundice to the evaluation of the patients
hematology, serum hepatic enzymes, and adjunct procedures
is a valuable approach. Accelerated destruction of erythrocytes is associated with a moderate to marked reduction in
the packed cell volume (PCV). Biochemically, a marked increase in the serum ALT and AST activities with a mild increase in the serum ALP activity indicates acute, severe hepatocellular injury.
Mild to moderate, variable increases in the serum ALT,
AST and ALP activities in association with hyperbilirubinemia suggest intrahepatic disease and the need for additional diagnostics. Ultrasonography is a valuable tool for assessing the liver and extrahepatic biliary system when a
marked rise in the serum ALP activity is concurrent with
hyperbilirubinemia.
Novel concept. Biliprotein (originally referred to as delta
bilirubin because of its location after separation of the total
serum bilirubin with high performance liquid chromatography) is a fraction of conjugated bilirubin that is irreversibly
bound covalently to albumin. Its formation as a consequence

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272

of cholestasis is not completely understood and the amount


formed is variable. In jaundiced dogs and cats, it can range
from very little to more than 90% of the total serum bilirubin concentration. Because of its irreversible binding to albumin, its degradation parallels that of albumin, approximately 10 to 14 days. Consequently, if it is the predominant
component of the total bilirubin, the decrease in the serum
total bilirubin concentration following resolution of the disease process will be protracted. Because some of the drychemistry reagent systems can directly measure biliprotein,
its determination along with the total bilirubin concentration
can provide useful information.

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Supplemental reading
Ishak K, (1993), Hepatic histopathology, In Schiff L, Schiff E (eds), Diseases
of the liver, 7th ed, J.B. Lippincott Company, Philadelphia, 145-160.
Kuhlenschmidt M, Hoffmann W, Rippy M, (1991), Glucocorticoid hepatopathy: Effect on receptor-medicated endocytosis of asialoglycoproteins. Biochem Med Metab Biol, 46:152-168.
Lawler DF, Keltner DG, Hoffman WE, et al., (1996) Benign familial hyperphosphatasemia in Siberian huskies. Am J Vet Res, 57:612-617.
Pappas NJ Jr, (1986), Source of increased serum aspartate and alanine
aminotransferase: Cycloheximide effect on carbon tetrachloride hepatotoxicity. Clin Chim Acta, 154:181-190.
Solter PF, Hoffmann WE, Hungerford LL, et al., (1993), Assessment of corticosteroid-induced alkaline phosphatase isoenzyme as a screening test
for hyperadrenocorticism in dogs. J Am Vet Med Assoc, 203:534-538.

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273

The effects of extrahepatic disease on the liver


Denny Meyer

For the study of medical diseases of the liver, it is essential that the pathologist be apprised of the clinical findings and the results of laboratory tests and radiographic studies. The correct diagnosis is most likely to be reached by the
pathologist and clinician working as a team. Kamal Ishak,
MD; pathologist.
Hepatic reaction to extrahepatic disease is being recognized with increasing frequency (Table 1). Both serum hepatic test and histomorphologic abnormalities can occur.
The secondary hepatic involvement poses two diagnostic
problems: (1) mimics primary hepatic disease and (2) diverts
attention from the primary extrahepatic disease process.
There are a variety of reasons why extrahepatic diseases secondarily involve the liver. These can be divided into anatomical and functional relationships. The liver has two blood
supplies, the hepatic artery and the portal vein. The former
provides nutrition and oxygen. The later, which comprises
approximately 80% of the total hepatic blood flow, delivers
substances absorbed from the gastrointestinal tract and hormones from the pancreas. Consequently hepatic integrity
and function can be altered secondary to cardiovascular insufficiency, anemia, portosystemic shunts, and exposure to
ingested xenobiotics and intestinal bacteria or their products
when the intestinal barrier is violated by disease.
Hepatocytes reside in acini composed of three diverse
metabolic zones. Blood flows from the portal triad passing
through zones 1, 2 and 3 before draining via the hepatic
vein. Consequently, hepatocytes in zone 3 are most susceptible to hypoxic conditions such as heart failure and shock.
The metabolic diversity of the hepatic zones is necessary to
accommodate the numerous homeostatic activities. Many of
these functions are related to the intermediary role of hepatocyte metabolism between dietary sources of energy and
extrahepatic tissue demands for energy. Therefore metabolic
diseases often involve the liver. Examples include hypera-

Table 1. Extrahepatic causes of morphologic


or histopathologic changes in the liver
Inflammatory intestinal disease
Extrahepatic infections (bacterial)
Rickettsial infections
Acute pancreatitis
Diabetes mellitus
Congenital portosystemic shunt

Prolonged protein-restricted diet


Septicemia
Shock
Right-sided heart failure
Hyperadrenocorticism

drenocorticism, diabetes mellitus, hyperthyroidism, perhaps


hypothyroidism and lipid disorders. One qualitatively specific hepatocyte function is bile formation. Another cell type
that plays a role in the extrahepatic manifestations of disease
is the Kupffer cell; a member of the monocyte-macrophage
system. It is involved in the hepatic immune response and
"filters" toxins and bacteria which enter the portal circulation. When this role is amplified in response to extrahepatic
disease, focal hepatitis can develop.

Cholestasis of sepsis
The uptake and excretion of bile acids by the hepatocyte
is the primary driving force for bile flow through the biliary
ductular system. Bile acids are a class of steroidal substrates
that are produced from cholesterol by the liver, carried by
the biliary system to the intestinal tract where they contribute to fat absorption. Upon reaching the ileum, bile acids
are efficiently absorbed into the portal circulation (< 10% of
the secreted bile acids are lost in the feces during any one enterohepatic cycle) and transported back to the liver where
their extraction from the sinusoidal blood is remarkably efficient (first-pass clearance is 75-90%). This liver - gut relationship, referred to as the enterohepatic circulation, is critical for understanding the diagnostic application for measuring the serum bile acid concentration for the recognition of
hepatic disease and abnormalities of the portal circulation.
Cholestasis or impaired bile flow can be classified as extrahepatic or intrahepatic. The accumulation of bilirubin in tissues, jaundice, is a clinical indication of abnormal hepatobiliary function when accelerated erythrocyte destruction is
eliminated. Differential considerations include lesions
which obstruct the flow of bile in the common bile duct
(physical impairment) and, most commonly, a variety of diseases that damage hepatocytes and violate the intrahepatic
architecture.
Intrahepatic cholestasis can develop in association with
extrahepatic bacterial infections. Clinically the patients are
icteric, biochemically the hepatic enzyme tests show only
mild to moderate increases despite a remarkable increase in
the serum bilirubin concentration and relatively unremarkable histologic findings. There may be accumulation of bile
pigment, including canalicular plugs, and a mild inflammatory cell component, often round cell and periportal. The intrahepatic architecture remains intact. Pathologic terms such

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274

as periportal hepatitis, focal hepatitis or hepatitis, chronic,


active with bile retention may be used to characterize the microscopic findings. The successful treatment of the extrahepatic infectious process is associated with spontaneous resolution of the cholestasis. The pathophysiologic mechanisms
causing this functional cholestasis are multiple and poorly
understood. Toxins derived from bacteria may directly or antibodies to bacterial cell wall components that cross-react
with the canalicular membrane may paralyze the energydependent transport systems of the membrane. It has also
been shown that selected acute-phase reactant proteins can
interfere with hepatocellular uptake of bile acids. The common pathophysiologic factor is the impaired excretion of bile
acids which are the primary driving force for bile flow.

Inflammatory bowel disease


Dogs and cats with chronic enteric disease often will
have concurrent hepatic changes. The nature of the hepatic
changes leads one to speculate that they are secondary to the
portal uptake of bacteria or their products. Observations by
Pavlov over 100 years ago identified that poisonous symptoms occurred when intestinal toxins are not detoxified by
the liver and this theory still remains valid today. The nature
of the inflammatory infiltrate (periportal) secondary to intestinal disease has led to the hypothesis that the changes are
secondary to bacteremia from intestinal bacterial translocation through the diseased intestinal tract. A concept now in
favor is that the endotoxin lipopolysaccharide (LPS), a component of the cell wall of gram negative bacteria, transit the
intestinal wall in significant amounts in states of intestinal
inflammation. The hepatic reticuloendothelial system
(Kupffer cell) is critical for LPS detoxification and impairment of this function may lead to hepatic injury/inflammation. Though endotoxins may directly damage hepatocytes,
evidence suggests that a release of a number of substances
from the macrophage mediates diverse biological effects.
The macrophage products include superoxides, toxic oxygen
radicals, tumor necrosis factor and platelet activating factor.
Serum hepatic enzyme tests may reflect intrahepatic
cholestasis and hepatocellular injury. Rarely will tests of hepatic function be altered. Changes are most often develop in
association with long standing intestinal disease. The most
common hepatic microscopic findings include mild to moderate periportal inflammatory cell infiltrates consisting of
lymphocytes, plasma cells macrophages and neutrophils;
these findings prompt the morphologic terms of hepatitis,
chronic, active. Inflammation primarily involving the bile
ducts is termed cholangitis. Cholangiohepatitis refers to inflammation surrounding bile ducts and extending into the
parenchyma. Fibrosis, if present, is usually mild and vacuolar changes.

Acute pancreatitis
Acute pancreatitis can secondarily involve the liver
through two pathologic processes: (1) impairment of bile
flow in the common bile duct and (2) direct intrahepatic

4th European FECAVA SCIVAC Congress

damage. There is a variable amount of peripancreatic inflammation associated with acute pancreatitis. When the
phlegmon is sufficiently severe, it encompasses the common
bile duct and can cause clinical, biochemical and histologic
findings compatible with extrahepatic cholestasis. If the inflammatory process resolves, often within 7 to 10 days, the
serum bilirubin will decrease. However, fibrous tissue formation associated with the resolving inflammation may permanently embarrass the extrahepatic flow of bile necessitating surgical intervention. Biochemical and microscopic
findings consistent with hepatocellular injury and intrahepatic cholestasis can also develop in association with acute
pancreatitis. There are mild to moderate increases in the hepatic enzyme tests with or without hyperbilirubinemia. Microscopically there may be focal necrosis, Kupffer cell hyperplasia, mild periportal inflammatory cell infiltrates and
hepatocellular accumulation of bile pigment. The pathophysiologic mechanism responsible for these changes is not
known. Since the portal circulation receives blood from the
pancreas, perhaps the release of proteases directly into the
portal circulation from the inflamed pancreas plays a pivotal
role. Alternately, toxic substances released by the injured
pancreas may be filtered by the Kupffer cell and stimulate
the release of cytokines which amplify intrahepatic injury.

Metabolic disease
A variety of metabolic diseases can cause abnormal liver tests and, in some cases, alter hepatic morphology. One of
the more widely recognized hormonally-associated diseases
that frequently affects the liver is hyperadrenocorticism. The
canine liver is uniquely responsive to glucocorticoids;
highlighted by moderate to markedly increased serum alkaline phosphatase activity (without hyperbilirubinemia) and a
foamy change in the hepatocyte cytoplasm caused by glycogen accumulation. The glycogen accumulation can be diffuse enough to cause hepatomegaly. Less frequently the
serum alanine aminotransferase and aspartate aminotransferase activities are mildly increased; presumably secondary
to drug-stimulated production. Insulin deficiency alters glucose and lipid metabolism. Patients with diabetes mellitus
may develop hepatic lipidosis with abnormal liver tests. Hyperthyroidism in cats can cause abnormal liver tests, including hyperbilirubinemia, which spontaneously resolves with
management. There is minimal to no microscopic hepatic lesions observed. In dogs with hypothyroidism, we have occasionally associated mild to moderately abnormal hepatic enzyme tests and hepatic hydropic degeneration and Ito cell
prominence. There is a complex and poorly understood relationship between thyroid function and hepatic UDP-glucuronosyltransferase (UDP-GT) activity, the enzyme involved in bilirubin metabolism. Multiple isoforms exist. Experimentally, both hyperthyroidism and hypothyroidism
have been shown to alter bilirubin metabolism via a UDPGT effect. There is a linear positive relationship between
bilirubin UDP-GT activity and the ratio of bilirubin di- to
monocongjugates present in bile. Serum T4 concentrations
correlate with UDP-GT activity; induction associated with a
decreased serum T4 concentration.

Congenital portal vascular anomalies


The presence of anomalous portal vessels that by-pass
the liver has been described in most domestic species. Hepatic encephalopathy, manifested by a wide variety of neurological signs clinically, is a common sequela. There may
be a mild to moderate increase in the serum hepatic enzyme
tests, a decrease in the biochemical markers dependent on
hepatic formation (albumin, BUN) and a moderate to
marked increase in the total serum bile acid concentration
without an abnormal serum bilirubin concentration. Histologically, there may be no obvious morphologic abnormalities, mild to moderate vacuolar change, or the apparent absence or paucity of a portal vein in the portal tracts plus an
increase in arteriolar-like structures. Lipogranulomata,
better referred to as foci of pigment-filled macrophages, occur with increased frequency of young dogs with congenital
portosystemic shunts. This histomorphologic change is common in older dogs (>10 years of age) without apparent liver
disease. The accumulation of hepatic iron is a common event
and may be related to the changes for the erythrocytic indices. The pigment-laden macrophage foci will stain notably
positive for the presence of iron. Since iron is a potent oxidant, it is possible that oxidative injury to the hepatic membrane is one factor in the formation of these foci. Variable of
nonsuppurative inflammatory cells may be associated with
the foci, consequently the incorporation of the term granuloma into the histologic terminology. However, they are not
a true granuloma. The histological finding of increased iron
in the hepatic biopsies of a relatively young dog should stimulate the differential consideration of a portosystemic shunt
especially if foci of pigment-laden macrophages are present.
Liver atrophy develops due to the decrease in total blood
flow and diversion of hepatotrophic factors. Microscopically, this is occasionally reflected by the increased proximity
of portal tracts and attenuation of the sinusoids and hepatocellular cords. It is unclear if the extrahepatic shunts always
develop independent of intrahepatic vascular changes or if
an intrahepatic vascular dysplasia predisposes to continued function of portal vessels that would normally be dormant. A hepatoportal microvascular dysplasia without extrahepatic shunts has been described in dogs. Most likely, multiple etiopathogeneses are involved in this syndrome. An increase in the plasma cortisol concentration, free cortisol concentration, and free cortisol fraction is present in dogs with
portosystemic shunts. Perhaps this metabolic derangement
is, in part, responsible for the increased plasma ALP activity, hepatic hydropic degeneration (vacuolar change), and
polydipsia/polyuria that develops.

Nodular hyperplasia
Although nodular hyperplasia is an intrahepatic event, it
is included because this relatively benign process may cause
an increase hepatic tests and histomorphologic changes that
may be suggestive of chronic hepatitis or an extrahepatic disease such as hyperadrenocorticism. The dog shows a propensity for the development of nodular hyperplasia of the liver.
It is not known if the proliferative change is a response to

275

previous hepatic injury or metabolic disorders. In human patients, nodule formation, which differs histologically somewhat from that described in dogs, has been associated with
altered hepatic blood flow and the use of azathioprine. In the
dog, the lesion is common and appears to be age-related suggesting, perhaps, a factor common to many dogs or a similar
type of hepatic response to a variety of factors. Nodules are
present by 6 years of age and, in one study, were present in
all dogs older than 14 years. The expansile process compresses existing parenchyma resulting in hepatocellular atrophy and approximation of the reticular fibers. Grossly, their
appearance mimics macronodular cirrhosis and neoplasia.
Microscopically, hepatocytes can develop a variety of cytoplasmic changes including lipidosis, hydropic degeneration,
and glycogen accumulation. This may be problematic in needle biopsy specimens since the identification of nodular regeneration is very difficult due to size limitations and the histomorphologic findings can be suggestive of a metabolic disorder. Nodular hyperplasia is associated with lipocyte prominence and the formation of lipogranulomata. Prussian blue
staining demonstrates an abundance of iron accumulation in
these foci of pigmented macrophages. We have associated an
increase in serum hepatic enzyme activities, notably alkaline
phosphatase, with nodular hyperplasia. The etiopathogenesis
may be a reflection of two physioanatomical processes. First,
the distorted hepatic architecture impairs bile flow and precludes adequate blood supply to hepatocytes and resulting in
cholestatic induction of enzyme synthesis (alkaline phosphatase) and compromised membrane integrity (leakage of
aminotransferases). Alternatively, the increase in at least the
aminotransferases may be directly related to the hepatocyte
proliferative process since an increase in the serum aminotransferase activities has been shown to be related to an increased production of these enzymes following an injury. Interesting, an increase in the serum alkaline phosphatase activity and was consistently present in the patients with azathioprine-associated nodular hyperplasia.

Supplemental reading
Andrzejewska A, Dlugosz J, Kurasz S, (1985), The ultrastructure of the liver in acute experimental pancreatitis. Exp Pathol, 28:167176.
Arai M, Mochida S, Ohno A, et al., (1993), Sinusoidal endothelial cell damage by activated macrophages in rat liver necrosis. Gastroenterology,
104:166-1471.
Bergman JR. Nodular hyperplasia in the liver of the dog: An association
with changes in the Ito cell population, (1985) Vet Pathol,
22:427438.
Fong TS, McHutchison JG, Reynolds TB, (1992), Hyperthyroidism and hepatic dysfunction. J Clin Gastroenterol, 14:240244.
Gross TL, Song MD, Havel PJ, et al., (1993), Superficial necrolytic dermatitis (necrolytic migratory erythema) in dogs. Vet Pathol,
30:7581.
Ishak K, (1993), Hepatic histopathology, In Schiff L, Schiff E (eds), Diseases
of the liver, 7th ed, J.B. Lippincott Company, Philadelphia, 145-160.
Lichtman SN, Sartor RB, Keku J, et al., (1990), Hepatic inflammation in
rats with experimental small intestinal bacterial overgrowth. Gastroenterology, 98:414423.
Meyer DJ, Harvey JW, (1994), Hematologic changes associated with serum
and hepatic iron alterations in dogs with congenital portosystemic
vascular anomalies. J Vet Intern Med, 8:5556.
Taboada J, Meyer DJ, (1989), Cholestasis associated with extrahepatic bacterial infection in five dogs. J Vet Intern Med, 3:216221.

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277

The liver biopsy: pitfalls and interpretation


of the report by the clinician
Denny Meyer

The establishment of an accurate diagnosis is dependent


on sampling an adequate amount of tissue and, most important, on a histologic interpretation by someone well versed
in liver histopathology. E. Schiff, M.D., L. Schiff, M.D.,
medical pathologists
The specimen of liver tissue can be obtained percutaneously by the use of a needle, at laparoscopy using a needle or a clamshell biopsy forceps, and at laparotomy. Each
approach has its advantages and limitations. Ultrasonography has increased the use of the needle for obtaining a guided biopsy specimen. There are two general types of hepatic
biopsy needles; suction/aspiration (Menghini, V. Mueller
Co, Chicago, IL; Jamshidi, Kormed Inc, St. Paul, MN) and
cutting (Vim-Silverman with Franklin modification, Baxter,
Deerfield, IL; Tru-Cut, Travenol Laboratories Inc, Deerfield, IL). The latter type is more commonly used and provides a more consistently adequate specimen with less fragmentation. The Tru-Cut is an economical, disposable needle
that can be gas sterilized and reused 2 to 3 times. It does require a relatively experienced operator for consistent success. Disposable, automated spring-driven cutting biopsy
needles are now available that are user-friendly tools and reduce the risk of tissue injury associated with the movement
of the diaphragm. These include Monopty (Bard Urological,
Covington, GA) and the Temno (Products Group International, Boulder, CO); the latter can be gas sterilized for
reuse. Another choice is the Biopty instrument; a reusable
gun combined with a disposable needle that can be gas sterilized and reused (Bard Urological, Covington, GA). These
biopsy needles can be used for most soft tissue biopsy needs.
Prior to obtaining a liver biopsy, it is prudent to evaluate
hemostasis. The following should be considered: identify
drugs that affect platelet function, determine if the breed is
predisposed to von Willibrands disease, scan a blood film
for platelet numbers (> 8 platelets/oil immersion field), and
assess the adequacy of the coagulation factors with either a
combination of a prothrombin time (PT) plus an activated
partial thromboplastin time (APTT) or a Thrombotest. Even
if the results are within the reference range, there is no
downside to the subcutaneous administration of vitamin K1
12 to 24 hours prior to the biopsy procedure, especially if
icterus is present.
Focal disease may be missed with a needle biopsy which
provides a core of tissue that represents approximately
1/50,000 of the whole organ. Multiple samples increase the
probability of detecting the lesion. Length of an intact nee-

dle specimen is another consideration. Studies in human patients indicate that a length of 0.5 cm can detect the changes
associated with acute viral hepatitis but is not reliable for
defining the findings indicative of chronic hepatitis. A length
of 1.5 cm is usually sufficient for recognition of the latter.
Bridging hepatic fibrosis is a important prognostic finding.
An intact needle biopsy that is at least 2 cm in length is suggested as minimally adequate for this assessment. A biopsy
needle may glance off of the fibrous septa of a cirrhotic
liver and obtain relatively normal appearing tissue of a regenerative nodule. The spring-driven cutting needles reduce
this possibility.
Because of its superficial location relative to blood supply, the margin of the liver is predisposed to fibrosis that
may mimic changes of hepatic fibrosis/cirrhosis. In this location, fibrous septa join portal tracts to the subcapsular connective tissue or to each other and are sometimes unusually
close, erroneously suggesting parenchymal collapse and hepatic fibrosis. A subcapsular specimen of limited depth may
give a misleadingly pessimistic impression of chronic hepatitis. Hepatic tissue obtained with a clamshell forceps or
an inadequate operative wedge biopsy could give this type
of misinformation. The former is also prone to crush artifact.
Regardless of the biopsy mode used, lack of uniformity in
selecting the biopsy site for repeat biopsies could affect subsequent evaluations for disease progression and therapeutic
efficacy.

When to biopsy the liver?


The biopsy is obtained to answer a question. The more
common ones are: Why are the serum hepatic enzymes persistently raised? Why is the patient icteric? Why is there a
transudative abdominal effusion? How bad is the liver disease (prognosis)? Is there copper accumulation in a predisposed breed of dog? Is the liver affected by an extrahepatic
neoplasm (staging)? What is the nodule or tissue discoloration observed during a laparotomy. What is the cause of
the hepatomegaly? Consider initially addressing the latter
question by the simpler procedure of fine-needle aspiration
biopsy for cytology.
How do the serum hepatic test findings aid in the decision to biopsy? When there are biochemical findings indicative of acute, severe hepatic injury, histologic assessment often does not provide additional diagnostic or prognostic in-

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278

formation. In fact, a biopsy may be contraindicated. Persistently raised serum aminotransferases (ALT, AST) and a rise
of the serum total bile acid concentration (BA) support the
value of assessing the liver histologically. The hepatic-intestinal recycling of bile acids is termed enterohepatic
circulation. The high extraction efficiency (75-90%) for
bile acids limits the quantity that escapes into the peripheral circulation. The serum BA is a reflection of the efficiency and integrity of the enterohepatic circulation. The
measurement of the serum BA aids in the detection of congenital portosystemic shunts (PSS), identification of chronic
hepatitis/cirrhosis prior to the development of jaundice, and
monitoring of the progression or resolution of hepatic disease with therapy. A relatively good positive predictive value of histopathologic changes is achieved with values of >
25 umol/L for the dog and > 20 umol/L for the cat. Raising
the cut-off of the upper end of the reference range enhances
the specificity at the expense of sensitivity. These cut-offs
suggest that there is sufficient pathology affecting the enterohepatic circulation of bile acids to be detected with contrast radiology (congenital PSS) or histologically (intrahepatic inflammatory disease) especially when linked with the
evaluation of the serum aminotransferase activity for the latter. A persistent mild to moderate rise of the serum ALT +/AST indicates active hepatocellular injury/repair (altered
cell membrane integrity). A concurrent rise of the serum BA
suggests that sufficient alteration of the intrahepatic architecture has occurred to be detected histologically.
What Information Should the Biopsy Report Contain?
The biopsy report should contain information that provides part or all of the answer to the question that prompted
the biopsy. However the histopathologic findings (summated as a morphologic diagnosis) may not provide sufficient
information to define a specific clinical diagnosis. In part,
this is because the liver responds to a variety of insults with
a limited number of morphologic changes. It is also secondarily involved in a variety of extrahepatic diseases that may
not be clinically apparent. If the information from the biopsy does not answer the question asked or its applicability to
the question asked is not considered helpful, the clinician
should discuss the findings with the pathologist in relation to
the clinicopathologic information and evaluate the patient
for extrahepatic disease. There is terminology that has important interpretative meaning relative to hepatic
histopathology. (Refer to Nomenclature and Tables 1 and 2)
As mentioned previously, the liver may exhibit a variety
of nonspecific secondary changes in response to disease
elsewhere in the body or the liver itself. These include a variety of systemic infectious and inflammatory diseases, gastrointestinal diseases, congenital portosystemic shunts, and
pancreatitis. Similar changes can occur in proximity to a hepatic abscess or metastatic neoplasms. Liver test abnormalities are usually mild and the serum bile acid concentration is
usually within the reference range. The general rubric of
nonspecific reactive hepatitis is used but replacing the term
hepatitis with changes is recommended by some authors
due to the connoted meaning of the former. The histologic
features encompass a variable combination of portal and
parenchymal changes that are usually of minor degree and
distributed in a patchy, uneven manner. The findings include

4th European FECAVA SCIVAC Congress

portal infiltration by mononuclear cells (primarily lymphocytes), fatty change, focal hepatocellular necrosis, and lobular inflammation. The latter may consist of enlarged or hyperplastic Kupffer cells (sometimes forming small granulomatoid or lipogranulomatoid clusters), small foci of other
macrophages, or lymphocyte aggregates. The distinction
from resolving acute hepatitis or a mild form chronic hepatitis may be difficult and arbitrary without clinical information. Photomicroscopic examples of these findings are
available.
Chronic hepatitis is a poorly defined syndrome in dogs
and cats that encompasses a spectrum of histologic activity.
A simplified grading system (Tables 1 and 2) has been proposed in human medicine to bring uniformity to the histological assessment of hepatic biopsies. Since the grading
system does not use an etiologic classification, it should be
applicable to veterinary medicine. The system facilitates the
categorization of the disease and can be used as prompts
when discussing the interpretation of the biopsy findings
with the pathologist.

Table 1. Degree of Activity in Chronic Hepatitis


Lesions and degree of injury

Category

Mild
mild, patchy
Moderate
moderate
Marked
marked
Very marked
marked

Spotty
necrosis

Bridging
&/or multiacinar necrosis

absent/mild
mild
moderate moderate
marked
marked

Portal area
inflammation

absent
absent
marked absent
marked present

Piecemeal
necrosis

Table 2. Degree of Fibrosis in Chronic Hepatitis


Component lesions

Category
Mild
Moderate
Marked
Very Marked

Fibrous expansion
of portal areas

Bridging
fibrosisa

absent or mild
moderate
marked
marked

absent
absentb
marked
marked

Bridging
with nodules
(cirrhosis)
absent
absent
absentc
present

Refer to nomenclature for the definition


Occasional bridging may be present
c
Occasional nodule may be present (incomplete cirrhosis)
b

Nomenclature
When I use a word, Humpty Dumpty said, in a rather
scornful tone, it means just what I choose it to mean-neither
more nor less. (Gardner)
Acidophilic body - condensed, deeply eosinophilic, refractile structure, with or without a pyknotic nucleus, that is
formed from a hepatocyte subsequent to apoptosis. It is a
non-specific finding indicative of hepatocellular injury in

many acute and chronic liver diseases.


Apoptosis - a form of cell death that results in the shrinkage and fragmentation. Sometimes referred to as self-programmed cell death, it occurs in many tissues as a normal
process but may be increased by inflammation. The larger
apoptitic bodies, sometimes containing nuclear fragments,
are frequently referred to as acidophilic bodies in the liver.
Acinus - an irregular, anatomical, functionally-derived
unit of hepatic parenchyma associated with the terminal hepatic artery and portal venule, likened to a cluster of grapes
with the stem representative of the vessels and the grapes
parenchymal cells. Three regions are defined going away
from the vessels to the periphery in decreasing order of vascular and nutrient perfusion: zone 1 (periportal), zone 2
(mid-zonal), and zone 3 (pericentral). The alternative, traditional, microscopic unit is the classic lobule in which the
central vein is defined as the center and the portal tracts are
located at the periphery. Similar descriptive terminology is
used to indicate the parenchymal location with the exception
that the term centrilobular replaces pericentral.
Activity - a histological expression of the magnitude (degree) of parenchymal damage and inflammation.
Autoimmune hepatitis - a type of chronic hepatitis characterized by a prominent lymphocyte-plasma cell hepatic infiltrate in association with serum antibodies against cellular
constituents, e.g., antinuclear antibody (ANA), microsomal,
smooth muscle directed against actin. It is a relatively less
common cause of chronic hepatitis in humans and is usually
responsive to immunosuppressive treatment. The syndrome
has not been characterized in veterinary medicine.
Bridging necrosis - confluent hepatocellular necrosis resulting in parenchymal collapse that links portal tracts
with terminal hepatic (central) veins or portal tracts to one
another. A reticulin stain is helpful for defining the event.

279

Bridging fibrosis - hepatocellular necrosis and inflammation with the subsequent deposition of new collagen that
links portal tracts with terminal hepatic (central) veins or
portal tracts to one another. A trichrome stain is helpful for
its recognition. Its presence denotes a poor prognosis.
Chronic hepatitis - persistent inflammation of the liver
(clinical, biochemical, histopathologic) for > 6 months in
humans; the temporal corollary has not been established in
veterinary medicine.
Ito cell - non-parenchyal cell that lies in the space of
Disse; stores vitamin A. It is prominent histologically when
distended with lipid. Most recently demonstrated to have the
potential to produce collagens that contribute to hepatic fibrosis. (lipocyte, fat-storing cell, stellate cell).
Piecemeal necrosis - the destruction of hepatocytes at an
interface between parenchyma and connective tissue, together with a predominantly lymphocytic or plasma cell infiltrate. This process often is seen at the borders of portal triads or along the edges of fibrous septa in cirrhotic livers or
zone of necrosis.

Supplemental reading
Schiff ER, Schiff L, (1993), Needle biopsy of the liver, In: Schiff L & Schiff
ER, eds. Diseases of the liver, 7th ed, J.B.Lippincott Co, Philadelphia, 216-231.
Ishak K, (1993), Hepatic histopathology, In Schiff L, Schiff E (eds), Diseases
of the liver, 7th ed, J.B.Lippincott Company, Philadelphia, 145-160.
Meyer DJ, (1996), Hepatic pathology. In: Guilford WG, Center SA,
Strombeck DR, et al, eds. Strombecks Small Animal Gastroenterology. 3rd ed, W.B. Saunders Co, Philadelphia, 633-653.
Ishak K, (1994), Chronic hepatitis: Morphology and nomenclature. Mod
Pathol, 7:690-713.
Gardner M. The annotated Alice. In: Carroll L, Alices adventures in wonderland and through the looking glass. York. Wings Books, 1960; 268.

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4th European FECAVA SCIVAC Congress

4th European FECAVA SCIVAC Congress

281

Management of liver disease: benefits


of ursodeoxycholic acid
Denny Meyer

The management of hepatic disease is based on four objectives: 1) treat the specific cause, 2) attend to the metabolic consequences of reduced hepatic function, 3) facilitate hepatocellular regeneration, and 4) impede the progression of
hepatic injury and pathologic changes.
Removal of known hepatotoxins, e.g., sulfa-containing
antimicrobials and anticonvulsant medications, and reduction of hepatic copper concentration and impairment of its
absorption are examples attendant to accomplishing the first
objective. Unfortunately, the etiopathogenesis of chronic liver disease is not known. Consequently, the recognition and
management of the consequences of chronic liver injury has
palliative importance.
Coagulation factor deficiencies are associated with
chronic cholestatic disease due to impaired absorption of vitamin K (needed for Factors II, VII, IX, and X). Periodic
subcutaneous administration of vitamin K1 may be required.
The abnormal intrahepatic architecture and disturbance of
sodium balance through poorly understood mechanisms can
cause portal hypertension with the resultant formation of ascites that may require periodic medication (e.g., spironolactone, furosemide). Gastrointestinal ulceration can cause insidious blood loss that may require the use of protectants
(sucralfate, H2-receptor antangonists). The blood loss itself
can provoke or contribute to an exacerbation of hepatic encephalopathy. Once hepatic encephalopathy develops, the
acute signs are managed with antibiotics and lactulose and a
diet change to a high quality protein diet is instituted for the
long term. The recommended protein amount is variable due
to several factors but 17 grams per 400 kcal metabolizable
energy is an approximation. However, protein of high digestibility and biologic availability, e.g., cooked eggs and
cottage cheese, should be given priority in the diet. Adequate
caloric intake is imperative to impede the skeletal muscle
wasting. Infections, uremia and hypokalemia should be
treated promptly as they exacerbate hepatic encephalopathy.
During stress, e.g., infections, surgical procedures, the
serum glucose concentration should be carefully monitored.
The livers ability to contribute to maintaining it normalcy is
comprised.
The good news pertinent to the liver is that it has the remarkable capacity for regeneration. The bad news is that
with chronic injury, the regeneration may take the form of
nodules that alter the intrahepatic architecture and probably
cannot adequately replace the deficient metabolic deficiencies. Nonetheless, every effort should be made to facilitate

the regeneration through adequate caloric intake. Carbohydrates, e.g., rice and pasta, should be the fuel for supplying
the majority of the caloric need. Linked to the dietary strategy is the protein considerations aforementioned.
Medical impediments to the progression of chronic hepatic injury are largely conjectural with few clinical studies
documenting their benefits. The benefits of prednisolone remain debatable as a first-line treatment for all types of
chronic hepatitis and has noteworthy side-effects. Antifibrotic agents, colchicine and zinc supplementation, and anti-oxidants, vitamins E & C, may offer positive contributions
to the long-term management of the consequences of hepatic injury as may ursodeoxycholic acid, a bile acid with
unique physiologic properties.
The primary bile acids are synthesized from cholesterol
in hepatocytes and secreted into the biliary system. Most of
the bile acids are usually stored in the gallbladder prior to secretion into the duodenum. Approximately 50 to 70% of the
newly formed bile is continuously secreted into the duodenum in support of bile acid recycling during the fasting period. This component contributes to the fasting serum total
bile acid (FBA) concentration. Within the intestinal lumen,
the primary bile acids, CA and CDCA, are dehydroxylated
by bacteria to deoxycholic acid (DCA) and lithocholic acid
(LCA), respectively. DCA and LCA are referred to as secondary bile acids. Intestinal bacterial enzymes also deconjugate a small percentage of the primary and secondary conjugated bile acids. The bile acids are efficiently reabsorbed by
the terminal ileum mediated by a sodium-potassium ATPase
active transport system. Only 5 to 10% of bile acids are lost
in the feces during any one enterohepatic cycle; the minimal
loss replenished by hepatic synthesis of primary bile acids.
After their reabsorption into the portal circulation, they
are carried to the liver and efficiently extracted from the sinusoidal blood by the hepatocytes located in zone 1 and reexcreted into the biliary system. The physio-anatomical
counter-flow relationship of the portal blood and bile in this
region of the liver facilitates this process. The relatively bile
acid-rich portal blood flows through zone 1 in one direction
while the relatively bile acid-poor bile flows in the opposite.
As the bile acids as actively transported against a gradient
into bile, its counter flow aids in whisking them out of the
liver (Table 1). The hepatic-intestinal recycling of bile
acids is termed enterohepatic circulation. The high extraction efficiency (75-90%) for bile acids limits the quantity
that escapes into the peripheral circulation. The concen-

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DVM, Dipl ACVIM, Dipl ACVP


NeXstar Pharmaceuticals, Boulder, Colorado - USA

282

Table 1. The enterohepatic circulation of bile acids


The primary bile acids (cholic acid and chenodeoxycholic acid) are
synthesized and conjugated by the hepatocyte --> excreted by the
canalicular membrane into the biliary system --> carried to the intestinal tract --> participate in the emulsification of lipids for absorption --> move to the ileum during which time bacteria dehydroxylate a portion of the primary bile acids forming secondary
bile acids (cholic acid to deoxycholic acid and chenodeoxycholic
acid to lithocholic acid) --> reabsorbed into the portal circulation -> carried to the liver and removed by the hepatocyte for "recycling". Hepatocellular excretion of bile acids into the biliary system
is the primary driving force for bile flow; termed bile acid-dependent flow.

tration of all the bile acids measured in the peripheral blood


following a meal is referred to as the postprandial serum total bile acid concentration (PPBA).
The FBA and PPBA concentrations are a reflection of the
efficiency and integrity of the enterohepatic circulation.
Their measurement aids in the 1) detection of congenital
portosystemic shunts, 2) identification of chronic hepatitis/cirrhosis prior to the development of jaundice, and monitoring of the progression or resolution of hepatic disease
with therapy. The most common indications for the determination of the serum total bile acid concentration include: 1)
increased serum ALT and/or AST in a patient with clinical
signs suggestive of hepatobiliary disease 2) persistently increased serum ALT (+/- AST) activity in the dog and cat, 3)
juvenile animals with clinical signs of hepatic insufficiency
(hepatic encephalopathy, poor growth, nonspecific neurological or behavioral signs) consistent with congenital portosystemic shunts, and 4) monitoring patients with known
hepatic disease. A hepatoportal microvascular dysplasia
without extrahepatic shunts has been described in dogs.
These dogs often do not have clinical signs of hepatic insufficiency, have few to no hematologic or serum biochemical
abnormalities, only mild to moderate rises in the serum total
bile acid concentration, and minimal to no histopathologic
changes depending on the hepatic lobe biopsied. A raised
serum PPBA concentration has been described in Maltese
dogs without congenital extrahepatic portosystemic shunts,
hepatic microvascular dysplasia, or inflammatory liver disease. It is possible that an unidentified substance in the
serum affects the reaction of a 3-a hydroxy bile acid in the
enzymatic spectrophotometric assay.

Cytotoxicity of retained bile acids


Prolonged retention of bile has been shown to be associated with a variety of deleterious subcellular events within
the hepatocyte (damage to mitochondria, endoplasmic reticulum, Golgi apparatus) which exacerbate intrahepatic injury.
Recently, this ultrastructural toxicity has been attributed to
selected bile acids. The more hydrophobic ones, defined by
their HPLC migration, have the greatest potential to cause
injury. The dihydroxy bile acids, chenodeoxycholic acid and
deoxycholic acid can attain high serum and intrahepatic concentration secondary to cholestasis. In vivo and in vitro stud-

4th European FECAVA SCIVAC Congress

ies have shown that these bile acids can cause hepatocelluar
dysfunction and necrosis at concentrations attained in prolonged cholestasis. Hepatocytes are at greatest risk of bile
acid-induced injury due to their function of concentrating
the bile acids prior to secretion through the canalicular membrane. By analogy, the liver can be considered to treat bile
acids as sticks of dynamite with burning fuses of varied
length. There is no harm if they are efficiently eliminated.
However, the longer they are retained within hepatic tissue
the greater the risk of injury.
Ironically, during studies to define the toxic role of bile
acids on cells, one bile acid was demonstrated not only to be
devoid of cytotoxicity but actually protected hepatocytes
from the toxic effects of the other bile acids. This bile acid,
ursodeoxycholic acid, has received considerable clinical attention for the management of chronic liver disease in human beings. The oral administration of 10-15 mg/kg body
weight once a day has been associated with encouraging results; improvement in the serum liver tests and clinical disposition. Published studies in the veterinary literature are
sparse. A recent case report described the use of ursodeoxycholic acid for the long term management of one dog with
chronic liver disease (histologically documented with a
serum bilirubin greater than 12 mg/dL (205 umol/L) for 3
months. The patient improved clinically and biochemically
(decreased serum liver enzyme tests and serum bilirubin
concentration - approximately 6 mg/dl). The patient did well
for approximately 8 months at which time it succumbed to
end-stage liver pathology. There have been no side effects
associated with the use of this drug in human beings or dogs.
While it is unknown if the drug facilitates resolution of existing hepatic fibrosis, it does appear to impede the progression of the microscopic changes if initiated early in the
course of the disease. Further studies using ursodeoxycholic
acid alone and in combination with other drugs in veterinary
patients with chronic cholestatic intrahepatic disease is
clearly warranted.
There are a variety of proposed mechanisms for the beneficial effects associated with the administration of ursodeoxycholic acid. The contemporary areas of investigation are: (1) hypercholeresis, (2) direct cellular protection
against the more hydrophobic bile acids or their displacement from the enterohepatic circulation, (3) antioxidant effect, and (4) immunomodulation. As mentioned previously,
bile acids provide the predominant driving force for bile
flow (choleresis). Unconjugated ursodeoxycholic acid has
been shown to actually cause hypercholeresis, amplified bile
flow compared to the physiologic effects of other bile acids.
This is thought to be related to its ability to enhance biliary
[HCO3] and excretion via a hypothetical mechanism referred to as cholehepatic recycling.
The displacement of cytotoxic bile acids from the enterohepatic circulation would theoretically decrease the prolonged exposure of hepatocytes to their high concentrations.
The high concentration of orally administered ursodeoxycholic acid has been shown to effectively compete with
chenodeoxycholic acid and deoxycholic acid for ileal absorption, thereby displacing them from the enterohepatic circulation. In the canine patient treated with ursodeoxycholic
acid, serial determinations of the serum bile acid profiles

4th European FECAVA SCIVAC Congress

the management of the complex pathophysiologic alterations associated with the diseased hepatobiliary microenvironment known as chronic liver disease.

Supplemental reading
Angelico M, Del Vecchio C, Nistri A: Effect of tauroursodeoxycholic acid
on serum liver enzyme and serum lipid levels in patients with chronic active hepatitis. Curr Therap Res 1995; 56:626-634.
Anwer MS: Mechanism of bile acid-induced HCO3 -rich hypercholeresis.
An analysis based on quantitated acid-base chemistry. J Hepatol
1992; 14:118-126.
Counsell LJ, Lumsden JH: Serum bile acids: Reference values in healthy dogs
and comparison of two kit methods. Vet Clin Pathol 1988; 17:71-74.
Hoffman AF: Pharmacology of ursodeoxycholic acid, an enterohepatic
drug. Scand J Gastroenterol 1994; 29:S1-S15.
Kurktschiev D, Subat S, Adler D, et al: Immunomodulating effect of ursodeoxycholic acid therapy in patients with primary biliary cirrhosis.
J Hepatology 1993; 18:373-377.
Rothuizen J, de Vries-Chalmers Hoynck van Papendrecht R, van den Brom
WE: Post prandial and cholecystokinin-induced emptying of the gall
bladder in dogs. The Vet Rec 1990; 126:505-507.
Schmucker D, Ohta M, Kanai S, et al: Hepatic injury induced by bile salts:
Correlation between biochemical and morphological events. J Hepatol 1990; 12:1216-1221.
Sokol RJ, Winklhofer-Roob BM, Devereaux MW, McKim Jr JM: Generation of hydroperoxides in isolated rat hepatocytes and hepatic mitochondria exposed to hydrophobic bile acids. Gastroenterology 1995;
109:1249-1256.
Solter P, Hoffmann W, Hoffman J: Evaluation of an automated serum bile
acids assay and the effect of bilirubin, hemoglobin, and lipid on the
apparent bile acid yield. Vet Clin Pathol 1992; 21:114-118.
Tisdall PLC, Hunt GB, Tsoukalas G, et al: Post-prandial serum bile acid
concentrations and ammonia tolerance in Maltese dogs with and
without hepatic vascular anomalies. Aust Vet J 1995; 72:121-126.
Vlahcevic ZR, Heuman DM, Hylemon PB: Regulation of bile acid synthesis. Hepatology 1991; 13:590-600.

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with HPLC demonstrated a remarkable increase in the ursodeoxycholic acid concentration and a decrease in the
chenodeoxycholic acid and deoxycholic acid concentrations.
Ursodeoxycholic acid may afford direct hepatocellular protection by partitioning into the lipid-rich membrane and
excluding the cytotoxic hydrophobic bile acids. In vitro
studies with ursodeoxycholic acid in rats have found a moderate to marked reduction of substances produced as a consequence of oxidative injury suggesting a potent antioxidant
effect.
The beneficial effects associated with ursodeoxycholic
acid in certain chronic liver diseases may be related to immunomodulation. Cytokines appear to be involved in the
initiation, modulation and/or perpetuation of the immune responses in the liver. Ursodeoxycholic acid has been shown
to reduce the aberrant major histocompatibility complex
class I expression on hepatocytes in human beings with primary biliary cirrhosis and other studies have shown suppression of interleukin-2, interleukin-4 and interferon-g using test systems which employed mononuclear cells from
the peripheral blood of human beings with primary biliary
cirrhosis.
In summary, the determination of the total serum bile
acid concentration provides an index of hepatobiliary function and assesses the integrity of the portal circulation. Beyond their use as a diagnostic test, recent research has
demonstrated that there are good and bad bile acids.
Prolonged retention of certain endogenous bile acids appears
to amplify intrahepatic pathology while others, notably ursodeoxycholic acid, appear to offer a novel alternative in the
management of chronic liver disease without adverse sideeffects. Ursodeoxycholic acid clearly generates excitement
with its potential multifaceted beneficial modes of action in

283

4th European FECAVA SCIVAC Congress

285

Early diagnosis of renal diseases


A.R. Michell
DSc MRCVS
Head, Centre for Small Animal Studies - Animal Health Trust - Newmarket, Suffolk - United Kingdom

Introduction

Chronic renal failure (CRF) is an insidious, progressive,


irreversible decline in renal function which results from loss
of nephrons. Because there are far more nephrons than are
needed to maintain normal plasma composition and sustain
the endocrine function of the kidney (e.g. production of erythropoietin), most renal function is already lost before clinical signs become evident; indeed most is lost before the usual markers of renal disease i.e. plasma urea and creatinine
rise convincingly beyond the normal range. Markers of renal damage, such as increased enzymes in urine or blood,
are more useful in acute renal damage rather than CRF. The
hallmark of CRF is the decline in glomerular filtration rate
(GFR) which accompanies the progressive loss of nephrons
(despite a compensatory increase in the individual GFRs of
surviving nephrons). A measure of reduced GFR (e.g. by
plasma clearance of technetium labelled EDTA, or iohexol
or creatinine) therefore offers the most sensitive alert to
compromised renal functions. If traditional markers (plasma
urea, creatinine) are used, the latter is more specific but allowance should be made for breed (differences in muscle
mass hence in creatinine production) and, ideally, as animals readings should be compared with those obtained from
it earlier in life, rather than comparing with the wide range
of book normals. Thus routine screening, e.g. at revaccination, would allow more sensitive detection of asymptomatic renal insufficiency - and alert practitioners to the increased risks associated with anaesthesia and/or dehydration in such cases. Fractional phosphate excretion (a very
indirect marker of secondary hyperparathyroidism) has recently attracted considerable veterinary attention but it is a
very insensitive test for CRF. Plasma phosphate, on the other hand, needs careful monitoring in established CRF since
it influences metastatic calcification and progression of the
renal diseases. Not all renal disease causes azotaemia;
glomerulo-nephritis, for example, may cause proteinuria
without azotaemia in the early stages. Equally, CRF need
not cause proteinuria. If we could detect CRF earlier, we
could manage it better e.g. by introducing specific diets earlier, when they are likely to be more acceptable, and we
could also be aware of the increased risk of decompensation
e.g. by dehydration, cardiac failure, hypotension, anaesthesia. We might also learn more about the factors which cause
or perpetuate it.

Chronic renal failure (CRF) is the outcome of an insidious, relentless, permanent loss of nephrons. It may take
years to progress to a stage where clinical signs are obvious.
Meanwhile, however, as nephrons are lost, the glomerular
filtration rate (GFR) of the animal falls. Paradoxically, the
GFR of intact surviving nephrons, individually, may rise as
part of the process of compensation which postpones the onset of clinical signs. Total GFR, however falls. The hallmark
of CRF, therefore, is an increasingly subnormal GFR2.
GFR is measured, classically, as the clearance of a substance excreted solely by glomerular filtration (i.e. neither
secreted elsewhere in the nephron nor metabolised elsewhere in the body) and which, once filtered, is not reabsorbed by the rest of the nephron. It represents the rate of excretion as the plasma volume per minute which could be totally cleared of the marker, thus if P = plasma concentration,
U = urine concentration and V = rate of urine production
GFR = U V (ml/min)
P
But, since U x V equals the excretion rate, GFR also
equals excretion rate per plasma concentration, thus it is a
measure of renal efficiency1. If the plasma concentration of a
natural metabole, e.g. creatinine, which is handled solely (almost solely) by glomerular filtration, is doubled, its rate of
excretion will be unchanged even when GFR is halved; the
reduction of filtration rate is offset by the increased concentration in the filtered plasma. Thus the key consequence of
CRF is not the reduction in the excretion of nitrogenous
waste but the prize paid for the increased plasma concentration at which excretion is maintained2. It is thus a failure of
the kidneys vital role in maintaining the normal plasma concentration of a range of molecules and ions. Clinically we
may detect the changes in plasma concentration or their consequences, including endocrine responses and, eventually,
clinical signs but nothing will adequately represent the extent
of the problem except a representation of GFR. This may be
either a true measurement, or an estimate based on the rate of
disappearance from plasma of a marker, frequently linked to
a radioactive isotope to facilitate measurement.
Advanced imaging techniques including ultrasound,
scintigraphy and MRI can also provide information relevant
to the diagnosis of renal disease, by detecting changes in renal form, function or perfusion. To a limited degree, excretion of enzymes in urine (rather than changes in their plasma

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Summary

286

composition) can provide adjunctive information but are


more likely to facilitate diagnosis of acute renal damage3,4.
Proteinuria is important in the detection of glomerulonephritis and may in itself promote the progression of CRF, increasing the importance of its monitoring (see elsewhere in
this volume). In the earliest stages of glomerulonephritis,
sensitive measures of proteinuria may detect disease at a
stage where GFR is still normal (or even above normal). It
is important to emphasise that CRF does not necessarily involve proteinuria. The reason that so much emphasis is
placed on proteinuria in the detection of human CRF is that
most human renal disease is glomerulonephritis. Of all the
important clinical effects of CRF, anaemia is probably the
least sensitive for its early detection. Finally, other indices of
renal function (e.g. phosphate excretion, concentrating capacity) are affected by CRF but too insensitively for either
early detection or quantitative monitoring of its progression.
Unfortunately the same is true of the two most readily available indices for general practitioners, plasma urea and creatinine. These issues are now examined in detail.

Plasma urea and creatinine1


If we rely purely on measurements of plasma urea and
creatinine, rather than their clearance, we assume not only
that glomerular filtration rate is the only factor affecting
their excretion but that both are generated at a constant rate;
neither is true and this flaw affects urea far more than creatinine. Creatinine, though imperfect, is the best endogenous
marker of a reduction in GFR. To illustrate its shortcomings,
let us consider the mathematics of CRF.
Suppose renal disease, of whatever cause, is progressing
slowly and linearly so that half or renal function is lost in the
first three years. During this period, GFR is halved and plasma creatinine doubles. That may scarcely take it above the
book-normal range; thanks to renal compensation the animal remains symptomless. In the next 18 months, GFR
halves again, plasma creatinine is now four times the animals own original normal value. Thus in this relatively
short time, compared with the duration of the disease the animal progresses from being symptomless to severely symptomatic. It progresses from a symptomless increase in plasma creatinine (azotaemia) to symptomatic renal failure
(uraemia). At any time in this period decompensation of renal function by dehydration, hypotension or drugs which reduce blood pressure or renal perfusion, could precipitate
acute onset of symptoms - acute on chronic renal failure,
which differs from acute renal failure (ARF) in that there has
already been a permanent loss of nephrons, whereas ARF
need not cause nephron loss. Another 4-5 months, with a further halving of GFR (to 12% of normal) bring the animal towards terminal uraemia and death.
There is thus a mathematical reason why plasma creatinine is so insensitive. The increase is logarithmic, exponential i.e. the early rise is unremarkable especially when compared with book normal ranges which encompass a variety of techniques and breeds. Significant breed differences
result from differences in muscle mass5 since creatinine is
generated from muscle. Moreover, in the late stages of CRF,

4th European FECAVA SCIVAC Congress

loss of muscle mass may reduce the rate of production and


moderate the increase in plasma concentration, compared
with the fall in GFR. In advanced CRF, the fact that a small
amount of creatinine may be secreted into the renal tubule
becomes important because the process may increase but also its relative magnitude is greater in comparison with the
reduced GFR. Since GFR itself is affected by time of day
and meal pattern it becomes clear that the only useful way of
screening plasma creatinine as an index of CRF would be
with regular samples after the overnight fast and comparison
with the animals own normal value (earlier baseline values
taken annually at the revaccination visit).
Since the rise in plasma creatinine concentration is exponential, a plot of the reciprocal concentration against time
tends to be linear. This has, therefore, aroused some enthusiasm as an index of the progression of CRF, both in humans
and dogs, but granted the problems with the underlying measurement6 it probably offers little advantage compared with
careful serial monitoring of creatinine itself.
Urea is a more popular measurement in practice because
of its wider availability in simple practice laboratories. It is,
however, horrifically imprecise as an index of renal function
because its excretion rate varies with that of water as both
tend to be reabsorbed simultaneously. Thus in dehydration,
urea rises more than creatinine2. Clearly, since it is subject to
variable reabsorbtion it can not be a valid marker for GFR.
Worse, its production rate depends on hepatic function and
dietary protein. If we place animals on a low protein diet
their blood urea should fall, not because renal function has
improved, but because of the reduced urea production which
accompanies a reduced protein intake. Plasma creatinine, by
contrast will not fall, reflecting the absence of an improvement in GFR. A drastic reduction in muscle mass, or meat
intake, could reduce plasma creatinine6.

Why seek early diagnosis?


With any screening technique it is a valid question; what
will we do with the information and how will the patient benefit. In my view there are essentially three benefits. Firstly,
the sooner renal disease is detected, the sooner dietary modification can begin and the more gradual it can be. This must
reduce the problem of non-compliance i.e. rejection by the
animal of a novel diet. Learned aversion (bait shyness in
rats) minimises the acceptability to many species of a novel
diet which is first experienced when the animal feels unwell.
The evolutionary benefit of this is obvious where the novel
diet (or a contained toxin) genuinely causes the nausea but it
clearly increases the problem of dietary manipulation once
an animal feels ill. The second advantage of early diagnosis
is that dietary manipulation (or other measures) apart from
postponing the onset of azotaemia and, eventually, uraemia,
may also genuinely slow the progression of the disease. That
is the subject of a separate contribution to this volume. The
third, and perhaps the greatest benefit of more regular renal
screening would be the early detection of animals with
symptomless but substantial renal insufficiency, making
them especially vulnerable to the effects of anaesthesia or
dehydration and especially the combination of both.

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The best marker now available for plasma clearance estimates of GFR is DTPA (which behaves very similarly to
the gold-standard marker, inulin) linked to radioactive technetium (Tc) which is readily measured by a gamma counter7.
The beauty of technetium is its safety; since it has a half-life
of six hours i.e. only one sixteenth of the original radioactivity survives the first day, few precautions are needed beyond the first voiding and this can safely be discarded after
24 hours. In fact, humans simply use the normal toilets with
no precautions at all.
For those without the ability to count radioactive emission there are two alternatives; iohexol has been validated in
dogs and is a very safe radiographic contrast agent8,9. The
only problems are the substantial volume needed in tiny animals and the viscosity which is reduced by warming; the
main problem is that the samples, though wonderfully stable
(hence suitable for posting to the laboratory) require expensive analytical equipment. The other alternative is exogenous creatinine but, at least in the UK, it is not available in
sterile form. Polyfructosan-S may offer a further choice
since it behaves similarly to inulin but is easier to dissolve
and may also be simpler to analyse6.

for the exposure of animals to procedures (e.g. anaesthesia)


and drugs (e.g. ACE-inhibitors, NSAIs) which can prejudice renal function in susceptible individuals, without at
least monitoring plasma creatinine before and after. In the
case of ACEIs, the minority of patients which react adversely improve with the withdrawal of the drug. The problem is that in veterinary medicine, with no coroners court, it
is too easy to attribute adverse effects and fatalities to the
disease rather than the treatment. With renal function today,
as with acid-base balance in previous years, the reason that
so few animals appear to die of decompensated renal insufficiency is probably, quite simply, that their death cannot be
attributed to changes which we do not measure. If we
sought, we would certainly find.

References
1.

2.

3.

Other indices
4.

There has been misplaced enthusiasm for fractional


phosphate excretion in recent veterinary literature. Essentially this amounts to an extremely insensitive index of secondary hyperparathyroidism resulting from CRF. As plasma
PTH levels rise they reduce the tubular reabsorbtion of phosphate and increase the fraction of the filtered phosphate
which is excreted. Since PTH assays are now available there
seems little reason to use this insensitive test1,10, except, perhaps, to confirm the effect of dietary phosphate restriction.

5.

6.

7.
8.

9.

Conclusion
Even if there are still practical and economic constraints
on regular renal screening in animals, there is little excuse

10.

Gleadhill, A. and Michell, A.R. (1996) Clinical measurement of renal


function. Ch 9 In: Manual of Canine and Feline Nephrology and
Urology. Ed. J. Bainbridge and J. Elliott. BSAVA, Cheltenham (UK)
107-116.
Michell, A.R. (1988) Renal function, renal damage and renal failure.
In Renal Disease in Dogs and Cats: Comparative and Clinical Aspects. Ed. A.R. Michell. Blackwell, Oxford pp 5-29.
Jung, K. (1992) Urinary enzymes in renal, renal-associated and
urological disorders. Ch. 12 In Urinary Enzymes. Ed. K. Jung,
H. Mattenheimer and U. Burchardt. Springer-Verlag, Berlin, pp.
170-187.
Kerr, M.G. (1989) Veterinary Laboratory Medicine. Blackwell Scientific, Oxford pp 109-120.
Gleadhill, A. (1996) Quantitative Assessment of Renal Function in
Domestic Animals; Measurement of GFR by the Plasma Clearance of
Tc-DTPA. PhD Thesis, Univ. of London.
Mitch, W.E. and Walser, M. (1996) Nutritional Therapy for the Uremic Patient. Ch 55 In the Kidney (5th Edn) Ed. B.M. Brenner, W.B.
Saunders, Philadelphia. pp 2382-2423.
Gleadhill, A., Peters, A.M. and Michell, A.R. (1995) A simple method
of measuring GFR in dogs. Res.Vet. Sci. 59:118-123.
Gleadhill, A., Michell, A.R. (1996) Evaluation of iohexol as a
marker for the clinical measurement of glomerular filtration rate in
dogs.
Heine, R. (1995) Renal damage in the dog evaluated by urinary enzymes and glomerular filtration rate using plasma clearance of iohexol. PhD Thesis, Norwegian College of Veterinary Medicine,
Oslo.
Gleadhill, A. (1994) Evaluation of screening tests for renal insufficiency in the dog. J. Sm. Anim. Pract. 35:391-6.

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Clearance measurements

287

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289

Management of renal diseases: have we progressed?


A.R. Michell
DSc MRCVS
Head, Centre for Small Animal Studies - Animal Health Trust - Newmarket, Suffolk - United Kingdom

Introduction: the nature of renal failure

Chronic renal failure (CRF) is the clinical presentation


of a variety of diseases, poorly characterised in dogs, but
featuring a relentless, irreversible loss of nephrons. As a result, there is a steady decline in glomerular filtration rate
(GFR). Since the kidneys have a large functional reserve capacity, i.e. far more nephrons than are needed for most normal functions, the majority of the nephron loss occurs over
months or years during which no clinical signs are detectable, thanks to the compensatory changes in the function
of surviving nephrons. While this initially benefits the patient it makes it harder to discover the originating cause - or
whether CRF is the outcome of a variety of repetitive insults, including disease or exposure to toxins, including
some drugs. In the 1980s a key tenet of renal medicine was
that the factors sustaining progression of renal disease may
be different from those which initiate it i.e. that at some
stage, CRF becomes a disease characterised by self-sustaining progression. If so, there was the hope that the factors influencing progression might be more amenable to investigation and treatment. In particular, dietary factors attracted
attention; lipids, phosphate, sodium and protein for example. Sodium was considered mainly in the context of hypertension, a factor which certainly sustains progression of
CRF. Like dietary protein, however, sodium raises GFR and,
granted that reduced GFR is the hallmark of CRF, this would
seem beneficial. For some 15 years, however, there was a
strong suspicion that the adaptive increase in the GFR of
surviving nephrons, while sustaining overall renal function,
ultimately accelerated their demise i.e. it accelerated progression. In that case, reduced dietary protein offered the
chance of not only reducing the effects of CRF (i.e. slowing
the increase of azotaemia and postponing the onset of
uraemia) but of actually ameliorating the progression of the
disease. Except in rats, this now seems increasingly improbable, indeed there is reason to doubt whether progression is
self-sustaining, rather than being the outcome of repetitive
renal insults. It is, therefore, timely to review current concepts of the factors which influence the progression of
chronic renal disease and, in particular, those that are likely to be relevant to dogs and cats. It is also appropriate to
consider the role of erythropoietin in alleviating the
anaemia of CRF and the present role of transplantation in
offering a substitute for lost renal function.

Chronic renal failure (CRF) is an insidious, relentlessly


progressive, irreversible disease characterised by progressive
loss of nephrons and the consequent fall in glomerular filtration rate (GFR). Clinically, most of the course consists of a
silent, asymptomatic phase (compensated renal insufficiency) during which there is a gradual onset of azotaemia (accumulation, in plasma, of the end products of protein breakdown, notably urea, creatinine, and a range of putative
uraemic toxins). This is followed by the onset of uraemia, the
symptomatic phase. An azotaemic animal may be pushed into symptomatic uraemia by dehydration (e.g. diarrhoea), hypovolaemia (e.g. haemorrhage), hypotension (e.g. anaesthesia, especially with dehydration) or renovascular effects of
drugs (e.g. ACEIs or NSAIs). This acute-on-chronic failure does not necessarily cause additional nephron damage
and may be reversible, but only to the pre-existing level of insufficiency. At present, the only way of restoring normal renal function to a patient with CRF is to provide a healthy
compatible replacement kidney. Whether it survives depends
on the immunogenetic match between recipient and donor,
the underlying disease, and the immunosuppresive regimen.

Progression
Progression is not necessarily slow, e.g. in rapidly progressive glomerulonephritis but typically, we believe,
months or more usually years separate the onset from the
clinical signs. That is why early diagnosis requires smoke
alarms which will detect smouldering renal insufficiency,
rather than awaiting the clinical signs; once flames break
through the roof the diagnosis is clear but it comes too late
for damage limitation.
The extended period of renal insufficiency reflects not
only the underlying pathology but also the huge functional
reserve capacity of the kidneys and also the ability of surviving intact nephrons to adapt. Thus while GFR declines,
the workload of the remaining nephrons, their single
nephron glomerular filtration rate (SNGFR) increases the reserve capacity and the adaptive power of a healthy kidney is
well illustrated by renal transplant donors who suffer no adverse effects following abrupt removal of half their
nephrons. While GFR is halved initially, it rapidly increases
to 75% of normal1.

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Summary

290

Adaptation or exacerbation?
The nature and consequences of this adaptive process in
CRF has become the central issue of nephrology since the
early 1980s. Previously the intact nephron hypothesis of
Bricker emphasised that the functions of the kidneys in CRF
are those of the surviving intact nephrons, with adaptive
changes, rather than the distorted function of damaged
nephrons. The kidney is perceived as a population of defunct, damaged, non functional nephrons and surviving, hyperfunctioning, hyperfiltrating nephrons, limiting the detectable abnormalities of renal function and postponing the
onset of detectable clinical signs. What changed in the
1980s, was the thesis of Brenner that the adaptive changes
in the surviving nephrons hastened their own demise, i.e.
that progression becomes a separate, self sustaining
process. Initially this was blamed on hyperfiltration itself,
more recently on increased intraglomerular pressure (which
is not necessarily linked to systemic hypertension)2.

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arise from mediators released during nephron injury which


then damage other nephrons; such mediators could also be
targets for pharmacological or dietary manipulation e.g.
prostaglandins via NSAIs or dietary lipids and specific evidence in dogs, cats, rats or humans; species differences appear to be important and it is possible that dogs are better
models for human CRF than rats3 (which are peculiarly
prone to glomerular sclerosis if they have glomerular hypertension).

Causes of progression3
Possible factors may include the following or interactions
between them
Hyperfiltration
Glomerular hypertension
Systemic hypertension
Glomerular hypertrophy

Renal disease
Uraemic toxins
Catabolism
Exogenous mediators
Growth factors
Proteinuria

Uric acid
PO4
Ca
PTH
NH3
Na

PCV
Lipids
Coagulation
Lipid peroxidation
Cholesterol

Clinical implications
The clinical implications of this hypothesis are spectacular
1. Elevated SNGFR is not benign compensation but an inherently lethal process for the kidney and ultimately the
patient: it postpones terminal renal failure but makes it inevitable.
2. On the other hand, if the perpetuation of CRF is a separate process from its initiation, there are grounds for optimism because, with its extended time - course, it is more
amenable to clinical investigation whereas the originating
causes may have occurred years earlier. Moreover, if dietary or pharmacological measures can slow or arrest progression, CRF could be halted at an acceptable stage, provided it was detected sufficiently early.
Central to this debate has been the role of protein in sustaining progression. The traditional reason for moderating
protein intake, reduction of azotaemia, remains unchallenged but merely offsets the effects of CRF. The new concept was that by reducing hyperfiltration, protein restriction
slowed progression. Certainly amino acids increase GFR so
the logic is plain. Until we remember that the core problem
of CRF is the fall of GFR and we remind ourselves that the
increase in SNGFR, before 1980, was regarded as adaptive.
We should not, therefore, restrict this increase in SNGFR
unless we are convinced that it hastens the demise of surviving nephrons. We should also remember that the distinction between the originating causes of CRF, shrouded in
mystery, and the sustaining causes of progression, while exceptionally attractive both scientifically and clinically, demands proof. Moreover loss of nephrons is part of the natural ageing of the kidney. The 21st century may regard ageing as a treatable disease but, for the moment, progression
could also be an intensification of renal ageing or, quite simply, the cumulative effect of a whole lifetime of nephropathic events, immunological, pharmacological and toxic. The
kidney, after all, is matched only by the liver in its exposure
to molecules at concentrations far above those which, in
plasma may be harmless. Self sustaining progression could

Hyperfiltration and glomerular hypertension


The increased SNGFR results from increased perfusion,
or increased intraglomerular pressure mediated by reduced
afferent tone or increased efferent tone, thus increasing the
filtration fraction (FF, the proportion of plasma converted into primitive urine). Efferent tone is increased by angiotensin
II hence angiotensin converting enzyme inhibitors (ACEIs)
reduce SNGFR whereas amino acids increase it by reducing
afferent tone. Diabetics are peculiarly vulnerable to
glomerular hypertension because their reduced afferent tone
exposes the glomerulus to higher pressure even when systemic pressure is normal; they also suffer hyperfiltration in
the early stages of their disease4. Thus a marginally hypertensive diabetic may have a damaging increase in glomerular pressure. The increased pressure also causes an increase
in the normally small degree of filtration of albumin and the
resulting trace albuminuria (microalbuminuria) provides a
sensitive warning of diabetic nephropathy in humans. The
problem in dogs is the wide range of normal urinary protein.
Experimentally, diabetic dogs have the reduce afferent tone
which underlies glomerular hypertension. A physical consequence of glomerular hypertension is enlargement and increased wall tension, predisposing to sclerosis3.
The main clinically controllable factor sustaining progression is systemic hypertension4,5. Nevertheless the beneficial effects of antihypertensives may depend on factors besides those on blood pressure. For example ACEIs slow progression of human diabetic nephropathy whereas beta-blockers giving similar blood pressure control do not3,6. Angiotensin has local effects on glomerular pore size, glomerular mesangial tension and is a renal growth factor; and
ACEIs also have various metabolic effects. Similarly, heparin and related drugs have renoprotective effects other than
those as coagulation. If control of blood pressure is important
in moderating progression of CRF it is likely to be in cats,
rather than dogs as hypertension is more common perhaps

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mineral by PTH is not accompanied by the appropriate increase in urinary phosphate excretion. That is because GFR
is so low that suppression of tubular phosphate reabsorbtion
by PTH, no longer promotes the necessary increase in excretion. The importance of phosphate restriction in ameliorating secondary hyperparathyroidism has also been shown
in humans with severe CRF14a.
Increased plasma phosphate is a major factor in metastatic calcification and for this and other reasons, it is an important determinant of progression in canine and feline CRF.
In humans with advanced CRF, those best able to excrete
phosphate were those whose disease progressed least3. Since
renal phosphate excretion is irretrievably compromised, limitation of dietary phosphate intake and of secondary hyperpathyroidism are key objectives in limiting the progression
of CRF15.

Sodium3
Proteinuria
Proteinuria is not only a marker of glomerular damage
(or, at trace concentrations, of increased glomerular pressure) but it is also an independent risk factor sustaining progression3,8. The link results from tubular injury leading to
release of cytokines directly or from inflammatory cells.
Proteinuria can also cause further glomerular damage. Loss
of plasma albumin predisposes to hyperlipidaemia which
may also sustain progression (see below). In dogs, both
ACEIs and calcium channel blockers reduce proteinuria
and glomerular hypertrophy, but only ACEIs reduce
glomerular pressure9. Hypercholesterolaemia, which accompanies hypoalbuminaemia (as in severe proteinuria)
may nevertheless be an independent risk factor for progression of CRF in humans10.

The role of sodium in CRF is both neglected and misunderstood. There is great enthusiasm for sodium restriction to
treat or prevent hypertension. Certainly dogs and cats generally receive a generous excess of dietary salt.
But in canine CRF hypertension is rare (see elsewhere in
this volume) and whereas a gradual drop in dietary salt may
be harmless, a sudden reduction could compromise residual
renal function.
A more persuasive reason to reduce dietary sodium
would have existed when hyperfiltration was seen as the mediator of progression; high sodium intake increases GFR.
Perhaps most important, and most neglected, is that sodium
reabsorbtion is the main energy consuming work of the kidney and the amount to be reabsorbed is dictated by GFR.
Thus while, much nonsense is talked about resting the kidney, the most effective way of doing it would be by reducing sodium intake, GFR and reabsorptive workload.

Changes in azotaemic plasma


Ammonia is a potent cause of compliment-mediated renal damage; normally the high osmotic concentrations in the
kidney are protective but they are reduce in CRF3. The acidosis which accompanies CRF, and lack of dietary antioxidants may both increase renal ammonia production. Azotaemic plasma shows evidence of increased lipid peroxidation and lipoprotein abnormalities11. These may be reduced
by dietary manipulation in humans12.

Calcium, phosphate and parathyroid


hormone (PTH)
Calcium could be involved in progression through its
role as an intracellular signal affecting vascular and mesangial tone as well as renin secretion. PTH increases intracellular calcium and has also been considered as a uraemic
toxin, apart from its role in exacerbating hyperphosphataemia13,14. The latter reflects the fact that in renal (secondary) hyperparathyrodisim, the mobilisation of bone

Growth factors and cytokines3


Increasingly, the power of molecular biology to identify
and synthesis mediators, receptors or receptor antagonists,
offers a future in which self perpetuating injury can be
blocked by attacking the underlying control mechanisms. In
doing so, it will be essential to distinguish between mediators of injury and mediators of repair and to remember that
most physiological control systems involve multiple feedback loops so that whatever interference is imposed, the effects may be blunted by counterregulation.
Among the cytokines and growth factors which have attracted most attention are interleukins, angiotensin II, endothelins, prostaglandins, tumour necrosis factor (TNF) and
growth factors including a IGF-1 (insulin-like growth factor)
angiotensin and PDGF (platelet derived growth factor which
is also produced by mesangial cells and increases their proliferation). While these factors essentially affect the local environment of and communication between cells, they may
be increasing in plasma concentration as a result of CRF.

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because, as long suspected in humans, glomerular disease is


more prevalent (and more likely to cause hypertension7).
Increased glomerular size is not the same as glomerular
hypertrophy. Neither hyperfiltration nor a raised glomerular
pressure per se seems sufficient to trigger or sustain progression but evidence from rats suggests that the combination of glomerular hypertrophy and systemic hypertension
does predispose. Both in rats and humans it is possible to
dissociate beneficial effects on glomerular sclerosis from reductions in hyperfiltration and once sclerosis occurs it is a
progressive change.
Mesangial cells are important because they alter their
tension in response to local and systemic hormones, thus affecting glomerular surface area and efferent tone, but also
because they affect local accumulation of macromolecules
and matrix synthesis. They release growth factors but their
activity is part of the repair process, rather than a cause of
sclerosis3.

291

292

Diet and progression


Two main dietary factors have attracted the spotlight in
recent research and debate on the management of CRF: they
are the role of proteins and lipids in sustaining progression.
In evaluating the evidence it is important to distinguish
not only between species but between spontaneous disease
and various induced models. These may involve primary
nephron loss (e.g. surgical remnant kidney), primary
glomerular damage (immune or nephrotoxic), hypertensive,
or spontaneous (genetic) models e.g. hereditary glomerulonephritis in Samoyeds3,16.
Perhaps the most discouraging evidence, both from clinical nephrectomy (e.g. for neoplasia) and experimental
subtotal nephrectomy, is that self-sustaining progression is
highly dependent on the severity of the nephron loss and only occurs when it is extreme. This suggests that far from
dominating the clinical course of CRF, self-sustaining progression may be merely a terminal event i.e. progression
may be the cumulative effect of various renal injuries, some
of which may be self-exacerbating. If so, models that depend
on acute intervention are unlikely to be representative
though they may throw light on contributory mechanisms.
Above all many of the models cause proteinuria or
nephrosclerosis without a progressive decline in GFR i.e.
in the sense associated with clinical CRF, these models do
not cause progression3. Thus in assessing evidence in these
controversies, as well as considering whether it relates to
models of clinical CRF, and in which species, the criterion
of progression is crucial. The problems of detecting and
monitoring CRF are considered elsewhere in this volume.
Serial measurements of GFR, with due precautions, are the
best but as clinical approximations, plasma creatinine or its
reciprocal are usually used as indirect indices. Neither is
sensitive or reliable.

Protein and progression


In non human primates, experimental reduction of GFR
to 30% of normal failed to cause progression and low protein diets affected neither blood pressure nor proteinuria but
caused a further fall in GFR.
In humans, the evidence on protein restriction is that it
does not significantly affect long-term progression, even
when the restriction is very severe (unless the patient is diabetic4,17,18 or in the advanced stages of the decline in GFR).
No benefit was seen in children with CRF19. For the moment, the situation is that evidence of efficacy is inconclusive, rather than there being proof of a lack of efficacy20,21.
In dogs, there is little defensible evidence for a beneficial
effect of protein restriction on the progressive decline in
GFR which characterises CRF3,22-24, though it limits the development of lesions in Samoyeds with hereditary glomerulonephritis16.
Most of the evidence on protein and progression arises
from rat models. Some of the benefits of protein restriction
may reflect an associated reduction of calorie intake, an independent factor in progression25.

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Unfortunately, while both CRF and hypertension are


probably both more prevalent in cats than dogs, evidence
concerning both is scarce in this species. A recent study by
Elliott and Barber26 suggests that anaemia was a particularly
important prognostic sign. It also indicated that rather than
progressing steadily, severe falls in GFR often occurred suddenly, late in the course of CRF. Neither in cats nor in dogs
are presenting signs and measurements a good guide to
prognosis27.
The influence of anaemia on progression of CRF is a
complex question. Clearly, humans benefit greatly from
treatment with erythropoietin but there is nevertheless the
fear that, at some level, a raised PCV becomes a risk factor
through the effects on renal haemodynamics and blood pressure28,29.

Lipids and progression


The focus of interest is on the ability of polyunsaturated
fatty acids (PUFA), notably those in fish oils or some plant
oils, to modify progression, perhaps by affecting the production of cytokines notably prostaglandins and thromboxanes3. Low protein diets may also influence cytokine production. Experimentally, PUFA from fish oils (menhaden
oil, omega-3 PUFA) preserved renal function in dogs with
induced CRF and humans with clinical CRF30,31,32 whereas
plant derived omega-6 PUFA were worse than saturated beef
fat. PUFA may also moderate systemic pressure and if so
this is likely to be important in cats rather than dogs, where
only a minority with CRF are hypertensive33.

Conclusion
One of the problems in advising on dietary management
of CRF in dogs or cats is not simply the scarcity and uncertainty of the relevant evidence but the lack of information on
the altered nutritional requirement in such patients, regardless of progression34. This problem is worst in cats because
they are obligate carnivores, unlike dogs, and they are more
prone to protein-losing nephropathy. Cats with CRF may, in
a minority encounter additional problems due to renal
potassium-wasting and the associated potassium depletion
may cause, as well as muscle damage, additional renal damage. Such patients require potassium gluconate supplements
though the suggested dose34,35 (2-6 mmol/d) seems remarkably low. For a 5 kg cat this is 1 mmol/kg or less, barely
equivalent to the extracellular potassium whereas the huge
majority, and the site of the main deficits is intracellular.
Recently there has been a reawakening of interest in the
use of oral adsorbents to remove uraemic metabolites and reinforce the dietary control of progression of CRF36.
For the moment, the main basis for dietary manipulation in CRF damage is to restrict the effects of azotaemia
and acidosis (which exacerbates azotaemia and bone damage37) and, perhaps through restriction of phosphate and
manipulation of specific unsaturated lipids, to moderate its
progression.

References
1.

Meyer, T.W., Baboolal, K. and Brenner, B.M. (1996) Nephron adaptation to renal injury. Ch.44 in The Kidney (5th Edn). Ed. B.M. Brenner. W.B. Saunders, Philadelphia pp 2011-2048.
2. Fine, L.G., Woolf, A.S. and Gallego, C. (1991) Of rats and men: the
need for more convincing clinical studies on progression of renal diseases. Am. J. Kidney Dis. 17: 258-260.
3. Michell, A.R. (1995) Progression of chronic renal failure: have we
progressed. Vet. Ann. 35: 159-176.
4. Neuringer, J.R. and Levey, A.S. (1994) Strategies to slow progression
of renal disease. Sem. Nephrol. 14:261-273.
5. Kes, P. and Ratkovic-Gusic, I. (1996) The role of arterial hypertension in progression of renal failure. Kidney Int. (Suppl) 55:S 72-74.
6. Ihle, B.U., Whitworth, J.A., Shahintar, S., Cnaan, A., Kincaid-Smith,
P.S. and Becker, G.J. (1996) Angiotensin converting enzyme inhibition in nondiabetic progressive renal insufficiency: a controlled double-blind trial. Am. J. Kidney Dis. 27: 489-495.
7. Buckalew, V.W., Berg, R.L., Wang, S.R., Porush, J.G., Rauch, S. and
Schulman, G. (1996) Prevalence of hypertension in 1795 subjects
with chronic renal disease: the modification of diet in renal disease
study baseline cohort. Am. J. Kidney Dis. 28: 811-821.
8. Burton, C. and Harris, K.P. (1996) The role of proteinuria in the progression of chronic renal failure. Am. J. Kidney Dis. 27: 765-767.
9. Brown, S.A., Walton, C.L., Crawford, P. and Bakris, G.L. (1993)
Long-term effects of antihypertensive regimes on renal hemodynamics and proteinuria. Kidney Int. 43: 1210-1217.
10. Washio, M., Okuda, S., Ikeda, M., Hirakata, H., Nasishi, F., Onoyama, K., Yoshimura, T. and Fujishima, M. (1996) Hypercholesterolaemia and the progression of renal dysfunction in chronic renal failure patients. J. Epidemiol. 6: 172-177.
11. Ong-Ajyooth, L., Ong, Ajyooth, S., Sirisalee, K. and Nilwarangkur,
S. (1996) Lipoproteins and lipid peroxidation abnormalities in patients with chronic renal disease. J. Med. Assocn. Thai. 79: 505-512.
12. Peuchant, E., Delmas-Beauvieux, M.C., Dubourg, L., Thomas, M.J.,
Perromat, A., Aparicio, M., Clerc, M. and Combe, C. (1997). Antioxidant effects of a supplemented very low protein diet in chronic renal
failure. Free Radic. Biol. Med. 22: 313-320.
13. Massry, S.G. and Smogorzewski, M. (1994) Mechanisms through
which parathyroid hormone mediates its deleterious effects on organ
function in uraemia. Sem. Nephrol. 14: 219-231.
14. Combe, C. and Aparicio, M. (1994) Phosphorous and protein restriction and parathyroid function in chronic renal failure. Kidney Int. 46:
1381-1386.
14a. Vanholder, R., DeSmet, R., Vogeleere, P. and Ringar, S. (1994) Uremic toxicity: the middle molecule hypothesis revisted. Sem. Nephrol.
14: 205-218.
15. Finco, D.R., Brown, S.A. and Crowell, W.A. (1996) Effects of dietary
protein and phosphorus on the kidneys of dogs. Recent Advances in
Canine and Feline Nutritional Research: Proc. 1996 Iams International Symposium. Ed. D.P. Carey, B.A. Norton and S.M. Bolser. Orange Fraser Press, Wilmington (Ohio, USA) pp 123-142.
16. Valli, V.E.O., Baumal, R., Thorner, P. et al (1991) Dietary modification reduces splitting of glomerular basement membrane and delays
death due to renal failure in canine x-linked hereditary nephritis. Lab.
Invest. 65: 67-73.
17. Klahr, S., Levey, A.S., Beck, G.J. et al (1994) The effects of dietary
protein restriction and blood pressure control on the progression of
chronic renal disease. New Engl. J. Med. 330: 878-884.

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Pedrini, M.T., Levey, A.S., Lau, J., Chalmers, T.C. and Wang, P.G.
(1996) The effect of dietary protein on the progression of diabetic and
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Holm, E.A. and Solling, K. (1996) Dietary protein restriction and the
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questions. Sem. Vet. Med. Surg. (Small Anim) 7: 237-243.
Kronfeld, D.S. (1993) Dietary management of chronic renal failure in
dogs: a critical appraisal. J. Small Anim. Pract. 34: 211-219.
Tapp, D.C., Kobayashi, S., Fernandes, G. and Venkatachalam, M.A.
(1989) Protein restriction or calorie restriction? A critical assessment
of the influence of selective calorie restriction on the progression of
experimental renal disease. Sem. Nephrol. 9: 343-353.
Elliott, J. and Barber, P.J. (1998) Feline chronic renal failure: clinical
findings in 80 cases diagnosed between 1992 and 1995. J. Sm. Anim.
Pract. 39: 78-85.
Cook, A.K. and Cowgill, L.D. (1996) Clinical and pathological features of protein-losing glomerular disease in the dog: a review of 137
cases (1985-1992). J. Am. Anim. Hosp. Assocn. 32: 313-322.
Lafferty, H.M., Anderson, S. and Brenner, B.M. (1991) Anemia: a potent modulator of renal hemodynamics in models of progressive renal
disease. Am. J. Kidney Dis. 17:2-7.
Abels, R. (1990) Rate of progression of chronic renal failure in predialysis patients treated with erythropoietin. Sem. Nephrol. 10: (Suppl 1) 20-25.
Brown, S.A. and Finco, D.R. (1996) Fatty acid supplementation and
chronic renal disease. Recent Advances in Canine and Feline Nutritional Research : Proc. 1996 Iams International Symposium. Ed. D.P.
Carey, S.A. Norton and S.M. Bolser. Orange Frazer Press, Wilmington (Ohio, USA) pp 159-170.
Brown, S.A., Brown, C.A., Crowell, W.A., Barsanti, J.A. and Finco,
D.R. (1996) Does modifying dietary lipids influence the progression
of renal failure? Vet. Clin. N. Am. (Sm. Anim Pract) 26(6) 1277-1285.
Cappelli, P., Di Liberato, L., Stuard, S., Ballone, E. and Albertazzi, A.
(1997) N-3 polyunsaturated fatty acid supplementation in chronic
progressive renal disease. J. Nephrol. 10: 157-162.
Michell, A.R., Bodey, A.R. and Gleadhill, A.G. (1997) Absence of hypertension in dogs with renal insufficiency. Renal Failure 19: 61-68.
Rubin, S.I. (1997) Chronic renal failure and its management and
nephrolithiasis. Vet. Clin. N. Am. (Sm. Anim. Pract) 27(6): 13311354.
Polzin, D.J., Osborne, C.A. and Lulich, J.P. (1996) Diet therapy
guidelines for cats with chronic renal failure. Vet. Clin. N. Am. (Sm.
Anim. Pract) 26(6): 1269-1275.
Dwada, A. and Shiigai, T. (1996) The effects of oral adsorbent AST120 concurrent with a low protein diet on the progression of chronic
renal failure. Am. J. Nephrol. 16: 124-127.
Price, S.R. and Mitch, W.E. (1994) Metabolic acidosis and uraemic
toxicity: protein and amino acid metabolism. Sem. Nephrol 14:
232-237.

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295

Canine hypertension:
a difficult but fascinating disease
A.R. Michell

Twenty years ago, few veterinary students would have


learned anything about canine hypertension, yet many medical students would have been aware that the dog was a classic species for the experimental study of hypertension. Now,
it is almost assumed that dogs with chronic renal failure
(CRF) will require antihypertensive therapy. Yet, only a minority will actually be hypertensive and, in those which are
normotensive, such therapy could well decompensate their
residual renal function. There has been real progress in recent years with canine hypertension. This comprises
1. Validation of non-invasive measurement techniques for
arterial pressure.
2. Establishment of a large epidemiological database - allowing normal values to be defined with regard to breed
and age and also showing differences with sex.
Most canine hypertension is secondary, unlike human
hypertension which is mainly primary hypertension (essential hypertension, EHT). Among the causes are diabetes
mellitus and Cushings Syndrome (as in man) and hepatic
disease (unlike man). Renal disease can also cause hypertension but, unlike man, the majority of dogs with renal insufficiency (reduced glomerular filtration rate) remain normotensive: the basis for this resistance to hypertension merits study. Certain breeds of dog (notably sight hounds)
have normal pressures in the human hypertensive range and
these breeds raise three questions:
1. Are they models for EHT?
2. Why are they resistant to the adverse effects of raised arterial pressure?
3. Is the increased pressure adaptive?
These questions will be explored, alongside the epidemiological features of hypertension in other breeds and the importance of sodium intake.

Acknowledgements
The primary investigator in this research is Dr Angela
Bodey and our work has been generously supported by
WALTHAM.

Introduction
Dogs have featured in the study of blood pressure and
hypertension since the earliest times; Hales in 1733 made

his pioneering observations on blood pressure measurement


not only in horses but also in dogs and the classic Goldblatt
model of hypertension was a dog model before it became a
rat model. Humans with hypertension are susceptible to renal damage and, independently, humans with chronic renal
failure (CRF) are likely to develop hypertension. It is not
surprising, therefore, that the last decade has seen increasing
concern with a hitherto neglected disease - canine hypertension. This has coincided with the availability of non-invasive methods for blood pressure measurement. Twenty years
ago, few veterinary students would have learned anything
about hypertension yet now many will be taught that dogs
with CRF require antihypertensive therapy, including salt
restriction.
The 1990s have seen a growing concern for evidencebased medicine i.e. based on scientific data rather than cumulative clinical experience (however well judged) or textbook assertions, however widely repeated. This review argues that hypertension is rare in dogs, even when they have
serious renal insufficiency and that treatment of an animal is
likely to further decompensate renal function. Similarly,
there is little reason for salt restriction, except insofar as
most canine diets present a nutritional excess of sodium; if
there is a reason it has more to do with renal energy demand
than with hypertension.

What is hypertension
The answer is less obvious than it appears. Blood pressure, contrary to the impression given in many textbooks, is
rapidly and widely variable1,2. In some sense it is remarkable
that patients offer any consistency in their readings especially when, as is often the case in humans, the measurement
consists of a single reading3.
Reproducible readings require a non-stressful technique,
quiet surroundings, a relaxed patient and, preferably, a consistent time of day. Once these are obtained, comparison
should be made with the appropriate population i.e. allowing
for age and breed. Hypertension is an elevation of resting arterial pressure which significantly exceeds the range for the
control population; the normal pressure for a middle aged
black American will be substantially higher than that for an
Italian child.

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DSc MRCVS
Head, Centre for Small Animal Studies - Animal Health Trust - Newmarket, Suffolk - United Kingdom

296

Measurement of blood pressure


Direct measurement of arterial pressure continues to be
the gold-standard but it is invasive and, while measurements made with telemetric signals from chronic catheters in
trained dogs are likely to be consistent1, acute intervention in
untrained dogs is almost certain to elevate the reading.
Moreover direct readings are only gold standard when
meticulous attention is paid to the transducer and to the
catheter, particularly the position and patency of its tip4.
Even subtle stress, let alone pain, elevates pressure as reflected in the concept of white-coat hypertension in humans i.e. pressures measured in the surgery are likely to exceed those measured at home. Similar considerations apply
in dogs5. Thus blood pressures measured in the clinic exceed
those measured in a neutral environment5,5a, transient stress
causes a protracted increase of systolic pressure in particular
and dogs rated as stress-prone have higher pressures than
more relaxed dogs5,6.
Indirect measurements are non-invasive; they depend on
an occluding cuff which alters the arterial pressure at the
measurement site and the detection of signals associated
with systolic, diastolic and mean arterial pressure. These signals may be sounds detected with a stethoscope, ultrasound,
or changes in oscillometric pressure patterns. The latter
forms the basis for the DINAMAP, the gold-standard noninvasive blood pressure monitor. Cuff inflation, deflation
and recording are automated and a reading usually takes 20
seconds to 1 minute.
The cuff-limb interface is crucial.
1. The inflatable cuff width must be correct for the limb circumference (w = 0.4c).
2. The site inherently affects the accuracy and reproducibility of readings (i.e. even in anaesthetised dogs).
3. In conscious dogs, some sites are less acceptable to the
animal and this also affects the speed and reproducibility
of the measurements.
Blood pressure, like adult height shows a wide normal
range, and hypertension is like being 2 metres tall; it may be
unusual but it is not necessarily harmful and attempts to reduce the measurement to normal are more likely to cause
harm. Moreover the normal pressure of a Deerhound
would be hypertensive for a Labrador and any attempt to reduce a Deerhounds pressure to that of a Labrador could well
be catastrophic.
The clinical definition of hypertension rests precisely on
the concept of the likelihood of adverse effects. Thus in humans 140/90 (systolic/diastolic) is widely regarded as normal but depends on age, race etc. What is implied is that
higher levels, according to a body of clinical evidence, are
likely to cause secondary damage e.g. strokes, coronary disease, cardiac hypertrophy, retinal and renal damage etc. In
fact most clinicians will consider a second, higher, threshold
at which the risk of immediate, rather than long-term damage is the concern and therapy becomes urgent.
The ability to detect a hypertensive individual depends
on the precision (reproducibility) of the measurement technique and the narrowness of the normal range with which
comparison is made. The continuing practice of defining canine hypertension with regard to a single book normal for

4th European FECAVA SCIVAC Congress

the entire species is, therefore, preposterous granted the


range of breed-specific variation7.
Indirect readings are seldom accurate i.e. they usually
differ from the gold-standard. This does not matter provided that the difference is predictable and reproducible. In
conscious animals, direct readings are unsuitable so what
matters about an indirect technique is its reproducibillity
(i.e. precision) i.e. its ability to give consistent readings,
characteristic of the individual patient. Above all, the more
reproducible the technique, the narrower the normal range is
likely to be and, therefore, the greater the sensitivity with
which abnormalities will be detected.
In dogs the preferred clinical technique for blood pressure measurement is now the use of the DINAMAP oscillometric monitor with an appropriate-sized tail cuff and at
least six readings; the first reading is discarded and the remaining five are meaned. Outliers (which are not usual since
the machine has internal controls for artefacts) are discarded. The dog should be standing comfortably, not forced into
recumbency, limb cuffs should only be used in conscious
dogs where a tail reading is unobtainable - usually in shortdocked individuals. This technique has been validated and
calibrated against direct arterial pressure in both anaesthetised and conscious dogs8,9. When the same technique is
used in humans, rather than the usual general practitioners
approach of using a single reading, much greater precision is
obtained3. This is hardly surprising, granted that the first
reading probably serves simply to properly bed the cuff
into place.
The use of a tail cuff in conscious dogs offers the greatest precision and compliance in the majority of dogs hence
its use is preferred in our standard technique to the proximal
fore limb cuff site, the best limb site in conscious dogs.
Readings are best taken in standing rather than recumbent
dogs, because of far better compliance and reduced stress9.

Blood pressure in normal dogs


In healthy dogs, systolic pressure depends on age, breed,
sex, temperament, diet, obesity and exercise regime7. The
rise with age is particularly interesting since it is characteristic of species, such as humans and dogs, which customarily
consume excessive dietary salt10,11. Recently Sansom and
Bodey (1998) have observed a similar age-related rise in cats
(Vet. Rec. In Press). In dogs average pressure ( SE) rises
from 108 2.2 below 6 m, to 121 1.6 by one year, to 130
1.3 by 4 years, 141 2.3 by 10 years, 145 2.5 by 13 years
and may continue to increase to 153 6.2 though in older
dogs, as in very old humans, pressure may fall. Two recent
surveys of British dogs (Edney12 and Michell13) suggest that
the average age at death is 13, with substantial breed variation. Heart rate also varies with breed, though the usual assumption that smaller breeds have higher rates in unreliable7.

Hypertension in dogs
Essential (primary) hypertension is rare in dogs, though
an interesting genetic model exists1. The main causes of hy-

4th European FECAVA SCIVAC Congress

Renal disease and canine hypertension


Although dogs are susceptible to hypertension, they are
naturally resistant to it, even when renal function is severely comprised. Thus among dogs with reduced GFR the
prevalence of hypertension was little higher (9%) than
among dogs with normal GFR (6%). Dogs with GFR less
than 33% of the normal lower limit (with an average GFR
equivalent to 10 ml/min in a 70 kg human) had arterial pressures not significantly above normal, and these dogs showed
no correlation between GFR and arterial pressure17. In humans, once GFR falls below 33% of normal (40 ml/kg) the
majority are hypertensive; these data were obtained from
310 patients who were normotensive prior to their renal disease18. A recent study of 1795 humans with chronic renal
disease found a significantly higher prevalence of hypertension among patients with glomerular disease19. As GFR declined, the prevalence of hypertension rose from 66% at 83
ml/min (b normal) to 95% at 12 ml/min (10% of normal).
It is therefore sad to find the continued repetition of the
myth that hypertension is a common complication of canine
renal disease, combined with an absurd defining threshold
of hypertension for all breeds (180/100) and advocacy of
the use of ACE-inhibitors without warning of their ability to
worsen renal function in a minority of patients20. In the absence of measured hypertension (compared with breed normals), using the standard technique, or of signs of hypertensive organ damage (e.g. retinopathy), it would be negligent to treat dogs with CRF for an assumed hypertension.
The most likely effect of lowering a normal arterial pressure
in a dog with CRF would be to decompensate what remains

of its renal function. The evidence is clear and, in the interests of welfare, it is time that we treated the CRF that is present in the dogs rather than the hypertension prevalent in the
textbooks.

References
1.

2.
3.

4.
5.

5a.

6.

7.
8.

9.

10.
11.
12.

13.
14.

15.

16.
17.
18.

19.

20.

Bovee, K.C. (1993) Genetic essential hypertension in dogs: a new animal model. In: The Advancement of Veterinary Science Vol. 4. Ed.
A.R. Michell, C.A.B. International, Wallingford. pp 185-194.
Michell, A.R. (1997) Long-term control of blood pressure and sodium
balance: is the baseline nocturnal? Perspec. Biol. Med. 40: 516-528.
Michell, A.R. (1996) Routine blood pressure measurement: application of the standard canine technique in a human. Blood Pressure
Monitoring 1: 385-387.
Michell, A.R. (1993) Hypertension in companion animals. Vet. Ann.
(Bailliere) 33: 11-23.
Vincent, I.C., Michell, A.R. and Leahy, R.A. (1993) Non-invasive
measurement of arterial blood pressure in dogs: a potential indicator
for the identification of stress. Res. Vet. Sci. 54: 195-201.
Kallet, A.J., Cowgill, L.D. and Kass, P.H. (1997) Comparison of blood
pressure measurements obtained in dogs by use of indirect oscillometry in a veterinary clinic versus at home. J.A.V.M.A. 210: 651-654.
Vincent, I.C. and Michell, A.R. (1996) Relationship between blood
pressure and stress-prone temperament in dogs. Physiol. Behav. 60:
135-138.
Bodey, A.R. and Michell, A.R. 91996) Epidemiological study of
blood pressure in domestic dogs. J. Sm. Anim. Pract. 37: 116-125.
Bodey, A.R., Young, L.E., Bartram, D.H., Diamond, M.J. and
Michell, A.R. (1994) A comparison of direct and indirect (oscillometric) measurements of arterial blood pressure in anaesthetised dogs
using tail and limb cuffs. Res. Vet. Sci. 57: 265-269.
Bodey, A.R., Michell, A.R., Bovee, K.C., Buranakurl, C. and Garg, T.
(1996) Comparison of direct and indirect (oscillometric) measurements
of arterial blood pressure in conscious dogs. Res. Vet. Sci. 61: 17-21.
Michell, A.R. (1989) Physiological aspects of the requirement for
sodium in mammals. Nutr. Res. RCVS. 2: 149-160.
Michell, A.R. (1995) The Clinical Biology of Sodium. Elsevier,
Oxford.
Edney, A.T.B. (1997) An observational study of presentation patterns
in companion animal veterinary practices in England. D.Vet.Med.
Thesis, Univ. of London.
Michell, A.R. (1998) Breed differences and other factors influencing
canine longevity (Vet. Rec., submitted).
Muirhead, E.E. (1994) Renal vasodepressor lipid:medullipin in:
Textbook of Hypertension Ed. J.D. Swales, Blackwell Scientific,
Oxford pp 341-359.
Michell, A.R. (1988) Renal function, renal damage and renal failure.
In: Renal Disease in Dogs and Cats: Comparative and Clinical Aspects. Ed. A.R. Michell, Blackwell Scientific, Oxford. pp 5-29.
Michell, A.R. (1994) Salt, Hypertension and renal disease: comparative
medicine, models and real diseases. Postgrad. Med. J. 70: 686-694.
Michell, A.R., Bodey, A.R. and Gleadhill, A. (1997) Absence of hypertension in dogs with renal insufficiency. Renal Failure 19: 61-68.
Buckalew, V.W., Berg, R.L., Wang, S.R., Porush, J.G., Ra. S. and
Schulman, G. (1996) Prevalence of hypertension in 1795 subjects
with chronic renal disease: the modification of diet in renal disease
study baseline cohort. Am. J. Kidney Dis. 28: 811-821.
Danielsen, H., Kornerup, H.J., Olsen, S. and Posborg, V. (1983) Arterial hypertension in chronic glomerulonephritis. An analysis of 310
cases. Clin. Nephrol. 19: 284-287.
Henik, R.A. (1997) Systemic hypertension and its management. Vet.
Clin. N. Am. (Sm. Anim. Pract) 27: 1355-1372.

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pertension - in the sense of a pressure significantly above the


normal mean - were, in order of importance, hyperadrenocorticism (155.84 4.4), hepatic disease (152.7 7.6), thyroid dysfunction (142.7 3.3), diabetes mellitus (142.6
3.9), renal disease (140.5 3.0), cardiac disease7. The link
with hepatic disease, though seen in only a small number of
dogs is interesting because it has not yet been reported in humans, it could perhaps reflect reduced hepatic activation of
a renal vasodepressor hormone called medullipin11,14.
As a percentage of the normal population, the dogs with
these conditions (other than cardiac disease) were few
(11.6%). The average age ranged from 7.2 (renal disease) to
10.3 (diabetes) for which the corresponding normal systolic
pressures were 133.2 1.8 and 140.2 2.6. The average
pressure and age for all normal dogs was 131.3 0.6, 4.4
years. Thus while renal disease raises average pressure beyond the expectation for age, the question remains whether
it is an important cause of canine hypertension. Our underlying hypothesis was that dogs were resistant to hypertension, even when they have renal disease15,16 and this proved
to be the case17.

297

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299

The most common viral, bacterial and parasitic


diseases of ornamental fish
Massimo Millefanti

I have often wondered why so few veterinarians in Italy


are interested in tropical fish medicine. While approximately
15 million cats and dogs give work to several thousand professionals, almost 30 million fish used for ornamental purposes, be they tropical, salt water or freshwater, or cold water
fish, stimulate the interest of only a few score of veterinarians.
There are, of course, many reasons some of which I list
here:
Fish live in water in structures specifically prepared for
them (aquaria, artificial lakes) and while the owner can see
them he does not come directly into contact with them. He
cannot stroke them nor take them for a walk as he could do
with his dog, cat, ferret, rabbit etc. Nor can he hear their
voice as he could do with his canary, mynah, parrot or other pet bird. It is extremely uncommon that fish are given
names. In the majority of cases the relationship between
the owner and a pet fish is fairly impersonal. A fish is usually considered as part of the furniture and if it dies, it can
be replaced without great sadness or difficulty. This indirect relationship is also the reason why the aquarium lover
frequently fails to realise that his fish has an active disease
and this has the consequence of delayed diagnostic and
therapeutic interventions by a veterinarian.
The majority of freshwater tropical fish are extremely
cheap while the cost of a consultation by a professional,
who must obviously be paid, is often much greater than the
commercial value of the patient to be cured. Due to difficulty in capturing and transporting fish, it is often the veterinarian who must go to the structure housing the sick
fish, thus further increasing the cost of the consultation.
The educational programme which leads to a degree in veterinary medicine covers this particular sector only partially and cursorily. The newly qualified veterinarian finds that
he must deepen his knowledge in a sector in which he is almost totally ignorant unless he has had a particular interest
in aquarium medicine. This may, in fact, be one of the reasons why many experts in aquariological sciences have degrees in subjects other than veterinary medicine.
Since there are still no veterinary clinics, at least in Italy,
which care for ornamental fish, numerous owners do not
know that in many cases their own sick animals could be
easily cured by appropriate, simple and cheap treatment.
Finding pharmacological remedies to use for therapy is often
not easy. The use of drugs which must be diluted and the
sometimes complicated calculations of the therapeutic doses
often discourage an owner from starting treatment of his fish.

A veterinarian is often called after other people have already given suggestions on what to do. This means the fish
to be treated are often debilitated by their disease and,
sometimes, their clinical signs have been altered or indeed
provoked (poisoning) by the attempted therapies.
Objectively it is sometimes extremely difficult to carry out
a treatment. I am thinking, for example, of the large marine
aquaria containing, besides fish from the coral reef, many
delicate invertebrates and rocks which create cavities in
which the patient can easily hide. It is not a simple task to
extract one or more sick fish in order to place them in a
nursing tank and furthermore the stress and possible lesions that we ourselves could provoke during the capture,
must be carefully evaluated.
Many aetiological agents of the common infective and infestive diseases of aquarium fish cannot be found on their
host, because they leave it rapidly, immediately after the
death of the fish. The process of decomposition of the delicate tissues of a dead fish, if this is left even for a few minutes in a tropical aquarium, begins very quickly and can
make the findings difficult to decipher. Freezing a dead
fish is of no post-mortem diagnostic help.
There are, however, many reasons why the organisers of
this veterinary medicine congress have included a section of
the programme devoted to ornamental fish. Let us now have
a look at some of these:
Many owners (especially young owners) of ornamental
fish, particularly goldfish (Carassius auratus) believe that
while their animal must live in captivity it has the right to
do so in a state of wellbeing and must, therefore, be cared
for as well as possible, including care from a veterinarian.
Many ornamental fish of incomparable beauty, for example some kinds of koi (Cyprinus carpio) or discus (Symphysodon discus), now have a commercial value of up to
several thousand euro. In these cases the aquarium lover
needs regular and qualified assistance from a veterinarian.
When active collaboration has been set up between professionals and importers of exotic fish, particularly as far
as concerns prophylaxis of common bacterial, viral, protozoal and parasitic diseases, true fish lovers can acquire
healthier fish.
Some zoonoses can be carried by tropical fish and the role
of the veterinarian in this field is of paramount importance.
One example of this problem is the transmission of myocbacteriosis from fish to immunodepressed humans.
New viruses are being isolated from captured sea fish which

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Med Vet
Private Practitioner, Milano - Italy

300

are then raised as ornamental fish. The potential pathogenicity of these viruses for humans is not yet known. In this case,
too, the veterinarian can be directly involved in studies.
In the light of the foregoing, associations which study the
science of aquaria ever more frequently require the collaboration of a veterinarian.
Before describing, albeit briefly, the main infective and
infestive diseases of aquarium fish, it is worth remembering
how important it is that the veterinarian who wishes to take
care of these animals has a basic knowledge of the anatomy,
morphology and biology of the various imported species
(and there are very many!), knowledge of the legislation
concerning their importation, sale and conditions of captivity and knowledge about the management and function of the
various types of aquarium available in shops, from importers
or enthusiasts.
Aquaria are often incorrectly maintained and the management of the animals within them poor. This is frequently
because the owner of an aquarium has not understood the
technical details of the filtering or lighting systems or has no
knowledge of the biology of the species in captivity.
Many diseases are associated with the presence of toxic
catabolic substances produced by the fish themselves within the aquarium and could be easily resolved once the cause
is understood (overcrowding, exposing the aquarium to direct sunlight for many hours a day, excessive amount or incorrect type of food administered, no control of the filtering
system, etc.).
A period of quarantine in specifically designed tanks for
tropical freshwater fish, particularly if the fish come from the
Asian market or are captured sea fish, can be the best weapon
for preventing the spread of the infective or infestive diseases
which are becoming ever more frequently diagnosed.
Cultivating aquatic plants which release natural bacteriostatic substances or which enhance the filtering of the water
(for example, the water hyacinth) and giving food containing natural polysaccharides (glucans) extracted from the cell
walls of some algae and yeasts which can improve the immune defenses of the reared fish, are useful strategies for
preventing diseases which are commonly encountered in
every day veterinary practice.

VIRAL DISEASES
The best known viral disease of ornamental fish, because
of its unmistakable feature, is lymphocystis or lymphocystis
virus infection. This disease is caused by an iridovirus and is
commonly found in sea fish (eg marine angelfishes) as well
as some freshwater fish such as the Asiatic belontiidae (bettas, paradisefishes and gouramis). The disease can be recognised easily; there are small pearl-like whitish or brownishgrey nodules which may be present in groups on the fins
and, but less frequently, on the body of the sick fish. The fish
may have lost weight and have a fluctuating appetite. This
disease is stress-related: indeed it is predominantly found in
sea fish captured from the coral barrier reef, imported and
then subjected to various changes of food and environment
during the transport from importer to buyer.
Once the fish with lymphocystis has been transferred to

4th European FECAVA SCIVAC Congress

a nursing tank, the nodules can be gently removed. Recurrences, however, are frequent.
Papillomata due to herpes viruses can be diagnosed in
goldfish, koi and sea fish. They present as predominantly
greyish-white nodules with a characteristic cauliflower appearance, localized to the head or fins of the ill fish.
Viral septicaemic disease or spring viraemia is a disease caused by Rhabdovirus carpio. The disease is very
common among cyprinides reared for ornamental purposes,
for example koi and goldfish. In this case, too, stress (that is,
an increase in water temperature or the reproductive period)
can favour the onset of the disease in aquaria but particularly in artificial lakes. The phisical examination reveal ocular,
gill and skin haemorrhages, cutaneous changes, and
(pathologie anatomy) bleeding in the internal organs (intestine, swimbladder) of the sick fish. It is often associated with
haemorrhagic bacterial septicaemia which will be described
later in this article.

BACTERIAL DISEASES
I shall start with the common haemorrhagic septicaemia
(or goldfish ulcerative disease) of cyprinides, caused by bacteria such as Aeromonas spp., Pseudomonas spp. and others,
which can be associated with a Rhabdovirus infection.
Haemorrhagic septicaemia can occur in other exotic freshwater fish, besides cyprinides, for example mollies,
gouramis and some cichlids.
This disease produces many clinical signs including ascites (gelatinous, yellowish fluid), exophthalmos, ulcers,
skin haemorrhages, erosions of the fins and pale gills with
puntiform haemorrhages.
The treaments of choice are nitrofuranic baths (eg. nitrofurazone at a dose of 10 mg/l for 6 hours for 5-7 days) or oral
furazolidone (administered in food) for 7-10 days. Personally, I have had excellent results in goldfish living alone in
simple bowls without filtering systems, for example fish
bought or won at fairs or markets, using a one week cycle of
daily 4-5 hour baths of solutions of sulphamethoxazole and
trimethoprim at doses of 50 and 10 mg respectively per litre
of water.
Columnaris disease, caused by the Flexibacter (ex Chondrococcus) columnaris bacterium, is very widespread particularly in mollies (eg black molly), cyprinides and young cichlids. The clinical signs are small whitish spots which, over
a few hours, coalesce to form raised mucus-rich areas (indeed another name for this disease is cotton wool disease)
at the mouth and caudal parts of the fish.
The treatment is oxytetracycline baths (10-50 mg/l) for 1
hour a day for one week.
The last bacterial disease I would like to mention is mycobacteriosis (or fish tuberculosis). This disease is caused by
Mycobacterium fortuitum, M. marinum and M. chelonei and
can affect both freshwater ornamental fish and salt water fish.
A fish with mycobacteriosis loses weight and is lethargic
and anorexic. It can have exophthalmos, ascites, skin ulcers
and sometimes deformation of the dorsal profile.
Post-mortem examination reveals greyish-white nodules
in the liver, spleen, kidneys and heart. Ziehl-Neelsen stain-

ing of histological preparations of these organs confirms the


presence of mycobacteria.
Fish tuberculosis is a chronic disease which can also be
very dangerous for immunodepressed humans who come into contact with the water from aquaria containing fish affected by the disease. When mycobacteriosis is suspected
(that is when a fish with symptoms similar to those just described is refractory to the most common antibiotic therapies) it is worth confirming the suspicion by a post-mortem
examination.
Since this bacterium is acquired through the gastrointestinal tract, a period of quarantine and correct alimentation
with hygienically safe food should prevent the onset of this
zoonosis.

PROTOZOAL DISEASES
These are the most widespread and well known diseases
to affect fish reared for ornamental purposes.
One protozoal disease which affects all freshwater fish is
ichthyophthiriosis or white spot or ich, caused by a
ciliated protozoon: Ichthyophthirius multifiliis. The diseased
fish presents with small raised whitish spots all over the
body and on the fins and continues to rub against objects in
the aquarium because of the pruritic symptoms.
The protozoon, with its typical main horseshoe shaped
nucleus, is an excellent swimmer, which penetrates the epidermis of the fish with circular movements provoking a cellular reaction manifested by the white spot.
The pharmacological treatment used (for example zinc
free green malachite at a dose of 0.1 mg/l poured directly into the aquarium) acts only on the free forms swimming in
the aquarium before they enter the fish or form reproductive
cysts.
Cryptocarion irritans causes a disease similar to the one
I have just described but different in that it affects salt water
fish. Besides the disseminated spots on the body and fins,
the diseased fish has characteristic opaque eyes and respiratory distress because the protozoa also invade the gills.
Treatment with copper sulphate (0.15-0.20 mg/l) for at
least one week is usually effective. It must be remembered,
however, that these concentrations of copper sulphate are fatal for invertebrates and toxic for many fish from the
chaetodontidae (butterflyfishes) and pomacanthidae (marine
angelfishes) families.
Amyloodinium ocellatum (sea fish), Oodinium pillularis
and O. limneticum (freshwater fish) are dynoflagellate protozoal aetiological agents of the velvet diseases or oodiniasis of ornamental fish.
Fish with these diseases have changes in skin colour, lose
weight, are anorexic, have pruritus, breathing problems (they
go to the column of air bubbles in the tank) and opaque eyes.
The skin takes on a characteristic velvety appearance which
can be seen easily if the fish is examined in an oblique light.
The treatment is similar to that advised for the white
spot.
The protozoon (sporozoon) Pleistophora hyphessobryconis, which is transmitted through the gastrointestinal tract
(cannibalism) causes pleistophoriasis in neon tetra

301

(Paracheirodon innesi) but also in other small cypridins and


exotic freshwater fish.
Neon tetra disease is a chronic disease with a very slow
evolution. The signs are weight loss, appetite changes, erratic swimming and changes in skin colour. The superb redblue colour of neon fish progressively fades giving room to
whitish marks with poorly defined, irregular margins.
There is not yet an effective treatment for this common
disease.
Hole in the head disease is nowadays considered a
multifactorial disease. The hypothesis that the primary (or
only) aetiological agent is a protozoon is now being challenged by some researchers. The disease is characteristic of
South American cichlids such as the discus, angelfish
(Pterophyllum scalare) and oscar (Astronotus ocellatus) but
can also be found in African cichlids. The sick cichlid has
skin erosions of the head, above the eyes, covered with
whitish mucus from which it is sometimes, but not always,
possible to isolate protozoa of the Spironucleus and Hexamita genera. Other signs are weight loss, appetite changes,
cloacal oedema and mucus in the faeces.
Quarantine and correct care (avoiding stress) of these
splendid fish remain the best strategies for prevention of the
disease.
The recommended treatment is metronidazole baths (1020 mg/l) for 3 days.
Other commmon protozoal dermatitides caused by
Ichthyobodo (ex Costia) necatrix, Chilodonella cyprini, Cycloachaeta spp. (ex Trichodina), Brooklynella hostilis (treatment: green malachite) and myosites due to Myxobolus spp
(for which there is no therapy) can be diagnosed. Further details of these diseases can be found in the works listed in the
references at the end of this article.

PARASITIC DISEASES
Trematodes of the Dactylogirus genus, transparent organisms less than a millimetre long, can infest the gills and
skin of many freshwater fish, particularly goldfish and koi.
Affected fish swim erratically because of pruritus, have
threads of mucus on the gills and laboured fast respiration
with the opercula raised.
Microscopic examination of the mucus confirms the suspected diagnosis.
Small leaf-shaped trematodes of the Gyrodactylus genus
preferentially affect cichlids and sea fish. These flukes predominantly localize in the skin causing increased secretion
of skin mucus and ulcers from pruritus and predispose to
secondary bacterial infections (erosion of the fins).
The treatment is baths of praziquantel (10 mg/l) for 3-5
hours or nitroscanate (0.1 mg/l) 2 or 3 times each week for
the Dactylogirus infestation because this worm (in contrast
to Gyrodactylus which is ovoviviparous) reproduces by laying eggs in the water.
The Camallanus cotti nematode infests many exotic freshwater fish (eg tetras, characins and mollies) and more rarely
sea fish. These reddish parasites, which are just over one centimetre long, live firmly anchored to the colonic mucosa of
the unfortunate host fish and emerge from the anal opening.

MAIN PROGRAMME

4th European FECAVA SCIVAC Congress

302

The treatment of choice for this parasitic disease are fenbendazole administered in food (0.25% or 250 ppm) or in
aquarium water (2 ppm) as initial therapy followed by another dose 2-3 weeks later, or baths of nitroscanate (0.5-1
mg/l) for 4-5 hours once a week for 3 to 4 weeks.
Lernaea cyprinacea is a copepod crustacean known as
the anchor worm. It reaches a maximum length of 2 cm.
While the male lives free in the water, the female of the
species attaches to the gills and skin of freshwater fish (particularly goldfish, koi and cichlids) using a peculiar cephalic structure. The female also has two yellowish ovigerous
sacs at her caudal extremity which make diagnosis easy.
Fish affected by lernea infestation have respiratory difficulties (raised opercula) because of the abundant mucus in
the gills, intense pruritus and secondary bacterial infection
(skin ulcers and fin erosion).
This disease can be cured by baths of sodium chloride (23 g per litre) for 3-5 minutes for 3 days or with formalin,
which is a 37% solution of formaldehyde (0.2 ml per litre of
water in a nursing tank), for one hour for 3 consecutive days.
If this parasitic disease is ignored, during the summer it can
decimate the fish population in a lake within a few days.
Finally, I shall finish this brief, schematic list of the
common diseases of ornamental fish with the infestations
by Argulus spp. These are small crustaceans, 5-6 millimetres long commonly called fish lice. They can be removed
from the skin of their hosts, which are preferentially goldfish and koi, by gently using tweezers. The skin is then disinfected with a solution of iodopovidone (1:10). There is a

4th European FECAVA SCIVAC Congress

fish, Gambusia affinis (mosquitofish), which eats these


crustaceans and can live in freshwater aquaria, that can be
used to eliminate the disease.
I would like to thank my colleagues Laura Torriani,
Roberto Granata, Giuseppe Mosconi, Alessandra Cappelletti and Elena Ferlini for their invaluable help.

References
1)
2)
3)
4)
5)

6)
7)
8)
9)
10)
11)

Buchter R.L., (1992), Manual of Ornamental Fish, BSAVA Cheltenham.


Carpenter J.W., Mashima T.Y., Rupiper D.J., (1996), Exotic Animal
Formulary: Fish, 13-29, Greystone Publ. Manhattan Kansas.
Herkner H., (1995), Zierfishe in Krankheiten der Heimtiere: 893-926,
Schltersche Hannover.
Millefanti M., (1996), Le malattie dei Pesci dAcquario, De Vecchi
Editore Milano.
Mosconi G. (1994), Linsorgenza delle Malattie nei Pesci Ornamentali in Atti del Corso SCIVAC di Medicina degli Animali Esotici: 15, SCIVAC Cremona.
Noga E.J., (1995), Fish Disease: Diagnosis and Treatment, Mosby
Saint Louis Missouri.
Scott P.W., (1991) Ornamental Fish in Manual of Exotic Pets: 272285, BSAVA Cheltenham.
Stoskopf M.K., (1993), Fish Medicine, W.B. Saucers Philadelphia.
Untergasser D., (1991), Malattie dei Pesci dAcquario: Diagnosi e
Trattamento, Primaris Milano.
Zupo V., (1990), le Malattie dei Pesci: come identificarle e curarle in
acquario, Ed.Olimpia Firenze.
Zwart P., (1992), Diseases Aspects in Ornamental Fish in XVII
WSAVA World Congress Proceedings, Volume I: 733-736, A.Delfino Editore Roma.

4th European FECAVA SCIVAC Congress

303

Alternatives in the treatment of coxarthrosis in dogs:


pectineomyectomy, tenotomy of the iliopsoas
and neurectomy of the joint capsule (PIN) as a
symptomatic treatment for coxarthrosis
Pierre M. Montavon
DVM
Veterinar Chirurgische - KI der Universitat Zurich - Switzerland

Technique

Abduction and extension of the hip are reduced in patients with coxarthrosis. Contracture of the pectineus muscle
and pressure of the tendon of the iliopsoas over the inflammed joint capsule is painful and reduce the abduction
and extension of the hip joint, respectively. Pectinectomy
and tenotomy of the iliopsoas result in clinical improvement
of the function of the hip joint. Neurectomy of the ventral aspect of joint capsule is aimed at reducing pain for a durable
period of time. This symptomatic therapy is relatively simple
and can be performed bilaterally. It also allows later insertion of a hip prosthesis. Clinical results are satisfactory.

Knowledge of the local anatomy is required to perform


this technique. Important structures in the vicinity are to be
respected, such as arteria and vena femoralis with their
branches, and the obturatorius and saphenous nerves.
Skin incision in form of T facilitates the overview and
approach of the deep structures in the proximal area of the
wound. First, the pectineus muscle is prepared, transsected
and resected, applying exact hemostatic techniques. Care is
taken of the obturatorius nerve located caudal to the origin
of the pectineus muscle. The arteria and vena femoralis profunda are preserved during the proximal transsection of the
pectineus muscle and the femoral vessels, including the arteria and vena femoralis caudalis during its distal transection
(Figure 1).
The pectinectomy discovers the iliopsoas muscle proximal to its insertion onto the trochanter minor which is palpable over the caudal edge of the proximal femur. The arteria and vena femoralis profunda are retracted proximally
over the joint capsule of the hip. The tendon of the iliopsoas
is searched from dorsal and under the iliopsoas muscle as
this is retracted in a distal direction. The tendon acts as a
string in immediate contact with and pressing strongly over
the medial joint capsule of the hip. It is retracted in a dorsal
direction, over the capsule with the help of a curved instrument such as a mosquito or Hohman retractor (Figure 2). Its
transection with a blade liberates the joint capsule of the hip

Coxarthrosis results from instability of the hip joint in


dogs. This degenerative disease is present bilaterally most of
the time and leads first to synovitis in younger growing animals (6-12 months of age). Patients may then experience
acute pain. Afterwards, the symptoms are reduced and affected dogs are able to compensate. Later, chronic
coxarthrosis with joint deformation takes place. Typically,
one side is more affected than the other. Concommittant degenerative processes may develop to the spine or the stifle
joints in older patients.
Pain leads to lameness associated with contracture of local muscular groups, resulting in decrease of the functional
range of motion of the affected hip joint. The abduction and
extension of the hip is reduced and painful. The medial aspect of the hip joint may be sensitive upon palpation and
contracture of the pectineus muscle is sometimes evident.
Pectinotomy1 and pectinectomy2 have been successful to
reduce the pain in coxarthrotic patients. The results have
been attributed to the decrease of the degree of hip subluxation, hence reduced tension on the inflammed joint capsule.
This intervention did not improve the degree of extension of
the affected hip joint.
The ventral aspect of the hip joint capsule is associated
to the pain in presence of dysplasia. This area is under the
greatest load during subluxation of the hip4, and receives a
substantial innervation5.
The technique presented here uses an iliopsoas tenotomy
and ventral neurectomy under visualization in adjunction to
the pectinectomy for treatment of coxarthrosis3. This results
in durable pain free and improved hip joint extension, in addition to the effet of a classical pectinectomy.

Figure 1 - Pectineus muscle transection, medial view.

MAIN PROGRAMME

Summary

304

4th European FECAVA SCIVAC Congress

Figure 2 - Iliopsoas tenotomy, medial view.

Figure 3 - Neurectomy of the ventral capsule of the hip joint, medial view.

and improves the extension of the joint. Partial neurectomy


of the joint capsule is achieved while preparing carefully its
ventral aspect with a periosteal elevator, attempting to severe innervation from the obturatorius nerve ventrocaudally
and from the femoralis nerve ventrocranially (Figure 3).
After control of the hemostasis, the superficial layers of
the wound are only closed in interrupted fashion.

older dogs with concommittant problems. Economical reasons may also lead to the choice of such surgical technique.

Results
This intervention can be performed bilaterally simultaneously. The use of this technique in 52 patients has been reported3. The results have been positive, improving immediately and durably the fonction of the operated hip joints to
the satisfaction of the owner of the animal. No side effects
have been observed. This intervention leaves the possibility
for the insertion of hip prostheses at a later date. Its indication is optimal in immature dogs affected bilaterally and in

Literature
1.

2.

3.

4.
5.

Wallace L.J.: Clinical investigations and surgery on the pectineus


muscle and its relationship to canine hip dysplasia. In: Scientific Proceedings AAHA, 38th Annual Meeting, Las Vegas: 384, 1971.
Richard D.A., Hinko P.J., Morse E.M.: Pectinectomy vs. pectinotomy
in the treatment of hip dysplasia. Vet. Med. Small Anim. Clin. 67:
976, 1972.
Ballinari U., Montavon P.M., Weiss R.: Die Pectineusmyektomie, Iliopsoastenotomie und Neurektomie (PIN) als symptomatische Therapie bei der Coxarthrose des Hundes. Schweiz. Arch. Tierheilk. 137:
251, 1995.
Gardner E.: The innervation of the hip joint. Anatomical Record 101:
353, 1948.
Peterson H.A., Winkelmann R.K., Coventry M.B.: Nerve endings in
the hip joint of the cat: their morphology, distribution and density. J.
of Bone and Joint Surgery 64: 333, 1972.

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305

Uncemented canine totale hip prosthesis:


development and clinical application
Pierre M. Montavon

Short summary
A cementless total hip prosthesis with screw fixation was
developed at the University of Zrich for treatment of
coxarthrosis in dogs. It has been used in over 60 clinical patients with excellent surgical success rate and clinical results. The results with now the longest follow up over 4 years
are characterized by absence of: pelvic nerve damage, long
term luxation and infection.
The procedure is reproducible and lasts less than 2 hours
with a trained operating team of 3 persons.

The hip joint is approached performing a craniolateral


approach on the dog in lateral recumbency. A T-shaped capsulotomy is made along and at the base of the neck. A burr
is used for the excision of the femoral head and neck, reducing the creation of stress riser areas and optimizing the
preparation of the proximal femur for insertion of the
femoral component. Preparation of this area with a special
rasp, acting also as a template, is necessary until the entire
instrument can be introduced, granting insertion of the
femoral component of the prosthesis.
The femur is then maintained caudally with the help of a
Mayo retractor and the joint capsule is retracted with finger
Meyerding retractors.

Cemented hip prosthesis has been successfully applied


for total hip joint replacements in dogs since 15 years1.
Several designs have been later introduced2, 3. Cementless
prostheses have also been studied based on the press fit
principle4, 5.
A cementless total hip prosthesis was developed at the
University of Zrich (Figure 1). The goals were:
1) to reduce the risk of nerve damage
2) to diminish the operative infection rate
3) to decrease the possibility of postoperative luxation
of the prosthesis
4) to simplify the technique and make acceptable to any
well trained orthopedic surgeon, and
5) to allow surgery of revision when necessary.
Twelve consecutive cases treated with the last generation
of this prosthesis are presented here, in the light of 49 cases
operated using the evolving designs of the same prosthesis.

Technique - Prosthesis, instrumentation


and implantation
After experimental and clinical testing, three different
sizes of prostheses resulted, using 3, 4 or 5 screws. This fixation guarantees primary and long-term stabilization of the
prosthesis (Figure 1). Titanium-aluminium-vanedium alloy
is used for all metal components.
The stem of the femoral component is anchored endosteally by a monocortical screw fixation to the medial cortex alone. Screws are inserted blind through access holes in
the lateral cortex with the aid of a drill guide fixed to the
stem. Tapered heads of the self-tapping screws lock in the
matched holes of the stem.

Figure 1 - Cementless total hip prosthesis with screw fixation.

MAIN PROGRAMME

DVM
Veterinar Chirurgische - KI der Universitat Zurich - Switzerland

306

The acetabulum is now prepared using a reamer of fitting


size, until the subchondral layer has been exposed. The cavity is cleaned of any soft tissue remnants and osteostyxis in
the caudal and cranial areas of the acetabulum is performed
with a drillbit mounted on oscillating device. This reduces
the risk of trauma of the nerves present on the medial aspect
of the hemipelvis (i.e. sciatic nerve).
Hemispherical acetabular cups have an ultra high molecular weight polyethylene insert within a perforated titanium
alloy shell, designed to improve osseointegration. They exist in four sizes: 26, 29, 32 and 36 mm outer diameter.
The cup mounted on an inserting device is then positioned into the acetabulum. The edge of the ventral half of
the cup should match the cranial, ventral and caudal border
of the prepared acetabulum. The cup is then hammered
down. A hole is drilled in oscillating fashion through the
hemipelvis, originating at the central hole of the acetabular
cup. A 4 mm cancellous titanium bone screw is positioned
for the fixation of the acetabular cup.
A guide is fixed onto the femoral component. Both are
positioned in slight anteversion (15) after insertion. The use
of drill inserts allows exact blind positioning of the holes for
the screws into the cortices. Oscillating device placed on the
drill machine and the use of three lips drill bits reduces the
soft tissue trauma, when exiting the medial cortex of the femur while drilling.
The screws are self-tapping and their conical heads lock
into the holes of the femoral component. This results in a
stable unit consisting of the femoral shaft of the prosthesis
and of the screws after their placement in the medial cortex.
Once the femoral component is fixed to the femur, the guide
is removed.
The femur is then moved in a physiological fashion and
the distance between the femoral and the acetabular component is evaluated. Femoral head and neck components exist
in three sizes of lengths for the neck: 5, 10 and 15 mm. The
minimal estimated length is first positioned over the conical
peg of the femoral component already in place. The prosthetic joint is reduced with the help of special retraction
three positions are tested for impingement and possibility of

4th European FECAVA SCIVAC Congress

luxation within the physiological range of motion: 1) abduction to test the clearance between medial greater trochanter
and the dorsal edge of the cup, 2) outward rotation of the hip
with flexed stifle at 90 for craniodorsal luxation of the prosthesis and, 3) full flexion and inward rotation of the hip for
caudoventral luxation of the prosthesis. In presence of any
problem, the prosthesis has to be tested with the next superior neck length, until the prosthesis is judged stable. Impingement of the caudal fibrous joint capsule may be carefully removed with a rongeur (cave: sciatic nerve). If instability of the prosthesis persists, the acetabular screw has to
be removed and the cup repositioned in order to cover the
area of luxation.
After copious flushing, the joint capsule is closed with 2
or 3 far-near-far-near stitches, with synthetic resorbable material (size 2-0). Fasciae, subcutaneous layers and skin are
closed in appositional fashion.

Results
The range of motion of the prosthesis is greater than the
physiological range. Success rate of the surgery and clinical
results are excellent. The technique is reproducible. Its duration is less than 2 hours, requiring ideally the presence of 3
persons at the table. Patients recover a normal gait within 46 weeks. If necessary, the second side can be operated after
an interval of 8 weeks.

Literature
1.

2.
3.
4.

Olmstead M.L., Hohn R.B., Turner T.M.: A five year study of 221 total hip replacements in the dog. J. Am. Vet. Med. Assoc. 183: 191,
1983.
Olmstead M.L.: The canine cemented modular total hip prosthesis. J.
Am. Hosp. Assoc. 31: 2, 109, 1995.
Bardet J.F., Letournel E.: Prothse totale de la hanche chez le chien.
Pract. Med. Chir. Anim. Comp. 30: 555, 1995.
De Young D.J. et al.: Implantation of an uncemented total hip prosthesis. Technique and initial results of 100 arthroplasties. Vet. Surg.
21: 168, 1992.

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307

The modification of the Slocums technique


for the repair of cruciate ruptures
Pierre M. Montavon

Short summary
A modified tibial plateau leveling osteotomy technique is
presented, combined with the creation of an aponeurotic fascial sling cranial to the proximal tibia. With this method,
partially torn cranial cruciate ligament can be preserved. It
is characterized with very good surgical success rate and
postoperative results. Radiographic follow-up shows practically no further postoperative evolution of gonarthrosis.

The craniocaudal slope of the tibia plateau leads to cranial tibial thrust of the tibia under compression1. The technique of leveling of the tibia plateau for deficit of the cranial
cruciate ligament has been described2 and successfully applied in large populations of clinical patients. A modification
of the technique is described here3. Its combination with the
creation of an aponeurotic sling cranial to the proximal tibia
with the medial and lateral fasciae during closure of the surgical wound4 gives very good results.
The goals of the modification of the technique presented
here are: 1) to make the surgery possible in any size of dogs;
2) to preserve the tibial insertion of the medial collateral ligament of the stifle intact; 3) to make the osteotomy and its
fixation with readily available instruments and implants and
4) to stabilize the persisting cranial drawer sign of the tibia
in order to avoid later meniscal damage.

Technique
A lateral approach to the stifle joint is performed with
parapatellar incision of the biceps fascia from proximal to
the patella until the middle of the tibia. The fascia is then
freed up and prepared. Lateral arthrotomy allows exploration of the stifle joint. Routine cleaning up of the joint is
performed. Partially ruptured anterior cruciate ligament5 is
left intact, removing only the torn parts. A parapatellar incision of the pes anserius is then made medially, from proximal to the patella to the middle of the tibia. It is prepared and
freed up, especially in the area of the medial femoral
condyle4.
The joint capsule is also opened on the medial aspect of
the stifle joint. The retropatellar fat pad is then totally excised, respecting the cranial aspect of the menisci as well as
the bursa located on the tibial tuberosity under the patellar

ligament. The insertion of the cranial tibialis and peroneus


longus muscles are elevated from the fossa extensoria and
the tendon of extensor digitalis longus is freed up from the
sulcus extensorius. Those structures are retracted caudally. A
transverse hole is then drilled through the tibia from its caudomedial aspect. The hole is located below the insertion of
the medial collateral ligament of the stifle. It is the basis of
an angle of 20-25 placed between the cranial aspect of
both menisci caudally, and the bursa of the patellar ligament
located at the proximal extremity of the tibial tuberosity cranially (Figure 1).
A template is helpful to first set landmarks over the medial tibial cortex. A transversal wedge defined by this angle is
then osteotomized in the proximal tibia using oscillating saw.
First a medial monocortical cut is carried out with a
smaller saw blade. A longer blade is then used to complete the
transverse osteotomy towards laterally, while sparring articular and periarticular soft tissue structures. The bony wedge is
then removed. After partial elevation of the M. popliteus, a
Hohman retractor is placed along the caudal cortex of the tibia to protect popliteal structures and vessels. Either holes are
drilled into caudal tibial cortex or a small cut with the saw is
placed at the caudomedial border of the tibia, slightly proximal to the summit of the osteomized wedge. It is then possible to fracture the proximal caudal tibial metaphysis towards
cranially, bringing it into contact with the tibial tuberosity, using bone holding forceps. Functional axes of the tibia have to
be respected during the leveling of the tibia plateau. Two interfragmentary bone screws of adequate size are placed in position function into a craniocaudal direction through the tibial
tuberosity into the caudal metaphyseal fragment in order to
stabilize the osteotomy (Figure 2). During the fracturing and
the fixation of the osteotomy, the tuberositas tibiae has to be
handled carefully in order to avoid fracture into it. The tibial
craniocaudal plateau orientation should now come close to
perpendicular to the anatomical axis of the tibia.
After copious flushing of the tissues, the lateral and medial arthrotomy is closed with monofilament resorbable sutures
in appositional cruciate pattern placed into the fibrous joint
capsule. The prepared medial and lateral fasciae of the stifle
are imbricated over the proximal cranial half of the tibia, using preplaced horizontal mattress suture pattern (Figure 3).
The proximal lateral fascia is then imbricated over the
patellar ligament tissues with a far-near-far-near pattern
(Figure 4). The rest of the fascial incisions, subcutaneous
layers and the skin are closed in appositional fashion.

MAIN PROGRAMME

DVM
Veterinar Chirurgische - KI der Universitat Zurich - Switzerland

308

4th European FECAVA SCIVAC Congress

Figure 1 - Medial aspect of the hindlimb. Transversal wedge to be osteotomized on the proximal tibia.

Figure 2 - Medial aspect of the hindlimb. Fixaton of the osteotomy with two
interfragmentary bone screws.

Figure 3 - Cranial aspect of the stifle. Creation of an aponeurotic sling during closure of the wound.

Figure 4 - Cranial aspect of the stifle. Completion of the aponeurotic sling.

4th European FECAVA SCIVAC Congress

Postoperative x-rays are made. A soft Robert-Jones bandage is applied for the first postoperative day. First control
x-rays 4-6 weeks postoperatively. In the meantime, the activity of the dog is restricted with a leash.

309

Iatrogenic fracture of the tuberositas tibiae can be avoided. When present in the patients of this series, it was successfully repaired with wire tension band.

Literature
Results of this surgery in over 60 patients will be related.
Typically, the technique offers good to very good results.
The gait was fully functional and the operated stifles stable
upon palpation 6 weeks after the surgery. The patients regain
the maximal musculature 4 to 6 months after surgery. Partial cruciate rupture did not evolute. Arthrosis appears minimal at later controls (1 year and more).

1.
2.
3.
4.
5.

Slocum B., Devine T.: Cranial tibial thrust: a primary force in the canine stifle. J. Am. Vet. Med. Assoc. 183: 456, 1983.
Slocum B., Slocum T.D.: Tibial plateau leveling osteotomy for repair
of cranial cruciate ligament rupture in the canine. Vet. Clin. North
Am. 23: 777, 1993.
Tepic S.: Personal communication.
Harrison J.W., Montavon P.M.: Technique extra-capsulaire de stabilisation de la motilit antrieure du tibia. Schweiz. Arch. Tierheilk.
123: 1, 1981.
Beck P., Montavon P.M.: Was diagnostizieren Sie? Schweiz. Arch.
Tierheilk. 129: 493, 1987.

MAIN PROGRAMME

Results

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311

Use of glucans as a nutritional supplement in fish


Giuseppe Mosconi

Introduction
There are numerous problems associated with the treatment of diseased fish, particularly if the specimens to be
treated are delicate and small as in the case of ornamental
tropical fish.
Treatment with medicated food is often not possible as
the diseased fish refuse to eat. The large number requiring
treatment (thousands or tens of thousands of fish per tank)
precludes individual treatment. The large capacity of the
aquatic environment in which the fish live also makes treatment of the water as a whole costly. Catching the fish and
placing them in a separate container for rapid bath treatment
often damages and stresses them to the point of neutralising
the benefits obtained from the treatment itself.
The condition of the fish must therefore be such as to enable them to react as efficiently as possible to disease and to
fight off the attack of the pathogenic germs by themselves.
All forms of stress must thus be eliminated and at the same
time their immune system must be reinforced. This enables
the infection to be cured, thus reducing the need for chemical treatments.

The immune system of fish


Fish have a number of different mechanisms or barriers
which assure them immunity to pathogens and thus resistance to disease.
Two types of immune mechanisms provide protection
against infectious and infesting diseases - non-specific defences and specific defences.
The difference between these two defence systems is that
in the first category, the defence mechanisms exert a general action not associated with recognition of a specific disease
causing agent and there is no memory enabling recognition of previously encountered pathogens. In the case of specific defences, however, these are aimed at one foreign agent
only and are triggered by the pathogen itself (adoptive defence). Alternatively they may be induced by administration
of vaccines which produce specific (targeted) resistance to
individual diseases.
In fish, the non-specific immune system is extremely important. It is based on the chemical characteristics of the skin
and mucous membranes, cells specialised in ingesting and
destroying pathogens and also various humoral factors with

an antimicrobial action. Non-specific immunity can be stimulated by the presence of pathogens or enhanced by the administration of immunostimulants.

Immunostimulant substances
Immunostimulants, otherwise known as immunomodulators, are substances which raise the immune defences of
the fish, increasing their resistance to disease.
There are many substances able to stimulate the immune
system and all induce a rapid response lasting for a number
of weeks.
According to their derivation, immunomodulators can be
divided into a number of groups:
Bacteria and bacteria-derived products (microbacteria,
lipopolysaccharides and endotoxins produced by gramgerms);
Complex carbohydrates (glucans);
Synthetic immunostimulants (levamisole, antiviral drugs,
etc);
Nutritional factors (vitamin C, vitamin E, lipids);
Polypeptides, animal extracts (fish extracts);
Cytokinin and thymic extracts;
Vegetable extracts and lecithin.
In fish farming, treatment based on various types of immunostimulants has been practised for a number of years. In
the case of ornamental aquarium or pond fish, the practice is
however much more recent. We therefore carried out a number of experiments, investigating the efficiency of a number
of plant-derived immunomodulators (glucans and some micronutrients). Glucans are extremely complex polysaccharides extracted from barley, yeast, fungi, a number of plants
and algae. The most interesting among the latter is Fucus
vesciculosus (which yields a particularly active glucan).
These complex sugars interact with vitamin C and a
number of micronutrients such as alginic acid and silicic
acid to act as catalysts and phase exchangers for oxygen.
The transferred oxygen molecules have been shown to
stimulate the non-specific immune system of the fish and
macrophage activity in particular.
Macrophage cells specialise in ingesting (phagocytising)
the most diverse of undesirable substances whether organic
(viruses, bacteria, protozoa, cell debris) or inorganic (minerals, carbon, silica, foreign bodies, etc) which they may encounter within the tissue.

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Med Vet, MS, Dipl ECVS


Private Practitioner, Bologna - Italy

312

Glucans in combination with the above micronutrients


and vitamin C stimulate the macrophages which become
more aggressive towards the pathogens, improving their capacity to neutralise and kill them. The activated
macrophages also stimulate the production of lymphocytes,
improving the antibody response to the infecting agents.
The result is a raising of the non-specific natural defences of the fish and greater resistance to disease.
To sum up, the main action of the glucans is to activate
the phagocytosis mechanisms of the white cells which form
part of the non-specific immune system and to enhance the
action of the lymphocytes, thus also improving the specific
antibody reaction. This opposes the immune deficiency
caused by stress (immunosuppression effect).

4th European FECAVA SCIVAC Congress

From the start of the test, the fish were fed with a daily
ration equal to 1% of live weight. Three tanks (2, 4 and 6)
received normal fish-food, while the other three (1, 3 and 5)
received flake food supplemented with immunostimulants Euro Life Immuno +.
The food was distributed by means of a mechanical feeder over a period of seven hours per day. Each day, the mortality rate in each tank was noted and subsequently reported
in a twice-weekly table.
At the end of the test, the surviving fish were examined
for typical symptoms of spring viremia or bacterial complications.

Results
Effect of the immunomodulator
EURO LIFE IMMUNO + in the prevention
of viral and bacterial diseases in goldfish
(Carassius auratus L.)
The main cause of disease in ornamental fish is stress.
Many specimens are the healthy carriers of diseases contracted in the past and show no signs of disease as they possess an efficient immune system which keeps these under
control. But if stress or a number of coinciding stress factors
weaken the immune system, the disease may emerge in its
full virulence.
We have carried out various tests on aquarium fish, administering Euro Life Immuno + flakes of food enriched
with 2% glucans. The most authoritative experiment was
carried out by Professor Paolo Melotti, Director of the Aquaculture Research Centre of the Faculty of Veterinary Medicine at the Universit di Camerino in collaboration with Andrea Dees and Oliviero Mordenti of the Zootechnical Institute at the Universit di Bologna with Giuseppe Mosconi,
Euraquarium SpA veterinarian.
The cycle of tests carried out on the goldfish using Euro
Life Immuno + was aimed at verifying the products efficiency in preventing the development of viral and bacterial
diseases affecting this species of ornamental fish.
The goldfish came from a breeding establishment where
spring viremia was endemic with regular spring and autumn outbreaks accompanied by the usual bacterial complications generally associated with microorganisms belonging
to the Aeromonas genus.
On draining a pool containing about 6,000 three-year-old
goldfish in April 1997, about 50% of the fish were found to
have symptoms typical of the disease characterised by skin
edema, hemorrhages and deep lesions also affecting the muscles. Microscopic examination of the remaining fish without
obvious lesions showed a high presence of exoparasites (protozoans and trematodes) affecting the skin and gills, which
were eliminated before the test by repeated treatments.
Out of this group, a random sample of 300 fish were chosen with a mean weight of 50 g 16. These were immediately divided into six 250 litre tanks (50 fish per tank), each
with a purification system consisting of a mechanical filter
and a biological filter. A thermostat system kept the water at
a temperature of 20 2 C.

Mortality data are given in Table 1 while the presence of


symptoms is given in Table 2.
As can be seen from Table 1, in all tanks receiving Euro
Life Immuno + food, mortality was considerably lower than
in the three tanks receiving normal fish-food without immunomodulators.
The results relating to the presence of typical symptoms
of spring viremia observed after 60 days in surviving fish
in the various groups were also extremely interesting. In this
case, the goldfish treated with Euro Life Immuno + were
found to have very few symptoms, unlike those not undergoing treatment (Table 2). This could be explained by the
gradual effect of the immunomodulator which is reinforced
over a period of time with prolonged administration of the

Table 1 - Death rate noted at twice-weekly intervals.

Table 2 - Presence of symptoms noted at 60 days from the beginning of


the test.

4th European FECAVA SCIVAC Congress

food. This theory is confirmed by mortality figures. Over the


sixty day period, the number of deaths among fish fed with
normal food tended to increase, unlike those fed with Euro
Life Immuno +.

313

7. To enhance colouring;
8. To reduce the quantity of undigested residues.

Characteristics of Euro Life Immuno +


immunostimulating food
The in-depth studies carried out by the Universities of
Bologna and Camerino into glucans and a number of natural micronutrients used in fish nutrition as immunomodulators have enabled Euraquarium to formulate an innovative
line of fish-food - Euro Life Immuno + basic, goldfish and
seafish - with the following aims:
1. To provide an appetising food with a high biological value;
2. To reduce or eliminate stress-induced disease;
3. To prevent known or suspected diseases by increasing the
resistance of the fish;
4. To help the healing process in the case of infection;
5. To increase the specific immune response;
6. To raise the index of food conversion and use;

Feeding aquarium fish with immunostimulants offers


considerable benefits, guaranteeing an immediate improvement in resistance to infectious and infesting diseases.
Prolonged administration further reinforces the immune
system, guaranteeing a wide-ranging and heterogeneous resistance to attack by pathogenic germs.
In the event of disease, the efficacy of chemical treatment is enhanced by using fish-food containing immunomodulators.
As a result of the wide range of positive factors inherent
in this type of fish-food (appetising, improved conversion of
the food, enhanced pigmentation, reduction of undigested
residues), natural substances with immunostimulating properties will be used more and more often in formulas of food
for ornamental fish, thus guaranteeing a tangible improvement in the quality of life for the inhabitants of the aquarium.

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Conclusions

4th European FECAVA SCIVAC Congress

315

Surgical treatment of rectal, anal, perianal


and perineal lesions
Gert Niebauer

Summary
An introduction to the general principles of anorectal
surgery will be given, including patient preparation, antimicobial prophylaxis and therapy, antisepsis and the use of surgical drains. The following conditions will be reviewed,
with emphasis on an update on disease mechanisms and surgical treatment techniques: congenital anomalies, trauma to
anus and rectum, anorectal stricture, anal sacculitis,
hidradenitis, perianal fistulae, rectal fistula, hyperplasia of
circumanal hepatoid (perianal) glands, neoplasms of perianal glands and anal sacs, neoplasms of the anus and rectum,
anal and rectal prolapse, rectal diverticulum and perineal
hernia; in the latter condition, a new pathogenic theory, advanced by the author, involving the insulin-like peptide hormone relaxin, will be discussed.

General principles of anorectal surgery


Congenital anomalies
Trauma to anus and rectum
Anorectal stricture
Anal sacculitis
Hidradenitis
Perianal fistulae
Rectal fistula
Hyperplasia of circumanal hepatoid (perianal) glands
Neoplasms of perianal glands and anal sacs
Neoplasms of the anus and rectum
Anal and rectal prolapse
Rectal diverticulum
Perineal hernia
General principles of anorectal surgery: anorectal surgical procedures are rarely emergencies; sufficient time is usually available for preoperative patient preparation; reduction
of stool content in the large intestines and antimicrobial prophylaxis can be initiated prior to most surgical procedures
that enter the rectal lumen10. Examples for pre- and postoperative treatment are: neomycin (25 mg/kg body weight) and
erythromycin (2 mg/kg body weight) given every 8 hours, or
metronidazole given alone (30 mg/kg body weight) once
daily for two days preoperatively. Systemic prophylaxis
should be initiated immediately prior to surgery and
chemotherapy (perhaps per os, if available), using the same

agents, should be continued for several days after surgery or


as long as deemed necessary. Antibacterial combinations also can be used: e.g., cefoxitin sodium (15 to 22 mg/kg body
weight) plus trimethoprim-sulfadiazine (30 mg/kg body
weight); or gentamicin (4.5 mg/kg body weight) plus clindamycin (10 to 40 mg/kg body weight); kanamycin (7.5
mg/kg body weight) plus clindamycin (10 to 40 mg/kg body
weight), gentamicin (4.5 mg/kg body weight) plus metronidazole (30 mg/kg body weight).
The use of surgical drains (e.g., Penrose rubber drains) is
recommended when a communication between the rectal lumen and the perirectal tissues existed preoperatively or had
been created during surgery.
Postoperative stool softeners may be used to help prevent straining to defecate after surgery.
Congenital anomalies: are rare in small animals; can either be an inadequately developed or absent anal orifice
(atresia ani, imperforate anus) or rectal aplasia (atresia recti,
segmental aplasia) in which the anal orifice is developed
normally but the rectum is interrupted by an atretic segment.
The mildest form of anal anomaly is congenital stricture. In
females with rectal and anal atresia, genitorectal fistulae
(rectovaginal fistula, anogenital cleft) may also occur.
Trauma to anus and rectum: anus or rectum can be injured from within or without. Ingested foreign objects, such
as needles or pieces of bone can become lodged in rectum or
anus, and may penetrate the mucosa and underlying tissue
layers due to sphincter contractions. Other causes include
improper rectal thermometry, rectal tearing during examination, improper use of and enema tubes, impalement or acts
of sadism. Laceration of the anus and rectum from without
can be due to severe trauma to the perineal region, such as
from dog bites, or pelvic fractures with dislocation of sharp
bone splinters.
Signs - tenesmus, dyschezia and hematochezia. Peritonitis might develop in cases of deep rectal perforation. Treatment - Rectal lacerations should be closed with simple interrupted sutures, preferably with a synthetic monofilament, absorbable material (e.g. polydioxanone). Drainage of the
contaminated areas and intensive antimicrobial treatment
with broad-spectrum antibiotics (see above) is necessary.
Most cases of rectal perforation are, however, retroperitoneal
(in the caudal half of the rectum) and usually heal well by
second intention. Closure per rectum of these defects should
not be attempted. Anorectal strictures or fecal incontinence
(damage to the anal sphincter muscles and/or their nerve sup-

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Med Vet, PhD, MS, Dipl ECVS


University of Pennsylvania, Philadelphia - USA - Clinica Veterinaria Dante, Orbetello - Italy

316

ply) may develop as sequelae to traumatic injuries.


Anorectal strictures: can be either functional or anatomical in origin. Functional constrictions (anorectal spasms)
can occur as transient or chronic spastic anal sphincter contractions, as a sequel of traumatic lesions or irritations of the
rectoanal area. Functional constrictions must be differentiated from strictures due to inflammation, fibrosis or neoplasia,
and from the normal narrowing of the rectal lumen, often
found on rectal palpation, just caudal of the colorectal junction (functional sphincter ani tertius). Pathologic idiopathic anorectal spasms can be seen in nervous excitable animals, especially German shepherd dogs. True, mechanical
anorectal strictures can occur as sequelae of traumatic or
inflammatory lesions of rectum, anus and/or anal sphincter,
chronic anal sac disease, perianal fistulae and/or previous
surgical procedures. Circumferential fibrosis causes tenesmus, dyschezia and chronic constipation, with or without
secondary megacolon. Rectal neoplasms, which also can
cause rectal constriction, must be differentiated from benign
rectal or anal stricture. Rectal examination, proctoscopy, radiographic and ultrasuonographic studies and biopsies are
helpful to distinguish between these two conditions. Treatment of strictures involves either bougienage, surgical
transection of the fibrous ring, or full thickness resection of
the scar. Lesions located near the anus can be excised per
rectum (intraluminal approach). For more cranial lesions, a
dorsal or lateral pararectal approach may be necessary to execute a full thickness 360 degree resection-anastomosis with
or without a pull-through procedure. A abdominal approach, with or without pelvic osteotomy (symphysiotomy
or pubic triple osteotomy), is indicated when rectal strictures
extend into the area of the rectocolonic junction.
Hidradenitis: is a pyogranulomatous inflammation of the
anal glands, apocrine sweat glands and sebaceous glands in
the cutaneous zone of the anus and the hairless anal disk. Although initially superficial, the chronic inflammation involves the deep connective tissues surrounding the circumanal hepatoid glands and is thought to be one of the initiating lesions in the development of perianal fistulae. In fact,
inflammation of the anal glands in the columnar zone, with
subsequent fistula formation in the anal sinuses, in most cases is found concomitant with hidradenitis of the cutaneous
zone. Treatment of hidradenitis consists of resection and/or
fulguration of the affected anal cutaneous zone including the
paired tail folds, if affected. However, since hidradenitis
most frequently is an early stage of perianal fistula formation, deeper hidden or developing fistulous tracts usually are
detected during surgery. Also, responsiveness of the lesions
to systemic corticosteroid treatment has led to the hypothesis that in certain breeds (German Shepherd) an autoimmune
mediated inflammatory process may be involved.
Anal sacculitis: In many cases it remains unclear
whether inflammation is the cause or the result of anal sac
disease. Anal sac ducts can become obliterated. Infection
aggravates the condition and abscessation of the sac occurs.
Anal sac rupture, chronic anal sac abscessation or perianal
fistulae are common sequelae of anal sacculitis. Complete
surgical excision of the anal sacs is indicated in cases of
chronic and recurrent impaction or abscessation, non-healing abscesses, and in all cases of perianal fistulation. Tem-

4th European FECAVA SCIVAC Congress

porary or permanent fecal incontinence or anorectal stricture


are rare potential complications of anal sac extirpation. This
might occur when by extensive dissection the nerve supply
to the external anal sphincter is inadvertently damaged (especially bilaterally), or if bilateral anal sacculectomy causes
undue trauma to the anal sphincter muscles.
Perianal fistulae: are chronic perianal inflammatory lesions of dogs. Their etiology is obscure. Pathogenically, infection, originating in the specific glandular structures, in
and around the canine anus (see above), seems to be the
most important initiating factor of the disease. Most commonly, mature dogs of either sex and of breeds with a long,
low-slung tail are affected. The lesion most frequently is
seen in German shepherd dogs.
Signs - tenesmus, dyschezia, bleeding and malodorous
purulent discharge from perianal fistulous tracts. Severe
pain is present in most cases of extensive fistulation. Chronic constipation with or without megacolon, lethargy, anorexia and weight loss can occur as complicating factors.
Treatment - The disease is progressive in nature and conservative treatment is frequently ineffective, although longterm treatment with systemic corticosteroids and broadspectrum antibiotics has been effective in selected cases.
The combination of surgical and medical treatment in early
stages of the disease yields the highest rate of cure. Several
methods of surgical treatment have been described. None is
fully satisfactory. Healing without recurrence can be
achieved in approximately 50% of severely affected animals4. The various methods include excision or exterioration
of all fistulous tracts, or their destruction by chemical or
thermal means. The method of choice depends largely on the
extent of fistulation and the preference of the individual surgeon. Regardless of the surgical method chosen, and because of the likelihood of involvement of the anal sacs in the
disease, bilateral anal sacculectomy should be performed
concomitantly (see above). Complete surgical excision is
potentially damaging to vital structures (nervous supply to
the anal sphincter and the sphincter itself). Thus, a combination of fistulectomy and fulguration and/or cauterization of
remaining tracts by caustic agents such as 10% Lugols solution has been advocated11. In very advanced cases, surgical procedures necessarily have to be a compromise between
completeness of excision and minimization of trauma to prevent fecal incontinence. Thermal or chemical destruction
leads to necrotic tissue and opposes the healing process, at
least temporarily, and may predispose to postoperative stricture formation. Laser therapy, however, seems to be a valuable alternative, where available3. Cryotherapy, was advocated by many investigators, but it is not more effective than
surgical excision and is potentially dangerous, resulting in a
higher incidence of post-treatment stricture than sharp and
blunt dissection.
The hypothesis that a broad based tail can prevent aeration of the anal region in certain breeds and that this contributes to the development and persistence of perianal fistulae has not been veryfied and thus, tail amputation is not recommended.
Rectal fistulae may occur associated with severe forms
of perianal fistulation. The fistulous tracts can extend cranially within either perirectal tissues or submucosally with-

in the rectum itself. Rectal fistulae may also develop without


perianal fistulation. German shepherd dogs seems to have an
anatomical predilection for this, as their anal sacs extend relatively far craniad and are in closer proximity to the rectum
than anal sacs in other breeds. Treatment consists of complete excision of the fistulous tract(s) by a pararectal approach, debridement of the mucosal lesion, closure of the
rectal defect with simple interrupted, absorbable sutures and
placement of a drain.
Hyperplasia of hepatoid circumanal (perianal) glands:
is a common phenomenon, usually seen in older male dogs.
A moderate degree of hyperplasia, without accompanying
lesions, is a physiologic response to androgenic stimuli. In
cases of extensive hyperplasia, secondary irritation of the
perianal skin with anusitis, hidradenitis and tenesmus might
develop. Frequently, hepatoid circumanal gland hyperplasia
is seen concomitantly with perianal adenomas. Anatomically, these glands are found in the hairless disk encircling the
canine anus and are scattered in the skin of the prepuce, inguinal area, hind limbs, sacral region and a well defined area
dorsally on the tail of dogs (tail gland)8.
Treatment - Because extensive hepatoid circumanal
gland hyperplasia (with or without tail gland hyperplasia) is
caused by androgenic stimulation, other diseases or lesions
related to sex hormone imbalances may be present concomitantly, e.g. prostatic hypertrophy. In male dogs, castration is
the recommended therapy for extensive hepatoid gland hyperplasia, and testicles should routinely be examined histologically; androgen-producing tumors (commonly Leydig
cell tumors) frequently are found. Occasionally, hyperplasia
of the hepatoid circumanal glands may be detected in older,
spayed bitches, probably associated with lack of estrogens
and a relative increase in androgen hormone concentration.
Neoplasms of perianal glands and anal sacs: tumors of
the perianal glands originate almost exclusively from hepatoid circumanal glands. Hepatoid circumanal gland tumors
are among the most frequently occurring canine tumors.
Development and growth of hepatoid gland tumors is related closely to plasma androgen levels. Thus, 85% of hepatoid
tumors are found in mature or aging male dogs. The majority of hepatoid circumanal gland neoplasms are benign, thus
well encapsulated and not invasive. Yet, hepatoid adenomas
often are ulcerated and infected secondarily. Mechanically
irritated ulcerating tumors can cause considerable bleeding
and their appearance can mimic malignancy.
Hepatoid adenocarcinoma shows aggressive local invasion and, occasionally, causes severe hemorrhage. Extension
of the malignancy into the perineal region and into the pelvic
canal is common and metastasis occurs to the regional
(sublumbar) lymph nodes.
Treatment - Prior to treatment, benign and malignant tumors have to be differentiated. Clinical distinction is not always easy and biopsy may be indicated. Surgical excision
(or cryotherapy) is necessary in cases of large, ulcerating
and hemorrhaging adenomas. Castration at the time of tumor
excision prevents regrowth, enhances involution of remaining tumor nodules and promotes regression of hepatoid
gland hyperplasia. Adenocarcinomas should be completely
excised, which only is achievable when tumors are fairly
small. Lymph node metastasis can be expected. Radiation

317

therapy as an additional treatment modality has shown some


effect in selected cases. Hormone therapy and/or castration
seem to be ineffective in cases of hepatoid adenocarcinoma.
Neoplasms of the anal sacs: canine anal sac tumors appear to be invariably malignant. Adenocarcinomas arise from
the apocrine glands of the anal sacs. Female dogs are affected in 95% of the cases. Anal sac adenocarcinoma is the most
frequent neoplasm of the perianal and perineal region in older (over 10 years of age) female dogs. Prior ovariohysterectomy seems not to affect the incidence. Most characteristically, anal sac adenocarcinomas (occurring in over 90% of
the cases) elicit hypercalcemia by producing a parathormonelike protein (paraneoplastic syndrome). Although the tumors
are metastatic, initially, they seem to remain confined to the
anal sac. At this stage they may be detected by routine rectal
examination. In later stages, when dogs are presented because of related clinical signs (dyschezia, ulceration, hemorrhage), lymph node metastasis to the sublumbar nodes and to
distant organs will usually have already occurred8.
Treatment - Surgical excision is not curative, in general.
Recurrence and/or metastasis, if not already present at the
time of surgery, can be expected within weeks to months after surgery. Complete surgical excision at early stages,
though not likely to prevent recurrence, reduces the elevated
serum calcium concentration and thereby alleviates, at least
temporarily, the metabolic effects of severe hypercalcemia.
Neoplasms of the anus and rectum: non-glandular tumors from the cutaneous part of the anus are rare. Anaplastic squamous cell carcinomas (cloacagenic type) and malignant melanomas have a very poor prognosis. Primary neoplasms of the rectum are also relatively rare and occur in
older dogs (mean age 8.5 years, range 2 to 14 years. Rectal
tumors, whether benign or malignant, usually originate from
the rectal mucosa. Other primary rectal neoplasms such as
leiomyomas (-sarcomas), hemangiomas (-sarcomas), lymphomas (-sarcomas) and plasmacytomas occur occasionally.
Epithelial tumors are categorized as benign proliferative
polypoid growths and infiltrative and/or ulcerative
adenocarcinomas. Adenomatous polyps are raised, broad
based, sessile, multiple or focal lesions of varied shapes and
sizes. Some rectal polyps invade the muscularis mucosa
histologically. In these instances, the polyp is regarded as
carcinoma in situ. Both, rectal polyps (adenomas) and adenocarcinomas can grow relatively slowly. Progressively intensifying clinical signs (tenesmus, dyschezia, hematochezia) over a period of several months or more, often are
part of the case history. Canine rectal polyps may be regarded as precancerous.
Adenocarcinomas feature a variety of growth patterns,
including proliferative, friable masses that fill the rectal lumen, and tumors that infiltrate the rectal wall, resulting in
stricture. In these latter cases a fibrotic annular (napkin)
ring can be digitally palpated or detected on positive contrast
radiography.
Signs - The primary clinical sign is hematochezia. Digital
rectal examination, proctoscopy and positive contrast (barium) radiographic studies usually are diagnostic. Infiltrative
and anaplastic carcinomas bear a very poor prognosis. Thus,
in cases suggestive of rectal cancer, a biopsy and thorough
clinical staging is recommended prior to surgical treatment.

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4th European FECAVA SCIVAC Congress

318

Treatment - Surgical treatment of invasive tumors circling the rectum usually (but not always) is only palliative as
these tumors frequently have metastasized to sublumbar
lymph nodes or beyond by the time of surgery12. In locally
confined rectal tumors, radical excision, following prior
biopsy, is recommended. Depending on location, size and
extent, an intraluminal or a pararectal approach, with or
without pelvic symphysiotomy or pubic triple osteotomy,
can be employed. Resection of histologically confirmed malignant tumors usually requires a trans-pelvic or pararectal
(dorsal) approach to maximize surgical exposure7. Despite
attempts to preserve the sphincter mechanism, fecal incontinence frequently is seen as a sequel to extensive rectal resection1. Sometimes, incontinence is transient. Severe
anorectal stricture, or a combination of stricture and incontinence might develop postoperatively. Thus, results of treatment are variable. In a study of 78 cases, the mean survival
time of dogs with colorectal carcinoma was 15 months without treatment and 22 to 24 months after surgical excision,
while other investigators report considerably shorter survival times2. In cases with infiltrative anaplastic rectal
carcinomas and annular lesions the prognosis is very poor.
Anal and rectal prolapse: straining to defecate or urinate
and any irritative lesion of the lower intestinal tract can
cause anal and/or rectal prolapse. Prolapse occurs most frequently in malnourished pups and kittens with intestinal
parasitism. In animals of any age, rectal and/or anal prolapse
also can occur in association with dystocia, prostatic disease,
perineal hernia (especially immediately after its repair), rectal neoplasia, rectal foreign bodies etc. The difference between anal and rectal prolapse is a matter of degree. In anal
prolapse, only anal mucosa, engorged and edematous, protrudes. In cases of rectal prolapse an oblong, cylindrical
mass, with a dimple, marking the reflecting rectal wall, protrudes from the anus.
Diagnosis - Rectal prolapse must be differentiated from
prolapsed intussusception. In the latter, a probe can be inserted and advanced far craniad into a circular space in between the cylindrical mass and the anal perimeter. In anal or
rectal prolapse, the probe cannot be inserted deep to the
anus, lateral to the tubular mass. Prolapsed mucosa is not appreciably sensitive to pain perception by superficial irritation. Thus, automutilation as well as necrosis of mucosal
surfaces often occur.
Treatment - Treatment should include elimination of
causes (e.g., antiparasitic therapy, improved nutrition, etc.),
in addition to reducing the prolapsed rectum or anus. After
reduction of an anal mucosa prolapse, a purse-string suture
can placed around the anus tight enough to avoid recurrence
but loose enough to allow defecation of soft feces. The purse
string sutures can be left in place for up to one week. In cases of repeated recurrence or severe swelling, the protruding
mucosa can be trimmed surgically. For rectal prolapse, the
tubular structure usually can be reduced manually. In cases
with severely damaged or necrotic prolapsed tissue, resection of the protruding mass may be necessary. Colopexy is
recommended to prevent future prolapse when an extensive
recurrent prolapse of healthy tissue has occurred. In cases of
prolapsed intussusceptions, no attempts should be made to
reduce the protruding mass per anus. Reduction should be

4th European FECAVA SCIVAC Congress

executed via an emergency laparotomy.


Rectal diverticulum: occurs unilaterally or bilaterally in
the caudal rectum of dogs. Almost always, these lesions are
seen in old male dogs in conjunction with perineal hernia,
due to breakdown of muscular support. Very rarely, diverticula may occur without apparent perineal herniation. Anal
sphincter musculature and rectal muscularis mucosae become atrophic and muscle fibers are separated by bulging of
the rectal mucosa.
Signs - Tenesmus, chronic constipation and fecal impaction. When rectal diverticula are chronically impacted
with fecal material, surgical repair should be attempted.
Treatment - Surgical treatment via pararectal approach.
In nearly all cases, the diverticulum is merely inverted into
the rectum, without opening the rectal lumen, and the defect
in the musculature is closed with absorbable sutures. If, during dissection, the lumen is entered, a Penrose drain is
placed to drain the wound. When the external and internal
anal sphincters are severely affected, such as in cases of coexisting perineal herniation and/or when megacolon exists,
the procedure is unlikely to restore normal defecation. In
general, surgical reduction will only be attempted when
large rectal deverticula are encountered during the repair of
a perineal hernia.
Perineal hernia: occurs spontaneously and almost exclusively in intact male dogs with animals between 7 and 13
years at highest risk6. Only a few cases are reported in older
males that were castrated during their first year of life, or in
female dogs or in cats. In affected animals, an idiopathic
process, probably associated with a hormone imbalance,
weakens progressively connective tissues and muscles of the
pelvic diaphragm. Neither testosteron nor estrogen-progesteron seem primarily responsible for the development of hernias, despite the fact that castration reduces the incidence of
recurrence after surgical repair. Nearly all dogs with perineal
hernia present with cystic prostatic hypertrophy. Recently,
the hypothesis of a relaxin-related pathogenesis was advanced by the author9. It was shown that relaxin is produced
in canine prostates; it might be that hypertrophic prostates
produce excess levels of relaxin which in turn might progressively weaken the pelvic diaphragm. Subsequently,
pelvic and abdominal structures and organs, lacking support,
herniate through the pelvic canal and lodge in subcutaneous
perineal pouches. Perineal herniae can be unilateral, bilateral or, less commonly, circumferential (in relation to the
anus). In cases with unilateral perineal hernia, the later appearance of a hernia on the opposite site is likely. Herniae
usually contain some peritoneal fluid and characteristic fluid or fat-filled cysts, linked to the prostate. In severe cases,
prostate, bladder and occasionally intestines can herniate
and incarceration or strangulation can occur. The herniated
tissues follow a route that is usually medial to the coccygeus
muscle and lateral to the rectum, either lateral between the
coccygeus and the levator ani muscle or medial between the
levator ani muscle and the rectal wall, coccygeoanalis muscle and the sphincter externus muscle, and the internal obturator muscle ventrally. The loss of lateral support to the rectal wall causes rectal deviation (rectal flexure), or rectal
sacculation (rectal diverticulum).
Treatment - Several surgical techniques have been de-

scribed for repair of perineal hernias. None of the methods


is free of failures, since herniorrhaphy techniques rely on suturing and healing of tissues that are affected by a degenerative process. The repair technique using the transposition of
the internal obturator muscle, has the lowest rate of
complications (less than 10%) compared to other described
procedures5. Castration of male dogs at the time of hernia repair is recommended strongly13.
Post-operative complications may include: infection of the
hernial region due to intraoperative contamination (proximity
of the surgical field to the anus); if the sacrotuberous ligament
is employed in the closure and sutures have been placed too
deep, inadvertent partial or complete ligation of the sciatic
nerve may occur; if the pudendal nerve is inadvertently severed (especially if the nerves are damaged bilaterally), fecal
incontinence will develop. Rectal prolapse may occur in animals intensively straining to defecate. Appropriate surgical repair and castration is curative in over 90% of cases.

319

3.

4.

5.

6.

7.

8.

9.

10.

References
1.

2.

Anderson GI, McKeown DB, Partlow GD, Percy DH, (1987), Rectal
resection in the dog - a new surgical approach and the evaluation of
its effect on fecal continence, Vet Surg 16:119-125.
Church EM, Melhaff CJ, Patnaik AK, (1987), Colorectal adenocarcinoma in dogs: 78 cases (1973-1984), J Am Vet Med Assoc,

11.
12.

13.

191:727-730.
Ellison GW, Bellah JR, Stubbs WP, vanGilder J, (1995), treatment of
perianal fistulas with ND:YAG Laser - results in twenty cases, Vet
Surg, 24:140-147.
Goring RL, Birght RM, Stancil ML, (1986), Perianal fistulas in the
dog - retrospective evaluation of surgical treatment by deroofing and
fulguration, Vet Surg, 15:392-398.
Hardie EM, Kolata RJ, Earley TD et al., (1983), Evaluation of internal obturator muscle transposition in treatment of perineal hernia in
dogs, Vet Surg, 12:69-72.
Hayes HM, Wilson GP, Tarone RE, (1978) The epidemiologic features of perineal hernia in 771 dogs, J Am Anim Hosp Assoc,
14:703-707.
McKeown DB, Cockshutt JR, Partlow GD, Kleer de VS, (1984), Dorsal approach to the caudal pelvic canal and rectum - effect on normal
dogs. Vet Surg, 13:181-184.
Niebauer GW, (1993), Rectoanal disease, In: Bojrab MJ, Disease
mechanisms in small animal surgery, 2nd ed, Lea&Febiger, Philadelphia, 271-286.
Niebauer GW, (1991) The potential role of relaxin in canine perineal
hernia, Proceedings, Federation of American Societies for Experimental Biology, 75th annual meeting, Atlanta, GA.
Penwick RC, (1988), Perioperative antimicrobial chemoprophylaxis
in gastrointestinal surgery, J Am Anim Hosp Assoc, 24:133-145.
Vasseur PB, (1984), Results of surgical excision of perianal fistulas
in dogs, J Am Vet Med Assoc, 185:60-62.
White RAS, Gorman NT, (1987), The clinical diagnosis and management of rectal and pararectal tumours in the dog, J Small Anim Pract,
28:87-107.
Wilson GP, Hayes HMJr, (1979), Castration for treatment of perianal
gland neoplasms in the dog. J Am Vet Med Assoc, 174:1301-1303.

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4th European FECAVA SCIVAC Congress

321

Clinical interpretation of ocular hemorrhages


Claudio Peruccio
Med Vet, Dipl ECVO
University of Torino - Department of Animal Pathology - Italy

Ocular hemorrhages are among the most frustrating


problems presented to the veterinary ophthalmologist.
They can be secondary to eye diseases such as glaucoma, uveitis, retinal detachment, trauma, eye surgery etc. or
the consequence of systemic diseases (i.e infection, toxicity,
neoplasia, vasculopaties, coagulopathies, immuno-mediated
disorders etc..).
The origin of vascularization in the different anatomical
sites where ocular hemorrhages can occur, their characteristics and evolution will be discussed. The differential diagnosis and treatment will be considered.

Origin of vascularization in the


different anatomical sites where ocular
hemorrhages can occur, their
characteristics and evolution
Among the domestic animals, the main supply of blood
to the eye and orbit is the internal maxillary artery (as a
branch of the external carotid artery) which after passing
through the alar canal, branches to give rise to the external
ophthalmic artery1.
The internal ophthalmic artery, a branch of the internal
carotid artery, is relatively small and less important than in
primates where it provides most of the circulation of the eye.
The venous drainage varies among the different species
and is mainly via the superior and inferior orbital veins.

If they are the consequence of trauma, their evolution depends upon the entity of tissue damage.

Cornea
Being avascular the cornea has no potentiality to develop
hemorrhages; just in case of keratitis a small collection of
blood can occasionally be localized within the corneal tissue.

Anterior chamber
Most intraocular hemorrhages are localized in the anterior chamber causing the so cold hyphema.
In many instances clotting is reduced by dilution of the
blood by aqueous and the release of plasminogen activator
by the surface of the iris. Unclotted blood sediment and exits via the filtration angle3.
When reabsorption doesnt occur in 3-4 days, the cause
of bleeding persists.
Sometime clotting occurs, depending on the cause of hyphema, and all the anterior chamber can be completely filled
by clotted blood. This is a more frequent finding when the
cause of hyphema are trauma, iridocyclitis and intraocular
neoplasia; it does not occur in autoimmune trombocitopenia
and in dicoumarin toxicity.
Hyphema is a common finding after trauma, severe iritis,
infectious diseases, anemia, trombocitopenia, hypertension,
retinal detachment, intraocular neoplasia, complications
during and after surgery, clotting disorders and chronic glaucoma3,5,6,7.

Conjunctiva
Conjunctival petechia and hemorrhages are a frequent
finding due to the extensive capillary network.
Conjunctival arteries come from the superficial temporary artery, the anterior ciliary artery and the malar and palpebral arteries2. Venous drainage is through the palpebral and
malar veins to the facial vein and from the angularis oculi
vein to the orbital plexus and superficial temporal vein2.
Around the limbus deep and superficial blood vessels
anastomose with each other.
Blood can easily diffuse within the conjunctiva giving
rise to apparently serious clinical situations that can disappear in one -two weeks.

Uvea
The uveal tract is the most vascularized ocular structure
and for this reason, it is the area of origin of most intraocular
hemorrhages. It is composed of iris, ciliary body and choroid.

Iris
The iris vasculature is composed of a major arterial circle from which the many vessels extend radially toward the
center and the periphery of the iris8.

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Summary

322

The major arterial circle is formed by two arteries that


originate from the lateral and medial long posterior ciliary
arteries; at the medial periphery of the ciliary zone each
artery branches superiorly and inferiorly to pass circumferentially toward the opposite artery.
Radial vessels passing retrograde anastomose with the
short posterior ciliary arteries and one another to form a
functional arterial circle; in the dog radial arteries to the
pupil poorly develop transverse anastomosis, so a minor arterial circle does not exist2,8.
The thick capillary network favours both bleeding and
reabsorbtion of blood; in the final stages the color of the iris
changes and is usually dark.

Ciliary body
The blood supply of the ciliary body is derived from the
two long posterior ciliary arteries and the anterior ciliary arteries that undergo several divisions which anastomose to
form the major arterial circle located either in the base of the
iris or anterior ciliary body8.
The vasculature of the ciliary processes is primarily supplied by the major arterial circle; in carnivores there is a well
developed capillary bed responsible for aqueous production.

Choroid
The choroid is composed mostly of large veins and scattered arteries.
Externally to internally the choroid can be divided into:
- large vessel layer with few arteries, mostly branches of the
short posterior ciliary arteries (to a lesser extent the
choroid also receives blood from the long posterior ciliary
arteries and the anterior ciliary arteries9 and many large
veins that merge centripetally into four or more prominent
vortex veins8;
- medium-sized vessel and tapetum layer: the vessels are
emissaries between a single sheet of capillaries and the layer of large blood vessels8;
- choriocapillaris, a thin layer of fenestrated capillaries.

Vitreous
The vitreous body in normal conditions is avascular and
hemorrhages can invade it if bleeding occurs in the surrounding structures (retina and uvea) or from the persistent
and patent hyaloid system in PHTVL cases.
According to their localization vitreous hemorrhages can
be classified into subvitreal (subhyaloid or preretinal) and
intravitreal hemorrhages1.
Preretinal hemorrhages are located in the space between
the posterior face of the vitreous body and the internal limiting membrane of the retina and they often have a boat
keel conformation due to the force of gravity.
Intravitreal hemorrhages can be concentrated regionally
into strands or sheets or diffused in the vitreous body1.
Resolution of intravitreal hemorrhages often takes sever-

4th European FECAVA SCIVAC Congress

al months and fibrous membranes can be found as a sequela;


traction on the retina and retinal detachment can follow.
Vitreous degeneration following vitreal hemorrhages can
cause syneresis and synchisis scintillans1. The main cause of
vitreal hemorrhages are trauma, retinal detachment, Collie
eye anomaly, retinal dysplasia, PHTVL, preretinal vascular
loops, retinal vasculopaty, retinitis, uveitis, chronic glaucoma, intraocular neoplasia, hemorrhagic systemic diseases,
toxicosis, hypertension.

Retina
Retinal arterial supply in domestic animals is via the
short posterior ciliary arteries (cilio-retinal arteries)8. At the
periphery of the optic disc they originate the cilioretinal arterioles, usually three in the cat and about 20 in the dog. A
very well developed capillary network provides nourishement to the inner retina, extending to the inner nuclear layer.
Four main factors can play a key role in the pathogenesis of retinal hemorrhages:
- the blood pressure within the vessels;
- the state of the circulating blood;
- the state of the vessel wall;
- the height of the extravascular / intra-ocular pressure.
It is probably exceptional for one single factor to be responsible, but there are cases in which for example elevation
of the blood pressure alone may be sufficient to cause hemorrhages from presumably healthy vessels.
When hemorrhage has coincided with a sudden rise of
blood pressure, the latter is the only or at least the principal
cause of the bleeding; whereas in cases where there has been
a slowly established pressure rise, the pressure element is of
comparative insignificance10.
In renal disease with general hypertension all the first
three factors are present.
Clinically, it is important to determine whether the
source of the retinal hemorrhage is to be found in the arterioles, the capillaries or the venules and in which retinal layer
it is located. The clinical appearance of retinal hemorrhages
varies according to the site of the extravasation of the blood.
They are usually most numerous centrally where the retina
is thickest and the capillary circulation is more complex
than in the periphery.
It is to be remembered that the vessels do not penetrate
more deeply than the external nuclear layer, the outer layers
being avascular. Therefore hemorrhages are confined to the
inner layers of the retina unless effusion of blood is large
enough to plough up all the tissues.
We commonly divide hemorrhages in pre-retinal, retinal
or sub-retinal according to their distribution.
Pre-retinal hemorrhages appear as dark-red masses, often initially circular in shape but tending to sink owing to the
action of gravity, assuming the shape of a boat-keel.
Retinal hemorrhages have different patterns according to
the layer where they occur.
If they have a striate character they must belong to the
nerve fiber layer or lie between that layer and the internal
limiting membrane.
Hemorrhages occurring within the loose retinal tissue

4th European FECAVA SCIVAC Congress

tend to assume the round droplet form natural of a free fluid; more often they are located externally to the inner nuclear layer, extending to the outer nuclear layer. Ophthalmoscopically they appear as dot and blot hemorrhages.
Sometimes they show other patterns, stellate and reticular for example, which indicate that the blood is at liberty to
wander horizontally among the vertically disposed neural
and supporting fibres.
Subretinal hemorrhages between the choriocapillaris and
the retinal pigment epithelium, are choroidal in origin; they
are dark red in color dimmed by the greyish bloom caused by
the overlying retina, they are usually rounded, raised and often extensive; over them the retinal vessels pass unaffected.

323

In intraocular surgery hemorrhage is a possible complication.


Coumarin derivatives and prostaglandin inhibitors can
affect hemostasis and cause intraocular hemorrhage.
V vasculopathies and other bleeding disorders
Vasculopaties are potential cause of ocular hemorrhages
as in hyperviscosity syndromes or hypertension. Hypertension per se is not so important in the pathogenesis of intraocular hemorrhage that can start a long time after the pressure
rise if and when concomitant vascular lesions are present at
the arterioles, venules, precapillary and capillary level10.

Causes of ocular hemorrhages


From the etiological point of view, to make a complete
differential diagnosis in case of ocular hemorrhages, we can
adopt the acronim DAMNITV.
D degenerative diseases
Coagulopaties can be secondary to hepatic degenerative
processes and a possible clinical sign are ocular hemorrhages.
Degenerative processes affecting the kidney can cause
hypertension and retinal hemorrhages.
A anatomical, congenital defects
Collie Eye Anomaly (CEA) and retinal dysplasia are
common causes of retinal detachment and secondary intraocular bleeding. The eye can be completely filled by blood.
M metabolic diseases
Diabetes mellitus is the main cause of retinal vasculopathy in man, causing microaneurisms, neovascularization and
hemorrhages.
Diabetic retinopathy has been described in the dog,
mainly caracterized by microaneurisms; the lesions can be
observed in histologic sections, but ophthalmoscopic findings are unusual.
N neoplasia
Primary or metastatic intraocular tumors are a possible
cause of hemorrhage.
Intraocular hemorrhages can be secondary to neoplasia
localized at different sites in the body when they cause coagulopathies (liver neoplasia), hypertension (feocromocitoma), anemia (many tumors), hyperviscosity syndrome
(myeloma), disseminated intravascular coagulopathy (paraneoplastic syndromes).
I inflammatory, infectious, immunomediated disases
Uveitis of any origin is a common cause of intraocular
hemorrhage.
Severe inflammatory processes affecting several organs
in the body (i.e. pancreatitis), can cause coagulopathies and
secondary intraocular hemorrhages.
Infectious diseases as rickettsiosis and leptospirosis in the
dog and infectious peritonitis in the cat or infestive diseases as
leishmaniosis are possible cause of intraocular hemorrhages.
Immunomediated diseases as autoimmune thrombocytopenia can have the same effect.
T diseases secondary to trauma and toxicity
Direct or indirect trauma to the eye can cause intraocular
bleeding, usually only in one side.

The treatment depends upon the cause of bleeding. The


animal must be kept quiet, if necessary by administering
tranquilizers. When necessary, symptomatic treatment is applied; anti-inflammatory drugs, mydriatics, miotics, tPA are
the possible choice.
The use of mydriatics and miotics is controversial and of
no proven value1,3:
- atropine 1% - cycloplegic action will reduce filtration angle outflow, therefore increasing danger of glaucoma, but
is important in the treatment of anterior uveitis3;
- pilocarpine 1%, maintains filtration angle outflow. Miotic
action increases the iris surface, enhancing fibrinolysin activity, but increasis the risk of posterior synechia3;
- intraocular tissue plasminogen activator (tPA) 25 micrograms, will dissolve clots and fibrin but, if the cause is not
removed, rebleeding is likely3;
- anti-inflammatory topical corticosteroids can be used in
case of uveitis. For the same reason prostaglandin inhibitors could be useful, but their use is not advised because many of them also prolong blood clotting7.

References
1.
2.
3.
4.

5.
6.
7.
8.

9.

10.
11.

K.N. Gelatt - Veterinary Ophthalmology - Lea & Febiger, Philadelphia, 1991.


Peruccio C. - Atlante di oftalmologia veterinaria - Edizioni Medico
Scientifiche, Torino, 1985.
Severin G.A. - Severins Veterinary Ophthalmology Notes - Severin
Edit., 1996.
Stades F.C., Wyman M., Boeve M.H., Neumann W. - Ophthalmology for the Veterinary Practitioner - Schlutersche GmbH & Co.KG,
Verlag und Druckerei, Hannover, 1998.
Barnett K.C., Crispin S.M. - Feline Ophthalmology - W.B. Saunders
Company Ltd, 1998.
Walde I., Schaffer E.H., Kostlin R.G. - Atlas of Ophthalmology in
Dogs and Cats - B.C. Decker Inc. Toronto, 1990.
Slatter D. - Fundamentals of Veterinary Ophthalmology - W.B. Saunders Company, Philadelphia, 1990.
Prince J.H.,Diesem C.D., Eglitis I., Ruskell G.L. - Anatomy and Histology of the Eye and Orbit in Domestic Animals - Charles C.
Thomas, Springfield Ill.USA,1960.
Torczynski E. - Choroid and Suprachoroid - In Biomedical Foundations of Ophthalmology, Vol.1, T.D. Duane and E.A. Jaeger Edit.,
Philadelphia, J.B. Lippincott, 1988.
A.J. Ballantyne, I.C. Michaelson -Textbook of the fundus of the eye
- E. & S. Livingstone, Edinburgh, 1970.
L.F. Rubin - Atlas of Veterinary Ophthalmoscopy - Lea & Febiger,
Philadelphia, 1974.

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Treatment

4th European FECAVA SCIVAC Congress

325

The eye in the ageing animals


Claudio Peruccio
Med Vet, Dipl ECVO
University of Torino - Department of Animal Pathology - Italy

As the years pass the tissues of the eye undergo ageing


processes which are similar to those which take place in other parts of the body
The risk of functional deterioration of the eye is increased by the concentration in a single small organ of various structures which are functionally interdependent on
each other.
It is very important that the vet is able to recognise the
clinical signs which are related to ageing of the ocular
structures, interpret them, explain the pathogenetic mechanism to the owner in simple terms and, above all, to make a
correct choice of therapy when there is one.

Changes in the eyelids


Neoplasms
Tumors on the eyelid margins are fairly common in elderly dogs, especially adenomas or sebaceous adenocarcinomas of the meibomian glands. Early and radical excision by
simple wedge resection is necessary in order to avoid having
to operate on larger masses requiring more complicated
surgery.
It is possible to remove up to 1/3 - 1/4 of the eyelid margin depending on the conformation of the palpebral fissure
and obtain a good repair. More extensive tumors require blepharoplastic with sliding skin grafts1.
Chronic blepharitis
Complicated chronic inflammatory processes can give
rise to the formation of pyogranulomas with marked deformation of the eyelid margin.
The involvement of the meibomian gland encourages the
formation of styes, tarsal cysts and chalazions and lead to
abnormal meibom secretion with a subsequent qualitative
tear deficiency1.
Treatment consists of hot compresses and antibiotics applied to the site of the lesion, if necessary. Once any infection has been eliminated, an antibiotic and cortisone combination should be applied locally in the form of eye solution
or ointment either to the fornix or the eyelid margin.
Massaging the eyelid margin 2-3 times a day for 10-15
days can also be very useful.

Changes in the tear film


and its distribution
It is fairly common for production of lacrimal fluid to decrease in elderly animals causing conjunctivitis and keratitis.
It is possible to measure tear production by using the
Schirmer Tear Test (STT); values below 9 mm/minute are
regarded as inadequate and establish a diagnosis of KCS2,
one of the most common condition in elderly dogs.
There are many causes of this condition resulting in reduced function or complete destruction of the lacrimal gland
tissue (idiopathic, immuno-mediated, neurogenic, hypothyroidism, lacrimotoxic drugs as phenazopyridine, sulphadiazine, sulphasalazine etc..).
The classical treatment is replacement therapy consisting
of instillation of artificial tears many times through the day,
in addition to antibiotic base eye ointments in cases of infection and corneal ulceration; corticosteroids are used in selected cases to control the inflammatory process, but may be
contraindicated by the presence of corneal ulceration which
are not always easy to distinguish.
One - two drops of pilocarpine may be administered
morning and evening with food in an attempt to induce
lacrimation, bearing in mind that this drug is toxic.
The most effective drug for treatment of KCS is now cyclosporine, available as a 0,2% eye ointment (Optimmune Schering Plough) or prepared in 1% suspension in corn oil3
applied twice a day.
In most cases tear production increases within a few
weeks, but if it not succesful the treatment should be continued as long as 12 weeks before giving up.
The Schirmer tear test should be performed on a regular
basis and additional symptomatic treatment may be necessary.
In a short term clinical field trial on the efficacy of cyclosporine eye ointment 80% of cases improved3.

Changes in the cornea


Corneal changes secondary to chronic irritation
In some elderly dogs, eyelid closure and distribution of
the precorneal tear film are not adequate and, in the parts
which are more exposed to ambient stimuli, the cornea can
become opaque.
This is the result of the incomplete protection of the eyelid and the tear film; clinically a slight opacity is observed in

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Summary

326

that area, with pigmentation and sometimes vascularization.


It is important to establish the cause of this change, when
possible, to prevent further deterioration.
Schirmer Tear Test should always be performed. In any
case the administration of artificial tears is indicated, to protect the cornea.
Mineralization of the cornea or superficial corneal dystrophy in the elderly dog, so called calcific keratopathy4,5.
In dogs of advanced age,usually between 13 and 18
years4, mineralization of some superficial areas of the cornea
can be observed, with calcium deposits in the superficial
stroma and in the subepithelial sector. The phenomenon may
be unilateral or bilateral.
In the initial stages the animal does not appear to be troubled but gradually, as the deposits increase in size and thickness, ulcers can appear and the eye becomes painful.
A chelating agent such as EDTA is used, initially every
2-4 hours, then 1-2 times a day. If a suitable
eye solution is not available, it is possible to dilute 1 ml
of ethylenediaminetetraacetic acid (EDTA) in 15 ml of artificial tears solution4.
In severe cases special attention should be paid to treatment of ulcers and uveitis; if treatment fails and the ulcers
persists, lamellar keratectomy must be performed.
Changes in the cornea following endothelial diseases5
The main functions of the corneal endothelium are the
maintenance of corneal transparency; it acts as an active
pump to dehydrate the stroma and as a barrier to prevent
penetration of the aqueous humour. If a certain number of
endothelial cells lose their function, the cornea hydrates, assuming a blue colour. This situation can occur in elderly
dogs when the corneal endothelium has been damaged as a
result of anterior uveitis (iridocyclitis), glaucoma, intraocular surgery, trauma etc.
Ageing by itself causes loss of cells and the number of
functioning cells can be inadequate for maintaining a state of
normality.
In some breeds of dogs (e.g. the Boston terrier, the Chihuahua etc..) another possible cause is endothelial dystrophy
of hereditary origin5.
Fluid within the corneal stroma may coalesce resulting in
bullous keratopathy with subsequent ulceration.
There is no reliable effective treatment: hyperosmotic
agents can be used to attract fluid from the cornea towards
the exterior; improvement in transparency is only temporary; only functional renewal of the endothelium can
change the situation.
Therapeutic soft lenses or collagen lenses can be used
when there are complicating corneal erosions.
A recent study has demonstrated the efficacy of thermokeratoplasty in the management of these situations6.
Recurrent superficial corneal erosions
These are more common in elderly dogs but not exclusively so; they may be secondary to the corneal edema described earlier, repeated trauma (e.g. through trichiasis, defects in the eyelid etc..), complicated by infection or following dystrophy of the epithelium and basement membrane (E-

4th European FECAVA SCIVAC Congress

BM-D), more frequently seen in Boxer dogs5. Healing is


slow and inadequate.
In all cases the objective of treatment should be to eliminate the cause of ulceration and to avoid complications. In
E-BM-D the margins of the epithelium do not adhere to the
basement membrane, need to be excised and debrided. If
necessary a grid or stippled keratotomy may be performed to
encourage subsequent epithelial adhesion.
Other treatment regimes used by veterinary ophthalmologists include therapeutic soft contact lenses, cyanoacrylate
adhesive, epithelial growth factors, aprotinin, conjunctival
flaps and stromal keratectomies5,7.

Changes in the uvea


Iris
In elderly dogs, especially small dogs and in particular in
the miniature French poodle, varying degrees of atrophy of
the iris are often observed with resultant changes in the diameter of the pupil and anisocoria1,4.
The sphincter muscle atrophies, the stroma iridis becomes thinner and, when retroilluminated, the fine iris network can be seen.
Ciliary body
A number of age related changes occur in the ciliary
body: the basement membrane of the non-pigmented and
pigmented epiteliums thicken greatly and have a multilaminar appearance8.
Also the stroma of the ciliary body thickens while the
non-pigmented epithelium thins and the degree of pigmentation of the pigmented epithelium lessens8.

Changes in the iridocorneal angle


Also the iridocorneal angle changes with age; these
changes appear to reduce the area available for aqueous humor outflow and might make older individuals more susceptible to any kind of insult that could lead to glaucoma8.

Changes in the lens


Senile sclerosis4
In the dog, as in other animals, the lens becomes more
dense with time. Throughout the animals life-time, lens fibres produced from the lens epithelium at the equator converge towards the centre substantially increasing the size of
the nucleus.
The nucleus becomes more dense with gradual changes
in the optical characteristics from the age of 6-7 years.
Senile sclerosis is frequently misdiagnosed as cataract.
When the ophthalmoscope is used correctly the back of
the eye can be very clearly observed through the dense nucleus and it is possible to exclude the presence of a nuclear
cataract.

4th European FECAVA SCIVAC Congress

Changes related to eye diseases


Glaucoma is one of the main causes of blindness in the
dog; the retinal changes induced by the presence of glaucoma can occur early but in case of chronic glaucoma complete blindness is often present in aged animals.
Vitreous syneresis can be an age related problem and is
a possible cause of retinal detachment.

References
1.
2.

Changes in the vitreous

3.

Asteroid hyalosis
Asteroid hyalosis is characterized by small, round bodies
composed of a calcium-lipid complex suspended in the vitreous humor. This condition occurs principally in old dogs9.

4.

Vitreous syneresis
Syneresis refers to an irreversible degenerative process
of the vitreous that is characterized by liquefaction.
Vitreous syneresis is seen occasionally in older dogs but
its incidence is low10.

5.
6.

7.

8.
9.

Changes in the retina

10.

Changes related to systemic diseases


Many systemic diseases may involve the retina and their
effects are more likely to be seen at a certain age.
Systemic hypertension may cause retinal detachment and
hemorrhage11,12; the main cause are renal failure, hypothyroidism and hyperviscosity syndromes.

11.

12.

P.J. Smith - Geriatric Ophthalmology - ASVO Proceedings March


1993.
F.C. Stades, M. Wyman, M.H. Boeve, W. Neumann - Ophthalmology for the Veterinary Practitioner - Schlutersche GmbH & Co.
KG,Verlag und Druckerei, Hannover, 1998.
ESVO & ECVO proceedings, Sept. 1994 - Cyclosporine, veterinary
applications in ophthalmic disease.
C.A. Fischer - Geriatric Ophthalmology - Vet. Clin.North Am. S.A.P.,
19, I, January 1989, 103-123.
K.L. Ketring - The aging canine cornea - ASVO proceedings, San
Diego, March 1997.
C.J. Murphy, T. BurlingS. Hollingsworth - Thermokeratoplasty for
the treatment of chronic bullous keratopathy in the dog - ACVO proceedings, October 1993, 21.
R.V. Morgan, K.L. Abrams - A comparison of six different therapies
for persistent corneal erosions in dogs and cats - V.C.O. 4, 1, 38,
1994.
B.K. Collins, C.P. Moore - Canine anterior uvea. In Veterinary Ophthalmology, K.N. Gelatt, edit, Lea & Febiger, Philadelphia, 1991.
L.F. Rubin - Asteroid Hyalosis in the dog -Am. J. Vet. Res. Nov.
1963, 1259-1261.
R. Curtis, K.C. Barnett, A. Leon - Diseases of the canine posterior
segment. In Veterinary Ophthalmology, K.N. Gelatt, edit, Lea &
Febiger, Philadelphia, 1991.
R.M. Gwin, K.N. Gelatt, T.G. Terrell, C.I. Hood - Hypertensive
retinopathy associated with hypothyroidism, hypercholesterolemia
and renal failure in a dog - J.A.A.H.A., 14, March/April 1978, 200209.
J. Sansom, K.C. Barnett, K.A. Dunn, K.C. Smith, R. Dennis - Ocular disease associated with hypertension in 16 cats - JSAP 35, 604,
1994.

MAIN PROGRAMME

Cataract1,4
The term cataractrefers to any opacity of the lens.
Vets frequently diagnose senile cataract in elderly dogs,
but the true incidence of its occurrence is not known because
there are many causes of opacification of the lens and very
often a localized but progressive cataract remains undetected for years. The opacity will become more evident with advancing age.
Surgical treatment of cataracts, including senile cataract,
has in recent years undergone the same evolution as in human
medicine; in each case a veterinary ophthalmologist should
evaluate the risk-benefit ratio and the presence of contraindications to make a correct selection of animals to be treated.

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329

Recent advances in the understading of generalised


progressive retinal atrophy
S.M. Petersen-Jones

Summary
The generalised progressive retinal atrophies (PRAs) are
a group of inherited primary photoreceptor and are a leading cause of blindness in pure-bred dogs but are less important in cats. Most forms are recessively inherited although
an X-linked form exists in dogs and a dominant form in the
Abyssinian cat. Recently advances in molecular techniques
have allowed the identification of gene defects causal for
two forms of PRA in the dog and led to the identification of
linked DNA markers for two other forms.
Rod cone dysplasia type 1 (rcd1) in the Irish setter was
found to be caused by a mutation in the gene encoding the beta subunit of cGMP phosphodiesterase. This led to a break
down in the phototransduction cascade in the rod cell and an
accumulation of the final substrate cGMP probably triggers
programmed cell death (apoptosis) of photoreceptors. A mutation in the alpha subunit of the same protein has recently
been implicated in PRA in the Cardigan Welsh corgi.
Linkage of genetic markers to the genes for progressive
rod cone degeneration (prcd) and early retinal degeneration
(erd) have been recently reported. Prcd is numerically the
most important form of PRA affecting miniature and toy
poodles, English and American cocker spaniels, the
Labrador retriever and the Portuguese water dog. A linkage
test for prcd will be a great step forward in the eradication
of PRA.

The generalised progressive retinal atrophies (PRAs) are


a group of inherited primary photoreceptor diseases which
result in similar clinical signs and ultimately lead to blindness. One recent survey listed 108 different breeds of dog as
suffering from PRA, although in many breeds the condition
has not been investigated. PRA is also recognised in cats although in far fewer breeds than in dogs.
Attempts are being made to develop genetic tests for
PRA which can identify which animals will become affected (important for the later-onset forms) and will detect carriers of the recessively inherited forms of PRA. These investigations have used two main approaches, the first has
been to make an educated guess, on the evidence, available
which gene could be abnormal and then screen that gene for
mutations. This is the candidate gene approach. The second
approach has been to use genetic markers to try and find a
marker which is linked to the disease gene. Recent collabo-

rations to map the dog genome have resulted in markers suitable for this purpose in the dog. A closely linked marker
could potentially be used to test for the presence of the disease gene. Both approaches have already had some success
in investigations of canine PRA, but there is still a lot of
work to be done.

Clinical signs
PRA initially causes night blindness, followed by a progressive loss of daytime vision until the affected animal is
totally blind. The age at onset of night blindness, and the rate
of progression of vision loss, varies both between and within the different forms of PRA.
Regardless of the form of PRA the ophthalmoscopic
signs are similar. The funduscopic changes result from thinning of the neuroretina, loss of ganglion cell axons, reduced
blood supply to the degenerating retina and pigmentary
changes involving the retinal pigment epithelium. The initial
ophthalmoscopic signs are often a granular appearance to
the peripheral tapetal fundus which then progresses into a
generalised tapetal hyperreflectivity. In some dogs radial
bands of variable reflectivity appear at the periphery of the
tapetal fundus, possibly due to variation in tapetal topography due to grooving from underlying choroidal blood vessels. Concurrent with retinal death and thinning, the superficial retinal blood vessels become attenuated. Initially the
smaller arterioles become more difficult to visualise and
then as the condition progresses larger vessels are obviously
thinned. The panretinal atrophy is accompanied by depigmentation in the nontapetal fundus resulting in a grey colour
to the fundus (originally described as pavement grey) with
interspersed areas of pigment clumping. The loss of the centrally projecting axons of the ganglion cells results in an obvious atrophy of the optic nerve head. This change is less obvious in cats.
Secondary changes include a reduction in the pupillary
light response and in dogs secondary cataract formation.
Secondary cataracts do not develop in cats with PRA.

Functional changes in the neuroretina


Electroretinography, the measurement of electrical activity from the retina resulting from light stimulation, is a sen-

MAIN PROGRAMME

DVO, Dipl ECVO, MRCVS


Department of Small Animal Clinical Sciences
College of Veterinary Medicine
Michigan State University, East Lansing - USA

330

sitive measure of generalised retinal function and in many


forms of PRA is useful for the detection of PRA prior to the
development of ophthalmoscopic changes. The electroretinographic changes vary between the different forms of
PRA and in some cases may give an insight into the failure
of retinal function associated with the disease.

Laboratory investigations of PRA


Detailed histopathological characterisation of some
forms of PRA has been reported, usually where a breeding
colony has been established allowing examination of several time points during the progression of the disease. Similarly electrophysiological investigations have been performed
on colony animals and give an insight in to the ongoing
pathological process.
Biochemical analysis of affected retinae has been performed in some cases. Abnormal elevation of cyclic guanine
monophosphate (cGMP) levels has been found in some forms
of PRA suggesting a breakdown in the visual transduction
cascade. Cyclic GMP is the final metabolite of the cascade
and accumulates when the cascade is non-functional.
Molecular biological investigations have been performed
in some forms of PRA. This includes the screening of potential candidate genes for mutations.

Investigation of individual forms of PRA


Canine PRA may be broadly divided into early-onset,
mid-onset and late-onset forms. Where more detailed histological investigations have been performed a number of the
early-onset forms have been further defined as photoreceptor dysplasias and some of the later-onset forms as degenerations. Detailed analysis of the course of the disease is only
reported in a small number of breeds, and breeding analysis
to show genetic heterogeneity has been performed in still
fewer breeds. The majority of forms of canine PRA are inherited in an autosomal recessive manner. An X-linked form
in the Siberian husky has been described. in the Abyssinian
cat a dominantly inherited form occurs.

Rod-cone dysplasia type one (rcd1)


in the Irish setter
The gene mutation for this form of PRA has been identified and a DNA-based test developed.
Rcd1-affected dogs show night blindness from as early
as six to eight weeks of age and ophthalmoscopic signs are
detectable shortly thereafter. Day vision may be lost by one
year of age although occasionally affected dogs can retained
vision up to about six years of age.
The electroretinograph of affected Irish setters is abnormal prior to retinal maturation with rod mediated responses
being rapidly lost. Histopathological investigations showed
that in rcd1 the retina develops normally for the first 13 days
of life after which photoreceptor differentiation becomes arrested. The photoreceptors then go on to degenerate. It ap-

4th European FECAVA SCIVAC Congress

pears that an abnormal accumulation of cGMP triggers this


stop in development of photoreceptors and leads them to die
by the process of apoptosis. Once the abnormal accumulation
of cGMP (the end metabolite of the visual transduction cascade) was identified this pointed to an abnormality in the cascade. Investigators turned their attention to the members of
the visual transduction cascade. The break through was the
finding that the messenger RNA for the beta subunit of
cGMP phosphodiesterase (cGMP-PDE) was abnormally
low before any alterations in the level of the messenger RNA
for other transduction cascade proteins. The gene for cGMPPDE gene was screened and the causal mutation identified.
This was a guanine to adenine transition at nucleotide 2420
altering codon 807 from encoding the amino acid tryptophan
to a stop codon. This is predicted to have the effect of producing a premature termination of the cGMP-PDE protein
by 49 amino acid residues. Once the gene mutation was identified DNA-based tests were developed which allowed the
identification of both rcd1-affected dogs, rcd1 carriers and
genetically normal dogs. The mutation which causes rcd1 has
not been demonstrated in any other breeds of dog.

PRA in the Cardigan Welsh corgi


PRA was first described in the Cardigan Welsh corgi in
the 1970s and is of early onset, causing blindness at about 2
- 3 years of age. Although not studied in any great detail by
electrophysiology or at the histopathological level it has been
the subject of a molecular genetic study. This study revealed
that the disease was due to a mutation in the gene encoding
the alpha subunit of cGMP phosphodiesterase. It is the second form of PRA for which the gene mutation has been identified and the second form involving a subunit of cGMP
phosphodiesterase. A DNA-based test is under development.

Rod-cone dysplasia type two in the collie


Rod-cone dysplasia type two (rcd2) in the collie shows
many similarities to rcd1. There is a similar age of onset and
a similar breakdown in visual transduction resulting in abnormally raised cGMP levels followed by photoreceptor
dysplasia then degeneration. Studies have shown it is not
due to the same gene mutation as rcd1. Despite detailed investigation of visual transduction genes the causal gene defect remains elusive.

Early retinal degeneration (erd) in the


Norwegian elkhound
Affected dogs are nyctalopic by six weeks of age and
blind by 12 to 18 months of age. The electroretinogram does
not develop normally, the b-wave is abnormal resulting in an
a-wave dominated response. The ERG is extinguished at
about one year of age. Histopathology shows that rods and
cones do not develop normally and have abnormal synaptic
termini, they then go on to degenerate. Defective synaptic
transmission from photoreceptors to bipolar cells could ex-

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Photoreceptor dysplasia in the miniature


schnauzer
Photoreceptor dysplasia (pd) is unusual in that the development of photoreceptors is abnormal from as early as 24
days of age and yet ophthalmoscopic signs of PRA are not
evident until later in life and vision is maintained until quite
late in the disease progression. The age at which an ophthalmoscopic diagnosis can be made varies from under two
years of age until over 5 years of age.
Changes in the ERG can be detected well before ophthalmoscopic changes. The rod and cone ERGs are abnormal
soon after completion of postnatal retinal maturation and
from then on deteriorate rapidly.
Screening of the opsin and 1-transducin genes failed to
find and mutation in pd affected dogs.

PRA in the miniature longhaired


dachshund
PRA in the miniature longhaired dachshund results in
ophthalmoscopically detectable changes from about six
months of age, although there is quite a wide range in both
age at onset and rate of progression. The ERG develops normally as the retina differentiates but by 17 weeks of age
some reduction in b-wave amplitudes are present and by 26
months of age the amplitudes are markedly reduced.
Screening a variety of genes for mutations has failed to
reveal the cause of this form of PRA.

PRA in the Tibetan terrier


PRA in the Tibetan terrier was first reported in Sweden
in 1974 and then in the UK in 1978.
Nyctalopia and ophthalmoscopic signs of PRA are present at about one year of age. Electroretinographic changes,
namely a reduction in b-wave amplitude, are detectable at
about 10 months of age. The electroretinographic changes
suggest that both rods and cones are affected at the same
time, but that rods are lost more quickly than cones.
Histopathological changes are recognisable in affected dogs
from as young as nine weeks of age.
Screening a variety of genes for mutations has failed to
reveal the cause of this form of PRA.

X-linked PRA in the Siberian husky


This recently described form of PRA is the only naturally occurring model for human X-linked RP. Retinal development appears to occur normally and affected males first
develop abnormal rod- and cone- mediated ERG responses

between six and 12 months of age. The ERG responses then


deteriorate rapidly. Ophthalmoscopic changes are present by
18 months of age. Histologically, hemizygous males develop lesions as early as 12 months of age. There is then a rapid
progression of the disease.
Carrier females have reduced ERG amplitudes and develop ophthalmoscopic evidence of patchy retinal thinning,
presumed to be due to random X chromosome inactivation.
Histologically the lesions range from scattered patches of
severe rod loss with partial to complete cone preservation, to
diffuse and random loss of cells and their nuclei in the outer
nuclear layer. Linkage studies are underway to try and localise the responsible gene on the X chromosome.

Retinal dystrophy in the Labrador


retriever
A photoreceptor dystrophy has been reported in
Labrador retrievers in Scandinavia. The first form of PRA
described in this breed was shown to be a progressive rod
cone degeneration (prcd) (see below). The condition described in Scandinavia would appear to be different on electrophysiological and histopathological grounds, although
test matings to show that two different defects are present in
the breed have not been performed. The Scandinavian dogs
with retinal dystrophy have ERG abnormalities at seven
months of age whereas prcd in the Labrador is reported to be
detectable by ERG at between one and 1.3 years of age, additionally animals heterozygous for retinal dystrophy, unlike
heterozygotes for prcd are recorded as having detectable
ERG abnormalities. Histological investigations of the Scandinavian dogs have shown that they have abnormalities of
their photoreceptors at any earlier age than the prcd
Labrador. Biochemical studies of the retinal dystrophy
Labradors has demonstrated that there are slightly raised
levels of cGMP at early stages of retinal differentiation, although unlike rcd1 in the Irish setter there was no demonstrable loss of cGMP phosphodiesterase catalytic activity.
Screening a variety of genes for mutations has failed to
reveal the cause of this form of PRA.

Progressive rod-cone degenerations


in the miniature and toy poodle,
cocker spaniels, Labrador retriever
and Portuguese water dog
Progressive rod-cone degeneration (prcd) was first
recognised in the miniature poodle, but is now known to occur in cocker spaniels (American and English), Labrador retrievers and Portuguese water dogs. Test breeding has shown
prcd to be caused by mutations at the same gene locus in
these breeds, although there are some differences in the disease progression between the breeds. Prcd is numerically the
most important form of PRA and has been studied in detail
in the poodle.
Histopathological examinations suggest that the photoreceptors develop normally and then go on to degenerate. The
earliest change detected has been a reduction in the rate of

MAIN PROGRAMME

plain the abnormal b-wave of the ERG. Molecular studies


have excluded a number of genes as the site for the erd mutation. Recently a genetic marker linked to erd has been
identified.

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renewal of the photoreceptor outer segments. Outer segments are shed from the distal tips of the photoreceptor and
reformed at the proximal end of the outer segment and it is
this which is slower in prcd dogs compared to normal animals. Changes in circulating lipid levels in prcd- affected
poodles has been observed although the significance of this
finding is not clear. The ERG of prcd dogs develops normally as the retina matures, but after then the amplitude of
rod responses reduce.
Molecular investigations have excluded an number of
genetic loci as being the site of the prcd mutation. Recently,
a linked marker to the prcd locus has been reported and this
is likely to lead to the development of a DNA-linkage diagnostic test and eventually to the identification of the causal
mutation(s).

Uncharacterised forms of canine PRA


As already mentioned there are many forms of PRA
which have not been investigated and await a detailed genetic, histological, electrophysiological and molecular biological investigation. Some may prove to be allelic to forms
of PRA already identified but others may represent different
gene defects.

Feline PRA
Progressive retinal atrophy occurs in two forms in the
Abyssinian breed and is suspected in some other breeds including the Siamese.
One form in the Abyssinian is dominantly inherited and
causes a rapidly progressive loss of vision which is obvious
from a few weeks of age. The affected kittens also have a
fine oscillatory nystagmus and sometimes a nodding head
movement. Fortunately this dominantly inherited form of
PRA is very rare in the pet population.

4th European FECAVA SCIVAC Congress

The second form of PRA in the Abyssinian breed is recessively inherited and affects adult cats. Ophthalmoscopic
signs are present from about 1.5 to 2 years of age and are
slowly progressive. This form of PRA is common in Scandinavia and occasionally seen in the UK. A later-onset form of
PRA is suspected in the Siamese breed, with affected cats
presenting at about 10 or 11 years of age.
The genetic cause of the various forms of PRA in the cat
have not yet been elucidated.

Future investigations
Future investigations to develop DNA-based tests for
PRA are likely to rely more heavily on finding linked genetic markers. Once the closest possible linkage to a marker has
been established this will allow screening of the chromosomal location for potential candidate genes to screen. Spin
offs from the human genome project should facilitate this
approach because there are similarities between the grouping of genes between species. However, even after linkage is
established it can still be a considerable amount of work to
find the actual mutant gene and within it the nucleotide
change which is ultimately responsible for loss of function
of the gene or its resultant protein.
We can anticipate the identification of many more PRA
causing gene defects and therefore the development of further DNA tests for PRA over the next few years.

Further reading
Clements PJM, Sargan DR, Gould DJ, & Petersen-Jones SM. (1996) Recent
advances in understanding the spectrum of canine generalised progressive retinal atrophy. Journal of Small Animal Practice 37, 155162.
Petersen-Jones SM. (1998) A review of research to elucidate the causes of
the generalized progressive retinal atrophies. The Veterinary Journal.
155, 5-18.

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333

An approach to sudden-onset blindness


S.M. Petersen-Jones

Summary
Sudden-onset blindness may result from serious intraocular disease or lesions involving the central visual pathways. Identification of the aetiology requires careful and
thorough examination and in some cases the use of specialist techniques such as electroretinography and advanced
imaging. The prognosis for return of vision in some instances is poor and in many is hopeless.

Sudden-onset loss of vision can result from a number of


different conditions. Often for the loss of vision to be obvious to the owner it will involve both eyes. The conditions
which can result in a sudden loss of vision can be divided into the following three categories:
those which result in ophthalmoscopic signs such as acute
glaucoma, acute uveitis, intraocular haemorrhage, retinal
detachment
those which result in blindness with dilated fixed pupils
e.g. sudden acquired retinal degeneration syndrome (dogs
only) and lesions involving both optic nerves, the chiasma
or both optic tracts
those resulting in blindness with normal pupillary light responses e.g. bilateral lesions of central visual pathways
from lateral geniculate nuclei to visual cortex.
The latter two categories can present a diagnostic challenge. In addition to a complete ophthalmic and neurological examination techniques such as electroretinography and
computed tomography or magnetic resonance imaging investigation can help identify the site of the abnormality.

The sudden loss of vision in a pet is a very distressing


event for owner and animal alike. To the veterinarian it can
present a diagnostic challenge, particularly if there are no
ophthalmoscopically detectable changes to account for the
blindness.

any other changes noticed, e.g. in appearance of eyes, in


behaviour?
was loss of vision associated with any particular event e.g.
trauma, illness?
did the owners notice the vision loss after their pet was
moved to different surroundings (many animals cope well
with failing vision in familiar surroundings)?
how much does the pet normally rely on vision i.e. is it a
working dog, a house-bound cat or a lap dog?
The owners assessment of vision is not always reliable.
Many cats and dogs which gradually lose vision cope surprisingly well in familiar surroundings and the owners may
not immediately realise there is a problem. In such cases if
the animal is moved to unfamiliar surroundings the loss of
vision becomes suddenly obvious and the owners assume it
is sudden onset.

EXAMINATION
Vision testing
An assessment of the animals vision should be made.
From the behaviour of the animal in the consulting room it
is usually obvious if it has suddenly lost vision. Additional
techniques employed to assess vision include an obstacle
course, visual tracking of cotton-wool balls dropped in front
of the animal, menace response and placing reactions.

Clinical assessment
A general physical examination should be performed as
should a thorough ophthalmic and neuro-ophthalmic examination. In cases where a central (CNS) lesion is suspected a
full neurological work-up should also be carried out.

Pupillary light reflexes


HISTORY
As usual a good history can be invaluable. The following
points may be useful to consider:
any previous ocular problems or systemic disease?
rate of progression of apparent loss of vision

The pupillary light reflex (PLR) can be an informative


part of the examination and should always be checked, however it must be remembered that it is not a measure of the
conscious perception of vision. Animals can have a normal
PLR and yet be blind due to cortical lesions or alternatively
can have an absent PLR e.g. due to atrophy of the pupillary

MAIN PROGRAMME

DVO, Dipl ECVO, MRCVS


Department of Small Animal Clinical Sciences
College of Veterinary Medicine
Michigan State University, East Lansing - USA

334

constrictor musculature and yet still have normal vision.


The extent and speed of pupillary constriction should be
noted for both the direct and consensual reflex of both eyes.
The direct PLR is the constriction of the pupil in the eye in
which the light is shone, the contralateral pupil should also
be checked (the consensual PLR). The consensual PLR can
be assessed by quickly swinging the examination light from
one eye to the contralateral one and if the reflex is normal
the pupil should already be constricted. The pupillary responses are often sluggish in normal animals when they are
initially examined, due to the action of circulating adrenaline. However, in most animals the speed of the pupillary responses return to normal after a few minutes.

REACHING A DIAGNOSIS
The results from the history taking, vision testing and
clinical examinations should enable a list of differential diagnoses to be made. The animal presenting with a true sudden loss of vision will fall into one of the following categories:
sudden-onset blindness caused by ophthalmoscopically detectable intraocular disease
sudden-onset blindness accompanied by dilated non-responsive pupils, but no other ophthalmoscopically detectable changes
sudden-onset blindness with normal PLR and no ophthalmoscopically detectable changes
These categories will each be considered in turn:

SUDDEN-ONSET BLINDNESS CAUSED


BY OPHTHALMOSCOPICALLY
DETECTABLE INTRAOCULAR DISEASE
There are a number of ocular conditions that can result in
a sudden-onset blindness:
Acute uveitis or glaucoma can render the affected eye
blind. Usually pain and the altered appearance of the eye
are the presenting signs rather than the loss of vision.
Cataracts. In some instances cataracts can progress rapidly and therefore cause a fairly rapid loss of vision. Diabetic cataracts are one example of this.
Intraocular haemorrhage. This can result in a sudden
loss of vision in the affected eye. Haemorrhage may result
from ocular trauma, neoplastic intraocular changes, bleeding from abnormal vasculature (remnants of embryonic
vasculature), or may be secondary to other intraocular disorders such as collie eye anomaly or retinal detachment.
Systemic disease including clotting disorders and hypertension, can also result in intraocular haemorrhage.
Retinal detachment. Complete retinal detachments results
in a sudden-onset vision loss. Unilateral detachments are
not always apparent to the owner and animals may only be
presented if the other retina detaches. Aetiologies to consider include trauma, inflammatory or neoplastic posterior
segment disease, retinal dysplasia, collie eye anomaly, retinal holes, and vitreous traction bands. Detachment also occurs secondary to systemic disease such as hypertension,

4th European FECAVA SCIVAC Congress

this is particularly common in older cats. Management


consists of treating any underlying conditions and, if their
use if not contraindicated, prescribing systemic corticosteroids. Bullous retinal detachments will often resolve with
treatment, in many cases restoring useful vision. However
the longer the retina has been detached the less likely it is
that a successful outcome will be achieved. Generally
speaking if a retinal tear or hole is present liquefied vitreous will gain access to the subretinal space through the
retinal defect and prevent reattachment. Surgical intervention in such cases may offer the only hope of achieving
reattachment, but as yet the success rate in animals is low,
the procedures are not widely practised and in some cases
the late presentation means that the retinal pathology is already too advanced for successful restoration of vision.
Papillitis. Inflammation involving the optic nerve head
(disc) will cause blindness in the affected eye and an absent direct and consensual PLR. The affected disc looks
swollen, reddened and may have surface hemorrhages.
There is usually oedema of the surrounding retina and possibly haemorrhage. The list of possible aetiologies includes
canine distemper, granulomatous meningioencephalitis,
and systemic fungal disease such as cryptococcosis. However, the majority of cases are idiopathic, and probably immune-mediated. Treatment is by administration of high
levels of systemic corticosteroids, unless contraindicated
(e.g. for the systemic mycoses). Prognosis is guarded as recurrence is common and eventual optic atrophy may result.

SUDDEN-ONSET BLINDNESS
ACCOMPANIED BY DILATED FIXED
PUPILS, BUT NO OTHER OCULAR SIGNS
The nerve fibres from the retina which form the afferent
arm of the pupillary light reflex accompany fibres for vision
along the optic nerve, through the optic chiasma and pass
along the optic tract before branching off just before the lateral geniculate body. Therefore lesions affecting the retina or
central visual pathways prior to the lateral geniculate body
will also alter pupillary responses. Bilateral complete lesions
result in dilated, fixed pupils. When the condition is unilateral, affecting only one retina or optic nerve there will be no
direct or consensual pupillary light response on the affected
side, and yet there will be a consensual response from the
other eye. When a unilateral optic tract lesion is present the
situation is more complicated because the vision and PLR
from both eyes is affected but not equally. The vision and
PLR of the eye contralateral to the optic tract lesion are more
severely compromised.
The differential diagnoses to consider are:
sudden acquired retinal degeneration syndrome
(SARDS). This condition typically affects middle-aged,
slightly obese dogs and causes a bilateral and rapid loss of
vision due to extensive retinal photoreceptor damage. Initially the fundus looks ophthalmoscopically normal, but
eventually changes resulting from generalised retinal degeneration become obvious. The aetiology of SARDS is
unknown and the resulting retinal damage is permanent.
SARDS must be distinguished from sudden-onset blind-

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dents can all affect the central visual pathways and can result in a rapid loss of vision. Advanced imaging techniques
such as computerised tomography and magnetic resonance
imaging, although expensive and not widely available, are
useful for demonstrating the presence of space-occupying
lesions impinging on the central visual pathways.

SUDDEN-ONSET BLINDNESS
WITH NORMAL PLR AND NO OCULAR
SIGNS
This results from bilateral lesions involving the higher
segments of the central visual pathways; the lateral geniculate nucleus, optic radiation or optic cortex. Bilateral lesions
may result from prolonged cerebral hypoxia, encephalitis
(e.g. chronic distemper) or hydrocephalus. Other severe neurological signs are likely to be present. Treatment and prognosis depend on the aetiology.

MAIN PROGRAMME

ness due to bilateral lesions of optic nerves or tracts, or lesions involving the optic chiasma. Optic neuritis involving
the retrobulbar portion of the optic nerves is probably the
main differential. An electroretinogram (ERG), which is a
test to measure the electrical responses of the retina as a result of light stimulation, is useful in making the diagnosis.
Dogs with SARDS do not have a recordable ERG, whereas lesions of the central visual pathways do not initially alter the ERG.
Retrobulbar optic neuritis. This typically presents as a
sudden loss of vision accompanied by dilated fixed pupils
and no funduscopic changes. It must be distinguished from
SARDS by electroretinography. The differentiation is important for prognostic reasons; optic neuritis will often respond to systemic corticosteroids whereas SARDS will
not. The potential aetiologies are the same as listed for papillitis and as with papillitis recurrence is possible.
Other lesions affecting optic nerves, chiasma or optic
tracts. Inflammatory lesions, neoplasms and vascular acci-

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337

Managing corneal ulceration in small animals


S.M. Petersen-Jones
DVO, Dipl ECVO, MRCVS
Department of Small Animal Clinical Sciences
College of Veterinary Medicine
Michigan State University, East Lansing - USA

Corneal ulceration is a common problem in small animal


ophthalmology. Ulcers may range from superficial (just involving the epithelium) to deep and even result in corneal
perforation. There are a number of possible causes including trauma, infection (herpesvirus as a primary infective
cause in cats or bacteria as a secondary complication in
cats and dogs) and secondary to other ocular disease. A full
examination of each case presenting with an ulcer should be
undertaken looking for predisposing factors and concurrent
disease.
Refractory or indolent ulcers just involve the epithelium
and require specific treatment to encourage healing. This
consists of removing all the loose epithelium and performing
a grid or punctate keratotomy. Deep or progressive ulcers
require a different approach. The possible involvement of
bacteria should be investigated and aggressive medical
therapy undertaken. Conjunctival pedicle grafts can be a
very successful way of dealing with ulcers that are either
deep or are progressing despite intensive medical therapy.

Corneal ulceration is a common presenting problem in


small animal ophthalmology. An ulcer is defined as a break
in integrity of the corneal epithelium. Ulcers range in severity from those which are superficial (just involving the epithelium) to those which may extend deeper into the cornea
and may even result in corneal perforation. When ulcers extend to Descemets membrane the resulting lesion is known
as a descemetocoele. The management indicated for the ulcer depends on the type and depth of the ulcer and the presence of concurrent ocular disease.

PRESENTING SIGNS
A break in the integrity of the corneal epithelium results
in exposure of corneal nerve endings and hence pain. A
trigeminal reflex arc can lead to an accompanying anterior
uveitis which adds to the discomfort resulting from some
corneal ulcers. The resulting ocular pain is typically manifest by increased lacrimation and blepharospasm. Superficial ulcers can be more painful than deeper ulcers because of
the greater number of nerve endings in the superficial layers
of the cornea.

In addition to the signs of pain, the owners may also notice the resulting change in appearance of the cornea.

SIGNALMENT & HISTORY


A good clinical history should be taken. This may indicate the possible cause of the ulcer, reveal the duration of
the problem and indicate if any treatment has already been
given.

EXAMINATION
As with every case a complete ophthalmic examination
must be performed and a general physical examination
should also be included. The examination should be both
methodical and thorough so as not to miss any predisposing
factors which might be contributing to, or even causing, the
ulceration. A darkened room and bright pen-torch or transilluminator are necessary for the examination. Unless there
is obvious profuse lacrimation a Schirmer tear test should
be performed to assess tear production. This test must be
performed prior to the addition of any fluid to the ocular
surface or undue manipulation of the eye. Confirmation of
the presence of corneal ulceration is by the application of
fluorescein.

Fluorescein staining
Use a fluorescein impregnated strip, apply one drop of
saline to the strip and apply this to the bulbar conjunctiva
- the minimum amount of dye should be applied;
flush the conjunctival sac well with sterile saline to avoid
any false impression of staining (particularly in eyes with
keratoconjunctivitis sicca);
fluorescein passes into any exposed corneal stroma staining it bright green. Use of a blue light enhances the fluorescent appearance of the dye;
fluorescein will not cross an intact (or superficially damaged) corneal epithelium;
fluorescein does not stain Descemets membrane;
fluorescein staining may not be obvious in very oedematous corneas.

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Summary

338

Other stains
Rose bengal stain can be used to demonstrate damage to
corneal epithelial cells. It is commonly use to demonstrate the
presence of dendritic ulcers in feline herpesvirus infections.

Magnification
Closer examination of lesions using magnification is
very useful. Without magnification is can be difficult to
judge the depth of ulcers and impossible to visualise significant abnormalities such as ectopic cilia. The biomicroscope
slit-lamp is the ideal instrument to provide this magnification. It can be used with a full beam of light to examine the
lids and conjunctival sac and survey the anterior segment of
the eye, but it can also be used with a narrow beam of light
directed at an angle from the microscope to achieve a so
called optical section of the cornea. This optical section is
particularly useful for judging the depth of ulcers. Other illumination techniques include the use of retroillumination
utilising light reflected from the fundus or the iris. This
technique silhouettes corneal opacities. Other ways of examining the cornea using magnification include using a direct ophthalmoscope with a high positive dioptre setting, or
a magnifying loupe.

Appearance of corneal ulceration


The changes visible on the cornea depend on the extent
and depth of the ulcer as well as its duration. In addition to
the ulcer itself which may appear as a slight roughening of
the cornea up to a large crater with liquefaction of surrounding corneal stroma there may be the following:
corneal oedema
corneal vascularisation (superficial and/or deep)
superficial corneal pigmentation
signs of an accompanying anterior uveitis
When examining the ulcer the depth and extent should
be assessed looking for evidence of corneal stromal liquefaction (due to protease release from bacteria, neutrophils or
from damaged keratocytes). Identification of intraocular involvement such as an accompanying anterior uveitis, hypopyon or even corneal perforation is important.

Further investigations
Collection of material from the ulcer edge for microscopic examination for the presence of pathogens, culture and possible use of other tests for the detection of pathogens (e.g.
polymerase chain reaction tests) may form part of the workup of corneal ulcers, in particular deeper or progressive ones.

AETIOLOGY OF CORNEAL ULCERATION


There are several possible aetiologies for corneal ulceration including:

4th European FECAVA SCIVAC Congress

Trauma
Foreign bodies e.g. grass seed under nictitating membrane.
Chemical injuries detergents, spirit, alkalis (tend to melt
corneal stroma and can rapidly deepen e.g. ammonia,
lime), acids (coagulate corneal protein and do not deepen).
Thermal injuries
Cilia abnormalities ectopic cilia (when present often
cause ulceration), distichiasis & trichiasis (dont often
cause ulceration).
Lid abnormalities entropion.
Tear film abnormalities keratoconjunctivitis sicca (ulceration is commonest with acute onset KCS), corneal drying during anaesthesia (e.g. cat anaesthetised with ketamine - this is really an exposure problem).
Exposure keratitis an inadequate blink can cause corneal
dry spot formation and ulceration.
Neurotrophic keratitis corneal anaesthesia (lesion of
ophthalmic branch of trigeminal nerve) will often cause a
superficial ulcerative keratitis of the area of cornea exposed within the palpebral fissure.
Secondary to other corneal disease e.g. lipid keratopathy, calcific corneal degeneration.
Refractory (non-healing) or indolent corneal ulcers
Some of these types of ulcer may be due to a form of
corneal epithelial dystrophy. The hemidesmosomes which
anchor the basal epithelial cells to the basement membrane
are reduced in number and the epithelial membrane itself
is abnormal. Dogs affected in this manner are considered
to have a true primary corneal epithelial dystrophy. Classically the boxer and corgi are described as suffering from
this condition. A clinically indistinguishable condition is
encountered quite commonly in a variety of breeds. These
ulcers involve the epithelium only. The surrounding epithelium is often nonadherent and may fold back on itself.
Infected corneal ulcers Feline herpesvirus infection can
result in classical dendritic ulcers. When seen such ulcers
are considered pathognomonic for herpes, however other
forms of ulceration possibly associated with stromal keratitis may also result from herpes infection. When herpes is
suspected collecting corneal material for viral culture or
preferably polymerase chain reaction tests to demonstrate
the presence of viral DNA can be useful. In some geographical locations corneal fungal infections can occur.
Most of the significant infective ulcers involve bacteria.
Primary bacterial pathogens are not recognised as a cause
of ulceration in cats and dogs, however bacterial contamination of corneal injuries can occur. Potentially pathogenic contaminating bacteria adhere to, and therefore colonise
damaged epithelial cells and stroma. This leads to infection
and possibly a progression of the ulcer. Material collected
from the edge of such an ulcer is useful for culture and also direct microscopic examination. One slide should be
stained with a stain such as Diff-Quik to demonstrate the
presence of bacteria and then a Grams stain performed on
a second slide to give a rapid guide as to the type of bacteria involved. Pseudomonas aeruginosa is notorious because of its association with melting corneal ulcers. These
are ulcers in which there is a rapid liquefaction of the
corneal stroma with a real risk of perforation. Proteases

4th European FECAVA SCIVAC Congress

MANAGEMENT OF CORNEAL ULCERS


Superficial abrasions will heal quickly without treatment
although a covering broad spectrum antibiotic is usually provided. When one of the predisposing factors listed above is
identified this should be treated appropriately.
Ulcers which are failing to heal or are deepening may
need more specific therapy and are considered below.

ated with gram-positive organisms a fortified solution of cefazolin (33mg/ml) or penicillin G (100,000 units/ml) can be
used. Agents to inhibit corneal melting have been suggested
and include EDTA and serum. Atropine may be given to treat
any concurrent reflex uveitis. Surgical intervention to apply a
conjunctival pedicle graft is a very useful line of management and should be used if medical therapy does not lead to
a rapid halting of the progression of a melting ulcer. Grafts
provides a blood supply (and hence antibacterials and antiprotease substances) and support for the affected cornea.
Third eyelid flaps still have a limited role but are not advisable for ulcers deeper than one half of the corneal thickness
or those that are progressing rapidly. DO NOT GIVE
STEROIDS until the cornea has re-epithelialised. Note that
deep ulcers may epithelialise leaving a corneal defect (facet).

Indolent ulcers
Conjunctival grafts
These are nonhealing ulcers that just involve the corneal
epithelium and show little tendency to heal. One potential
cause is an epithelial basement dystrophy. The ulcers fail to
heal because the epithelium does not form the proper junctions to anchor it to the basement membrane. Indolent ulcers
are commonest in dogs but can occur in cats. They can be
very frustrating to deal with unless the appropriate management is undertaken.
Treatment Indolent ulcers typically require surgical intervention to encouraging healing. The first stage is to strip
all the nonadherent epithelium off the cornea. A dry cotton
bud can be used for this or a #15 blade (employing a brushing motion rather than a cutting motion). Following removal
of all nonadherent epithelium small puncture wounds are
made into the anterior stroma using a 23 gauge needle
(punctate keratotomy). Alternatively a grid pattern of superficial scratches can be made over the exposed corneal stroma (grid keratotomy). A contact lens can be applied as an adjunct to this therapy.

Deeper ulcers or deepening ulcers


Bacterial infection of the corneal surface can lead to progressive ulceration, some initial injury is usually required to
allow bacteria to adhere to the ocular surface as the preliminary step in causing infection. Release of proteases from
bacteria, polymorphs or corneal keratocytes can lead to liquefaction of corneal stroma and rapid progression of some
ulcers. The most severe cases can progress over a matter of
hours and are described as melting ulcers. When overlying
stroma is removed, Descemets membrane may bulge forward (descemetocoele). Note that Descemets membrane
does not take up fluorescein. A descemetocoele is easily ruptured so a surgical repair will be required.
Investigation Swabs for bacteriology and cytology
should be performed
Treatment Progressive deepening ulcers should be treated aggressively with an appropriate antibiotic applied frequently. If a gram-negative infection is suspected
ciprofloxacin may be useful, this is initially applied hourly
for six hours then every two hours. For serious ulcers associ-

Conjunctival grafts, free or more usually attached, are


very useful for the management of serious sight threatening
corneal ulcers and can be readily performed using a minimum of specialised equipment.

Indications for conjunctival grafts


Conjunctival grafts are usually reserved for the treatment
of corneal ulcers which are deeper than one half of the
corneal thickness or where satisfactory healing without surgical intervention is unlikely. Conjunctival grafts can be
used to save vision in eyes with descemetocoeles, melting
and even perforated ulcers. They offer very significant advantages over techniques such as third eyelid flaps and tarsorrhaphies.
The advantages of conjunctival grafts are that they:
provide support for weakened cornea;
provide an immediate blood supply to the ulcer (except for
free grafts);
serum contains anticollagenases which are useful for melting ulcers where proteases are active;
serum supplies antibacterial substances;
with the exception of total conjunctival flaps, continued
visualisation of the cornea and intraocular structures is
possible;
are readily performed and highly successful;
are useful following keratectomy for feline corneal sequestrum removal and it is suggested that they reduce recurrence of the sequestrum.
The main disadvantage of their use is the resulting area
of corneal opacity at the ulcer site, however this is a minor
drawback compared to the risks of corneal perforation and
loss of the eye if grafting is not performed.

Types of conjunctival graft


The selection of graft depends on the extent and position
of the ulcer and the health of the surrounding cornea (for suture placement). The most versatile and useful graft is the

MAIN PROGRAMME

produced by the bacteria are blamed for this melting effect.


However, proteases can also be released from polymorphs
and some melting ulcers (from which bacteria are not isolated) are presumed to be due to release of these proteases.

339

340

pedicle graft which can be used on large and even perforated ulcers. Other patterns of conjunctival graft include;
bridge, hood and total grafts and free island grafts.

Technique of applying conjunctival grafts


Prior to placement of the graft the ulcer site should be
gently cleaned or debrided to remove necrotic corneal stroma. Any corneal epithelium which has started to grow down
into the depths of the ulcer crater should be removed by gentle scraping using a #15 scalpel blade, taking care to avoid
the depths of the ulcer. Failure to do this can mean that the
conjunctival flap may detach from the ulcer site. Conjunctival flaps or grafts should be fashioned so that they are as thin
as possible and while dissecting them it should be possible
to see the dissecting scissors through them. When suturing
the conjunctiva to the cornea the sutures should pass to approximately 3/4s of the depth of the cornea.
After placement of the graft the conjunctiva will heal into the ulcer site and provide a good blood supply to encourage corneal healing within two to three weeks. After this
time the flaps may be trimmed or dissected free. Total and
hood flaps usually need to be dissected free as the conjunctiva will have adhered to areas of the cornea which is not epithelialised. Conjunctiva should be left over the deep part of
the ulcer to act as a plug for the defect to confer strength to
the weakened cornea. Over the subsequent months some degree of remodelling of the remaining graft will occur.

4th European FECAVA SCIVAC Congress

repairing the corneal defect. The graft is then cut just above
the ulcer site and the conjunctival pedicle left to retract and
remodel. A piece of conjunctiva will have been left in situ
within the ulcer site.
In cases with corneal perforation a conjunctival pedicle
graft can effect a good repair. Prolapsed iris should be freed
from the cornea and replaced into the anterior chamber. The
graft should be fashioned and sutured in place. Balanced salt
solution (Alcon Ltd) or sodium hylauronate (Healonid,
Pharmacia Ltd) can be used to reform the anterior chamber.
It can be difficult to achieve a water-tight seal between the
graft and the edge of the corneal defect. If this is not
achieved aqueous leakage occurs, the anterior chamber can
collapse possibly leading to an iris-cornea adhesion (anterior synechiae). A continuous suture pattern may help achieve
a water-tight seal.

Other surgical techniques for managing


corneal ulcers
Small deep ulcers with healthy surrounding cornea may
be closed by direct suturing. Larger defects can be repaired
by performing a corneoscleral transposition. The advantage
of this technique is that is successful there will be less
corneal opacity than with a conjunctival pedicle graft. The
disadvantage is that the technique does not provide a blood
supply to help heal the ulcer and halt any protease action.
Other techniques include the use of grafts of frozen
cornea.

Conjunctival pedicle grafts


Conjunctival pedicles may be fashioned either by dissecting a pedicle of conjunctiva from bulbar conjunctiva
parallel to the limbus and then rotating it onto the cornea, or
by dissecting a pedicle at 90 degrees to the limbus which extends into the fornix and then is advanced over the cornea.
Which ever approach is used the graft should be slightly
wider than the defect and be able to reach and cover the defect without being under tension. The sutures to hold the
graft in place (e.g. 8/0 Vicryl) are passed into the walls of the
ulcer crater ensuring that they pass into relatively healthy
cornea. After 3 weeks the graft should have healed in place

FURTHER READING
Champagne ES & Munger RJ (1992) Multiple punctate keratotomy for the
treatment of recurrent epithelial erosions in dogs. J Am Anim Hosp
Assoc 28:213-216.
Hakanson N, Lorrimer D & Meredith RE (1988) Further comments on conjunctival pedicle grafting in the treatment of corneal ulcers in the dog
and cat. J Am Anim Hosp Assoc 24:602-605.
Hakanson NE & Meredith RE (1987) Conjunctival pedicle grafting in the
treatment of corneal ulcers in the dog and cat. J Am Anim Hosp Assoc 23:641-648.
Parshall C (1973) Lamellar corneal-scleral transposition. J Am Anim Hosp
Assoc 9:270.

4th European FECAVA SCIVAC Congress

341

Ocular manifestations of feline eosinophilic complex


in the cat
Stefano Pizzirani

Ocular manifestations of feline eosinophilic complex are


several and they involve different ocular structures of the anterior segment (single or associated) and of the orbit.
Similar diseases happen in human beings, being included in Histyocitosis X.
No obvious link is yet considered with Feline
Eosinophilic Granuloma Complex (EGC). Nevertheless
some references have been hypothesised with Eosinophilic
Plaque (EP)3, Collagenolytic Granuloma (CG)2 and Indolent
Ulcer (IU)1.
Eosinophilic reaction patterns in cats are multiple and
not everyone of them must be included in the EGC. This
could be only one of the manifestations or reactions possible
in a larger and more complex problem11,20,21.
Cause are unknown. Food allergy, atopy and parasite reaction are the most frequent hypothesis and the group of lesion is believed to be an immune mediated reaction (type I
or IV hypersensitivity reaction).
Clinical manifestations are:
- blepharitis
- blepharo-conjunctivitis
- conjunctivitis
- keratoconjunctivitis
- keratitis
- orbital granuloma (?).
Lesions may be mono or bilateral. No sex or breed or age
incidence has been described which was statistically significant. But two authors report higher incidence of
eosinophilic keratitis in male castrated cats1,9. Maybe a more
determined clinical grading with reference to single aspects
would be more rewarding.
Palpebral lesions show erosive or ulcerative dermatitis,
well demarcated, which interests the skin of the lid. The lid
margin becomes leukodermic because inflammatory cells
infiltration. The palpebral conjunctiva may be interested by
an inflammatory process as well. Blepharospasm and ocular
discharge may be present.
Conjunctival forms present redness, chemosis and/or
tickening of the conjunctival layers. Blepharospasm and ocular discharge come along primarily with the oedematous
form. We had a case with a severe keratoconjunctivitis sicca
because obstruction of the lacrimal ducts. Anyway no investigation was done to ascertain the presence of a lachrymal
adenitis too.
Nodular raised conjunctival localised proliferations can
be met on the outer surface of the nictitans. We had three

cases all in Persian cats as was the only one in literature2 but
these data are too few to predict a breed predisposition.
Cornea is invaded by proliferative tissue, with neovascularization. It can be localised or diffuse. Usually it is confined to the supero temporal quadrant, starting from the limbus. Ocular pain is rare but sometime the third eyelid is
slightly prominent, especially if compared to the normal eye.
Fluorescein test is negative but sometime, small positive
erosion are seen over the proliferative tissue, corresponding
at small disepithelialized foci14. Whitish to yellowish deposits are often seen on the corneal surface. Less commonly
on the conjunctiva.
Orbital deposition of eosinophilic cells infiltrate cause
exoftalmia7.
Pruritus is not common, except for those lesions referred
as EP.
Peripheral eosinophilia is not a consistent finding8,9,10.
Contemporary clinical syndromes referred as EGC are
rarely seen.
No strict relationship has been showed to exists between
this group of lesions and FeLVhg or FIV, or internal parasites.
Some Authors advocate FHV-1 infection as one of the
predisposing factors4,9.
Diagnosis is made with cytology or biopsy. Cytology is
less invasive, more rapid and usually diagnostic and show an
high number of eosinophils with few mast cells. Neutrophils, lymphocytes and plasma cells are also be a possible
finding. Variable pattern may be encountered, probably as
different evolutions of time. Chronic phases tend to be fibrovascular with increasing number of mononuclear cells
and decreasing number of eosinophils.
A thorough examination should be performed and dietary elimination trails, intradermal skin tests and/or serological tests (RAST or ELISA)12,22,23 should be proposed.
Differential diagnosis include: Chlamidia, FHV-1 and
Mycoplasma infections, granulation tissue from corneal ulcer
healing, mycotic blepharitis, orbital cellulitis and neoplasia.
Treatment uses local and systemic corticosteroids. Cats
need higher dosage regimen than other animals because the
few corticosteroid receptors. Prednisolone seems to be preferred at prednisone and the dosage stays around 4.4 mg / kg
once a day. Methylprednisolone acetate may be used as deposit drug and 4-5 mg/kg should be given every 15-20 days.
It is used usually for non treatable animals and chronic therapies. We still anyway prefer for long standing therapies to

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Med Vet, Dipl ECVS


Private Practitioner, Firenze - Italy

342

4th European FECAVA SCIVAC Congress

use if possible, injectable prednisolone once or twice a


week. Cases of iatrogenic Cushing syndrome are reported.
Megestrol acetate seems to have greater efficacy. This is
clinically reported but not scientifically proven. This seems
also to be the preferred drug by Oculists and the damned one
by Dermatologists and Internists. Many side effects have
been claimed as adrenocortical suppression, diabetes mellitus, mammary fibroadenomatous hyperplasia, mammary
neoplasia, pyometra, personality changes, poliphagia, polydipsia1,3,9,10,16,17,18,19.
Anyway many side effects have been also reported with
long standing high-dosage corticosteroids treatments.
We use Megestrol acetate as first preferred treatment. Its
efficacy is clinically better than corticosteroid one and
sometime it is efficacious where cortisone was not. We use
5 mg/cat for 2-3 days, than reduce at 5 mg/cat twice a week
for 1-2 weeks, 5 mg/cat once a week for 2-4 weeks and then
5 mg/cat every two weeks for 2-4 times. Differences are because different clinical situations and different responses.
It should not be used for chronic treatment. Diabetic animal and pregnant female should not be treated.
Cyclosporine has variable efficacy and there is no literature on it about the disease. We use it in combination with
topical dexamethasone, especially when the Schirmer tear
test is low. Very few times we have used it topically as the
only treatment but its efficacy was low.
Immune modulators have been reported to be used in the
treatment of the EGC13,15.
Therapeutical response vary. Some lesion never appear
again, some do. Some need chronic treatment. Similarly this
happens for different degrees of EGC.
To understand the cause, making a good staging and grading of the disease, knowing more about immunological status
of the patient, proposing a therapeutic protocol could be the
way to match the problem and to have good data to interpret.
Unfortunately the rarity of the ocular disease makes
prospective studies too difficult and retrospective ones too
limited.

References

3.
4.
5.
6.
7.

8.

9.

10.
11.
12.

13.
14.

15.

16.

17.

18.

19.

20.
21.
22.

1.

2.

Paulsen M.E., lavach J.D., Severin G.A., Eichenbaum J.D. Feline


Eosinophilic Keratitis: A Review of 15 Clinical Cases. JAAHA, vol.
23, N 1, 63-69, 1987.
Keil S.M., Olivero D.K., McKeever P.J., Moore F. Bilateral Nodular
Eosinophilic Granuloma of the Nictitating Membrane of a Cat Pro-

23.

ceedings of the ACVO Meeting 1995.


Latimer C., Dunstan R.W. Eosinophilic Plaque Involving Eyelids of
a Cat JAAHA, Vol. 23, N 6, 649-653, 1987
Nasisse M. Personal Communication. ISVO Meeting 1997.
Kipnis R.M. Corneal Eosinophilic Granuloma Fel. Pract., Vol. 9,
N6, 49-53, 1979.
Pentlarge V.W. Eosinophilic Conjunctivitis in Five Cats JAAHA,
Vol. 27, N 1, 21-28, 1991.
Dziezyc J., Barton C.L., Santos A. Exoftalmia in a Cat caused by an
Eosinophilic Infiltrate Prog. In Vet. & Comparative Ophthalm., Vol.
2, N 2, 91-93, 1992.
Center S.A., Randolph J.F., Erb. H.N., Reiter S. Eosinophilia in the
Cat: A Retrospective Study of 312 Cases (1975 to 1986) JAAHA,
Vol. 26, N 4, 349-358, 1990.
Morgan R.V., Abrams K.L., Kern T.J. Feline Eosinophilic Keratitis:
A Retrospective Study of 54 Cases: (1989 1994) Vet. & Comp.
Ophthalm., Vol. 6, N 2, 1996.
Bedford P.G.C., Cotchin E. An unusual chronic keratoconjunctivitis
in the cat J.Small Anim. Pract. (1983) 24, 85-102.
Rosenkrantz W. Eosinophilic Granuloma Complex (Confusion)
Veterinary Focus, Vol. 1, N 1, 29-32, 1989.
Power H.T., Ihrke P.J. Selected Feline Eosinophilic Skin Diseases
Vet. Clinics of North America, Small Anim. Pract., Vol. 25, N 4,
833-850, 1995.
Song M.D. Diagnosing and treating feline eosinophilic granuloma
complex Veterinary Medicine, pp. 1141-1145, 1994.
Prasse K.W., Winston S.M. Citology and Histophatology of Feline
Eosinophilic Keratitis Vet. & Comp. Ophthalmology, Vol. 6, N 2,
74-81, 1996.
McEwen E.G., Hess P.W. Evaluation of Effect of Immunomodulation on the Feline Eosinophilic Granuloma Complex JAAHA, Vol.
23, N 5, 519-526, 1987.
Mansfield P.D., Kemppainen R.J., Sartin J.L. The Effects of Megestrol Acetate Treatment on Plasma Glucose Concentration and Insulin
Response to Glucose Administration in Cats. JAAHA, Vol. 22, N 4,
515-518, 1986.
Chastain C.B., Graham C.L., Nichols C.E. Adrenocortical suppression in cats given megestrol acetate Am.J.Vet.Res., 42, 2029-2035,
1981.
Kraus M.S., Calvert C.A., Jacobs G.J., Brown J. Feline Diabetes
Mellitus: A Retrospective Mortality Study of 55 Cats (1982 1994)
JAAHA, 33, 107-11, 1997.
Middleton D.J., Watson A.D.J. Glucose intolerance in cats given
short-term therapies or prednisolone and megestrol acetate
Am.J.Vet.Res., Vol. 46, N 12, 1985.
Neer T.M. Hypereosinophilic Syndrome in cats Compendium,
Vol.13, N 4, 549-555, 1991.
Harvey R.G. Feline hypereosinophilia with cutaneous lesions
J.Small Anim.Pract. (1990), 31, 453-456.
Halliwell R.E.W. Efficacy of Hyposensitization in Feline Allergic
Disease Based Upon Results of in vitro Testing for Allergen-Specific
Immunoglobulin E JAAHA, 33, 282-288, 1997.
Roudebush P., McKeever P.J. Evaluation of a Commercial Canned
Lamb and Rice Diet for the Management of Cutaneous Adverse Reactions to Food in Cats. Vet. Dermatology, Vol. 4, N 1, 1-4, 1993.

4th European FECAVA SCIVAC Congress

343

61
Lens dislocation
Stefano Pizzirani

The lens maintains its anatomical position due to the suspensory apparatus, which is the zonule, lens equator and ciliary body. Every disease involving these structures may be
responsible for partial or total dislocation of the lens (subluxation / luxation). Lens displacement may be congenital,
primary (hereditary transmitted) or secondary.
Congenital aetiologies are represented by microspherophachia, are rare and often included in multiple ocular
anomalies.1,2,3,6,10
Hereditary causes are more frequent in particular breeds
as Terrier breeds8, Shar peis12, Border collies9 and Italian
Volpino*.
However many other breeds can be involved. Curtis describes altered zonular anatomy as main cause in terrier8.
Collagen diseases are the basis for similar conditions in human beings4,5.
Terriers may show the disease ranging from 3 to 8 years,
while Shar peis can be involved earlier.
Glaucoma, trauma, cataract, uveitis and senile degeneration13 may cause secondary lens displacement. Early diagnosis is important for reproductive and therapeutic purposes.
Clinical signs are reddish limbal conjunctiva and sclera,
vitreous hernia, aphachic crescent, variations in the pupillary
shape, alterations in the PLR for pupillary block, variations
in the IOP and depth of the anterior chamber, with irido and
phacodonesis. Later glaucoma develops. Four main mechanisms have been avocated in the pathogenesis of glaucoma
in human beeings4: pupillary block caused by an anterior
luxated or subluxated lens, peripheral anterior synechiae,
postcontusion angle deformities and phacolytic glaucoma
(which has not been yet reported in veterinary medicine).
Primary glaucoma usually does not exhibits a completed
luxated lens. It stays attached at a side of the ciliary processes usually. In primary luxation usually the lens is free at 360.
Anterior luxation is often an acute case with pain and
discomfort (increased lacrimation and blepharospasm).
Sometime a superficial examination, with a narrowed palpebral fissure, may not be able to recognise the non cataractous
lens in the anterior chamber. In our experience it can happen
more easily in the cat. A recurrent anterior luxation must be
suspected when a central posterior corneal oedema is present. When a complete corneal oedema comes with anterior
luxation, ultrasound may be helpful for diagnostic purposes.

*Personal data

Diagnosis can be easily achieved with a slit lamp. Use of


a mydriatic agent is strongly advised to pick up the early
cases. The other eye must be always thoroughly examined.
A gonioscopy must be achieved in the other eye when a
glaucoma and lens displacement is present in one eye. It is
important to educate the pet owner about the high risk for
the normal eye in primary displacement and the importance
to have it examined early in case of clinical signs.

i
SLIT LAMP EXAMINATION.
NORMAL EYE.

K CORNEAL SLIT
I IRIDAL SLIT
L ANTERIOR CAPSULE SLIT

i
k

SUBLUXATION

i
k

POSTERIOR LUXATION

Treatment varies depending on the site and degree of the


lens displacement.
Surgical indications are:
Anterior and posterior chamber luxation.
Mature or hypermature cataract.
Lens induced uveitis.
Inadequate visual function caused by the displaced lens.
Increased subluxation of the lens.

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Med Vet, Dipl ECVS


Private Practitioner, Firenze - Italy

344

In case of subluxation conservative treatment may be decided. The animals physical activity should be reduced and
clinical monitoring should be advised. Myotics may be contraindicated because Blood Acqueous rupture and uveitis,
and increasing possibilities of pupillary block. Locally applied NSAID may be used. Flurbiprofen 0.03% was shown
to be the most effective topical agent in preventing a rise in
IOP along with inflammatory diseases.7
Surgery maybe an option. ICLE is the rule. A 160 keratotomy must be performed to have enough room to extract
the lens without damaging the corneal endothelium. Cryoestraction is the preferred method and in this cases the posterior capsule is still well anchored to the patellar fossa and a
huge anterior vitrectomy must often be accomplished. An
automated vitrector allows best results, decreasing retinal
traction and detachment.
When the lens is anteriorly luxated an ICLE is mandatory. A partial anterior vitrectomy is usually necessary and the
surgery should be made early because pupillary block may
develop. Anterior luxations have a less favourable long term
prognosis in respect of the posterior luxations.
In order to achieve a postoperative emmetropia, intraocular lenses can be inserted with ciliary sulcus fixation.11,14
The most recent lenses have a larger optic part, in order to
mechanically maintain the vitreous body at its place.
Surgery is not commonly performed with posterior vitreal luxations.
Very important is the use of a myorelaxant non-depolarizing agent (atracurium besylate) during anaesthesia. Anaesthesia has to be assisted for ventilation and thoroughly monitorized. This allows a natural esposition of the globe, without any traction or pression on the globe from forceps, stay
sutures or extraocular muscles, decreasing the incidence of
vitreous prolapse and retinal damages during surgery.
Postoperative complications are frequent and widely
constituted by glaucoma. Retinal detachments and degenerations are also possible. Cataract develops after a lens displacement.
Glaucoma is the main concern in veterinary medicine as

4th European FECAVA SCIVAC Congress

well in human cases, making a long term prognosis quite poor.


Long term follow-ups are lacking in veterinary field.
Among the few data available1, the longest follow up was after 12 months on 15 cases out of 57. 47% of these had poor
exit, most of them represented by glaucoma development.

References
1.

2.
3.

4.

5.

6.
7.
8.
9.
10.
11.

12.

13.
14.

Glover T., Davidson M.G., Nasisse M.P., Olivero D.K The intracapsular Extraction of Displaced Lenses in Dogs: a retrospective Sudy of
57 cases (1984-1990) JAAHA 1995, Vol. 31, 77-81.
Martin C.L. Zonular defects in the dog: a clinical and scanning electron microscopic study. JAAHA 1978, 14, 571-579.
Molleda J.M., Martin E., Ginel P.J., Novales M., Moreno P., Lopez R.
Microphakia Associated With Lens Luxation in the Cat. JAAHA
1995, 31, 209-212.
Jaffe N.S., Jaffe M.S., Jaffe G.F. Lens Displacement in Catarct
Surgery and its Complications Jaffe N.S., Jaffe M.S., Jaffe G.F. 6th
Ed., 1997, Mosby Year Book.
Wheatley H.M., Traboulsi E.I., Flowers B.E., Maumenee I.H., Azar
D., Reed E.P., Whittum-Hudson J.A. Immunohistochemical Localization of Fibrillin in Human Ocular Tissues Arch. Ophthalmol. Vol.
113, 1995, 103-109.
Aguirre G.D., Bistner S.I. Microphakia with lenticular luxation and
subluxation in cats. Vet. Med. Sm. An. Cl., pag. 498, Maggio 1973.
Opremcak E.M. Antiinflammatory Agents in Mauger T.F., Craig
E.L. Haveners Ocular Pharmacology 6th. Ed. 1994, Mosby.
Curtis R. Lens luxation in the dog and cat Vet. Cl. of North Am.
Sm. An. Pract. 20, 3, pp 755-773, 1990.
Foster S.J., Curtis R., Barnett K.C. Primary lens luxation in the Border Collie. J. Small Anim. Pract., 27, pp. 1-6, 1986.
Priester W.A. Congenital ocular Defects in Cattle, Horses, cats, and
Dogs JAVMA, vol. 160, N 11, June 1, 1972, 1504- 1511
Nasisse M.P., Glover T.L., Davidson M.G., Nelms S., Sullivan T.
Technique for the Suture Fixation of Intraocular Lenses in the Dog.
Vet & Comp. Ophthalmology, vol 5, N 3, 146-150, 1995.
Lazarus J.A., Pickett P., Champagne E.S. Characterization and Heritability of primary Lens Luxation in a Related Family of Non-Inbred
Chinese Shar Peis Proceedings of the 28th ACVO Meeting, Santa
Fe, November 15-18 1997.
Fischer C.A. Geriatric ophthalmology Vet. Clin. of North Am., 19,
1, pag. 103, 1989.
Nasisse M.P., Glover T.L. Surgery for Lens Instability Vet. Cl. Of
North Am., Small An. Pract., Vol.27, N 5, 1175-1192, 1997.

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345

Thoraco-lumbar disc disease


Stefano Pizzirani

The commonest site for intervertebral disk disease


(IVDD) is the thoraco-lumbar area. Janssens reports 1-2% of
all dogs exhibits clinical signs of thoraco-lumbar disk disease (TLDD) during their life time and that 50% of dogs examined at the pathology table have some degree of TLDD.
65-75% of TLDD involves the T11-L2 spaces and T12-T13
and T13-L1 are the commonest.
Chondrodistrophic breeds show the highest incidence
but even in the non-chondrodistrophic breeds this pathology
is becoming frequent because the attention and diagnostic
skill is increasing. Anyway the Dachshund accounts for the
45-65% of cases.
Hansens classification has become too simplistic. Many
different ways of IVDD is encountered in all breeds.
Protrusion (acute): sudden collapse of the intervertebral
space with annular protrusion or intrannular estrusion. The
IV space may be reduced or not. This kind of disease is seen
in chondrodistrophic and non- chondrodistrophic breeds.
Symptoms are acute, with back pain and different degree of
impaired limb function. Myelographic signs show different
degrees and extension of cord oedema with tapering of subaracnoidal space.
Protrusion (chronic): older patients are usually involved. Large breed dogs are usually more commonly interested but it is not uncommon to see this pathology in chondrodystrophic breeds too. Usually signs are much less severe
than those encountered with acute protrusion, and often are
episodic findings during myelograms performed for other
purposes. It is common to find multiple chronic protrusion,
especially in the thoracolumbar area and they can be challenging a diagnosis for ataxia in large breed dogs suffering
with lumbosacral DJD also and suspected to have also Degenerative Myelopathy. Quite often multiple chronic protrusion are found cranial or caudal to an acute extrusion. Stiffness of the column in the tract interested by multiple chronic protrusion may favour the dynamic stress of the adjacent
IV space. Myelographic signs are spinal cord compression,
with diminished spinal cord width but with normal evidence
of the corresponding subaracnoidal space filled with the dye.
Intrannular or subligamentous extrusion: the torn annulus fibrosus is partially or completely invaded by nucleus
material, which stays anyway under the dorsal longitudinal
ligament (DLL). It is an acute or chronic phenomenon.
Acute ones come along with acute trauma to the spinal cord,
confined at the intervertebral junction. The extrusion may be
perfectly central, that is the main reason because it stays un-

der the DLL. In these cases surgery may be challenging and


asks for a dorsal fenestration and decompression; damage to
the spinal cord must be reduced to a minimum, but the cord
has to be moved and touched anyway in order to cut the windows in the dorsal annular ligament. Surgery is easier for
paramedian extrusion.
Chronic ones can undergo calcific metaplasia with ossification of the mass in the neuronal channel. They are not a
good indication for surgery.
Extraligamentous extrusion: nucleus polposus material
invades the neural channel, contacting the dura and migrates
at different levels long the dorsal bodies of the vertebrae.
Most of them are very acute. Some migrate in days or
weeks, pointing out it is not the amount of material which it
is important for the clinical signs or the prognosis but the velocity with which it hits the spinal cord.
In the sagittal plane Protrusion/Extrusion (PE) can be
median (1), paramedian (2), lateral (3) and foraminal (4).
(Fig 1).
Median and paramedian PE are usually under the DLL.
Lateral are usually extruded with nucleus material migrating
inside the neural channel. Foraminal are less frequent; they
show lateral back pain if T-L. A root signature (lameness,
limb movement pain) is evident if L4-L5 or caudal spaces
are interested.. Neurological signs are not so evident, because one root involvement only.
The division is mainly theoretical and mixed forms may
be possible.
Clinical signs may vary depending on several parameters. The most important is the velocity with which the PE
hits the cord. Some protrusion are more invalidating of slow

v v

12

Figure 1

3v

MAIN PROGRAMME

Med Vet, Dipl ECVS


Private Practitioner, Firenze - Italy

346

progressive massive extrusion.


Depending on the severity of neurological signs, patient
are divided into different classes:
Class 1. Only back pain. No neurological signs. Animal
show kifosis, reluctance to move, abdominal muscle contraction that can be erroneously misdiagnosed as acute abdomen. Around 10% of spinal cord compression can be
detected at myelography in these cases, especially in the
chronic ones.
Class 2. Proprioceptive deficits, mild ataxia, ambulatory
paraparesis.
Class 3. Non ambulatory paraparesis. If helped can stand.
Continent with normal pain sensation.
Class 4. Severe paraparesis/plegia with possible loss of
continence. Deep pain sensation is maintained.
Class 5. Paraplegia with incontinence and loss of pain
sensation.
Perhaps each of the previous classes should be divided
into another subclass time related:
A. peracute. Signs appeared within 12 hours.
B. acute. Signs appeared between 12-48 hours
C. subacute. Signs present for more than 48 hours.
D. chronic. Signs present for more than 7 days.
In class (4) 5 it is of prognostic relevance the time has
past since the occurrence of clinical signs, with less
favourable prognostic fate for a time >36-48 hours.
Myelomalacia may be a complication in the more severe
cases.

Diagnosis
Myelography is mandatory. Surgical approaches should
not be chosen without a myelogram. 28 32 % of fault is
reported in correct intervertebral space identification on
plain radiograph only. Then, in acute cases, lateralization
based on clinical signs shows 35% of inaccuracy, as many
are controlateral extrusions.
Lumbar puncture is the preferred method for TL-IVDD.
L7-L6 space or crania till L4-L5 are the preferred sites. 0.3
0.4 ml/kg of ioexol or iopamidol or iotrolan 240 mg/ml (also ioexol or iopamidol 300 mg/kg can be used) are used with
slow progression injection. We use lateral positioning of the
patient and take our first films after _ - 1/3 of the total calculated dosage, leaving the needle in position with extension
tube to the syringe. This allows to finely delineate the contour of the lesion. If high compression force is felt on dye
progression, we stop and take an exposure film. This allows
not to have epidurography confusing the image obtained.
Then we continue to inject the dye until the complete dosage
is given.
The dye can be forced beyond the compression site, allowing the delineation of the lesion. This cannot be possible
with the myelogram performed by cisternal puncture. A
swollen cord can avoid the progression of the contrast medium and if the swelling is remarkable, the dye can stop few
sapaces before the one interested by the PE.
Cisternal puncture may be necessary in cases of large
breed dogs with DJD of the articular facets of the lumbar vertebrae, with osteophytes interfering with needle insertion.

4th European FECAVA SCIVAC Congress

Lateral, ventro dorsal and bilateral oblique projections


are necessary to determinate the precise localisation of the
compression. When cord swelling does not allow the left or
right side, we look at the VD projection and chose the side
where the dye column is longer cranially and caudally (see
the picture 2).

PE side

Figure 2

Treatment
Conservative treatment is usually adopted for cases included in class 1 at the first episode. Conservative treatment
means cage rest for at least 3-4 weeks. This is not easy to
obtain from pet owners who have less tendency to apply the
rule of a strict confinement especially after few days or a
week when the animal gets better and starts to behave physically normal. Limitation of movement should be adopted
for 2 months (leash control, avoiding sport performances
and heavy work).
Analgesics, NSAID and corticosteroids, although beneficial, may have contraindication in case of free movement. .
In fact they reduce pain and the animal looses the spontaneous limitation of movement. They start moving normally
and several time this greatly aggravates the case. Theoretically then corticosteroids slow down collagen healing of annular fibers.
In acute cases methylprednisolone sodium succinate (30
mg/kg) should be used into the first 8 hours as free radical
scavenger. Then 15 mg /kg must be given every 6 hours within the 24 hours from the event in acute grave spinal trauma.
40-48% of relapses are reported in case of conservative
treatment.
Decompressive surgery should be used for dogs with
neurological signs.
Surgical therapy consists in different choices and techniques:
Dorsal laminectomy: consists in drilling away dorsal
lamina of the interested vertebrae. Articular facets should be
saved in order to avoid fibrous tissue compression postsurgically. If lateral facets are drilled away it is a very destabilising technique. With this approach it is almost impossible to
get access to a ventral disc. Decompression is mostly
achieved by giving dorsal room to the cord.
Hemilaminectomy: the lateral articular processes are
drilled away. The approach at the disc is lateral so a correct
rmyelographic localisation is mandatory. Allows often complete disc removal without damaging the cord. In case of intrannular/subligamentous estrusion it is possible to perform
a dorsal fenestration.

4th European FECAVA SCIVAC Congress

Prognosis
Prognosis varies upon different factors:
Clinical class
Time past since episode
Weight of the patient and his attitude
Relapse
A success rate of 80-96% is reported for classes 2,3,4 if
surgery performed within 48 hours from the episode. This
rate lowers to 56% for class 5 if within 12 hours, to 25%
from 12 to 36 hours and goes to 5% or less if surgery in class
5 is performed after 48 hours.
Relapses are from 2.67% to 26.55 for those underwent
surgery. 48% for those treated conservatively. These high
variations depend on techniques adopted. Standardisation in
clinical grading and surgical choices has not been yet
achieved. Neuroradiological skill, clinical grading and surgeons skills and techniques are factors influencing the outcome.

References
1.
2.

3.

L.A.A. Janssens Thoracolumbar disc herniation in the dog Vlaams


Diergeneeskd Tijdschr 59, 128-136, (1990).
N.D. Jeffery Treatment of acute and chronic thoracolumbar disc disease by minihemilaminectomy. J. Small Anim. Pract. (1988) 29,
611-616.
S.T. Simpson Intervertebral disc disease Vet. Cl. Of North Am. Sm.
An. Pract. 22, 4 889-897, 1992.

4.

S.H.Levine, D.D.Caywood Recurrence of neurological deficits in


dogs treated for thoracolumbar disk disease J.A.A.H.A. 20, 6, 889894, 1984.
5. J.Harari, S.L.Marks Surgical treatments for intervertebral disc disease. Vet.Cl. of North Am., Sm.An.Pract., 22, 4, 899-915, 1992.
6. R.M.Kirberger, C.J.Roos, A.M.Lubbe The radiological diagnosis of
thoracolumbar disc disease in the dachshund Vet. Rad. & Ultrasound, Vol. 33, N 5, 1992 255-261.
7. A.M. Lubbe, R.M. Kirberger, F.J.M. Verstraete Pediculectomy for
thoracolumbar spinal decompression in the duchshund JAAHA, vol.
30, N 3, 233-238, 1994.
8. S.J. Butterworth, H.R. Denny Follow-up study of 100 cases with
thoracolumbar disc protrusions treated by lateral fenestration J. Sm.
Anim. Pract., (1991), 32, 443-447.
9. J.D. Smith, S.M. Newell, S.C. Budsberg, R.A. Bennett Incidence of
contralateral versus ipsilateral neurological signs associated with lateralised Hansen type I disc extrusion J. Sm. Anim. Pract., (1997) 38,
495-497.
10. J.C. Yovich, R. Read, C. Eger Modified lateral spinal decompression
in 61 dogs with thoracolumbar disc protrusion J. Sm. Anim. Pract.,
(1994), 35, 351-356.
11. J.M. Fingeroth Treatment of canine intervertebral disk disease: recommendations and controversies in Bonagura J.D. Kirks Current
veterinary Therapy XII Small Animal Practice 1995, W.B. Saunders Co, Philadelphia.
12. J.M. Fingeroth Fenestration: Pros and Cons in Thacer C. Intervertebral Disc Disease problems in vet. Med., Vol. 1 N 3, 445-466, 1989.
13. T.L. Walker, C.W. Betts Intervertebral Disc Disease in Slatter D.H.
Textbook of Small Animal Surgery 1985, W.B. Saunders Co,
Philadelphia.
14. J.P. Toombs, M.S. Bauer Intervertebral Disc Disease in Slatter,
D.H. Textbook of Small Animal Surgery 2nd Ed., 1993, W.B.
Saunders Co., Philadelphia.
15. R.M. Jerram, R.C. Hart, K.S. Shulz Postoperative Management of
the Canine Spinal Surgery Patient part I Compendium, Vol. 19, N
2, 147-161, 1997.
16.R.C.Hart, R.M.Jerram, K.S.Shulz Postoperative Management of the
Canine Spinal Surgery Patient - part II Compendium, Vol. 19, N 10,
1133-1146, 1997
17. H.R. Sukhiani, J.M. Parent, M.A.O. Atilola, D.L. Holmberg Intervertebral disk disease in dogs with signs of back pain alone: 25 cases (1986-1993) JAVMA, Vol 209, N 7, 1275-1279, 1996.
18. J.P. Bray, H.M. Burbidge The canine intervertebral disk- part one:
structure and function JAAHA, Vol.34, N 1, 55-63, 1998.
19. J.P. Bray, H.M. Burbidge The canine intervertebral disk part two:
degenerative changes nonchondrodystrophoid versus chondrodystrophoid disks JAAHA, Vol. 34, N 2, 135-144, 1998.
20. N.J. Olby, J. Dyce, J.E.F. Houlton Correlation of plain radiographic
and lumbar myelographic findings with surgical findings in thoracolumbare disc disease J. Sm. Anim. Pract., (1994), 35, 345-350.
21. R.G. Prata Neurosurgical Treatment of Thoracolumbar Disks: the
rationale and Value of Laminectomy with Concomitant Disk Removal JAAHA, Vol. 17, N 1, 17-25, 1981.
22. P. Muir, K.A. Johnson, P.A. Manley, R.T. Dueland Comparison of
hemilaminectomy and dorsal laminectomy for thoracolumbar intervertebral disc extrusion in dachshunds J. Sm. Anim. Pract. (1995),
36, 360-367.
23. A. Schulman, C.L. Lippincott Dorsolateral hemilaminectomy in the
treatment of Thoracolumbar Intervertebral Disk Disease in Dogs
Compendium, Vol.9, N 3, 305-310, 1987.
24. H.W. Scott Hemilaminectomy for the treatment of thoracolumbar
disc disease in the dog: a follow-up study of 40 cases J. Sm. Anim.
Pract. (1997), 38, 488-494.
25. S.J. Wheeler, N.J.H. Sharp Small Animal Spinal Disorders. Diagnosis and Surgery Mosby-Wolfe, London, 1994.

MAIN PROGRAMME

Durotomy: Dura opening is performed when cord oedema or myelomalacia or intradural hematoma is suspected.
Inspection and swelling relief may be possible. It is important to open the dura as long as 1 o 2 vertebral body length.
Pediculectomy (minihemilaminectomy): Less destabilising technique. Removal of vertebral accessory process is a
less invasive technique but allows very limited channel exposure and inspection. Can be associated at the former
hemilaminectomy when multiple sites are present.
Fenestration: prophylactic procedure.. Very controversial
subject. Often personal choice of the surgeon. Should be
completely performed from T11-T12 to L3-L4. It is not a
easy procedure. Aortic damage is possible. Some authors use
this a s only treatment method. It is not a decompressive procedure. Some authors claim same reoccurrence statistics
without it.
Postoperative treatment:
Postoperative attention should be devoted to:
Pain control and treatment
Continence management and treatment
Physiotherapy
Possible complications refers to:
Gastrointestinal complications
Wound complications

347

4th European FECAVA SCIVAC Congress

349

Diagnosis and treatment of hypothyroidism


AD Rijnberk

Summary
Hypothyroidism at young age in both dogs and cats is
usually a congenital disorder, due to an enzyme deficiency
that prevents synthesis of thyroid hormones. The diagnostic
challenge in these rare disorders is the elucidation of the inborn error.
In most adult dogs with hypothyroidism it is a primary
thyroid disorder, whereby progression of an autoimmune
process leads to lymphocytic infiltration and disappearance
of thyroid tissue. The combination of a low thyroxine concentration and a high TSH concentration in plasma is diagnostic of primary hypothyroidism. However, in a number of
cases the thyroxine concentration is low without a concomitantly elevated TSH concentration. In some cases a
thyroid biopsy may be needed for a definite diagnosis. With
appropriate substitution therapy the long-term prognosis is
excellent.

Introduction
In the dog and cat the thyroid glands are separate lobes
lying beside the trachea from about the third to the eigthth
tracheal ring. They are covered ventrally by the sternohyoid
and sternothyroid muscles. Normal thyroid glands are not
palpable.
The basic functional unit of the thyroid is the follicle, a
hollow sphere of cells, about 30-300 m in diameter. The
wall of the follicle is a single layer of thyroid epithelial cells.
These follicular cells are cuboical when quiescent and
columnar when active. The lumen is filled with a proteinaceous colloid that contains a large glycoprotein called thyroglobulin, within the sequence of which the thyroid hormones are synthesized and stored.
Hormone synthesis and secretion. The main secretory
hormonal product of the thyroid gland is L-thyroxine or
3,5,3,5-L-tetraiodothyronine (T4). The other thyroid hormone, 3,5,3-L-triiodothyronine (T3), is secreted in much
smaller quantities (about 20% of that of T4). Most of the
circulating T3 is produced in peripheral tissues by outer
ring deiodination of T4.Inner ring deiodination results in
the metabolically inactive 3,3,5 triiodothyronine (reverse
T3, rT3).
Iodide, the main building block of the thyroid hormones,
is actively transported (trapped) from the extracellular flu-

id into the thyroid follicular cells, resulting in thyroid/plasma-concentration ratios of around 25. Tissues other than the
thyroid, such as gastric mucosa, salivary glands and choroid
plexus, also have an active transport mechanism for iodide.
In contrast to the thyroids, these tissues do not have the capacity for organic binding of iodide.
All of these iodide-concentrating tissues are also capable
of concentrating other structurally related monovalent anions such as thiocyanate (SCN), perchlorate (ClO4) and
pertechnetate (TcO4). However, unlike iodide, these ions
are also not organically bound in the thyroid and hence their
duration within the thyroid is short. This property together
with its short physical half-life, makes the radioactive isotope of pertechnetate (99mTcO4) a valuable radionuclide for
imaging the thyroid by scintillation scanning.
Once within the thyroid cell, inorganic iodide is rapidly
oxidized by thyroid peroxidase in the presence of H2O2 into a reactive intermediate that is then incorporated into tyrosine residues of acceptor proteins, mainly thyroglobulin.
These iodotyrosines (MIT and DIT) in thyroglobulin can
combine to form iodothyronines. Both organic binding of
iodide and coupling of iodotyrosines can be inhibited by
thiourea compounds, which are used in the treatment of hyperthyroidism. The thyroglobulin is iodinated at the apical
(follicular) border of the cell and is then brought into the
colloid by exocytosis.
For secretion, thyroglobulin is resorbed into the thyroid
cell via pinocytosis of colloid droplets. Each colloid droplet
is enclosed in a membrane derived from the apical border.
This is combined with a lysosome and as the phagolysosome
moves toward the basal aspect of the cell the droplet becomes smaller and more dense with progression of the hydrolysis of the thyroglobluin by the lysosomal proteases.
Regulation of thyroid function. Thyrotropin or thyroidstimulating hormone (TSH), a glycoprotein secreted by the
anterior lobe of the pituitary, promotes thyroid hypertrophy
and hyperplasia, and stimulates the synthesis and secretion
of thyroid hormones. This TSH secretion by the pituitary is
inhibited primarily by T3, that is produced locally from T4 by
Type II deiodinase (catalyzes deiodination exclusively at the
5-position) and also by T3 derived from the pool of free T3.
The setting of this T4/T3-TSH feedback loop is modulated by
a hypothalamic tripeptide, TSH-releasing hormone (TRH),
that stimulates TSH release, whereas somatostatin and possibly other neuropeptides inhibit TSH release.

MAIN PROGRAMME

DVM PhD
University of utrecht - The Netherlands

350

4th European FECAVA SCIVAC Congress

Hypothyroidism in young animals


Early in life the presence of thyroid hormones is crucial for
growth and development of all body tissues and particularly
the skeleton1. Hence in addition to the signs of adult-onset hypothyroidism, disproportionate dwarfism may be a prominent
sign of congenital or juvenile-onset hypothyroidism.
Juvenile-onset hypothyroidism can be congenital or acquired. Among the causes of the latter is the classic iodine
deficiency, which occurred in times when owners took too
literally the notion that dogs and cats are carnivores. A diet
consisting of meat alone is deficient in many respects and
certainly in iodine. This entity is no longer seen in countries
in which it is customary to feed manufactured diets, which
are rather rich in iodine.
Another, although also very rare, cause of acquired juvenile-onset hypothyroidism is lymphocytic thyroiditis. This is
the common cause of primary hypothyroidism in the adult
dog. Rarely the process of autoimmune destruction of the
thyroid glands occurs during adolescence and as a consequence the animal may be slightly retarded in growth, in addition to developing the signs of hypothyroidism of the adult.
Apart from the extremely rare condition of thyroid dysgenesis, congenital hypothyroidism may also occur, in both
dogs and cats, because of an enzyme deficiency that prevents
synthesis of thyroid hormones. Among these the defective
peroxydase activity is not uncommon in kittens. Animals
with this so-called organification defect concentrate iodide in
the thyroid glands but have limited ability to use this iodide
in thyroid hormone synthesis. The disorder appears to be heterogenous, for in some animals the defect is complete and no
iodide peroxydase activity can be demonstrated, while in
others it is partial. In the latter case the defect may be an abnormal localization of the enzyme within the thyroid cell.
The clinical hallmark of these defects is the combination
of goiter and hypothyroidism. The severity of both the goiter
and the hypothyroidism may vary considerably and it may
also be difficult to palpate a goiter in a very young animal.
Diagnosis. The diagnosis of hypothyroidism can be
made by measuring the concentration of circulating thyroxine. When a goiter is detected, stimulation with TSH is redundant, as the goiter is already evidence of increased endogenous TSH secretion.
The diagnostic challenge is the elucidation of the defect
in thyroid hormone synthesis that is causing the increased
TSH secretion. This requires in vivo studies with radioiodine.
In some cases there is rapid uptake of radioiodide by the thyroid but the iodide remains nonorganified, as is readily
demonstrated by the precipitous discharge of the accumulated radioactivity from the thyroids when an ion that competes
for uptake, such as perchlorate or thiocyanate, is given.2
Treatment. As in all forms of juvenile hypothyroidism except that caused by iodine deficiency, treatment consists of
oral administration of thyroxine (see next section). This will
lower the TSH secretion and as a result the goiter will shrink.

Hypothyroidism in adult animals


Hypothyroidism is the clinical syndrome resulting from

deficient production of thyroid hormone. At adult age in approximately 95 % of cases it is a primary thyroid disorder.
Only in 5 % or less of cases the disease is of (supra) pituitary
origin, i.e., secondary hypothyroidism.

Primary hypothyroidism
Pathogenesis. In the spontaneous form a progressive autoimmune process leads to lymphocytic infiltration and disappearance of thyroid tissue. Also the so-called idiopathic
forms, in which there is thyroid atrophy without inflammatory infiltrate, are generally regarded as the end result of an
autoimmune disorder. These immune-mediated destructions
are slow processes. Clinical manifestations of hormone deficiency will become evident only after a considerable amount
of tissue has been destroyed.
Although rare, there may coexist another hormone deficiency syndrome such as diabetes mellitus3. These multiple
autoimmune endocrine deficiencies are known as polyglandular failure syndromes. The combination of hypothyroidism and hypoadrenocorticism is known as Schmidts
syndrome4.
In dogs with hypothyroidism and dogs with lymphocytic
thyroiditis with or without overt hypothyroidism, circulating
antibodies to thyroglobulin (Tg), a second colloidal antigen
and to a thyroid microsomal antigen have been identified.
These autoantibodies and especially those against the microsomal fraction may initiate the complement cascade or antibody-dependent cell-mediated cytolysis resulting in further
release of thyroid antigens.
Although they may not be of great pathogenetic importance, autoantibodies against Tg may have some virtue as
markers of autoimmune thyroiditis. Circulating antibodies to
Tg have been detected in over 50 % of hypothyroid dogs.
These Tg antibodies may also occasionally interfere with radioimmunoassays used to measure plasma concentrations of
thyroid hormones, and especially T3. The occasional occurrence of T3 autoantibodies is due to antibodies recognizing a
T3-containing epitope of Tg that is different from the epitopes involved in eliciting the predominant population of canine Tg-autoantibodies5,6. These rarely (< 1 % of samples
sent to diagnostic laboratories) occurring T3 autoantibodies
may cause falsely elevated or decreased (depending on the
assay) values. T4-autoantibodies are encountered much less
frequently than T3-autoantibodies; in routine diagnostic laboratories they are observed only once in several years.
Apart from spontaneous hypothyroidism there is the iatrogenic form. This is especially seen in cats as a result of
the treatment of hyperthyroidism, a condition frequently occurring in this species. The hypothyroidism may be the result of radioiodine therapy or bilateral thyroidectomy.
Clinical manifestations. Acquired primary deficiency of
thyroid hormone is a condition of young and middle-aged
dogs (1-6 years). Dogs of larger breeds are more frequently
affected than smaller dogs. The incidence is equally distributed between male and females. So far there is only one convincing description on the occurrence of spontaneous primary hypothyroidism in the adult cat7.
The classical clinical picture of overt hypothyroidism in-

volves simultaneous manifestations from nearly all organ


systems. However, even in severe cases symptoms from a
single organ system (e.g. locomotor system) may dominate
in such a way as to distract from the causative disease. Nevertheless, centrally in the syndrome usually there is the history of slowing of mental and physical activities. Most dogs
with hypothyroidism have some degree of mental dullness,
lethargy and disinterest in exercise. These signs are gradual
in onset, often subtle and may not be recognized by the owner until after treatment has been started. Changes of hair and
skin are also common observable signs.
Differential diagnosis. As indicated above the presenting
symptoms may vary widely and therefore the most common
pitfall in the diagnosis of hypothyroidism is undoubtedly to
overlook the possibility that the presented problem(s) could
be due to hypothyroidism. For example, it is not uncommon
that dogs with hypothyroidism are presented in specialty areas such as cardiopulmonology (lethargy misinterpreted as
decrease in exercise tolerance) or orthopedics (locomotor
disturbance). With regard to the most common problem,
lethargy, the disease may be mistaken for metabolic (hepatoencephalophathy) or neurologic (encephalitis, hydrocephalus) cerebrocortical disease. As far as the atrophy of
skin and adnexa is concerned, conditions such as estrogen
excess, hyperadrenocorticism and growth hormone deficiency may also be considered.
Diagnosis. In man a low T4 level in plasma combined
with a high concentration of TSH establishes the diagnosis
of primary hypothyroidism. This approach has been impossible in the dog until recently, as a valid canine-specific assay for TSH was not available. Therefore the diagnosis of
hypothyroidism is still strongly based upon measurements of
T4 concentrations in plasma. As a measure of thyroid function T4 has to be preferred over T3, as T4 is only produced
from the thyroid gland. T3 concentrations in plasma are
largely derived from peripheral conversion and may remain
within normal limits in moderate hypothyroidism and may
be low in many non-thyroidal diseases. In addition the T3
measurements are more often than T4 measurements subject
to artifactuallly high or low results due to autoantibodies.
However, there are also many factors that can affect
basal T4 concentrations in euthyroid dogs, often leading to
a false lowering and consequently a false positive diagnosis of hypothyroidism. Of these factors, concurrent illness
and drugs (glucocorticoids, antiepileptics and analgesics)
are the most relevant. Drugs such as glucocorticoids have
multiple effects on peripheral T4 and T3 transfer, distribution and metabolism8. These effects include altered T4
binding to plasma carrier proteins, resulting in altered free
fraction levels of T4. Probably due to the multiple character of these drug- and disease-induced effects, measurements of free T4 concentrations in dogs have not provided
improvement of the diagnostic accurary above that of measurements of total T48.
Thus, where available, the TSH-stimulation test continues to be a conclusive test for the diagnosis of primary hypothyroidism. The test will distinguish depression of basal
T4 concentrations due to drugs and illness from advanced
primary hypothyroidism, but not from secondary hypothyroidism and early stages of primary hypothyroidism. Here

351

scanning with 99mTcO4-, radioiodine-uptake studies and/or


thyroid biopsy may provide the final diagnosis.
Now in many countries bTSH is no longer available the
TSH-stimulation test is disappearing from the diagnostic
scene. It has been tried to replace this test by a stimulation
test with the supra-pituitary stimulant TRH. However, the
rise in plasma T4 concentrations in healthy control dogs is
insufficient to allow any discrimination.10
The recently introduced immunoassays for the measurment of canine TSH are an important step forward. In cases
of (experimentally induced) primary hypothyroidism the expected combination of a low plasma T4 concentration and a
high TSH concentration has been found.11,12 However, in a
number of cases of primary hypothyroidism the T4 concentration is low without a concomitantly elevated TSH concentration, whereas also in euthyroid dogs elevated circulating TSH concentrations can be found.13,14,15 The lack of response of endogenous TSH to TRH stimulation may become
a useful adjunct for the diagnosis of canine hypothyroidism.15,16,17 When still in doubt about the definite diagnosis minor surgery and thyroid biopsy usually will give a definite answer. It is worth pursuing until a definite diagnosis
has been established because the decision for (life-long!)
substitutution therapy should be on solid ground.
Treatment. Although T3 is the metabolically active thyroid hormone, it is not the supplement of choice. A primary
advantage of providing the prohormone T4 is that the body
is given the opportunity to regulate the amount of T3 generated by normal physiologic mechanisms. In fact appropriate
T4 therapy results in normal levels of both T4 and T3.
Both T4-production rates and parenteral L-T4 replacement doses required to maintain euthyroidism are around 5
g per kg body weight per day. However, when T4 is administered orally the bioavailability is low and variable, due
to incomplete and variable gastrointestinal absorption. Oral
supplementation with synthetic L-thyroxine is started at a
dose rate of 10 g/kg twice daily. After two months a control examination is carried out. When blood is collected at
10-12 h after the last dose the T4 level in plasma should be
20 nmol/l. If not, the dose should be adjusted. Because of the
individual variation in intestinal absorption of T4 further
control examinations and adjustments may be needed.18
With increasing experience also the lowering of the circulating TSH concentrations may turn out to be a useful variable
for establishing the replacement dose of thyroxine.19
Prognosis. Hypothyroidism is one of the most gratifying
diseases to treat, because of the ease and completeness with
which it responds to treatment. With appropriate treatment
and follow-up examinations (every half year) all of the alterations associated with hypothyroidism are reversible. The
long-term prognosis is excellent.

Secondary hypothyroidism
In secondary or central hypothyroidism the thyroids are
not primarily affected but deprived of stimulation by TSH.
On histological examination there are no losses of follicles
but rather characteristics of inactivity. The condition is rare
compared to primary thyroid failure. The spontaneous forms

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in adult animals usually result from a tumor of the pituitary


or adjacent regions. Central hypothyroidism may also result
from surgical removal of pituitary tumors, whereby there is
of course also the possibility that it was present initially.20
Clinical manifestations. The clinical picture is similar to
that of primary hypothyroidism, although generally less pronounced. There may be lethargy and some alopecia, but the
tendency to thickening of the skin is less pronounced. Often
there is accompanying impairment in the secretion of other
pituitary hormones such as growth hormone and gonadotrophins.
Not uncommonly, the lesion causing low TSH secretion
is a hormone-secreting tumor (e.g., ACTH). The symptoms
and signs that arise from such a pituitary tumor may precede,
accompany, and even obscure the manifestations of pituitary
failure. In the example of an ACTH-secreting tumor the central hypothyroidism may only become manifest when the associated hyperadrenocorticism has been cured.
Diagnosis. Suspicion of central hypothyroidism should
arise in case of low plasma concentrations of both T4 and
TSH. This is with the condition that in all likelihood the low
T4 concentration is not caused by illness or drugs.
Apart from thyroid function, diagnostic evaluation
should include (1) the secretion of other pituitary hormones21 and (2) the pathomorphology of the pituitary and
adjacent areas by diagnostic imaging.
Treatment. Treatment with L-thyroxine can be the same
as in primary hypothyroidism. In addition, hypofunction of
other endocrine glands resulting from pituitary hormone deficiencies should be corrected.
Prognosis. In the spontaneous forms the prospects are
completely dependent upon the course of the causitive lesion
in the hypothalamus-pituitary area. In the iatrogenic form,
i.e., following total hypophysectomy, supplementation with
thyroxine (and glucocorticoids!) may enable the animal to
live a healthy life for several years.

4.

5.

6.

7.
8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

References
18.
1.

2.

3.

Saunders MH, Jezyk PK, (1991), The radiographic appearance of canine congenital hypothyroidism: Skeletal changes with delayed treatment. Vet Radiol 32:171-177.
Sjollema BE, den Hartog MT, de Vijlder JJM, van Dijk JE, Rijnberk
A, (1991), Congenital hypothyroidism in two cats due to defective organification: data suggesting loosely anchored thyroperoxidase. Acta
Endocr 125:435-440.
Eigenmann JE, Van der Haage MH, Rijnberk A, (1984), Polyendocrinopathy in two canine littermates: Simultaneous occurrence of
carbohydrate intolerance and hypothyroidism. J Am Anim Hosp Ass
20:143-148.

19.

20.

21.

Kooistra HS, Rijnberk A, van den Ingh ThSGAM, (1995), Polyglandular deficiency syndrome in a Boxer dog: thyroid hormone and glucorticoid deficiency. Vet Quart 17:59-63.
Young DW, Haines DM, Kemppainen RJ, (1991), The relationship
between autoantibodies to triiodothyronine (T3) and thyroglobulin
(Tg) in the dog. Autoimmunity 9:41-46.
Gaschen F, Thompson J, Beale K, Keisling K, (1993), Recognition of
triiodothyronine-containing epitopes in canine thyroglobulin by circulating thyroglobulin autoantibodies. Am J Vet Res 54:244-247.
Rand JS, Levine J, Best SJ, Parker W, (1993), Spontaneous adult-onset hypothyroidism in a cat. J Vet Int Med 7:272-276.
Kaptein EM, Moore GE, Ferguson DC, Hoenig M, (1992), Effects of
prednisone on thyroxine and 3,53-triiodothyronine metabolism in
normal dogs. Endocrinology 130:1669-1679.
Nelson RW, Ihle SL, Feldman EC, Bottoms GD, (1991), Serum free
thyroxine concentration in healthy dogs, dogs with hypothyroidism,
and euthyroid dogs with concurrent illness. J Am Vet Med Ass
198:1401-1407.
Frank LA, (1996), Comparison of thyrotropin-releasing hormone
(TRH) to thyrotropin (TSH) stimulation for evaluating thyroid function in dogs. J Am Anim Hosp Ass 32:481-487.
Williams DA, Scott-Moncrieff JC, Bruner J, Sustarcic D, PanosianSahakian N, Unver E, Said El Shami A, (1996), Validation of an immunoassay for canine thyroid-stimulating hormone and changes in
serum concentration following induction of hypothyroidism in dogs.
J Am Vet Vet Med Ass 209:1730-1732.
Rushig S, Kraft W, (1996), Determination of canine thyroid stimulating hormone (cTSH) in blood serum of dogs and its reaction to the
TRH stimulation test. Tierrztl. Prax 24:479-483.
Melian C, Peterson ME, Nichols CE, (1997), Evaluation of free T4
and endogenous TSH as diagnostic tests for hypothyroidism in dogs.
J Vet Int Med 11:120 (ACVIM Abstract 68).
Dixon RM, Graham PA, Harvie J, Mooney C, (1997), Comparison of
endogenous serum thyrotropin (cTSH) concentrations with bovine
TSH response test. Results in euthyroid and hypothyroid dogs. J Vet
Int Med 11:121 (ACVIM Abstract 69).
Hoppen HO, Lohmann P, Schlote S, Gnzel-Apel AR, Mller-Knig
A, Grnau B, Hmmerling R, Leidingern K, Morisse B, Nolte I,
(1997), Die Messung von caninem TSH zur Diagnostik der Hypothyreose des Hundes. Prakt Tierarzt 78:13-17.
Hoenig M, Ferguson DC, (1997), Comparison of TRH-stimulated
thyrotropin (cTSH) to TRH- and TSH-stimulated T4 in euthyroid, hypothyroid, and sick dogs. J Vet Int Med 11:121 (ACVIM Abstract 71)
Scott-Moncrieff JC, Nelson RW, (1997), Response of serum canine
thyrtropin (cTSH) to stimulation by thyrotropin releasing hormone
(TRH) in euthyroid dogs, hypothyroid dogs, and euthyroid dogs with
concurrent disease. J Vet Int Med 11:121 (ACVIM Abstract 70).
Rijnberk A, (1996), Clinical Endocrinology of Dogs and Cats. Kluwer Academic Publishers, Dordrecht/Boston, 43-48.
Ferguson DC, Hoenig M, (1997), Re-examination of dosage regimens for l-thyroxine (T4) in the dog: Bioavailability and persistence
of TSH suppression. J Vet Int Med 11:121 (ACVIM Abstract 72).
Meij BP, Mol JA, Bevers MM, Rijnberk A, (1997), Residual pituitary
function after transsphenoidal hypophysectomy in dogs with pituitary-dependent hyperadrenocorticism. J Endocrinol 155:531-539.
Meij BP, Mol JA, van den Ingh TSGAM, Bevers MM, Hazewinkel
HAW, Rijnberk A, (1997), Assessment of pituitary function after
transsphenoidal hypophysectomy in beagle dogs. Domest Anim Endocrinol 14:81-97.

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353

Diagnosis and treatment of hyperadrenocorticism


AD Rijnberk

Summary
The diagnosis of hyperadrenocorticism can be made according to two principles: (1) to test the integrity of the feedback system, and (2) to measure cortisol production. In the
first approach the sensitivity of the pituitary-adrenocortical
system to suppression is tested by administering dexamethasone in a dose that discriminates between healthy animals
and animals with hyperadrenocorticism, that is the low-dose
dexamethasone suppression test (LDDST). In the second approach an integrated reflection of the corticoid production is
obtained by measuring urinary corticoids (largely cortisol)
in relation to the creatinine concentration, known as the urinary corticoid/creatinine ratio (UCCR). Pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to
adrenocortical tumor can be distinguished with the highdose dexamethasone suppression test (HDDST), in which either plasma cortisol levels or UCCRs can be used. The latter has the advantage of combining both the diagnosis and
the differential diagnosis in one test procedure..
Also for the treatment of pituitary-dependent hyperadrenocorticism two principles can be followed: (1) elimination of the stimulus for the augmented production of cortisol,
i.e., the pituitary lesion causing excessive ACTH secretion,
and (2) elimination of the glucocorticoid excess. In the first
approach hypophysectomy is the best option, but it requires
a team of (super)specialists (neurosurgeon, endocrinologist,
radiologist and pathologist), whereby the skill and the experience of the neurosurgeon are crucial. The glucocorticoid
excess can be eliminated by bilateral adrenalectomy or by
adrenocorticlysis with o,p-DDD.

Introduction
Synthesis and release of glucocorticoids (and androgens)
by the two inner zones of the adrenal cortex is almost exclusively controlled by the pituitary hormone ACTH. The production of aldosterone in the outer zone (zona glomerulosa)
is regulated by the volume and potassium status of the organism by a complex, multifactorial and almost exclusively
extrapituitary control system, the renin-angiotensin system.
Glucocorticoid and especially cortisol secretion is directly dependent on the plasma concentration of ACTH or corticotropin. Chemically ACTH is a single-chain peptide comprising 39 amino acid residues. In the anterior lobe (AL) it

is synthesized from a well-characterized precursor molecule


pro-opiomelanocortin (POMC), which also gives rise to a
number of other peptides that are co-released with ACTH. In
dogs and cats the pars intermedia (PI) contains two cell
types that also can synthesize POMC. One cell type is similar to the corticotropic cells of the anterior lobe. In the other
cell type ACTH is cleaved into ACTH1-14 (precursor of MSH) and corticotropin-like intermediate-lobe peptide.
ACTH secretion by the anterior pituitary is regulated by
the hypothalamus and central nervous system via neurotransmitters that cause the release of hypophysiotropic hormones such as corticotropin-releasing hormone (CRH) and
arginine-vasopressin (AVP). In this neuroendocrine control
four mechanisms can be distinguished: (1) episodic secretion and possible diurnal rhythm of ACTH, (2) response to
stress, (3) feedback inhibition by cortisol, and (4) immunological factors.
Central nervous system events regulate both the number
and magnitude of ACTH and -MSH bursts. The ACTH
bursts range in the dog from 6 to 12 per 24-h period1 and the
-MSH bursts from 1 to 11 per 24 h2. ACTH and cortisol are
secreted within minutes following the onset of stresses such
as surgery and hypoglycemia. Stress responses originate in
the central nervous system and cause an increased release of
the hypothalamic hypophysiotropic hormones such as CRH
and AVP. These stress responses are reduced or totally abolished by prior high-dose glucocorticoid administration and
also less pronounced in spontaneous hyperadrenocorticism3.
Dogs and cats differ considerably in their responses to
stress. In dogs several emotional or neurogenic stresses do
not result in stimulation of ACTH secretion or MSH secretion.4 In cats, on the other hand, mild stresses such as handling and intradermal skin testing cause impressive increases
in the plasma concentrations of cortisol, ACTH and -MSH. In
contrast to dogs, cats appear to have a more actively secreting pars intermedia that is strongly responsive to stress5.

Adrenocortical hyperfunction;
Cushings syndrome
Hyperadrenocorticism is defined as the complex of physical and biochemical changes that is the result of chronic
glucocorticoid excess, whatever its cause. Apart from the exogenous form of the disease due to glucocorticoid therapy,
there are two endogenous forms in both the dog and the cat:

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DVM PhD
University of utrecht - The Netherlands

354

(1) ACTH-dependent, and (2) ACTH-independent.


In the ACTH-dependent form there is chronic ACTH hypersecretion, resulting primarily in hypersecretion of cortisol
and in hyperplasia of the two inner zones of the adrenal cortices. In this form, which accounts for about 85% of cases,
the ACTH excess originates form the pituitary; an ectopic or
paraneoplastic ACTH syndrome has not been recognized in
dogs and cats so far. Thus for these two species the name for
this category can be more specific: pituitary-dependent hyperadrenocorticism. ACTH-independent hyperadrenocorticism is due to autonomous glucocorticoid-secreting adrenocortical adenomas or carcinomas and comprises about 15%
of cases. The simultaneous occurrence of both pituitary-dependent hyperadrenocorticism and autonomously hyperfunctioning adrenocortical tumor has been described.6

Pituitary-dependent hyperadrenocorticism
There is increasing evidence that the ACTH excess is the
result of a process of tumorigenesis, that may be a multi-step
process requiring more than one mutation in the protooncogenes involved in hormone production and/or cell proliferation. An inherited aberration may be the earliest step7. The
process does not seem to be dependent upon continuous hypothalamic stimulation8. In about one-fourth to one-fifth of
cases an adenoma in the PI is found, but tumors in both lobes
may also occur9. This is of clinical interest not only because
the PI tumors tend to be larger than the AL tumors9, but also
because of the specific hypothalamic control of hormone
synthesis in the PI. The PI is under direct neural control.
This is principally a tonic dopaminergic inhibition, which
suppresses the expression of glucocorticoid receptors. This
explains why cases of pituitary-dependent hyperadrenocorticism of PI origin are resistant to suppression by dexamethasone10. However, this is not an absolute difference from AL
lesions, as pituitary lesions causing hyperadrenocorticism
may not maintain the regulation characteristics of the lobe of
origin. There does not seem to exist a dichotomy in the suppressive effect of dexamethasone, but rather a sliding scale.
The degree of insensitivity to glucocorticoid feedback is correlated with the size of pituitary corticotrophic adenomas.11
Clinical manifestations. Many of the signs and symtoms
can be related to the actions of glucocorticoids, that is, increased gluconeogenesis and lipogenesis at the expense of
protein. In dogs the cardinal physical features are centripetal
obesity and atrophy of muscles and skin with adnexa. In addition polyuria and polyphagia are often dominating features.
In dogs the polyuria is known to be due to both impaired osmoregulation of vasopressin release and interference of the
glucocorticoid excess with the action of vasopressin.
In cats the situation is somewhat different from that in the
dog. The cutaneous manifestations are initially less pronounced than in the dog. Furthermore glucocorticoid excess
gives rise less readily to polyuria/polydipsia in this species
than in dogs, and it may become obvious only when diabetes
mellitus develops. Cats seem to be much more susceptible
than dogs to the diabetogenic effects of glucocorticoids. In
the vast majority of the described cases of feline hyperadrenocorticism the disease was associated with diabetes mel-

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litus and the suspicion of hyperadrenocorticism has often


arisen specifically because of insulin resistance encountered
in the treatment of diabetes mellitus. Only about 10% of dogs
with hyperadrenocorticism develop overt diabetes mellitus.
Among the routine laboratory data a consistent finding
(in dogs only!) is an elevation of the plasma concentration of
alkaline phosphatase (AP)13. This is due to the induction of
an isoenzyme which has greater stability at 65 oC than other
AP-isoenzymes and is therefore easily measured by a routine laboratory procedure. It is also noteworthy that in the
majority of dogs with hyperadrenocorticism decreased T4
concentrations are found, which seems to be a consequence
of altered transport, distribution, and metabolism of T4,
rather than hyposecretion.
Diagnosis. There are two ways to make the diagnosis:
(1) to test the integrity of the feedback system, and (2) to
measure urinary corticoid excretion.
In the first approach the sensitivity of the pituitaryadrencortical system to suppression is tested by administering a synthetic glucocorticoid in a dose that discriminates
between healthy animals and animals with hyperadrenocorticism. A potent glucocorticoid such as dexamethasone is
used in order that the administered compound may be given
in such small amounts as not to contribute significantly to
the steroids to be analyzed. In this so-called dexamethasone
screening test or low-dose dexamethasone suppression test
(LDDST), 0.01 mg dexamethasone per kg body weight is
administered intravenously in the morning. Blood for cortisol measurement is collected 8 h after dexamethasone administration. In healthy animals the plasma cortisol concentrations are still depressed at this time, whereas in animals
with hyperadrenocorticism they have remained high or may
have escaped from initial suppression.
This LDDST is increasingly replaced by the second approach, i.e., the measurement of urinary corticoids. In this
way an integrated reflection of the corticoid production is
obtained, thereby adjusting for fluctuations in plasma levels.
The urinary corticoids (largely cortisol) are measured by radioimmunoassay and related to the creatinine concentration,
thus providing the urinary corticoid/creatinine ratio (UCCR). This test requires little time from the veterinarian, is
not invasive (no blood collection), has a high diagnostic accuracy and easily allows follow-up examination for the purpose of documenting remission and recurrence.14,15 In addition the test procedure has the advantage of combining a test
for basal adrenocortical function and a dynamic test for differential diagnosis (see below). The test can be used in both
dogs and cats, albeit in cats with higher reference values
than in dogs.16
Once the diagnosis of hyperadrenocorticism has been
made it is necessary to distinguish between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to
adrenocortical tumor. Despite a decreased sensitivity to suppression by glucocorticoids, the ACTH secretion of most animals with pituitary-dependent hyperadrenocorticism can be
suppressed with a 10-fold higher dose of dexamethasone, resulting in a decreased cortisol secretion. The autonomous
hypersecretion by adrenocortical tumors will not be influenced by the high dose of dexamethasone. Two procedures
are used, one employing plasma cortisol as a reflection of

adrenocortical secretion and the other urinary corticoid/creatinine ratios. In both, a greater than 50% decline from baseline values is regarded as diagnostic for pituitary-dependent
hyperadrenocorticism.17
When suppression is less than 50%, the hyperadrenocorticism may be due to either an adrencortical tumor or a pituitary ACTH excess that is extremely resistant to dexamethasone suppression.18 For the differentiation between these two
forms, measurements of endogenous ACTH are necessary.
In the great majority of the dogs with adrenocortical tumor
the basal ACTH values are completely suppressed.
In the rare situation of questionable ACTH values, which
for example might be due to the simultaneous occurrence of
both entities6, further studies are required. These may include
a CRH-stimulation test17 and visualization of the adrenal
glands and the pituitary. It may also be helpful to measure
plasma concentrations of -MSH. High values may be found
especially in cases of intermediate lobe tumors, which tend to
be dexamethasone resistant and rather large (see also above).
Once the biochemical work-up indicates the presence of
pituitary-dependent hyperadrenocorticism, the pituitary is
visualized if possible. This visualization is imperative in institutions where hypophysectomy or pituitary irradiation are
options for treatment. If this is not the case then visualization still gives insight into the prognosis.
Treatment. The treatment of pituitary-dependent hyperadrenocorticism should be directed at the elimination of the
stimulus for the augmented production of cortisol, i.e., the
pituitary lesion causing the excessive ACTH secretion. Particularly because there is increasing evidence that these lesions are of primary pituitary origin (see above) and not the
result of increased hypothalamic stimulation8, hypophysectomy is being revisited19. Visualization techniques have become available that enable presurgical insight into the size
and expansion of the lesion. This in combination with improved surgical and anesthetic techniques now permits removal of rather large tumors. Also because in this approach
the causative lesion is removed, this may become the
method of choice in dogs and cats, as it is in man. The animals need lifelong replacement therapy with thyroxine and
cortisone. In addition there may be transient diabetes insipidus, requiring treatment for some time.
Other approaches are directed at the elimination of the
glucocorticoid excess, either by bilateral adrenalectomy or by
chemotherapy. With total adrenalectomy the cure is 100%
and the prognosis with glucocorticoid and mineralocorticoid
replacement is good, unless the expansion of the pituitary lesion gives rise to neurologic signs. Details on the peri- and
postoperative medication are given in section. Probably because of the effectiveness and relative convenience of
chemotherapy with o,p-DDD, bilateral adrenalectomy is
hardly used in dogs. As o,p-DDD in cats does not give satisfactory results, in this species bilateral adrenalectomy has
been used most often to treat pituitary-dependent hyperadrenocorticism. It is often successful but from the experience
with the few cats that have been operated it has been concluded that long-term prognosis is guarded20. As in dogs, hypophysectomy may become a more attractive approach.
Currently the most common form of treatment of pituitary-dependent hyperadrenocorticism in the dog is still the

355

administration of the adrenolytic drug o,p-DDD (Lysodren, Bristol Laboratories). Many schedules aim at the selective destruction of the adrenal cortices, i.e., the destruction of the zona fasciculata and zona reticularis, while sparing the zona glomerulosa. However, in 5-6% of the dogs the
zona glomerulosa is destroyed to such an extent that iatrogenic hypoadrenocorticism occurs21 In more than half of
cases there are one or more relapses of hyperadrenocorticism during treatment21.
In order to circumvent these complications a treatment
schedule has been introduced that is aimed at the complete
destruction of the adrenal cortices and substitution therapy
for the induced adrenocortical insufficiency22:
- 50 to 75 mg o,p-DDD/kg per day is given for 25 days.
This daily dose should be divided into three or four portions and administered with food.
- On the third day, supplementations begins:
Cortisone, 2 mg/kg per day
Fludrocortisone, 0.0125 mg/kg per day
Sodium chloride, 0.1 g/kg per day
All doses are divided into at least two administrations.
After 25-30 days, a follow-up examination is made. The
cortisone dose is reduced to 0.5-1.0 mg/kg per day. Fludrocortisone and/or salt are adjusted according to the results of
measurements of Na and K in plasma.
Owner compliance is imperative for good results; written
instructions for owners should be provided.23 During the first
month the owner is requested to report by telephone at least
once a week and as often as questions or problems arise. The
owner is also instructed very clearly to stop o.p-DDD administration when partial or complete inappetance develops,
but with equal emphasis, to continue adrenocortical hormone
substitution. If this measure is taken, the owner should also
contact the veterinarian, who may increase the cortisone substitution temporarily. When a reduction in appetite is neglected and the o,p-DDD treatment is continued the dog may
start to vomit, refuse substitution therapy, and develop a hypoadrenocorticoid crisis. However, with good instructions
this is rare and usually the o,p-DDD administration can be
resumed after a few days without further problems.
As compared with treatment schedules that aim at the selective destruction of the two inner zones of the adrenal cortex, while trying to spare the zona glomerulosa21, the above
described schedule has the advantage that the disease is
stopped completely soon after initiation of the treatment and
is not merely suppressed. In addition, lifelong substitution
therapy is provided for the resulting primary hypoadrenocorticism and hence there is less risk of sudden, unexpected
adrenocortical insufficiency. Finally, concurrent diabetes
mellitus is more easily managed.24
Despite this drastic treatment schedule, recurrences do
occur in about 30% of cases within one year. The owner may
call because the animals appetite and water intake have increased. Omitting the cortisone substitution may ameliorate
the signs temporarily, but the possible recurrence should be
investiged by asking the owner to send urine specimens for
measurements of corticoid/creatinine ratios. Two morning
urine samples are collected at an interval of 4 to 5 days, each
time omitting the cortisone and fludrocortisone administration on the preceding evening. Ratios exceeding the upper

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limit of the reference range indicate glucocorticoid excess,


and o,p-DDD therapy is then started for another 25 days,
followed by once weekly administration of o,p-DDD for 8
weeks. Substitution therapy and follow-up examinations are
carried out as in the first course. In the rare case of a second
recurrence, this procedure is repeated and the weekly o,pDDD dose is continued for half a year.
Another therapeutic option, although an expensive one,
could be the inhibition of adrenocortical steroidogenesis by
ketoconazole, a synthetic imidazole analogue used as a
broad-spectrum antifungal agent. The major limitations in
using ketoconazole in dogs are (1) the need for continuing
twice daily administration, (2) the expense, and (3) the failure of some dogs to respond. In cats the results have been
unpredictable and variable.
Finally, two treatment options should be mentioned that
so far have been used infrequently. First there is radiation
therapy for pituitary macroadenomas. This may lead to some
decrease in the tumor mass and peritumoral edema, but concurrent adrenocortical suppression treatment is needed.
Probably still based upon the the abandoned concept of a hypothalamic origin of the disease the neuropharmacological
approach has been reintroduced recently with the
monoamine-oxidase inhibitor selegiline. This drug is not effective in ameliorating signs such as pu/pd and does not affect cortisol secretion.25

4th European FECAVA SCIVAC Congress

ful removal of the tumor will result in complete recovery


without the need for continuing medication. Because of the
atrophy of the contralateral adrenal, due to the longstanding
glucocorticoid excess, glucocorticoid substitution is needed
initially. At the time of anesthesia, when intravenous fluid
administration is started, 5 mg hydrocortisone or 1 mg prednisone per kg body weight is added to the first bottle and this
amount is administered over a period of 6 h. Subsequently
0.5 mg hydrocortisone/kg is administered at 6 h intervals until oral medication is possible. This will consist of 1 mg cortisone/kg body weight of twice daily, which is gradually decreased and then stopped 6-8 weeks after surgery6.
Dogs with irresectable tumor or recurrence of disease after adrenalectomy can often be treated successfully with
o,p-DDD, thereby initially employing the same schedule as
for pituitary-dependent hyperadrenocorticism (see above).
After 25 days of daily administrations of 50-75 mg o,pDDD/kg, this chemotherapy is continued for at least three
months by once weekly administrations of the same daily
dose.23 This approach often leads to complete and permanent
cure of the hyperadrenocorticism, and ultrasonographic examinations may reveal that the size of the tumor has decreased considerably. Even lung metastases may disappear,
although it may also happen that this tumor dissemination
cannot be affected.

References
Hyperadrenocorticism due to
adrenocortical tumors
Adrenocortical tumors causing hyperadrenocorticism occur in both the dog and the cat Most are unilateral solitary
lesions. The left and the right adrenal glands are affected
about equally. Bilateral tumors occur in about one out of 10
cases6,26. Histological types range from small well-encapsulated adenomas to large carcinomas with liver and lung
metastases. However, it should be noted that miscroscopic
examination of a seemingly benign looking tumor may reveal expansion of tumor tissue into vessels6.
Diagnostic imaging. Ultrasonography is the first choice
for the visualization of adrenal glands. The technique allows
good estimates of the size of the tumor and may reveal information about its expansion. In individual cases it may be difficult to distinguish between macronodular hyperplasia and
adrenocortical tumor. In these instances additional visualization with CT may be needed, and especially in these cases the
observations should be interpreted in conjunction with the results of the biochemical studies, i.e., basal plasma ACTH
concentrations and if necessary extended by a CRH test.21
Once the presence of an adrenocortical tumor has been established, the possibility of distant metastases should be considered. During the abdominal ultrasonography for the identification of the adrenals also the liver can also be investigated for metastases. In cases of suspicion of liver metastases an
ultrasound guided biopsy can be performed to test this this
supposition. In addition thoracic radiographs should be made.
Treatment. When the preoperative investigations have
revealed that it is likely that there is a resectable unilateral
tumor, it should be treated by surgery, because the success-

1.

2.

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Kemppainen RJ, Sartin JL, (1984), Evidence for episodic but not circadian activity in plasma concentrations of adrenocorticotrophin, cortisol and thyroxine in dogs. J Endocr 1984;103:219-226.
Kooistra HS, Greven SH, Mol JA, Rijnberk A, (1997), Pulsatile secretion of -MSH and the differential effects of dexamethasone and
haloperidol on the secretion of -MSH and ACTH in dogs. J Endocrinol 152:113-121.
Meijer JC, de Bruijne JJ, Rijnberk A, Croughs RJM, (1978), Biochemical characterization of pituitary-dependent hyperadrenocorticism in the dog. J Endocr 1978;77:111-118.
Kemppainen RJ, Sartin JL, (1987), Differential regulation of peptide
release by the canine pars distalis and pars intermedia. Front Horm
Res 17:18-27.
Willemse T, Vroom MW, Mol JA, Rijnberk A, (1993), Changes in
plasma cortisol, corticotropin, and -melanocyte-stimulating hormone
concentrations in cats before and after physical restraint and intradermal testing. Am J Vet Res 54:69-72.
Van Sluijs FJ, Sjollema BE, Voorhout G, van den Ingh TSGAM, Rijnberk A, (1995), Results of adrenalectomy in 36 dogs with hyperadrenocorticism caused by adrenocortical tumour. Vet Quart 17:113116.
Scholten-Sloof BE, Knol BW, Rijnberk A, Mol JA, Middleton DJ,
Ubbink G, (1992), Pituitary-dependent hyperadrenocorticism in a
family of Dandie Dinmont terriers. J Endocr 135:535-542.
Van Wijk P, Rijnberk A, Croughs RJM, Voorhout G, Sprang EPM, Mol
JA, (1992), Corticotropin-releasing hormone and adrenocorticotropic
hormone concentrations in cerebrospinal fluid of dogs with pituitarydependent hyperadrenocorticism. Endocrinology 131:2659-2662.
Peterson ME, Orth DN, Halmi NS, Zielinski AC, Davis DR, Chavez
FT, Drucker WD, (1986). Plasma immunoreactive proopiomelanocortin peptides and cortisol in normal dogs and dogs with Addisons disease and Cushings syndrome: Basal concentrations. Endocrinology 119:720-730.
Orth DN, Peterson ME, Drucker WD, (1988), Plasma immunoreactive proopiomelanocortin peptides and cortisol in normal dogs and
dogs with Cushings syndrome: Diurnal rhythm and responses to various stimuli. Endocrinology 122:1250-1262.

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Kooistra SH, Voorhout G, Mol JA, Rijnberk A, (1997), Correlation


between impairment of glucocorticoid feedback and the size of the
pituitary gland in dogs with pituitary-dependent hyperadrenocorticism. J Endocrinol 152:387-394.
Biewenga WJ, Rijnberk A, Mol JA, (1991), Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: A
study in dogs with hyperadrenocorticism. Acta Endocr 124:583-588.
Teske E, Rothuizen J, de Bruijne JJ, Rijnberk A, (1989), Corticosteroid-induced alkaline phosphatase isoenzyme in the diagnosis of
canine hypercorticism. Vet Rec 125:12-14.
Meij BP, Mol JA, Bevers MM, Rijnberk A, (1997), Residual pituitary
function after transsphenoidal hypophysectomy in dogs with pituitary-dependent hyperadrenocorticism. J Endocrinol 155:531-539.
Guptill L, Scott-Moncrieff JC, Bottoms G, Glickman L, Johnson M,
Glickman N, Nelson R, Bertoy E, (1997), Use of the urine
cortisol:creatinine ratio to monitor treatment response in dogs with
pituitary-dependent hyperadreancorticism. J Am Vet Med Ass
210:1158-1161.
Goossens MMC, Meyer HP, Voorhout G, Sprang EPM, (1995), Urinary excretion of glucocorticoids in the diagnosis of hyperadrenocorticism in cats. Domest Anim Endocrinol 12:355-362.
Galac S, Kooistra HS, Teske E, Rijnberk A, (1997), Urinary corticoid/creatinine ratios in the differentiation between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to adrenocorticial tumour in the dog. Vet Quart 19:17-20.
Van Wijk PA, Rijnberk A, Croughs RJM, Wolfswinkel J, Selman PJ,
Mol JA, (1994). Responsiveness to corticotropin-releasing hormone

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and vasopressin in canine Cushings syndrome. Eur J Endocrinol


130:410-416.
Meij BP, Voorhout G, van den Ingh TSGAM, Hazewinkel HAW,
vant Verlaat JW, (1997), Transsphenoidal hypophysectomy in beagle
dogs: Evaluation of a microsurgical technique. Vet Surg 26:295-309.
Duesberg CA, Nelson RW, Feldman EC, Vaden SL, Scott-Moncrieff
CR, (1995), Adrenalectomy for treatment of hyperadrenocorticism in
cats: 10 cases (1988-1992). J Am Vet Med Ass 207:1066-1070.
Kintzer PP, Peterson ME. Mitotane (o,p-DDD) treatment of 200
dogs with pituitary-dependent hyperadrenocorticism, (1991), J Vet
Int Med 5:182-190.
Rijnberk A, Belshaw BE. O,p-DDD treatment of canine hyperadrenocorticism: an alternative protocol. In: Kirk RW, Bonagura JD,
eds. Current Veterinary Therapy XI. Philadelphia: WB Saunders
1992:345-349.
Rijnberk A, (1996), Clinical Endocrinology of Dogs and Cats. Kluwer Academic Publishers, Dordrecht/Boston, 61-88.
Den Hertog E, Braakman JCA, Teske E, Kooistra HS, Rijnberk A,
(1997), Treatment of pituitary-dependent hyperadrenocorticism in the
dog by non-selective adrenocorticolysis with o,p-DDD. Vet Quart
19:S17.
Steffen T, Hrauf, Reusch C, (1997), Selegiline HCl (L-Deprenyl) for
treatment of canine pituitary-dependent hyperadrenocorticism. J Vet
Int Med 11:122 (ACVIM Abstract 74).
Ford SL, Feldman EC, Nelson RW,(1993), Hyperadrenocorticism
caused by bilateral adrenocortical neoplasia in dogs: Four cases
(1983-1988). J Am Vet Med Ass 202:789-792.

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Supraventricular tachycardia in the dog


Karsten Schober

Summary
Supraventricular tachycardia (SVT) is a common rhythm
disturbance in dogs. It is almost always a rapid, narrow
complex tachycardia. SVT may be a complication of cardiac
disease but may also occur in normal hearts. Reentry, altered automaticity, or triggered activity have been elucidated as the underlying electropathophysiologic mechanisms of
SVT. The different types of SVT may be distinguished according to onset and cessation, duration, P wave configuration, regularity, ventricular rate, response to vagal maneuvers and antiarrhythmic drug therapy. However, the surface
electrocardiogram alone may be inadequate for the complete differentiation of a specific mechanism. Sinus tachycardia and atrial fibrillation are the most important types of
SVT in dogs. Owing to the high heart rates, SVT may lead to
clinical signs such as weakness, tachypnea, syncope, systolic and diastolic cardiac failure, and death. Management
aims at termination of acute episodes of SVT, convertion into sinus rhythm and prevention of recurrence. Precordial
thumps, vagal maneuvers, and antiarrhythmics may be tried.
In dogs with heart disease and SVT (particularly atrial fibrillation, atrial flutter, or atrial tachycardia), reduction of
ventricular response rate is the primary therapeutic goal.
Digitalis glycosides, beta-adrenergic blocking agents, and
calcium antagonists are most often to be used. However,
restoration of sinus rhythm is highly improbable.

Supraventricular tachycardia (SVT) is a reletively


common rhythm disturbance in the dog.1,2 It should be considered in any patient with extremely rapid, narrow QRS
tachycardia.3-6 However, SVT with bundle branch block

(Fig. 1) as well as ventricular pre-excitation may lead to


wide QRS complexes.7 The P waves may be buried within
the ST-T complex and be virtually invisible. This is termed
a wide QRS supraventricular tachycardia. Ventricular tachycardia with narrow QRS complexes may also occur but this
is a very rare condition (arrhythmogenic substrate is ventricular but located very close to the AV node) and accounts for
less than 1 % of narrow complex tachycardias in humans.4
SVT may be classified according to their site of origin
and the underlying mechanism.8,9 Functional or anatomical
reentry, altered automaticity and, less frequently, triggered
activity (delayed after depolarizations) have been elucidated
as the fundamental mechanisms of SVT (Tab. 1).3,6,8-10 The
surface electrocardiogram alone may be inadequate for the
differentiation of a specific mechanism,6,9,10 however, an understanding of electrophysiology will better enable us to categorize and manage these arrhythmias. SVT may be further
subdivided according to their duration into sustained (> 30
s) or nonsustained.3,7 However, a working definition of 10 or
more consecutive beats to characterize sustained SVT seems
to be more practical.3 According to onset and offset, SVT
may be paroxysmal (sudden onset and cessation) or nonparoxysmal (gradual acceleration and deceleration). Paroxysmal SVT is suggestive of reentry whereas nonparoxysmal
SVT usually characterizes automatic rhythms.8
Automatic supraventricular tachycardia develops within
the sinus node or the atrial or junctional myocardium. Altered automaticity, particularly increased spontaneous depolarization rates may occur in response to catecholamine
stimulation, ischemia, infection, electrolyte disturbances,
enlarged atria, myocardial fibrosis and digitalis intoxication.8,9 Typically, a warm-up phenomenon characterizes automatic rhythms,11 i.e. the heart rate gradually accelerates

Figure 1 - Atrial fibrillation with left bundle branch block pattern (160 beats/min) in an 11 years old male giant snauzer with DCM. Paper speed, 50 mm/s; 5
mm = 1 mV.

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DVM, Med Vet


Department of Small Animal Medicine (Head: Prof. Dr. G. Oechtering)
Faculty of Veterinary Medicine, University of Leipzig - Germany

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Table 1. Classification of supraventricular tachycardia


according to their site of origin and mechanism4,6,8
delayed after
abnormal
reentry depolarizations automaticity
sinus tachycardia
atrial tachycardia
- paroxysmal
- permanent
atrial flutter
atrial fibrillation
AV nodal reentrant tachycardia
junctional tachycardia
AV reentry tachycardia (WPW)

(+)

+++

+++
(+)
+++
+++
+++

+++

(+)

(+)

+++

+++

WPW, Wolff-Parkinson-White syndrome; AV, atrioventricular; +++, common mechanism; (+), rare or questionable mechanism

and decelerates. Automatic rhythms are usually not as rapid


as reentrant rhythms.
Sinus tachycardia is the most common type of benign
SVT seen in dogs (Fig 2). Fear, pain, hypovolemia, hypotension, shock, hyperthermia, anemia, thyreotoxicosis,
treatment with atropine or catecholamines may lead to excess sympathetic stimulation which is the driving force for
this arrhythmia.10 Normal P waves on ECG which are sometimes hidden in the previous QRS-T complex, a regular
rhythm and heart rates up to 300/min are typical ECG features. Treatment is usually directed towards the correction of
the underlying, often non-cardiac problem. Vagal maneuvers
do little to slow down the heart rate.10 The temporary use of
-blockers may be indicated.
Atrial tachycardia arises from abnormally increased automaticity or reentry within the atrial myocardium.5 Automatic atrial tachycardia is nonparoxysmal and not as rapid as
reentrant rhythms. Typically, discrete P waves are seen on
ECG, although they are different in configuration compared

to sinus P waves. P-R interval and the ratio between P waves


and QRS complexes depend on the site of origin in the atrium, the rate of impulse formation, and atrioventricular (AV)
nodal transmission characteristics.8 Atrioventricular block
can occur and may confirm the suspicion of primary atrial
tachycardia.5 Atrial automatic tachycardia is often very resistant and nonresponsive to treatment; vagal maneuvers,
drugs, overdrive pacing or electrical cardioversion rarely
abolish the arrhythmia.5,8 It is usually observed in patients
with myocardial disease but little is known about the initiating events.6 The persistant nature of the tachycardia and the
inability to control the ventricular rate may virtually result in
dilated (tachycardia induced) cardiomyopathy.6,8,12
Atrial reentrant tachycardia occurs less commonly (Fig.
3). This arrhythmia is a regular, very rapid (180-500
beats/min) and paroxysmal tachycardia that is rather responsive to antiarrhythmic therapy. Class Ia agents, digitalis or blockers can be used to control the arrhythmia.10 About 20 %
of paroxysmal atrial tachycardias in people is assumed to
base on triggered activity resulting from delayed after depolarization.13
Automatic junctional tachycardia arises from in or near
the His bundle/AV junctional tissue, occurs nonparoxysmally and may be regular or irregular, depending on autonomic
tone.9 Negative P waves preceding the QRS complex may be
seen as well as P waves occuring within the QRS complex.
It may coexist with atrial fibrillation (AF) and may result in
regular ventricular response despite AF.10,14
Reentrant supraventricular tachycardia may develop
within the sinus node, the atrial myocardium and the AV
nodal tissue (functional reentry) or between the atria and the
ventricles via accessory pathways (anatomical reentry).
Reentry is thought to be the most common cause of
supraventricular tachydysrhythmias. Requirements for reentry include: 1) an available circuit (two pathways), 2) an area
of slow conduction, 3) an area of unequal refractoriness
(functional unidirectional block), and almost always 4) an

Figure 2 - Sinus tachycardia (195 beats/min) in a 5 years old male Pyrenean mountain dog. P-waves are fused with the preceeding T-wave (12th to 19th QRSTcomplex). Paper speed, 25 mm/s; 10 mm = 1 mV).

Figure 3 - Paroxysmal atrial reentrant tachycardia (480 beats/min) in a 9 years old female German shorthaired pointer. Paper speed, 50 mm/s; 10 mm = 1 mV.

Table 2. Drugs commonly used in the management


of supraventricular tachycardia in dogs1,8,9,24,38
Drug

Route

Adenosine
Amiodarone
Ajmaline
Atenolol
Quinidine sulfate
Diltiazem
Endrophonium
chloride
Esmolol
Flecainid
Metildigoxin

IV
PO
IV
PO
IV
PO
IV
PO
IV

0.05-0.30 mg/kg (fastest bolus)


2 mg/kg q 8 h
0.5-1.5 mg/kg (bolus)
0.2-1.0 mg/kg q 24 h
2-10 mg/kg (slow bolus)
10-20 mg/kg q 6-8 h
0.10-0.25 mg/kg (slow bolus)
0.5-2.0 mg/kg q 8-12 h
0.15 mg/kg mg (slow bolus)

IV

0.25-0.50 mg/kg (bolus) or


0.1-0.2 mg/kg (constant infusion)
1 mg/kg (bolus)
0.01-0.02 mg/kg (divided into 4
aliquots, each given hourly)
0.005-0.010 mg/kg q 12 h (or 0.22
mg/m2 BSA)
0.2-1.0 mg/kg q 12-24 h
6-8 (-25) mg/kg (very slow bolus)
10-20 (-40) mg/kg q 6-8 h
0.02- 0.10 mg/kg (very slow bolus)
0.25-1.0 mg/kg q 8 h
1-2 mg/kg (bolus)
0.008 mg/kg/min (constant infusion)
1-5 mg/kg q 8 h
0.5-2.0 mg/kg q 8-12 h
0.05-0.10 mg/kg every 10-30 min to
effect (slow bolusus, do not
exceed 0.20 mg/kg), 0.002-0.010
mg/kg/min (constant infusion)
0.5-2.0 (-5.0) mg/kg q 8 h

IV
IV
PO

Metoprolol
Procainamide

Propafenone

PO
IV
PO
IV
PO
IV

Sotalol
Verapamil

PO
PO
IV

Propranolol

PO
BSA, body surface area

General Dose Schedule

361

excitable gap within the circuit.10,15-17 When the circuit is


tiny, such as within the AV node, it is termed micro-reentry.
When the circiut traverses a longer path, the term macroreentry is used.10
Of all sustained supraventricular tachycardias, atrial fibrillation (AF) is by far the most common and most important. It is usually not difficult to diagnose AF from the surface electrocardiogram. Typically, the ECG shows rapid, irregular atrial activity in absence of P waves and rapid irregularly irregular ventricular response (Fig. 4 and 5). Exceptions can be found in dogs with concurrent AV nodal conduction disease or junctional tachycardia, where the ventricular response may be regular in rhythm.10,14 Atrial fibrillation
commonly accompanies other disorders such as mitral valve
disease, congenital heart defects, congestive heart failure,
hypertrophic cardiomyopathy, or hyperthyroidism,17 most
often associated with extremely large left atria. Toxins, autonomic dysbalance, trauma, anesthesia, or other tachycardias may also induce AF.14,17,18 Atrial fibrillation with a normal ventricular response rate in the absence of known structural heart disease is well described in men14,17,19 and
dogs20,21 and is termed lone atrial fibrillation. AF may be
paroxysmal, persistent (conversion into sinus rhythm possible) or permanent (incessant; conversion into sinus
rhythm impossible).16 The latter one is the most common
type of AF in dogs.
The electrophysiologic basis of atrial fibrillation has
been ascribed primarily to the multiple wavelet hypothesis.22,23 The wavelet theory is based on continuous multiple
intra-atrial reentry. Interlacing wavelets are able to reexcite
areas that have been activated by other wavelets. There is a
continuous changing pattern of excitation with AF, with 4 to
6 simultaneous reentrant wavelets necessary to maintain
atrial fibrillation.17,23 Leading circle reentry may be responsible for multiple wavelets, but an excitable gap has recently been demonstrated in one type of AF.17 However, limited
information is available on the pathological, electrophysio-

Figure 4 - Atrial fibrillation (230 beats/min) in a 12 years old male dachshound with mitral valve endocardiosis and ruptured chordae tendineae. Paper speed,
50 mm/s; 10 mm = 1 mV.

Figure 5. Atrial fibrillation (210 beats/min) in a 4 years old male Doberman pinscher with dilated cardiomyopathy. Paper speed, 25 mm/s; 5 mm = 1 mV.

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4th European FECAVA SCIVAC Congress

362

logical and initiating mechanisms of AF.12,17 Over the past


few years it became obvious that atrial electrophysiological
remodeling and regional electrical heterogeneity may be the
electrophysiologic basis for the development of AF. A heart
that is electrophysiologically homogeneous probably cannot
fibrillate.17 Multiple profibrillatory events can contribute to
the development of electrical heterogeneity and thus atrial
fibrillation:6,15,17
A. autonomic effects
B. atrial stretch
C. a single discharging focus
D. atrial remodeling.
Autonomic effects. Vagal stimulation has been shown to
cause unequal shortening of refractoriness in the atria and
thus creates electrophysiologic heterogeneity in experimental dogs.24 Elevated catecholamine and angiotensin II levels
produce structural changes in the myocardium (hypertrophy,
collagen accumulation, fibrosis) which might facilitate the
onset of AF by directly modifying electrophysiologic atrial
properties.25 Paroxysmal atrial fibrillation may be vagally
initiated (vagally-sensitive type) or catecholamine-induced (catecholamine-sensitive type) in otherwise normal,
healthy athletes.8,26
Atrial stretch. Increased atrial stretch, a common feature
in dogs with volume overloaded left atria, prolongs atrial refractoriness. This increase in refractoriness occured heterogeneously as shown in dogs with acute atrial distension.
Thin areas of the atria were more stretched than thick areas
resulting in heterogeneous prolongation of refractoriness
and increasing the dispersion of atrial effective refractory
period resulting in more easily inducable AF.6,27
Focal atrial fibrillation. A single rapidly discharging focus, similar to a pacemaker, as a cause of AF has been
shown in humans.28 Rapid atrial activation may lead to fragmentation of excitation, electrical heterogeneity and thus
atrial fibrillation.
Atrial remodeling. Rapid atrial activation as shown in
dogs12 causes time-dependent nonuniform electrophysiological remodeling of the atrial myocardium. Effective refractory period decreases as well as conduction velocity and wavelength, which, along with increased regional heterogeneity
and vulnerability, provide a substrate for AF.9,12 Thus, fast
heart rates created by supraventricular tachycardia leads to
electrophysiological remodeling that favours its own maintenance (AF begets AF).12,29
A critical mass of myocardium seems to be necessary to
maintain AF.23 The larger the heart the easier it is to sustain

4th European FECAVA SCIVAC Congress

atrial fibrillation.10 However, recent data suggest that sustained AF may also occur spontaneously in very small animals such as chickens.30
Atrial flutter is a relatively rare form of SVT in dogs. It
is different from AF and is most likely based on a single
macro-reentrant circuit of activation with an excitable gap
located in the right atrium, while the left atrium behaves as
a bystander not incorporated in the circuit.3,15 It may present
as brief paroxysms or as a sustained event. The classical
sawtooth pattern of atrial activity (undulating F waves) is the
ECG hallmark of this tachyarrhythmia. AV conduction is
usually less than 1:1, often 3:1 or 4:1 and thus appears to be
more regular.8,10 Atrial flutter can be paced terminated in
contrast to AF.9
Sinus nodal reentry is a rare condition in dogs. The pathway of reentry is confined within the sinus node or between
the sinus nodal and the surrounding atrial tissue. The arrhythmia starts paroxysmal (in contrast to sinus tachycardia)
and shows P waves that are very similar to sinus P waves.9
Increases in vagal tone or antiarrhythmic drugs may interrupt the reentry.
AV nodal reentrant tachycardia is a common cause of
SVT in people.6,8 The reentrant circuit is composed of two
pathways within the AV node (dual AV node): antegrade
conduction occurs in functionally differentiated fibers with
slow conduction and a short refractory period (slow -pathway), and retrograde conduction occurs in fibers with rapid
conduction and a long refractory period (fast -pathway).10,11
Atypical AV nodal reentrant tachycardia is assumed to use
the two pathways in the opposite direction.26 The paroxysmal tachycardia is regular with normal QRS complexes on
surface ECG and is initiated by a premature impulse (Fig.
6).6,8,26 The negative P waves are either completely hidden in
the QRS complex or distorting the terminal portion of QRS.
Increased vagal tone or drugs that slow AV conduction or increase effective refractory period may terminate the arrhythmia.5,6,8-10
Atrioventricular reentrant tachycardia (synonyms: bypass-tract reentrant tachycardia, circus movement tachycardia, reciprocating tachycardia) is well recognized in young
human patients4-6 but is less common in the dog.2,31,32 It represents a macro-reentry because the reentrant circuit is large
involving the AV node, the His-Purkinje system, ventricular
and atrial myocardium, and the bypass tract (the bundle of
Kent, James fibers, or Mahaim fibers).10,31 The bypass-tract,
an embryonic muscular remnant, may be very short (some
millimeters in length) and extremely thin (hair-sized in di-

Figure 6 - AV nodal reentrant tachycardia (480 beats/min) in a 11 years old male dachshound with syncope but without echocardiographically detectable organic heart disease. Paper speed, 50 mm/s; 5 mm = 1 mV.

ameter).3,16 In man, 60 to 70% of AV pathways are left


sided.26 AV reentrant tachycardia may be orthodromic or antidromic.6,9 Ventricular pre-excitation occurs when the impulse from the SA node bypasses the AV node through the
accessory pathway to the ventricles. As impulse conduction
in the bypass tract is faster than in the AV node, the impulse
conducted through the accessory pathway stimulates a portion of the ventricles prematurely with the rest of the ventricles being activated in the normal sequence through the AV
node. The Wolff-Parkinson-White syndrome consists of
ventricular pre-excitation with episodes of paroxysmal SVT
(Fig. 7). When the accessory AV connection conducts antegrade during sinus rhythm, ventricular pre-excitation is
manifested by the presence of delta waves, short PR interval
and prolonged QRS duration on surface ECG (Fig. 8). A
concealed bypass tract (which has only ventriculo-atrial conduction) is inapparent on the ECG during normal sinus
rhythm.2,9,31,32 SVT can be induced by premature atrial or
ventricular beats31,32 and is often very fast (> 300 beats/min).
Usually, QRS complexes are narrow (except antidromic impulse conduction) and retrograde P waves are to be seen
within the ST segment.6,26 Unfortunately, P waves are often
difficult to discern, especially with very rapid heart rates.31
Medical therapy aims at slowing AV conduction or at increasing refractoriness of the accessory pathway to ameliorate the arrhythmia.9,10,31

Management
Supraventricular tachyarrhythmias are important when
they result in clinical signs, when they lead to further deterioration of heart function or when they may be a marker or indicator of patients at risk for collapse or sudden death. Clinical signs resulting from tachycardias may include tachypnea,

363

worsening or development of congestive heart failure, weakness, reluctance to exercise, collapse, and syncope.
Atrial fibrillation is by far the most relevant type of SVT
in dogs. Dilated cardiomyopathy, severe chronic valvular
disease, or congenital malformations (patent ductus arteriosus, mitral valve dysplasia) usually account for AF in dogs.
Rapid ventricular rates during AF increase myocardial oxygen consumption, decrease diastolic filling and thus, result
in myocardial ischemia, stiffness and arrhythmia, reduce
cardiac output, leading to hypotension and congestive heart
failure.14,33 AF also causes myocardial electrophysiological
remodeling that itself maintains AF and may lead to tachycardia-induced cardiomyopathy.6,17 Treatment of AF depends on the stability of the patient and the underlying problem. Lone atrial fibrillation in giant breed dogs with slow
ventricular response rate (< 120 beats/min at home) should
not necessarily be treated.21 Sustained or suddenly observed
AF with a fast ventricular response but without structural
heart disease may be converted to sinus rhythm pharmacologically using class Ia (procainamide, quinidine), Ic
(propafenone), II (esmolol, metoprolol), or III (amiodarone,
sotalol, dofetilide) drugs14,20,33-35 or treating the initiating
problem. Antiarrhythmic agents change the refractory period, conduction velocity, or wavelength.9 Thump on chest
can be tried but rarely restores sinus rhythm (Fig. 9).
The primary goal in the management of AF (or atrial flutter) in dogs with heart disease is to reduce ventricular response rate, unload the heart and to correct neurohumoral
activation.6,9 The optimal heart rate in experimental dogs
with AF has been reported to be approximately 130 to 145
beats/min but this is rarely to be reached.36 The drug of
choice in animals with ventricular myocardial failure is digitalis although response to digoxin is often unpredictable. It
has positive inotropic action, prolongs AV refractoriness,
and decreases AV conduction.10,14 Digoxin shows ventricular

Figure 7 - Supraventricular tachycardia with WPW syndrome (334 beats/min) in a 2 years old male Siberian husky dog with recurrent episodes of weakness.
Note the retrograde P-waves in the ST-segment. Paper speed, 50 mm/s; 5 mm = 1 mV.

Figure 8. Ventricular pre-excitation and sinus rhythm (100 beats/min) in a 2 years old male Siberian husky dog with Wolff-Parkinson-White syndrome. Deltawaves are to be seen before onset of the R-wave. Paper speed, 50 mm/s; 5 mm = 1 mV.

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Figure 9. Conversion of atrial fibrillation (300 beats/min) into sinus rhythm (150 beats/min) following precordial thump (applied at the 7th QRS complex on
ECG) in a 3 years old female Great Dane with fever and increased sympathetic activity. Paper speed, 50 mm/s; 10 mm = 1 mV.

response predominantly by augmenting vagal tone,6,9,14,33


therefore, digoxin is relatively ineffective in situations
where sympathetic drive predominates, causing failure to
control ventricular rates with excitement or exercise.6,9,33
Hence, additional drugs may be required, if the rate control
is not satisfactory, eg. calcium channel blockers or -blockers. As the latter are negative inotrops, careful monitoring
during therapy is necessary.14 In dogs with preserved systolic
function, calcium antagonists, -blockers, or propafenone
may be used without digitalis for rate control. Diuretics and
angiotensin converting enzyme inhibitors are beneficial in
decreasing preload and thus left atrial size and profibrillary
myocardial stretch.6
Radiofrequency catheter ablation of the AV node, direct
current cardioversion, implantable atrial defibrillators, or biatrial pacing have been suggested to interrupt AF and prevent recurrences of atrial fibrillation in humans.14,17 However, such sophisticated therapeutic means are still under investigation and not routinely available for veterinary use.37
WPW-syndrome. Asymptomatic ventricular pre-excitation or infrequent, non-life-threatening and self-terminating
episodes of SVT do not require treatment. In sustained
symptomatic SVT with heart rates often above 300/min therapeutic intervention is mandatory. In these cases, SVT is a
life-threatening rhythm disturbance.38 Acute treatment aims
at the termination of the tachycardia whereas long-term
treatment aims at prevention of recurrences. Initial management of SVT, irrespective of mechanism, should start quickly and follow a logical progression:
1) Vagal maneuvers. Reflex vagal maneuvers (gentle
bilateral ocular pressure, carotid sinus massage, facial emersion in ice-water, external application of abdominal pressure) increases parasympathetic nervous (vagal) input that
may transiently impair AV conduction to the point of second
degree AV block resulting in abrupt termination of bypass
tract tachycardia.5,6,31 Emetics such as apomorphine may also abolish the tachycardia via increases in vagal tone.31
2) Mechanical termination. Precordial thumps in fast
tachyarrhythmias should initially always be tried although
abolition of the tachycardia mechanically is often not very
successful.31
3) Pharmacological cardioversion. Calcium channel
blocking agents such as verapamil or diltiazem slow conduction and prolong the refractory period of the AV node.31
Bypass tract refractoriness may be shortened. Beta-blockers
such as esmolol or atenolol have the same effect on the AV
node beside its antisympathetic activity.10 Adenosine, an ul-

trashort-acting endogenous nucleoside (plasma half-life


about 1.5 seconds), slows AV conduction, increases AV
nodal refractoriness, is negative inotrop, and has antiadrenergic actions.6,39 It should be given as a rapid bolus dose followed by a saline flush.39 Adenosine may terminate the vast
majority of junctional tachycardias and re-entrant tachycardias involving the AV node within seconds.39 Edrophonium
is a transient cholinesterase inhibitor, that produces a response similar to vagal maneuvers.6 Procainamide and
quinidine lengthen the refractory period of the accessory
pathway.31 Propafenone increases conduction time of the accessory pathway and the AV node and can be used acutely
and long-term.31 Digitalis glycosides depress AV nodal conduction but may shorten refractory period of the bypass
tract. As the conduction via the accessory pathway may be
favoured with digitalis, verapamil, or adenosine, administration of these drugs is usually avoided in humans with WPWsyndrome and atrial fibrillation because of the risk of rapid
ventricular response and subsequent ventricular fibrillation4,5,31
4. Transesophageal stimulation.
5. Direct current cardioversion.
Long-term management of WPW-syndrome can be accomplished by slowing conduction or prolonging refractoriness in either arm of the reentrant circuit. To the authors experience, procainamide, -blockers, and propafenone may
be used successfully.
Curative radiofrequency ablation of bypass tracts is the
ultimate in management strategies in people3,4 and has also
been reported in dogs.2,32

References
1.
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3.
4.

5.

6.

Bonagura JB, (1989), Atrial arrhythmias, In: Kirk RW (ed), Current


Veterinary Therapy X, WB Saunders, Philadelphia, 271-278.
Atkins CE, Kanter R, Wright K et al., (1995), Orthodromic reciprocating tachycardia and heart failure in a dog with a concealed posteroseptal accessory pathway, J Vet Int Med, 9:43-49.
Campbell RWF, (1996), Supraventricular tachycardia. Occasional
nuisance or frequent to treat?, Eur Heart J, 17:21-25.
Grimm W, Menz V, Hoffmann J et al., (1996), Elektrokardiographische Differentialdiagnose tachykarder Rhythmusstrungen. Teil I:
Tachykardien mit schmalem QRS-Komplex, Herz/Kreisl, 28:109-117.
Paul T, Pfammatter JP, (1994), Supraventrikulre Tachykardien im
Suglings- und Kindesalter. Diagnostik und Therapie, Monatsschr
Kinderheilkd, 142:774-780.
Van Den Berg, MP, Tuinenburg AE, Crijns, HJGM et al., (1997),
Heart failure and atrial fibrillation: current concepts and controversies, Heart, 77:309-313.

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Grimm W, Menz V, Hoffmann J et al., (1996), Elektrokardiographische Differentialdiagnose tachykarder Rhythmusstrungen. Teil II:
Tachykardien mit breitem QRS-Komplex, Herz/Kreisl, 28:157-163.
Wellens HJJ, (1996), The value of the ECG in the diagnosis of
supraventricular tachycardias, Eur Heart J, 17 (Suppl C):10-20.
Moise SN, (1992), Mechanisms of supraventricular arrhythmias,
Proc 10th ACVIM Forum, San Diego, 605-607.
Lunney J, Ettinger SJ, (1995), Cardiac arrhythmias, In: Ettinger SJ,
Feldman EC (eds), Textbook of Veterinary Internal Medicine, 4th ed,
WB Saunders, Philadelphia: 959-995.
Zipes DP, (1988), Specific arrhythmias: diagnosis and treatment, In:
Braunwald E (ed), Heart Disease. A Textbook of Cardiovascular
Medicine, 4th ed, WB Saunders, Philadelphia: 658-716.
Gaspo R, Bosch RF, Talajic M et al., (1997), Functional mechanisms
underlying tachycardia-induced atrial fibrillation in a chronic dog
model, Circulation, 96:4027-4035.
Rosen MR, (1988), The links between basic and clinical cardiac electrophysiology, Circulation, 77:251-263.
Baer M, Goldschlager N, (1995), Atrial fibrillation: an update on new
management strategies, Geriatrics, 50:22-29.
Mary-Rabine L, Mahaux V, Waleffe A et al., (1997), Atrial flutter:
historical backround, J Cardiovasc Electrophysiol, 8:353-358.
Campbell RWF, (1997), personal communication.
Zipes DP, (1997), Atrial fibrillation: from cell to bedside, J Cardiovasc Electrophysiol, 8: 927-938.
Russell LC, Rush EJ, (1995), Cardiac arrhythmias in systemic disease, In: Bonagura JD (ed), Kirks Current Veterinary Therapy XII,
WB Saunders, Philadelphia, 161-175.
Kopecky SL, Gersh BJ, McGoon MD et al., (1987), The natural history of lone atrial fibrillation. A population-based study over three
decades, N Engl J Med, 317:669-674.
Edwards NJ, (1993), Atrial fibrillation rate control in three groups of
patients, Proc 11th ACVIM Forum, Washington DC, 408-410.
Harpster NK, (1994), Cardiac arrhythmias in the Irish Wolfhoud: preliminary study, Proc 12th Forum ACVIM, San Francisco, 319-321.
Moe GK, (1962), On the multiple wavelet hypothesis of atrial fibrillation, Arch Int Pharmacodyn Ther, 140:183-188.
Allessie MA, (1995), Reentrant mechanisms underlying atrial fibrillation, In: Zipes DP, Jalife J (eds), Cardiac Electrophysiology: From
Cell to beside, WB Saunders, Philadelphia, 562-566.
Zipes DP, Mihalick MJ, Robbins FT, (1974), Effects of selective vagal stellate ganglion stimulation on atrial refractoriness, Cardiovasc

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Res, 8:647-655.
Borzak S, Goldstein S, Sabbah HN, (1993), Hemodynamic and neurohumoral predictors of the development of atrial fibrillation in dogs
with chronic heart failure, Circulation (Suppl I), 88:18.
Josephson ME, Schibgilla VH, (1996), Athletes and arrhythmias:
clinical consideration and perspectives, Eur Heart J, 17:498-509.
Satoh T, Zipes DP, (1996), Unequal atrial stretch in dogs increases
dispersion of refractoriness conductive to developing atrial fibrillation, J Cardiovasc Electrophysiol, 7:833-842.
Haissaguerre M, Marcus FI, Fischer B et al., (1994), Radiofrequency
catheter ablation in unusual mechanism of atrial fibrillation: report of
three cases, J Cardiovasc Electrophysiol, 5:743-751.
Wijffels MC, Kirchhoff CJ, Dorland R et al., (1995), Atrial fibrillation begets atrial fibrillation: a study in awake chronically instrumented goats, Circulation, 92:1554-1568.
Mukai S, Machida N, Nishimura M et al., (1996), Electrocardiographic observation on spontaneously occuring arrhythmias in chickens, J Vet Med Sci, 58:953-961.
Atkins CE, (1994), Supraventricular tachycardia associated with
atypical accessory pathways in dogs, Proc 12th ACVIM Forum, San
Francisco, 325-327.
Scherlag BJ, Wang X, Nakagawa H et al., (1993), Radiofrequency
ablation of a concealed accessory pathway as treatment for incessant
supraventricular tachycardia in a dog, J Am Vet Med Assoc,
203:1147-1153.
Riley RD, Pritchett ELC, (1997), Pharmacologic management of atrial fibrillation, J Cardiovasc Electrophysiol, 8:818-829.
Stroobandt R, Stiels B, Hoebrechts R et al., (1997), Propafenone for
conversion and prophylaxis of atrial fibrillation, Am J Cardiol,
79:418-422.
Falk HR, Pollak A, Singh SN et al., (1997), Intravenous dofetilide, a
class III antiarrhythmic agent, for the termination of sustained atrial
fibrillation or flutter, J Am Coll Cardiol, 29:385-390.
Hamlin RL, (1995), What is the best heart rate for a dog in atrial fibrillation?, Proc 13th ACVIM Forum, Lake Buena Vista, 1072-1074.
Wright KN, Bright JM, Cox JW et al., (1996), Transcatheter modification of the atrioventricular node in dogs, using radiofrequency energy, Am J Vet Res, 57:229-235.
Keene B, (1991), Emergency management of cardiac arrhythmias,
Proc 9th ACVIM Forum, New Orleans, 13-15.
Oates JA, Wood AJJ, (1991), Adenosine and supraventricular tachycardia, N Engl J Med, 325:1621-1629.

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367

Therapeutic considerations in dogs with dilated


cardiomyopathy
Karsten Schober
DVM, Med Vet
Department of Small Animal Medicine (Head: Prof. Dr. G. Oechtering)
Faculty of Veterinary Medicine, University of Leipzig - Germany

Etiology

Dilated cardiomyopathy (DCM) is a primary heart muscle disease of unknown etiology characterized by gradual
ventricular dilation, loss of contractility and often symptoms
of congestive heart failure. It occurs predominantly in middle aged, male large breed dogs. Despite the development of
new treatment strategies it remains an important cause of
morbidity and mortality in dogs. Long-term prognosis depends on disease stage and breed but is, in general, poor.
The primary goals of management in dogs with DCM are
stabilization of the patient, improvement of quality of life
and prolongation of survival. Inotropic support (digitalis
glycosides, sympathicomimetics, phosphodiesterase F-III
inhibitors, calcium sensitizers), pre- and afterload reduction
(diuretics, vasodilators), heart rate control (beta-adrenergic
blocking agents, calcium antagonists) and arrhythmia suppression (class I, II, and III antiarrhythmics) are the basic
principles of management. Supportive therapy (rest, oxygen
supply, chest or abdominal draining, low salt diet, exercise
regimen, carnitine, taurine, or coenzyme Q10 supplementation) are complemental to drug therapy. Dynamic cardiomyoplasty, growth hormone administration, and immunosuppressive drug therapy are still under investigation.

The causes of idiopathic DCM in dogs are still unknown.


Evidence suggests that DCM represents end stage myocardial failure resulting from a variety of disorders. Investigations into the pathogenesis of the disease have focused on
four basic mechanisms: (1) familial and genetic factors, (2)
viral myocarditis and other cytotoxic insults, (3) immune
mediated abnormalities, and (4) metabolic, energetic, and
contractile abnormalities.11-16 It is likely that more than one
primary disease processes can induce the same functional
and morphologic abnormalities that are clinically recognized in DCM.

Idiopathic dilated cardiomyopathy (DCM) is a primary


heart muscle disease of unknown etiology, characterized by
left ventricular or biventricular dilation and impaired systolic function.1,2 The disease is reportedly the second most
common cause of congestive heart failure in the dog3 and,
despite the development of new treatment strategies, it remains an important cause of morbidity and mortality in dogs
as well as humans. Idiopathic DCM is a condition usually affecting large breed dogs between one and five years of age
and is common in males.4 DCM seems to be a term that
rather represents different syndromes in different breeds or
even individuals within one breed than a uniform disease entity. The natural history of the disease is not well established
and differs in certain breeds, the clinical signs vary, the disease progression may be different as well as the response to
treatment. Specific cardiomyopathies in Doberman pinscher
dogs,5,6 boxer dogs,7 Dalmatians,8 English cocker spaniels,9
and Irish Wolfhound dogs10 have been described. To the authors experience, giant snauzers may also develop a special
type of DCM.

Pathophysiology
Impaired systolic ventricular function is the primary
pathophysiologic abnormality in most dogs with DCM. Reduced stroke volume may result in signs of low cardiac output manifested as weakness, syncope, exercise intolerance,
or cardiogenic shock. Compensatory mechanisms are activated early in the course of the disease that attempt to normalize cardiac output and maintain arterial blood pressure.
The neurohormonal compensatory changes in heart failure
include increases in sympathetic nervous tone, activation of
the renin-angiotensin-aldosterone system (RAAS), and the
release of vasopressin and other vasoactive peptides (endothelins, atrial and brain natriuretic peptides, neuropeptide
Y, gamma2-melanocyte-stimulating hormone, dopamine,
prostaglandins, endogenous opioids)17 or cytokines.15 The
long-term consequences are increased pre- and afterload,
myocyte injury,18 muscular, vascular and interstitial ventricular remodelling19 and, therefore, further aggravation of
heart failure.13 Diastolic function may also be abnormal in
dogs with DCM.20
In a small subset of human patients, diastolic dysfunction may occur before onset of systolic disturbance.21
Markers of diastolic abnormality correlate strongly with
congestive symptoms as pulmonary edema, pleural effusion, ascites, or cachexia. Other factors contributing to further deterioration of ventricular performance include valvular insufficiency secondary to atrial and ventricular dilation
and dysrhythmias such as atrial fibrillation or ventricular
ectopy.20

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Summary

368

Clinical diagnosis
Dilated cardiomyopathy is a progressive disease, usually
characterized by a subclinical, occult stage that lasts for
months or even years (asymptomatic DCM) and the stage of
overt cardiac failure (symptomatic DCM). The spectrum of
clinical signs exhibited by dogs with DCM is similar in all
breeds but considerable differences between various breeds
in the frequency and severity of these signs and the outcome
may be observed.2,20,22 Occult DCM has been described predominantly in Doberman pinschers,3,23 boxer dogs7,24 and
Irish Wolfhounds.10,20 Ventricular or supraventricular arrhythmias may be observed frequently in these dogs despite
normal echocardiographic systolic indices. Some of the dogs
eventually develop heart failure, some die suddenly.20,23
Physical examination. In dogs with clinical signs of
DCM, forward failure results in tissue hypoperfusion and is
seen as weakness, lethargy, exercise intolerance, syncope,
anorexia, pale mucous membranes, and hypothermia. Backward failure leads to tachypnoea, dyspnoea, jugular distension, ascites, muscle wasting and peripheral edema. Cardiac
auscultation may reveal muffled heart sounds, pulmonary
crackles, soft and often variable regurgitant systolic murmurs, arrhythmias, and gallop sounds. Weak arterial pulses,
pulse deficit, and pulsus alternans also indicate myocardial
failure.2,20,22,25
Biochemical analysis. Clinical pathologic changes in
dogs with DCM may be as follows: prerenal azotemia, hepatic enzyme elevations, mild metabolic acidosis, mild hypoproteinemia, hyperkalemia or hyponatremia. Serum thyroid concentrations are often depressed.20 Serum markers of
myocardial cell injury like cardiac troponin I concentrations
or the MB bands of creatinine kinase are elevated in most
dogs with DCM.18
Electrocardiography. High amplitude or widened QRS
complexes, widened P waves, and ST segment coving may
be discovered. Small R wave amplitudes occur in pleural or
pericardial effusions. Of greater clinical importance is the
high prevalence of cardiac dysrhythmias in dogs with DCM.
Atrial fibrillation or atrial tachycardia, ventricular premature
depolarizations, and ventricular tachycardia are common
whereas conduction disturbances may be observed less frequently.20,22 Holter ECG monitoring (24-hour ambulatory
ECG) is a very useful method to detect ventricular arrhythmias in dogs with occult DCM.23,24,26
Radiography. Cardiac silhouette enlargement (due to
cardiomegaly or pericardial effusion), left atrial enlargement, pulmonary venous congestion, alveolar and interstitial
edema, pleural effusion, distended caudal vena cava, hepatosplenomegaly, or ascites may be evident in congestive
heart failure.19,20
Echocardiography. This method has become the gold
standard used to document and quantify myocardial dysfunction and to exclude other causes of heart disease. Atrial
and ventricular dilation, ventricular hypokinesis, asymmetric chamber contraction, decreased mitral valve excursion,
mitral or tricuspid valve regurgitation, decreased cardiac
output, pseudonormal or restrictive flow patterns of ventricular filling, prolonged or shortened ventricular isovolumic
relaxation interval, and pericardial effusion may be observed

4th European FECAVA SCIVAC Congress

in dogs with DCM.10,20,27


Angiography and endomyocardial biopsy are invasive
diagnostic methods that are restricted in its use to research
and referral centres.

Management
The prognosis for survival in dogs with DCM is, in general, poor. However, prognosis in the individual case is difficult to predict.12,27 Death results from worsening cardiac
failure or malignant arrhythmia. The ideal in any treatment
regimen is to identify the etiology of the disease so specific
therapy can be instituted. As the cause of idiopathic DCM is
unknown, specific therapy is not possible.2 Management
rather than therapy is aimed at the consequences of DCM
like congestive heart failure or dysrhythmias but not at the
primary cause.11,12 Unfortunately, there is no single therapeutic regimen that can be instituted for each patient with
DCM. Every dog has existing and evolving individual requirements according to the nature and severity of clinical
signs. Managing asymptomatic patients differs from that of
symptomatic dogs, and therapy of acute congestive cardiomyopathy differs from long-term treatment of DCM.
Therefore, the therapeutic plan must be tailored to each patient and its individual needs.2,11,28,29
The primary goals of management in dogs with DCM are
to stabilize the patient, to improve the quality of life, and to
prolong survival. Cure is highly improbable. Inotropic support, preload and afterload reduction, improvement of peripheral tissue perfusion, arrhythmia control, and inhibition
of further myocardial remodelling are the aims of therapeutic intervention. Drugs, currently used to manage dogs with
DCM, include positive inotrop agents, diuretics, angiotensin-converting enzyme (ACE) inhibitors, vasodilators,
and antiarrhythmics including beta-adrenergic receptor
blocking agents and calcium channel antagonists (Tab.
1).12,20,29 Supportive therapy (rest, oxygen supply, chest or
abdominal draining, diet, salt restriction, and exercise regimen) are complemental to drug therapy. More sophisticated
treatment strategies include dynamic cardiomyoplasty, dual
chamber pacing, counter-pulsation (augmentation of diastolic function), or heart transplantation but these are not routinely available for veterinary use.

Positive inotrops
Inotropic support is the backbone of therapy.2,12,20 Digitalis is indicated in dogs with DCM and signs of heart failure or supraventricular rhythm disturbances.12,20 Digoxin
was shown in humans to improve exercise capacity and to
decrease signs and symptoms of heart failure.2,30,31 It increases the amount of calcium binding by the intracellular
structures thus acts as a positiv inotrop. Digoxin may also be
effective for slowing the ventricular rate in patients with
supraventricular tachyarrhythmias, reduces systemic vascular resistance, decreases myocardial oxygen consumption,
and improves diastolic function.30,32,33 In recent years, evidence in man has emerged that digoxin additionally has a

Table 1. Drugs commonly used in the management


of canine DCM
Drug

Route

Atenolol

PO

Bumetanide
Carnitine
Diltiazem
Dobutamine

PO
PO
PO
IV

Dopamine

IV

Enalapril
Esmolol
Furosemide
Furosemide
Hydralazine
Metildigoxin
Metoprolol

PO
IV
IV/SC
PO
PO
PO
PO

Nitroglycerin

TransC

Nitroprusside

IV

Pimobendan
Propranolol

PO
PO

Spironolactone
Taurine

PO
PO

General Dose Schedule


6.25-12.50 mg/dog q 24 h
(start very low)
0.025-0.100 mg/kg q 12 h
50 mg/kg q 8 h
0.50-1.25 mg/kg q 8 h (start low)
2.5-10.0 g/kg/min constant infusion
(24-72 h)
2.0-7.0 g/kg/min constant infusion
(24-72 h)
0.5 mg/kg q 12-24 h
0.25-0.50 mg/kg (single dose)
2.0-4.0 mg/kg bolus, q 6-12 h
1.0-4.0 mg/kg q 8-24 h
0.2-0.5 (-1.0) mg/kg q 12 h
0.005-0.010 mg/kg q 12 h
(do not exceed 0.25 mg BID)
0.05-1.00 mg/kg q 12-24 h
(start very low)
2.5-10.0 mg/24-h patch: 12 h on/12 h
off
2.0-10.0 g/kg/min constant infusion
(monitoring!)
0.25 mg/kg q 12 h (not licenced yet)
0.05-1.00 mg/kg q 8 h
(start very low)
2.5 mg/kg q 12 h
250-500 mg/dog q 8-12 h

variety of positive effects on neuroendocrine activation: (1)


reduction of sympathetic tone, (2) increase of parasympathetic activity, (3) normalization of impaired baroreceptor
mediated mechanisms with partly restoration of the impaired
circadian pattern of heart rate variability, and (4) decrease in
serum norepinephrine concentration and plasma renin activity.30,32,34 The action of digitalis is dose-dependent. Low doses primarily exert neurohumoral and autonomic effects,
whereas higher doses mainly have hemodynamic action.
The inotropic effect appeared to be greater among patients
with lower contractility and more severe heart failure. However, in asymptomatic patients or patients with milder stages
of DCM and sinus rhythm, digoxin in long-term was beneficial as well.32,34,35 In contrast to studies with other positive
inotrops in people, Digoxin was shown to have a neutral effect on total mortality.36 At lower doses, the number of side
effects, particularly serious arrhythmias, will decrease. In
most patients, slow oral digitalization is adequate.16,18 Loading doses should be avoided. Larger breed dogs (in particular Doberman pinschers) tend to tolerate less digoxin, and
the lower end of the dosage scale should be employed. Care
should be taken when giving the drug intravenously. Digitalis may cause peripheral and coronary vasoconstriction
and malignant arrhythmias.35 Administration of digoxin intravenously should, if necessary, be performed as follows:37
The total dose (0.01-0.02 mg/kg of BW) is divided into 4
aliquots to be administered at hourly intervals by slow (over
10-15 min) IV injection. Digitalis may aggravate the clinical

369

condition in the setting of cardiogenic shock and, therefore,


dobutamine or dopamine should initially be used instead.30
Sympathicomimetics. Both catecholamines, Dopamine
and Dobutamine, provide potent inotropic strength to the
failing myocardium. Dobutamine is a synthetic agent with
selective 1-activity, mild 2- and dose dependent -adrenergic effects. It is the preferred positive inotrop for the initial
treatment of severe systolic dysfunction associated with cardiogenic shock. At low doses (2-8 g/kg/min), it increases
cardiac output and decreases systemic vascular resistance
much more than digitalis. Its use is limited to intravenous
constant infusion (24 to 72 h). The effective as well as the
toxic dose of dobutamine in dogs may be very individual.
Careful cardiac monitoring is, therefore, imperative as higher doses may cause vasoconstriction and severe tachyarrhythmias. If arrhythmias develop or heart rate elevates
(> 20%), the infusion should be temporarily halted. The blocking agent esmolol may additionally be used to antagonize the arrhythmogenic effect of dobutamine. In humans38
as well as in dogs with DCM (particularly in Doberman pinschers; own experience) short periods of infusion have been
associated with long-term (several weeks) improvement in
cardiac performance.
Dopamine is a endogenous precursor of norepinephrine
and has dose dependent effects as well. At low doses (1-3
g/kg/min), it activates dopaminergic receptors and causes
selective peripheral vasodilation. At moderate doses (3-7
g/kg/min), -receptor activation results in positive inotropic effect. At higher doses (7-10 g/kg/min), predominantly adrenergic stimulation leads to peripheral vasoconstriction
and positive chronotropy.39,40 Dopamine is indicated to support cardiac function and blood pressure in cardiogenic shock
and to support renal function in oliguric or anuric states.
A newer class of positive inotropic agents, the selective
phosphodiesterase F-III inhibitors (Amrinone, Milrinone, or
Enoximone), is currently under investigation regarding its
suitability for clinical use in patients with DCM.
Pimobendan exerts its positiv inotropic effects partially
by sensitization of contractile proteins to intracellular calcium. It also causes venous and arterial vasodilation and positive lusitropy. It may increase exercise duration and quality
of life in humans with moderate to severe heart failure41,42
but was shown to increase mortality.42 Studies in dogs are
rare but promising.43,44,45 Pimobendan (beside standard therapy) did not affect mortality in Cocker spaniels with DCM
(n=10) but improved quality of life and survival in Doberman pinschers with DCM (280 days in the pimobendan
group vs. 72 days in the placebo group) in a double-blind
placebo controlled study.43

Diuretics
Furosemide, a loop diuretic, is generally considered in
dogs with congestive heart failure. It decreases preload and
retention of sodium and water. It is an effective diuretic, is
rarely truely toxic, is cheap, and easily manipulated to effect.
Intravenous administration will rapidly reduce systemic venous pressure thus preload. The potential to cause electrolyte
disturbances in dogs is low. Administered long-term at ap-

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4th European FECAVA SCIVAC Congress

370

propriate doses, it may decrease cardiac output, may cause


prerenal azotemia, and may early activate the RAAS.46
Furosemide can be used in combination with thiazides or
spironolactone (an aldosterone antagonist) particularly in refractory cases of fluid accumulation.2,11,12,17,20,22 Bumetanide,
another loop diuretic, may technically be more potent and
seems to offer advantage in a small number of patients resistant to furosemide, but is more expensive.

Vasodilators
Controlled clinical trials have shown that dogs with
DCM treated with diuretics and digoxin benefit from additional use of ACE inhibitors.47,48 Enalapril, Ramipril,
Quinapril, or Benazepril inhibit the conversion of angiotensin I to II, which is a potent vasoconstrictor. They reduce aldosterone and ADH release, decrease the degradation
of vasodilating kinins, reduce myocardial remodelling and
sympathetic tone. Clinically, ACE-inhibitors improve exercise tolerance, breathing, appetite, stage of heart failure, and
survival in dogs with DCM. The incidence of side effects is
low: hypotention, renal failure, hyperkalemia, and gastrointestinal signs have been described predominantly at higher
doses.20,47-49 Care should always be taken in using ACE inhibitors in compensated renal disease. As activation of the
RAAS occurs early in the course of DCM asymptomatic patients may benefit from early ACE inhibition.2
Nitrates (glycerol trinitrate, isosorbide dinitrate, sodium
nitroprusside) are often used in dogs with acute pulmonary
edema in conjunction with standard therapy. Nitroglycerine
is purely a venodilator. Tolerance develops rapidly in dogs.
Sodium nitroprusside is an ultrashort acting arteriolar and
venodilator mainly used in life-threatening left heart failure
and pulmonary edema. Because of its potency to cause severe hypotention, arterial and venous blood pressure should
be monitored during continuous intravenous infusion.20,49
The use of direct-acting arterial vasodilators, such as hydralazine, may be useful adjunct therapy for dogs with persistant signs of heart failure despite treatment with digoxin,
furosemide, and ACE inhibitors. Combination therapy with
nitrates is an acceptable alternative as well. Hydralazine
may activate neurohormonal reflexes resulting in tachycardia, sodium and water retention, hypotention, and alimentary disturbances.12,20,49
Beside dopamine, ibupamine, an orally active dopamine
analogue that causes vasodilation, diuresis, and natriuresis
has investigationally been described in man as additional
drug for congestive heart failure.50,51 Data on the use of
ibopamine in dogs are currently not yet available.

4th European FECAVA SCIVAC Congress

antisympathetic, and antidysrhythmic effects. Myocardial


oxygen consumption is reduced. Therapy for congestive
heart failure with -blockers in humans has always been
controversial since their beneficial effects were reported
firstly 23 years ago52. As therapies for heart failure have
shifted away from the simple correction of hemodynamic
abnormalities and have moved toward the long-term correction of excessive neurohormonal activation, the importance
of drugs like ACE inhibitors or -blockers has gained increasing interest. Because of the dose-dependent negative
inotropic action of -blockers, therapy must be initiated at
very low doses after initiation of standard therapy and stabilization of the patient, and then titrated slowly (in weekly intervals). Improvement of ventricular function does not occur
until one month of therapy.48,49,52-56 Beta-blockers may cause
acute detrimental hemodynamic and clinical effects in patients with severe heart failure and should, therefore, be
avoided in critically ill patients. Nonetheless, -blockers
may improve symptoms, exercise capacity, left ventricular
ejection fraction and may prolong life in patients with less
severe heart failure as shown in people.49

Antiarrhythmics
The use of antiarrhythmic drugs like procainamide,
quinidine, mexiletine, or tocainide in dogs with ventricular
arrhythmias secondary to DCM is controversial. There is no
evidence that any antiarrhythmic drug but beta-blockers reduce the risk of sudden death and prolong life in people.
Moreover, some antiarrhythmic drugs (in particular class I
agents) may increase mortality in patients with heart failure.57 All antidysrhythmics have profound negative inotropic and proarrhythmogenic effects and should exclusively be
used in life-threatening ventricular rhythm disturbances.
Carnitine, Taurine, or Coenzyme Q10 supplementation may be helpful in a subset of patients with DCM.12 Immunosuppressive drugs or growth hormone administration were tried in humans, however, effects were rather poor.

References
1.
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3.
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373

Nutrition and nutritional diseases of pet birds


Peter W. Scott

Summary
The diversity of species and the lack of detailed understanding of the requirements of most species of captive birds
has lead to a progression by trial and error. While the vast
majority of captive birds are fed semi-natural diets, so
called complete diets have also been developed. Much of the
data supporting these is held in house but many of these
diets perform well, whether they supply the nutritional needs
of birds is one aspect of the debate, the other major aspect
is their apparent failure to cater for the behavioural aspects
of feeding. Practical diets and nutritional deficiencies will
be reviewed.

Wild birds, like wild mammals, eat to meet their normal


energy requirement. Obesity would be a dangerous condition in the wild for many birds. Captive birds however may
become obese. This may be simply due to overeating because of greater availability of food or it may be a behavioural problem to relieve boredom, or finally it may be due
to a physiological drive to attempt to balance other nutrients
which may be deficient in the captive diet.
If the ratio of energy to protein is correct, and the amino
acid profile and mineral and vitamin levels are suitable,
birds do not generally become obese. Such well fed birds
look good, with good plumage, good disease resistance, and
spend a reasonable part of the day in normal feeding activities, hopefully preparing for breeding. Consideration given
to providing the right foods to provide the essential nutrients
is vital in any captive breeding project.
Deficiencies occur when birds are fed a restricted diet;
they then often develop fads and further restrict their own
diet. Pet psittacines are often kept indoors and denied access
to natural light; this causes vitamin D3 deficiency, unless additional dietary vitamin D3 is provided.
The basic diet types of many of the commonly kept
species are summarised in Table 1. Table 2 gives some information on the nutrient balance of various dietary items.
The two tables can be use together for improving a diet.

PRACTICAL DIETS FOR BIRDS


Formulating these cannot be an exact science, as much of
the necessary data is not available. There are various obser-

vations relating to particular species. Many psittacines, such


as macaws and cockatiels, perform well on approximately
20% protein for growth; macaws seem to require a higher fat
level than cockatiels. Quite low levels of protein seem to be
sufficient to maintain body weight in adult cockatiels.

Diets for larger parrots


Complete pelleted diets
There are several of these now available in the Europe,
(eg. Hagen, Pretty Bird, Roudybush, Kaytee). Most are well
researched products which appear nutritionally adequate,
they are certainly better on a purely nutritional level than
many of the pure seed diets fed to pet parrots.
Many birds eat nothing but seed simply because it is
more convenient for the owner. For these birds, when owner convenience is a major factor, there is sound justification
for converting them to pelleted diets. A pelleted diet will almost always be better than the purely seed diet fed to many
pet parrots. Experience suggests that seeds are used mainly
because many owners think that is what parrots eat, because
pet shops sell it to them. The main problem seems to be one
of education.
Some recommend that they be supplemented with restricted amounts of fresh food. It is important to realise that
complete diets are not usually formulated as part diets,
if they are designed as complete diets this is how they should
be used, adding fresh foods unbalances them.
The major disadvantages with pelleted diets appear to be
cost (which is balanced by convenience), that they appear to
perform not as well as a balanced natural diet, and perhaps
the most important disadvantage that they are eaten too
quickly - they totally ignore the birds relatively high intelligence and inquisitive nature.

Natural diets
Commonly used natural diets used by aviculturists are
often along the lines of:
One third: Carrots, apples, beetroot in equal amounts.
One third: Soya beans, chick peas, field/garden peas,
maize, maple peas.
One third: Pearl barley (hulled), whole sunflower, wheat.

MAIN PROGRAMME

Msc, BVSc, FRCVS


RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

374

4th European FECAVA SCIVAC Congress

Table 1. Summary of dietary requirements of commonly kept psittacines


Main groups

Commonly kept species

Notes on diet

Australian Parakeets

Budgerigar.

Small seeds, eg. hemp, canary seed, millet.

Cockatiel.

As budgerigars plus some larger seeds. Fruit, especially apples,


pears, orange, grapes. Groats, wheat, lettuce, carrot, chickweed.
Sprouted pulses.

Kakariki

Sunflower seed, larger parrot mix (sunflower, safflower, pumpkin


seeds etc). Look out for selective feeding.

Lovebirds

Large seeds, small nuts, berries, apple and carrot. Green foods are
popular. Soft fruits.

Ring necked parrots

Moustache parakeets,
Slaty-headed parakeets, Alexandrines,
Indian Ringnecks.

Large seeds, small nuts, berries, apple and carrot. Green foods
are popular. Soft fruits.

Cockatoos

Moluccan, Goffin and the various


sulphur crested cockatoos.

Large seeds (roseate cockatoos are prone to obesity so with these


it is often better to use small seeds). Fruit, greens, soaked pulses.
Provide wood to strip.

Conures

Sun conures, Green cheeked and maroon


bellied conures.

Mixed seeds; enjoy fruit; like to bathe in large water bowls.

Brush tongued parrots

Lorikeets. These have a long extensible


tongue which is covered in papillae to
collect pollen. They often crush flowers
and lick nectar.

Nectar, pollen, soft food, seeds, berries. Commercial lory diets

Macaws

Scarlet, Blue and Gold, Greenwing


(Red and Green), Dwarf macaws such
as Hahns, Severe and Illigers.

Large seeds, nuts in moderation, small pine nuts for interest.


Enjoy soft fruit.

Amazons & Pionus

Amazons eg. Blue fronted, red lored,


yellow headed, Cuban, Pionus eg.
Blue headed, Dusky

Large seeds, nuts in moderation, small pine nuts for interest.


Mixed pulses, fruit & vegetables. Enjoy soft fruit.

Eclectus

Vosmaeri.

As amazons, but with more fruit.

African Greys

Congo and Silver Greys, Timneh Greys.

As amazons taking particular care to keep the diet balanced,


avoiding fads. In particular avoid exclusively sunflower seed diets.

Non-nutritional food items are very important. Cockatoos like to strip wood - any fruit branches are suitable provided that they have not been sprayed with
garden chemicals. It is sensible to give them a good scrub with an antibacterial cleanser such as Ark-Klens (Vetark) to avoid introduction of infection from wild
birds. Hide dog chews can be drilled and hung from chains etc.

Plus

Plus sprinkling of small high quality pine nuts


in the afternoon/evening. Plus an appropriate
vitamin/mineral supplement such as Avimix
(Vetark).
The legumes and grains are soaked overnight to allow
some germination. The pearl barley does not sprout but
soaking loosens the hulls which then can be washed off.
Sunflower does seem to show some activity. During the
summer, sprouted components are best fed in the mornings
when the temperatures are cool; this avoids rapid spoilage.
In practical terms a bird eating to a particular energy intake ingests more protein, and has a better calcium:phosphorus ratio when fed the aviculturists diet than the seed
(high protein/high energy) diet. As an additional benefit it is

also taking in a wider range of micronutrients. Appropriate


vitamin/mineral supplementation is still valuable.

Handrearing mixes
This is an area where ready made diets have become extremely useful. There are a number of diets available
(Aviplus, Pretty Bird, Hagen) which all appear to perform
well. The person carrying out the handfeeding can greatly influence performance, but changing diets can still cause problems. It is not unusual for an experienced handrearer using a
home-made blend to experience serious problems when
changing to a prepared diet. This is not a poor reflection on

4th European FECAVA SCIVAC Congress

375

Table 2. Information on dietary items


Typical ingredients

Comments

Small seeds

Hemp, millet, canary seed.


Millet sprays when birds have reduced
appetite, or when young are fledging.

Lower fat and higher carbohydrate than the larger seeds.

Large seeds

Sunflower, safflower, pumpkin.


Grains - wheat, oats, buckwheat, groats.

Cereals are fairly low in protein (corn and wheat have 9 - 10%,
oats and barley contain 11 - 12%) but have a high energy value
due to their starch stores. Vitamins A, D3, B6, and B12 are quite
low or absent, corn is the only grain which contributes towards
vitamin A requirements. Cereals are also low in calcium, and their
phosphorus is mainly in the form of phytate.
These mixtures are of very variable quality, some being extremely
poor. Seeds need to be looked at carefully for fungal growth;
webby seeds need to be avoided. Aspergillus flavus can grow
on such food and can produce aflatoxin which may cause chronic
hepatitis and other problems. Oil seeds need to be rationed; birds
develop fads and often will eat nothing but sunflower seed.

Nuts

Brazil nuts are generally popular with


Fed in moderation, tiny pine nuts are ideal therapy, birds enjoy
macaws. Most parrots enjoy pine nuts,
spending time opening them for the high fat taste, but actually
from the giant Chinese ones to the tiny ones. get relatively little nutritionally from them. Batches of nuts should
be checked by opening a few prior to using them. Harvesting
followed by storage while damp encourages fungal growth.
Peanuts in shell often harbour Aspergillus, these are best avoided.

Fruit

Apples are popular with most psittacines;


soft fruit from berries to grapes are also
usually well received, as is pomegranate.

Must be fresh, or it wont be eaten and if left will encourage


growth of Aspergillus. In general the fruit isnt eaten, it is
squeezed to release pulp and juice. Orange is enjoyed and orange
juice can be used to flavour new foods or medicines.

Vegetables

Any fresh vegetables can be given.


Grated carrots, sweetcorn and celery
are popular.

Frozen mixed veg is a very useful standby. Beetroot is enjoyed


but will stain the faeces red.

Sprouted
and soaked pulses

Various beans such as haricot, soya,


mung, black eyed and maple, chick peas
and green peas, and lentils.

Legumes (peas, beans, and pulses) are concentrate feeds with


protein levels in the range 22 - 31%, fat level in the 1 - 6% range,
and carbohydrate 58 - 68%.
Oilseeds may have even higher protein levels, such as soybeans at
43%; they can be up to 55% fat. Soybeans are also the best
balanced in terms of amino acids. Sprouting is a very important
way of improving palateability and digestibility. Nutritional value
improves a little.

Animal protein

Cooked bones, such as chicken or lamb.

These are always enjoyed, but the fatty remnants should


be removed or high blood cholesterol levels and atherosclerosis
may result.

the diet. Changes to handrearing diets should only be made


very cautiously. A general analysis of 18 - 20% protein and
5% fat seems to be acceptable and produces good results.

Nectar feeding parrots


In the wild, psittacines consuming nectar take in fairly
large amounts of pollen. There is evidence, however, than
much of this passes through the psittacine gut undigested.
Some digestion occurs in the nestling bird, and in adults
overnight. Some species may be better than other at digest-

ing pollen. Pollen is a rich source of protein, typically 15 20% protein, 20 - 35% carbohydrates and 1 - 3% oils. Nectar consists mainly of sugar (depending on the source 13 60%, with most approximately 35%), with trace amounts of
organic acids, oils, dextrin, protein, and enzymes. The main
sugars are sucrose, fructose, and glucose.

Processing/Treatment of food
Sprouting of legumes and pulses raises the digestibility
of the components. Some of the fairly indigestible carbohy-

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Dietary classes

376

drate, such as starch, is converted into more digestible dextrins etc, and even into proteins as the sprout grows. The vitamin levels also rise slightly, especially vitamin C, although
not enough to be relied on as a major source. Sprouting also
makes the seeds of legumes safer, by reducing some of the
toxic or anti-nutritive factors present in them; soybeans, for
instance, contain a trypsin inhibitor which reduces the digestion of proteins. The act of soaking also makes it easier
for birds to break up the seed for digestion. Water used for
sprouting/soaking of seeds should be changed every couple
of hours as some of the nutrients will enter solution and encourage bacterial growth. For the same reason seeds should
be well rinsed and drained before feeding.

Converting Seed Junkies


Estimate the amount of seed normally eaten in a day and
give half of it; monitor the birds condition whilst trying
the following: weed the mixture, changing the balance
of seeds away from sunflower seed.
Use a top quality mix. The hulled blends available, such as
Ultra Mix and Tidy Mix, are ideal. Importantly, they are
fresh and palatable and can be top dressed with vitamins
using a little peanut oil or orange juice.
Use non-threatening forms of food. Shredded carrot is
less suspicious to a bird than a whole one!
Try introducing new items in amongst the seed.
Sprout seeds and pulses - they taste much better.
Introduce a soft-food, baby cereal, fruit pulp, or proprietary mixes (CeDE or EMP). Again, this will give a vehicle for vitamins.
Consider interval feeding. Instead of leaving food in the
cage all day try introducing meal times; 30 - 60 minutes
access three times a day.
Move the cage; place new food items such as corn on the
cob close to favourite toys.
Monkey see, Monkey do. Birds will often take and investigate titbits which they see the owner eating. Being
able to see other birds eating a better diet may also help.
Change the photoperiod. The natural photoperiod for
many birds is 12 hours light, 12 hours dark. In captivity
this is extended in the home by early risers and late night
television. Covering the cage from 9pm till 9am can
change a birds behaviour and sometimes help with establishing new feeding patterns.
Consider hospitalisation, or boarding out. A new regime
may be more acceptable under new management where
everything else is new.
Remember - owners have starved birds to death trying
to change their diet!

NUTRITIONAL DISEASE
Protein and Essential Amino Acid (EAA)
Deficiency
Protein required for growth is limited by the availability
of the various essential amino acids. To obtain sufficient

4th European FECAVA SCIVAC Congress

amounts of the limiting amino acids, the bird on a poor diet


is forced to overeat and then eliminate the excess nitrogen.
Protein levels in excess of that which can be used, are broken down as an energy source and may result in obesity, or
gout due to the formation of urates. The pathogenesis of gout
is not clear, water deprivation and nephrosis, even very short
term may make a considerable difference.
Although birds can manage on low protein levels, this
does not apply to periods of special need. When birds are
producing eggs, a low protein diet will stop production and
also can inhibit new feather growth. Choline, lysine and tyrosine deficiency all lead to colour abnormalities. Methionine deficiency has been linked with stress lines in feathers.
Lysine levels are low in seeds, therefore purely seed-fed
birds often develop poor feathering. The requirement for lysine is estimated at between 1 - 2% (high percentage of a low
protein diet). Poor matrices within the bones are another result of protein or amino acid deficiencies. EAA deficiencies
in general will lead to fatty liver problems. These are compounded due to the high fat diets often fed.

Vitamin A deficiency
This is the most common vitamin deficiency seen in parrots. The pathogenesis includes squamous metaplasia of the
epithelial surfaces of the oropharynx, renal tubules, reproductive tract, and air sacs. Poor condition or chronic upper
respiratory problems are the commonest presenting signs,
although nephrosis is also linked to the renal tubule changes.
Feather colour changes, hyperkeratosis of the feet, and general poor feathering are also involved.
The efficiency of the conversion of -carotene (in the
fruit or vegetables) into vitamin A is uncertain in psittacines,
but it is likely that due to the overabundance of carotenes in
their normal diet, conversion is not particularly efficient.
The relatively high requirement of vitamin A by psittacines
may be met by -carotene in fresh vegetables, carrot, cornon-the-cob, iceberg lettuce, green beans, celery, apricots, oranges, papaya etc. Supplementation is generally required,
ACE-High or Avimix (Vetark). This is particularly important
once signs of deficiency have been seen.

Metabolic Bone Disease


(Calcium and Vitamin D3 problems)
Calcium deficiency in adult birds can result in:
acute hypocalcaemic fits (especially African Greys)
the production of soft shelled eggs
eggbinding due to poor muscular function
a cessation in breeding.
Conversion into vitamin D3 requires exposure to sunlight. It may be this factor which is most important in deficiencies seen in captive birds. African Greys, in particular in
breeding establishments, are normally bred indoors and often spend most of their time in the nestbox, perhaps only
coming out for food. Birds kept indoors need regular supplementation, particularly breeding birds. Nutrobal (Vetark)
provides an appropriate balance of calcium and vitamin D3.

4th European FECAVA SCIVAC Congress

Vitamin E deficiency
Deficiency of vitamin E may come about through rancidity. Commonly fed seed mixes may contain seeds stored
far too long, in which levels of vitamin E have fallen and
fats have become somewhat rancid. Signs of disease (especially myopathies) are particularly seen in birds which are
also deficient in selenium or sulphur-containing amino
acids. Supplementation of these poor diets is essential, eg.
ACE-High (Vetark). Vitamin E also has an important part in
disease resistance.

Fat and essential fatty acids


Fat related problems, often associated with vitamin E deficiency, are common among pet birds. These are often the
result simply of overeating on a high calorie, low quality diet. In birds the liver is very active in lipogenesis. Linoleic
and arachidonic acids are essential: when they are lacking, a
fatty liver can develop due to impaired fat metabolism. Any
hepatic pathology which inhibits proper fat metabolism may
also lead to fatty liver.
Diets high in saturated fats can lead to atherosclerosis
and fatty liver syndrome, and are usually linked with a hypercholesterolaemia. Excessive amounts of cheese or too
frequent titbits of lamb bones have both been seen to lead to
these problems.

B Vitamin deficiencies
The high fat diets of pet psittacines are normally low in
B vitamins. Deficiency syndromes are poorly understood
but poor growth, general unthriftiness and poor feathering

are major features. They may be quite important. Classic


single B vitamin deficiencies are associated with:
Thiamine (B1) - opisthotonus, fits.
Riboflavin (B2) - curled toes, dry skin, poor feather pigmentation, fatty livers.
Pyridoxine (B6) - perosis, jerky movements, convulsions.
Pantothenic acid - dermatitis around eyes and mouth, wiry
down, ataxia.
Biotin - brittle feathers, swollen feet, ataxia, chondrodysplasia, fatty liver.
Folic acid - poor feathering, white or brittle feathers, beak
deformities.
Choline - perosis.

Vitamin C deficiency
Any form of stress, or physical, nutritional, toxic or infectious disease tends to deplete endogenous stores of vitamin C. Supplementation produces positive effects on egg
quality so even though a specific deficiency syndrome is not
reported in psittacines there is good reason for including vitamin C in general supplements, especially those used when
birds are under stress. ACE-High (Vetark) is particularly
useful in this regard.

References
BAUCK, L. (1995) Nutritional problems in pet birds. In. Seminars in Avian
and Exotic Pet Medicine. 4, (1).
BRUE, R.N. (1994). Nutrition. in Ritchie, B.W., HARRISON, G.J. &
HARRISON, L.R. eds. Avian Medicine. Principles and Application.
Wingers Publishing.
CLUBB, S. (1997). Us eof psittacine handrearing formulas. Basic Day Proceedings of the 4th Conference of the European Committee of the Association of Avian Veterinarians. EAAV,1997. London.
HAGEN, M. (1992) Nutritional observations, hand-feeding formulas, and
digestion in exotic birds. In. Seminars in Avian and Exotic Pet Medicine. 1, (1).
ROUDYBUSH, T.E. (1997) Nutrition. In: Avian Medicine and Surgery.
(Eds R.B.Altman, S.L.Clubb, G.M.Dorrestein & K.E.Quesenberry.
W.B.Saunders, Philadelphia.
SMITH, J.M. & ROUDYBUSH, T.E. (1997) Nutritional Disorders. In:
Avian Medicine and Surgery. (Eds R.B.Altman, S.L.Clubb,
G.M.Dorrestein & K.E.Quesenberry. W.B.Saunders, Philadelphia.
SCOTT, P.W. (1996) Nutrition of Psittacines. BSAVA Manual of
Psittacines. Pub. British Small Animal Veterinary Association.

MAIN PROGRAMME

In African Greys it is often also necessary to supplement using calcium lactate in drinking water. Marginal hypocalcaemic birds may show clinical disease during or following
medication with oxytetracycline on other binding agents.
Hypervitaminosis D3 has been reported in several species
in the USA, macaws appear particularly featured. Cases are
generally associated with over-supplementation of already
supplemented commercial diets.

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4th European FECAVA SCIVAC Congress

379

Avian skin disease: your worst nightmare


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary

stratum corneum

Avian skin disease presents many problems for the veterinarian. Causes will usually have a nutritional component,
often a behavioural component or possibly an untreatable viral component. Reaching a diagnosis can be complex, and
attempting treatment an be frustrating, correcting nutritional
diseases takes months, the new plumage must appear before
any improvement is seen (this may take a year). Topical
treatments are generally not appropriate because birds preen
them off. Behavioural changes are extremely difficult to implement due to poor client compliance.

Clinical anatomy
Birds have a thinner, more delicate skin than mammals,
it may be almost transparent. There is an epidermis, dermis
and subcutis. The dermis is very thin with few blood vessels
and contains the feather follicles and their supportive muscles which run to adjacent body prominences. Skin haemorrhage is rare. Bird skin has virtually no glands other than the
holocrine glands of the external ear canal and the uropygial
gland, however the whole skin surface of the bird can be regarded as a gland - it is lipogenic.
The uropygial gland is a large bilobed gland situated dorsally at the base of the tail, it is common in birds, all

s. intermedium
s. basale
basal membrane
dermis

psittacines except amazon parrots (Amazona spp) have one,


it is most developed in aquatic species and absent in ratites.
The gland produced a lipoid sebaceous material which the
bird spreads over its feathers when preening. Perhaps surprisingly the uropygial gland produces less than 10% of the
plumage sebum, the rest comes from the skin itself.
At the time of breeding many birds show a thickened
dermis - the brood patch, this is much more vascular and
may bleed if injured, breeding birds will often pluck a patch
over this area. the subcutis is mainly loose connective tissue
with fat.
Hormone control of feather growth is not fully understood, in some species oestrogens retard feather growth, in
others they promote it, generally testosterone has little effect
and thyroxine initiates growth. Birds cannot rear and moult
at the same time, generally they moult before or after a rise
in sex steroids.
Once adult plumage is developed most birds moult once
a year, usually after breeding. In most species this occurs in
waves through the feather tracts so that the bird is not made
flightless, although many water birds and flamingos do become flightless.

Feathers
Feathers are of epidermal origin growing around a feather follicle from the dermis, they grow in distinct feather
tracts and in several types depending on their location in the
body. Feathers are held in place in the mature telogen
phase at least partially by tension of the non-striated feather
muscles between follicles.

MAIN PROGRAMME

s. transitivum

Avian dermatoses almost all have a nutritional component since the majority of parrots are fed incorrectly or inappropriately, the clinician must review the diet of the bird
looking both at the nutritional content and the recreational
aspects of actually eating it. Many dermatoses have a behavioural component since we are often keeping pet
psittacines in situations which are abnormal, flock/social
birds taken from the wild and bred even a dozen generations
in captivity (which would be unusual) are not domesticated.
The majority of pet parrots are less than two generations
from the wild. Their instincts are those of wild birds and social influences such as flock structure, companionship, mutual preening, time spent foraging for food and avoidance of
potential predators all have parallels in captivity. This paper
will review the various causes of avian dermatoses highlighting common ones and discussing practical techniques
for diagnosis and treatment.

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4th European FECAVA SCIVAC Congress

distal barbule
hamuli
rachis

barb

proximal barbule

hypopenna

The primary remiges (wing feathers) arise from the


manus, and the secondaries from the ulna. They are linked
by the interremigeal ligament which has some smooth muscle components, and the primaries in particular firmly attached to bone. The tail feathers (remiges) are paired, most
birds have 6 pairs.
Contour
Flight
Body (includes the coverts which cover the bases of the
flight feathers)
Semiplumes - especially waterbirds
Others
Down - especially chicks, not in ratites, pigeons, and
passerines
Powder down - especially cockatoos, cockatiels &
african greys
Hypopennae - very large in ratites
Filoplumes - not found in ratites
Bristles

lice are common and said to be rarely a problem, many


birds carry a load with no problems they do appear to
be linked with untidy feathers in a number of birds, especially recent imports
mites are common eg. Cnemidocoptes in scaly leg/face
Dermanyssus gallinae the red mite does occur
Myialges nudus (mange mite) in Brotogeris - canarywinged parrakeet, mainly the head affected
Fungal
fungal causes are not common, but Aspergillus is seen
Viral
Psittacine Beak & Feather Disease (PBFD) - Psittacine
circovirus. This is a major problem and has spread from
its natural hosts the Australian parrots and parakeets
to cause serious disease in a wide range of psittacines
including amazons, african greys and macaws. This
probably responsible for most cases of French moult
polyomavirus / papovavirus. Like PBFD this is not uncommon, its natural host seems to be the budgerigar
where it causes Budgerigar Fledgling Disease and in
some countries appears to be the major cause of
French moult
avian poxvirus - papules or proliferative masses, secondary infections are common
herpes virus in psittacines, proliferative lesion
Bacterial
not common
Staphylococcal pyodermas
pododermatitis especially canaries, raptors nestling
psittacines
pansystemic infections sometimes manifest as skin
conditions

Non-infectious
semiplume

flight feather

filoplume
bristle
vane

down
feather

rachis
scapus
distal
umbilicus
calamus
proximal
umbilicus

Disease
Infectious
Parasitic
roundworms, tapeworms,
giardia is reported as a cause of pruritis, especially
cockatiels,

Genetic / Congenital
little or no feather growth
deformities eg. straw feather, chrysanthemums
feather cysts
beak deformities
wing-web dermatitis in lovebirds
amazon mutilation syndrome - dorsal surface of the feet
preening though instinctive appears to also require an
element to be taught, hand-reared birds may simply do
it badly
Nutritional
Poor diets will lead to poor feathering, to have a new
healthy plumage it is vital that the diet is corrected. There is
little point addressing behavioural factors or pathogens in a
bird being fed poorly. Low protein diets will generally adversely affect new feather production, a sudden improvement in protein level using cooked rabbit or chicken or egg
foods may often trigger a moult. Vitamin supplementation is
important with natural diets.
choline, lysine & tyrosine deficiency all lead to colour
abnormalities.
Lysine deficiency in seed diets. Lysine in legumes is often high, making up for the relatively low levels in
seeds/cereals. The cereals on the other hand tend to pro-

vide good levels of the sulphur-containing amino acids


methionine and cystine which are low in the legumes.
Vitamin A deficiency in psittacines is the common vitamin deficiency - poor condition and chronic upper respiratory problems are the main signs, although nephrosis is also linked due to renal tubule changes. Feather
colour changes, hyperkeratosis of the feet and general
poor feathering are also involved. The relatively high
levels of vitamin A needed by psittacines may be met
by -carotene in fresh vegetables, carrot, corn-on-thecob, iceberg lettuce, green beans, celery, apricots, oranges, papaya etc. Supplementation with ACE-High or
AVIMIX (Vetark) is recommended
folic acid - poor feathering, white or brittle feathers
pantothenic acid - dermatitis around eyes and mouth,
wiry down
biotin - brittle feathers
faults through illness like stress lines
Hormonal
age- brown hypertrophy of the cere in female budgies
sexual brood patch - it is suggested that sexually related plucking is often in the clavicular region or the tops
of the wings, certainly cockatoos may extend the brood
patch.
oBald male canaries need testosterone!
thyroid hypothyrodism in amazons, poor moult &
feather regrowth
Environmental
Toxic
stress lines - also following hormone use?
Exposure to cigarette smoke, or nicotine on owners
hands
Psychological
separation anxiety in handreared birds
very common, encouraging results with use of anxiolytics such as haloperidol, or naltrexone
Aggression
wounds
beak injuries
lost toes
wire damage - to the tails of wire hangers
frost bite
post wing clip, especially if done badly
Neoplastic
lipomas, xanthomas
fibrosarcomas
haemangiomas & haemangiosarcomas
basal cell tumours & squamous cell carcinoma
adenomas of the uropygial gland
Allergic / Hypersensitivity
cockatiels & macaws in USA

Diagnostic approach to feather picking


Discuss the diet
Correct it as appropriate, seed is completely unbalanced in
most cases. Balance seed with soaked/spouted pulses, introduce fruit and vegetables - grated is often more palatable and
less threatening/abnormal in appearance. Use supplements, it

381

is impossible to provide the variety available in nature.


Complete diets are available and may be better than
some made diets, compensation for lack of non-nutritional
stimulation of a natural diet may be necessary.
Give the bird a full clinical examination
Check birds skin for parasites
Biochemistry looking especially for indications of
hepatopathy
Haematology, serology as appropriate
Check faecal sample for parasites as appropriate
PCR tests for PBFD / Polyomavirus - not actually
chewers but look similar, also PCR faeces for Chlamydiosis
Feather follicle cytology - should be sterile
Biopsy
infectious causes
bacterial / fungal dermatitis / folliculitis
PBFD
allergy
endocrine disorders
neoplasia
Treatment will be based on the diagnosis reached but
may include:
specific treatment of infections - antiparasiticides,
antibiotics
behavioural modification
anxiolytics
Patience - some birds may take 2 years to moult damaged
feathers, few will look better quickly.
At worst PBFD or Polyomavirus may warrant euthanasia.

Behavioural modification
for feather pickers
Provide the largest cage that the room and wallet will
accommodate, this allows room to move and also allows you to create different areas.
Move the cage around, presenting a different view from
time to time, presenting a busy view when the bird is to
be left stimulates a curious bird. The majority of birds
benefit from being part of the family. Most parrots are
social birds and do not enjoy isolation.
Allow a good rest period, many birds require the cage
to be covered at night, this helps establish a routine. At
least 12 hours dark is important, for birds which are seriously plucking starting out with 16 hours dark is useful then gradually extending the daylight to a 12/12
regime.
Spray the bird regularly, a fine mist from small house
plant spray is ideal, birds will spend time cleaning and
drying feathers rather than pulling them out. This simulates the regular natural rainfall which most parrots
are exposed to in the wild.
Spend more time with the bird, talk to it more often, eat
with it and give it food/titbits, take it from room to
room.
Leave a radio, tape, or TV on when you are out.
Some birds will chatter away, dance, or generally be
stimulated.

MAIN PROGRAMME

4th European FECAVA SCIVAC Congress

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4th European FECAVA SCIVAC Congress

Create a theme park in the cage, acrylic toys, hide, fruit


tree (eg apple) branches from the garden, swings, bells
etc all provide recreation. Some birds are used to
spending all day foraging for food, to have all meals
provided ad lib inside a small cage is extremely boring
and leaves a lot of free time for vices.
Provide nibbles such as carrots, broccoli and other
vegetables. Small pine nuts given as a titbit are good,
birds spend ages trying to open them.
Consider a training program, there are good videos
available to help and in some countries specialists who
can advise you.
Review the diet and ensure that you provide a balanced
diet which encourages healthy feather growth, old unmoulted feathers in a poor skin are itchy and encourage
feather pecking. Sometimes increasing the protein level will induce a moult. Use appropriate supplements
such as ACE-High or AVIMIX (Vetark).

References & reading list


Cooper, J.E.,& Harrison, G.J. (1994). Dermatology in Ritchie, B.W., HARRISON, G.J. & HARRISON, L.R. eds. Avian Medicine. Principles
and Application. Wingers Publishing.
FLAMMER, K. (1991). Diseases of the Integument of Cage & Aviary
Birds. in Avian Medicine. TG Hungerford. Refresher Course for Veterinarians. Post Graduate Committee in Veterinary Science, University of Sydney. 431-442.
HILLYER, E., QUESENBERRY, K.E., & BAER, K. (1989). Basic Avian
Dermatology. Proceedings of the Annual Conference of the Association of Avian Veterinarians. Seattle. 101-121.
KING, A.S., & McLelland, J. (1984). Birds, their structure and function.
2nd ed. Baillire Tindall, London.
Latimer, K.S., Rakich, P.M., Niagro, F.D., Ritchie, B.W., Steffens, W.L.,

Campagnoli, R.P., Pesti, D., and Lukert, P.D. (1991) An updated review of Psittacine Beak and Feather Disease. J.Assoc. Avian Vet. 5,
(4) 202-206.
MADILL, D.N. (1991). Feather problems & bald birds. in Avian Medicine.
TG Hungerford. Refresher Course for Veterinarians. Post Graduate
Committee in Veterinary Science, University of Sydney. 87-92.
Niagro, F.D., Ritchie, B.W., Latimer, K.S., Lukert, P.D., Steffens, W.L., and
Pesti, D.: Polymerase chain reaction detection of PBFD virus and
BFD virus in suspect birds. In Proceedings of the Annual Conference
of the Association of Avian Veterinarians. Phoenix: 25-37, 1990.
Perry RA. Gill, J, & Cross, GM. 1991. Disorders of the Avian Integument.
in Pet Avian Medicine. Veterinary Clinics of North America 21, (6)
1307-1328.
REAVILL, D.R. (1996) Ed. Dermatology. in. Seminars in Avian and Exotic Pet Medicine. 4, (4).
Ritchie, B.W., Niagro, F.D., Latimer, K.S., DAVIS, R.B., Pesti, D., and
Lukert, P.D. (1991) Avian polyomavirus: An Overview. J.Assoc.
Avian Vet. 5, (3)147-153.
Ritchie, B.W., Niagro, F.D., Latimer, K.S., DAVIS, R.B., Vernot, J., Pesti,
D., Campagnoli, R.P. and Lukert, P.D. (1991) Polyomavirus Infections in adult psittacine birds. J.Assoc. Avian Vet. 5, (4) 202-206.
ROSSKOPF, W. & WOERPEL,R. 1996. Feather-picking and therapy of
skin and feather disorders. In Diseases of Cage and Aviary Birds. 3rd
ed. Editors ROSSKOPF, W. & WOERPEL,R. Williams & Wilkins.
Baltimore.
SCOTT, P.W. (1993) DNA Technology: Practical applications for the avian
veterinarian. in Proceedings of the 1993 European Conference on
Avian Medicine & Surgery. Utrecht, Netherlands. European Committee of the Association of Avian Veterinarians. 178-190.
SCOTT, P.W. (1994). Psittacine Polyomavirus in Britain. Veterinary
Record. Aug 13.
SCOTT, P.W. (1996) Nutrition of Psittacines. BSAVA Manual of
Psittacines. Publ. British Small Animal Veterinary Association.
Pearman, R.I.C. & Hardy, J.A. (1985). Integument. in Form and Function
in Birds. Vol 3. eds KING, A.S. & McLelland, J. Academic Press.
London. 1-56.
WILSON, L. 1996. Non-Medical Approach to the Behavioural Feather
Plucker. In Proceedings of the Annual Conference of the Association
of Avian Veterinarians. Tampa: 3-9, 1996.

4th European FECAVA SCIVAC Congress

383

Anaesthesia and surgery of pet fish


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary

Kidney
Spleen

Dorsal fin

Swimbladder

MAIN PROGRAMME

Fish are an uncommon animal presented to the veterinarian, anaesthesia is a simple technique which makes certain aspects of examination and treatment much more
straightforward. Fish as diverse as koi carp, goldfish, sharks
and marine puffer fish all respond to the same basic approach. Surgical techniques will be discussed, including removal of external neoplasms, radiosurgery, and intra-abdominal surgery.

Gonad

Operculum
Heart
Gill
arches

Anal fin
Gall
bladder

Pectoral
fins

Pelvic fin

Liver

Anaesthesia of fish is a sometimes joked about topic.


Sadly it is one which many koi keepers have adopted, almost
as a routine, yet which many veterinarians havent even considered. It can provide a very useful way of obtaining samples, scrapings or biopsies, or even tackling serious surgery.
Much becomes possible if the veterinarian is prepared to undertake anaesthesia.

Artery
Gill lamella

Vein

Water flow

ONE GILL ARCH


ONEGILL FILAMENT

Anatomy
In general fish anaesthetics are administered via the water in which the fish is swimming, the drug enters and leaves
the fish via the respiratory surfaces of the gills (eg. gaseous
anaesthesia in birds and mammals). In just the same way that
a bird or mammal is assessed prior to anaesthesia this should
be done with the fish. Compromised gills (not uncommonly
affected with degrees of hyperplasia) may mean that uptake
and elimination are slowed, increasing the risk, especially of
deep anaesthesia.

marking or tagging
surgery/debridement eg. removal of neoplasms
long distance transportation
handling of - valuable fish
dangerous fish
particularly large fish
The needs of these various tasks are different so care must
be taken with all applications. The transition between stages
of anaesthesia can be very rapid so great care is needed.

Reasons for anaesthesia


Handling of fish, in or out of the water, is physically difficult and not without risk to the fish, and in some circumstances to the handler. Anaesthetics are useful in making
any necessary handling procedures as non-stressful as
possible.
There are a variety of reasons why anaesthesia may be
required:
handling broodstock for stripping, blood sampling, treatment etc
vaccination by injection

Responses
The individual response of a fish to an anaesthetic and its
transition between the various stages is dependent on a number of factors:species: gill area to body weight ratio
size and weight: metabolic rate
lipid content: season, sex, maturity, diet
condition
disease

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4th European FECAVA SCIVAC Congress

Levels of anaesthesia

STAGE

PLANE

SIGNS/INDICATORS

Light sedation

slight loss of reactivity

Deep sedation

total loss of reactivity except


to strong pressure, equilibrium
normal

Partial loss
of equilibrium

erratic swimming, increased


opercular rate

Total loss
of equilibrium

reactivity only to deep


pressure stimuli

Loss of reflex
activity

total loss of reactivity, very


shallow opercular movements

Medullary
collapse

gasping followed by cessation


of opercular movements

The transition between these stages is dependent on several factors, particularly dose used, species and activity.
Stages 2/3 are often ideal for simple procedures, when the
head and tail of the fish can be wrapped struggling is minimised. The aim is generally to maintain the fish at the level
of minimal activity which can be considered sedation rather
than anaesthesia.
In general use a low level of anaesthetic until you are confident. Fish react differently, trout will be very agitated and
very active then suddenly roll over, carp will often tend to
settle quietly and unless you are observant may overdose.
When possible keep the fish moving using your hands or
a net, this way you can judge its depth of anaesthesia. My
own preference is not to use gloves, except for venomous
species some other veterinary surgeons always use surgical
gloves which they claim do less injury to the fish skin than
human hands.

Benzocaine
Benzocaine is probably the cheapest of the available
anaesthetics and it seems to work just as well as MS222
without the pH caused by that compound. Unfortunately it is
not very water soluble. A stock solution can be made up in
acetone or methanol (40g per litre). This can be kept at least
3 months in a dark bottle (necessary to prevent the formation
of toxic compounds).
stock solution
per 2 gall (9 litres)
gentle handling
25ppm
5.5ml
deeper surgical anaesthesia 50ppm
11ml
The figures above should be considered guidelines for
providing a safe sedation in an acceptable period of a few
minutes; experience will allow higher doses to be used for
more rapid effect. When this is done, however, great care
should be taken, as fish can easily be overdosed and irreversible medullary collapse may occur. All anaesthetics carry a degree of risk. Benzocaine is not licensed.
There is considerable interspecies variation and one
should always err on the side of caution. Relatively sedate
species such as carp are slower to succumb than trout, and
can become very deeply anaesthetised without the operator
always appreciating it.

Phenoxyethanol
This has been used at a concentration of 0.1-0.5 ml/litre
(100-500 mg/litre) as an anaesthetic. It also has bactericidal
effects and may therefore be of some use when handling
broodstock in reducing surface contamination. As an antibacterial it has been sold for aquarium use for over 40
years. There is an increased safety margin at lower temperatures since the lower doses can be used.
The lower level (0.1 ml/litre) is reported useful for prolonged sedation. At a concentration of 1 ml/litre (1000
mg/litre) it gives rapid anaesthesia and fish must be removed
quickly when anaesthetised or they will die.
Care needs to be taken when advising its use. It is reported to elute toxins from activated carbon in filters.

MS222 (Tricaine methylsulphonate,


Sandoz)

Specific surgery

At present MS222 is the only anaesthetic licensed in the


United Kingdom for fish, it also has the benefit of being
water-soluble.
Depth of anaesthesia needs to be watched carefully and
the fish removed when the desired plane is reached. Its disadvantage is that it causes pH changes and may cause irritation. MS222 is fat soluble so there may be some residual depression in large adult fish with well developed fat.

TYPE

COMMENTS

Arterial cannulation

Normal dose:
1:10,000 solution ie. 1g/10 litres ie. 100ppm for anaesthesia
1:20,000
1g /20 litres ie. 50 ppm for tranquillising
1:50,000
1g/30 litres ie. 33ppm for transport

Laparotomy

Experimental procedure in
salmonids cannulating the dorsal
aorta via the roof of the mouth
This has been carried out in sharks
to obtain biopsies for
diagnostics. Insufflation is
generally necessary
Gonadectomy has been carried
out, both experimentally and for
behavioural control. Usually a
ventral midline approach but indi-

Laparoscopy

4th European FECAVA SCIVAC Congress

from Stoskopf (1993)

Preparing for surgery


There are a few points to consider when planning
surgery:
have the client bring the fish in a manageable container of
water, another container of the same amount of water
should be available for recovery. For koi carp plastic dustbins are often ideal!
starve the fish pre-operatively if possible for 12 hours. This
avoids any potential regurgitation which in a small container may damage the gills.
unless you have set up a recycling system, plan to complete
the surgery quickly
use the lowest level of anaesthesia consistent with the
surgery
ensure that wherever possible you research the anatomy of
the species, if you cant then take extra care! There are over
20,000 species of fish which might be kept in private or
public aquaria and anatomy varies considerably.
most fish surgery will be performed with the fish out of
water positioned on a suitable surface which presents the
fish in the chosen fashion
fish skin is not mobile, repairing skin deficits post-operatively following tumour removal will be difficult/impossible
cryosurgery works well with skin neoplasia
electrosurgery using the Ellman Surgitron has proved highly effective in larger fish
tissue adhesives or superglue have been used successfully
for skin closure and for waterproofing sites.
antibiotic injections at the time of surgery avoid the need
for stressful repeat anaesthetics or restraint
polyglycolic acid sutures have been used successfully for

wound closure, care must be taken to knot the sutures securely, especially in seawater which seems to loosen them,
steel wire has been used in sharks as have other standard
non-resorbable sutures
Good surgical loupes are useful for work with small ornamental fish
Prolonged anaesthesia presents problems beyond the
scope of this paper but which are covered by Brown (1994)
and Stoskopf (1994).

Resuscitation
Fish are normally placed into a container of the same water which they were kept in and moved gently to encourage
a flow of water across the gills, a finger placed ventrally just
behind the lower jaw will keep the mouth open. It is worthwhile when planning to anaesthetise a fish to have the client
bring a container with the fish in water and another spare
container with enough water to transport the fish home.
With large fish a pump recycling tank water through the
gills can be useful, and (where appropriate) a diver can assist the fish in early attempts at swimming on recovery.

Euthanasia of fish
Humane anaesthesia is possible by administering a gross
overdose of anaesthetic and leaving the fish in the water for
a longer period. It is possible to sedate the fish using a water soluble anaesthetic and even then use the intravenous approach to administer barbiturates.

References
BROWN, L. (1992). Restraint, Handling and anaesthesia. In. Manual of Ornamental Fish. Ed. R.L.Butcher. British Small Animal Veterinary Association, Cheltenham.
BROWN, L. (1994). Anaesthesia and Restraint. In: Fish Medicine. Ed
M.K.Stoskopf. W.B.Saunders Co, Philadelphia.
SCOTT, P.W. (1992). Clinical examination of fish. In. Manual of Ornamental Fish. Ed. R.L.Butcher. British Small Animal Veterinary Association, Cheltenham.
SCOTT, P.W. (1992). Therapeutics. In. Manual of Ornamental Fish. Ed.
R.L.Butcher. British Small Animal Veterinary Association, Cheltenham.
STOSKOPF, M.K. (1994). Surgery. In: Fish Medicine. Ed M.K.Stoskopf.
W.B.Saunders Co, Philadelphia.

MAIN PROGRAMME

Ulcer debridement

vidual species anatomy may alter


this. Tumour removal may be possible. Be aware that in cyprinids
the abdominal organs are all
adherent and may make such an
intervention unlikely to succeed.
Routine, allows thorough
cleansing, potential to pack with
barrier cream. Remove material
which may act as foreign body and
then allow epithelialisation.

385

4th European FECAVA SCIVAC Congress

387

Management of peritonitis - Current update


Daniel D. Smeak

Summary
Peritonitis is a complex disease condition that results in
many pathophysiologic alterations affecting multiple organ
systems. Surgeons must possess a thorough understanding
of the pathophysiology of this disease so that effective
treatment can be made. Treatment should be directed at
eliminating the cause of peritonitis and preventing the resulting pathophysiologic responses. Peritoneal injury triggers many physiologic responses that are intended to control the peritoneal irritant. Although these responses are
beneficial initially to the patient, as they progress they often have deleterious effects. The purpose of this seminar in
review current information about treatment of peritonitis in
small animals.

these lymphatics into the thoracic duct. The peritoneum


functions as a by-directional barrier to the diffusion of water
and low molecular weight substances.

Peritoneal fluid
Peritoneal fluid is constantly produced and reabsorbed. It
provides lubrication for the movement of abdominal organs
within the peritoneal cavity. Although the peritoneal fluid
has minimal antibacterial properties, it does contain fibronectin a bacterial opsonizing protein. Fibrinogen is
not present, so normal peritoneal fluid will not clot.

Particulate matter and microbial


absorption
Introduction
Peritonitis is a complex disease condition that results in
many pathophysiologic alterations affecting multiple organ
systems. Surgeons must possess a thorough understanding
of the pathophysiology of this disease so that effective treatment can be made. Treatment should be directed at eliminating the cause of peritonitis and preventing the resulting
pathophysiologic responses. Peritoneal injury triggers many
physiologic responses that are intended to control the peritoneal irritant. Although these responses are beneficial initially to the patient, as they progress they often have deleterious effects.
The purpose of this seminar in review current information about treatment of peritonitis in small animals.

Peritoneal physiology
Peritoneal cavity
The peritoneal cavity is the largest preformed extravascular space in the body. It is lined by a single surface layer
of mesothelial cells. On the visceral surface of the diaphragm special lymphatic vessels are present under the
mesothelial membrane. Small spaces between mesothelial
cells called stomata function as channels for lymphatic
drainage from the peritoneal cavity. Contraction and relaxation of the diaphragm results in influx and emptying of

Particulate matter in the peritoneal cavity is absorbed


through the diaphragmatic lymphatic channels that drain via
several series of lymph nodes and empty into the thoracic
duct. Particles such as bacteria are rapidly absorbed from the
peritoneal cavity. Red blood cells are also rapidly cleared
from the peritoneal cavity.

Intra-peritoneal circulation
Intra-peritoneal fluid and particulate matter move along
a definite path in dogs. There is a general movement of fluid in a cranial direction towards the diaphragm. The intraperitoneal circulation of a contaminate appears to be influenced by diaphragmatic movement, gravity, and the site of
origin of the contaminate. A contaminate originating from
the cranial portion of the peritoneal cavity is dispersed
throughout the peritoneum within 15 minutes, while a caudal intra-peritoneal contaminate requires almost an hour for
complete dispersion. Increasing the viscosity of the contaminate will also reduce its rate of dispersion.

Peritoneal injury and healing


The peritoneal mesothelium is easily damaged and will
undergo permanent damage after minimal exposure to air or
saline. Regeneration of this mesothelial lining occurs rapid-

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DVM, Dipl ACVS


Professor, Head of Small Animal Surgery
The Ohio State University, College of Veterinary Medicine,Columbus, Ohio - USA

388

ly. Within hours of injury, the defect is covered with round


cells originating from circulating mesothelial cells within the
peritoneal fluid. Peritoneal defects will heal at the same rate
regardless of the size of the original defect. Certain injuries
to the peritoneum result in formation of adhesions. When the
mesothelial lining is damaged, normal release of plasminogen activator by the mesothelial cells is inhibited, so plasmin
is not available to break down fibrin. Fibrin then persists and
provides a framework for fibroblasts and deposits of collagen that leads to fibrous adhesion formation. The reason for
formation of adhesions following some injuries and not of
others is unclear, but it is thought to be related to tissue injury and serosal anoxia, and the presence of foreign material. The presence of foreign material within the peritoneal
cavity is a consistent cause of adhesions. Peritoneum responds to foreign material as it does to ischemic tissue; inflammation, granulation tissue formation, and finally adhesion formation. The intensity or strength of the inflammatory action and the amount of adhesions produced is dependent
on the stimulant. Adhesion inflammation may be controlled
by reducing the initial injury, preventing coagulation of fibrinous exudate, dissolving coagulated fibrin, and counteracting the fibroblast proliferation. Proper surgical technique including prevention of tissue damage, meticulous hemostasis,
careful suture placement, and complete removal of foreign
debris will help reduce subsequent adhesion formation.

Pathophysiology of peritonitis
Peritonitis, or inflammation of the peritoneum, is induced by a contaminate or irritating agent. Peritonitis can be
classified as primary or secondary, acute or chronic, localized or generalized, and aseptic or septic. Primary peritonitis (such as feline infectious peritonitis) in animals is much
less common then secondary peritonitis. Secondary peritonitis usually results from a prior disease or an acute lesion
causing contamination of the peritoneal cavity. Contamination may be septic or aseptic; however, aseptic or chemically-induced peritonitis usually progresses to septic peritonitis. Peritoneal contamination results in an inflammatory response characterized by influx of protein rich fluid and
white blood cells into the peritoneal cavity. The protein rich
fluid is thought to dilute the contaminate while the cells are
important for phagocytic and bactericidal activity. Compliment and other immune agents also enter the peritoneal cavity and aid in this activity. Bacteria and other particles are
cleared rapidly from the peritoneal cavity via the diaphragmatic lymphatics. Fibrinous adhesions isolate the contaminate initially and seal small perforations in hollow organs.
The omentum is important in assisting the isolation of bacteria and sealing of perforations. Inflammation around the
intestine induces an ileus condition which is thought to be
mediated by the sympathetic nervous system. This state of
paralysis of the intestines helps to localize the contamination
by slowing the intra-peritoneal circulation reducing direct
spread from the leakage area. Peritoneal irritation also causes increased rigidity of the abdominal musculature which inhibits respiratory movements and subsequently reduces intra-peritoneal circulation. Initially these responses to conta-

4th European FECAVA SCIVAC Congress

mination are helpful to the host, but they may progress to


have harmful affects. Rapid lymphatic clearance of bacteria
may induce septicemia and the exudation of protein rich fluid and cells can induce hypovolemia and hypoproteinemia.
Excessive intra-peritoneal fluid will exceed the lymphatic
resorptive capacity and allow bacteria to remain in the cavity and eventually proliferate. The oxygen tension in the fluid is reduced and this inhibits neutrophil activity and promotes proliferation of anaerobes. Bacteria suspended in fluid are not readily phagocytized since neutrophils function
best on a fixed surface. Fibrinous adhesions occlude diaphragmatic lymphatics and protect bacteria from white
blood cells and humoral agents. The protected areas then
form abscesses and become organized into fibrinous adhesions that obstruct or strangulate organs after weeks of disease. Ileus causes sequestration of large amounts of fluid
within the bowel and exacerbates the hypovolemia. Bacteria
proliferate as the bowel continues to distend and this potentiates the effects of endotoxin and septic shock. Cardiovascular alterations reflect the hypovolemia and endotoxic
shock. Eventually from hypovolemia and endotoxic shock,
visceral blood supply is reduced, metabolic acidosis ensues,
and tissue hypoxia results. An increased metabolic rate and
massive protein loss in the peritoneal cavity results in an
overwhelming catabolic state of the patient with peritonitis.
Reduced kidney profusion can cause insufficiency that reduces clearance of toxic by-products of metabolism and inflammation. Acute renal failure may result. Disseminated intravascular coagulopathy (DIC) may occur with septic peritonitis. Blood sludging within the microvasculature secondary to peripheral vasoconstriction and hemoconcentration predisposes the peritonitis patient to DIC.

Chemical peritonitis
Chemical peritonitis is the result of the presence of a
non-septic irritating substance within the peritoneal cavity.
The degree of inflammation depends on the chemical contaminate. Contamination by bile will produce intense peritoneal irritation. The presence of bacteria in the peritoneal
cavity with bile markedly increases the severity of the disease. Bile salts have an enhancing effect on bacterial proliferation, and they also reduce the activity of neutrophils. Bile
also lyses red blood cells and this releases hemoglobin
which has an enhancing effect on bacterial proliferation.
Gastric juices and pancreatic secretions are more irritating
than bile and cause immediate cellular damage. Intra-peritoneal urine may or may not be contaminated with bacteria
initially, depending on the status of the urinary tract before
the injury. Although urine peritonitis can produce profound
uremia subsequent to the absorption of urinary constituents
across the peritoneum, urine causes a relatively minor irritating response from the cavity provided heavy bacterial
contamination is not present. When combined with the contents of bile, bariums toxic effect is greater than either contaminate alone. Morbidity and mortality of peritonitis induced by barium has been related to the volume of barium
into the peritoneal cavity. Water soluble contrast agents are
less toxic but are still associated with a high morbidity with

4th European FECAVA SCIVAC Congress

Management of peritonitis The role of the surgeon (Hosgood)


Diagnosis
Peritonitis should be suspected in patients that develop
abdominal pain and or distension, fever, and leukocytosis
following abdominal surgery or trauma. Depending on the
severity, leukocytosis may be characterized by neutrophilia
with a left shift, or leukopenia. Hypoproteinemia is common
and this occurs due to the exudation of large amounts of protein rich fluid into the peritoneal cavity. Blood glucose levels may be increased, decreased, or normal but extremely
high or low levels are associated with high mortality rates.
Abdominal radiographs are usually characterized as a
ground-glass appearance with lack of contrast of serosal surfaces which suggests free intra-peritoneal fluid. Free intraperitoneal gas may be present if rupture of a hollow viscus
has occurred. Ileus may be evident by the presence of dilated gas-filled loops of bowel. The most useful aid in reaching
a definite diagnosis of peritonitis is cytologic examination of
intra-peritoneal fluid. Abdominocentesis can be performed
with a 20-gauge 1 1/2 needle. The accuracy of diagnosis
can be increased dramatically with diagnostic peritoneal
lavage (Kolata).
With this technique, saline is infused into the peritoneal
cavity, and the cavity is washed or allowed to circulate
with the cavity. The fluid is then collected by gravity flow
and analyzed cytologically and chemically. Fluid findings
that are indications for exploratory celiotomy include: high
white blood cell count (degenerative neutrophils), presence
of bacteria, vegetable or meat fibers suggestive of bowel
perforation, increased creatinine levels or increased bilirubin
levels.

Treatment
Treatment of peritonitis is based on four important
principles:
1. Patient stabilization
2. Treatment of infection
3. Correction of the cause of peritonitis
4. Abdominal drainage

Patient stabilization
Patients with generalized peritonitis are usually hypovolemic due to the exudation of large volumes of fluid into the
peritoneal cavity. Adequate fluid therapy is very important
and a balanced electrolyte solution should be administered at
a rate sufficient to replace the patients blood volume (90 ml
per kilogram body weight in one hour). Although fluid therapy is the most important element in the treatment of shock,
corticosteroid administration may also be indicated. The
beneficial effects of corticosteroids include preservation of
vascular and lysosomal membranes, positive cardiac inotropic affect, dilation of pre-capillary sphincters, increased
regional blood flow, prevention of bowel mucosa ischemia,
and reduction of adhesion formation. I prefer to use a rapidly acting glucocorticoid; prednisolone sodium succinate administered intravenously. Administration of a cyclo-oxygenase inhibitor such as flunixin meglumine is also beneficial
to the peritonitis patient in endotoxic shock. Flunixin administration (1.0 mg/kg, IV) has also been shown to block production of damaging prostaglandins which may contribute to
multiple organ failure.

Infection treatment
Systemic antibody therapy should be initiated as soon as
the diagnosis of peritonitis is made. A broad spectrum antibiotic combination should be given initially until microbial
culture and susceptibility results are known. Antibiotics selected should be effective against gram-positive and gramnegative aerobic bacteria and anaerobic bacteria. Although
some controversy exists over the use of bacteriostatic versus
bactericidal antibiotics, only the bactericidal antibiotics have
shown efficacy in the treatment of septic shock. Most recommended antibiotic regiments have been a combination of
an aminoglycoside (for its gram negative aerobic activity), a
penicillin (for their gram positive aerobic and anaerobic activity), and either clindamycin or metronidazole (for their
broader spectrum anaerobic activity). In more recent years,
development of new antibiotics such as the third generation
cephalosporins and new synthetic penicillins have been
shown to be as successful as multiple antibiotic regimens in
acute, uncomplicated peritonitis. A new group of antibiotics
that may have some application in the prolonged treatment
of peritonitis is the quinolones. The quinolones such as enrofloxin or trade name, Baytril, are broad spectrum bactericidal drugs that have good gram negative and gram positive
aerobic activity and are particularly effective against
Pseudomonas spp. These drugs however, have poor activity

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concurrent bacterial contamination. Powders and other foreign surgical material particles such as lint, will induce a severe inflammatory reaction. Talc has been replaced as a
glove powder by corn or rice starch which are less irritating.
Blood itself causes minimal irritation of the peritoneum and
is completely absorbed from the peritoneal cavity, often
within one day. Residual peritoneal blood enhances bacterial proliferation and also this blood contains fibrin which
may occlude diaphragmatic lymphatics and enhance formation of fibrous adhesions. These adhesions block lymphatic
clearance of bacteria and isolate bacteria. Severity of peritonitis from gastrointestinal leakage is related to the site of
the leakage and the type of bacterial contamination from the
site. Mixed bacterial populations are present in the GI tract,
but the quantity of bacteria and the prevalence of anaerobic
species increase distally in the GI tract. Higher bacterial
numbers seen in the distal GI tract increase mortality if leakage occurs. Initially, aerobic bacteria proliferate rapidly in
septic peritonitis. As the peritonitis progresses, bacterial synergism between aerobic and anaerobic species is evident.
Gram-negative aerobes particularly E coli are responsible
for early mortality while the anaerobes such as Bacteroides
fragilis predominate in the later stages.

389

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against anaerobes and should, therefore, be used in combination with clindamycin or metronidazole for adequate spectrum of antimicrobial activity. Some surgeons advocate intra-peritoneal administration of antibiotics for treatment of
peritonitis. Remember, most antibiotics reach therapeutic
concentrations in the peritoneal fluid following systemic administration. It is generally recommended that intra-peritoneal administration of antibiotics is not necessary if appropriate systemic antibiotic therapy is administered.

Determination and correction


of the cause of peritonitis
In small animals, peritonitis is usually a surgical disease.
Most cases of peritonitis are secondary to inciting problem
and exploratory celiotomy is indicated to determine and correct the cause of the problem. At the time of the exploratory
surgery the extent of the peritoneal contamination should be
reduced by peritoneal debridement and irrigation, and peritoneal drainage should be established. Specimens should be
taken for aerobic and anaerobic cultures.

Peritoneal debridement
Peritoneal debridement reduces intra-peritoneal bacterial numbers by removing bacteria sequestered in fibrinous
material and by removing exudate, blood clots, and necrotic tissue that enhance bacterial growth. Adhesions act as
barriers to fluid and antibiotic penetration and should be
broken down. During peritoneal debridement and breakdown of adhesions there is a potential risk of spreading infection throughout the peritoneal cavity and creating more
damage to the peritoneal mesothelium; however, this presents as less of a clinical problem than the potential for abscess formation. Remember to control hemorrhage during
adhesion breakdown because intra-peritoneal blood will enhance bacterial growth. Debridement should be complete as
possible; however, in patients with chronic abscess formation or fibrinous peritonitis complete debridement may be
impossible. In critical patients with extensive adhesion formation, less aggressive debridement in conjunction with
thorough peritoneal irrigation may be indicated initially.
Repeat debridement can be performed after the patients
condition has improved.

Intra-peritoneal irrigation
Following peritoneal debridement, irrigation should be
performed to aid in the removal of bacteria and particles that
enhance bacterial proliferation. Irrigation is most effective if
used within hours of contamination before fibrin traps bacteria. Irrigate the peritoneal cavity with warm, sterile normal
saline solution until the fluid suctioned from the cavity is
clear. Remove as much of the irrigation fluid as possible because residual intra-peritoneal fluid enhances bacterial proliferation and reduces neutrophil function. Even though irrigation could spread infection to adjacent areas, copious irri-

4th European FECAVA SCIVAC Congress

gation and complete removal of intra-peritoneal fluid is considered much more important. The need for antiseptic or antibiotic additions to the irrigation fluid is generally not
thought to be necessary. Antiseptics such as povidone-iodine
are potent inhibitors of neutrophil function and may actually
damage peritoneal surfaces and exacerbate sepsis. The addition of antibiotics to the irrigation fluid will initially deliver
higher antibiotic levels to the peritoneal cavity but systemic
administration is required for maintenance of adequate levels in the serum and intra-peritoneal fluid. We currently recommend intra-operative irrigation with warm, sterile normal
saline in conjunction with systemic antibiotic administration.
Administration of heparin systemically or in the irrigation
fluid can prevent drain occlusion and adhesion formation.
Clinical studies have not proven the efficacy of this therapy.
Heparinization may be contraindicated in the early stages of
peritonitis because it may limit the hosts ability to isolate the
infection by reducing and limiting adhesion formation.

Peritoneal drainage (Greenfield)


After debridement and irrigation of the peritoneal cavity,
peritoneal drainage should be established with either an intra-peritoneal drain or open peritoneal drainage.

Intra-peritoneal drains
Intra-peritoneal drains are usually indicated to drain localized fluid collections such as abscesses. One of the major
problems with intra-peritoneal drains is that they are rapidly
encased by omentum and this reduces drain function as early as several hours after placement. The sump-Penrose drain
appears to be several times more efficient than closed or passive penrose drainage of the peritoneal cavity. The sump
drain consists of a double lumen tube in which the second
lumen serves as an external airvent to break the intra-peritoneal vacuum. The drain can act passively or be connected
to a continuous suction vent. A triple lumen sump drain can
be constructed easily from a modified Foley catheter and a
fenestrated Penrose drain. A 22 French Foley catheter is
modified by removing the bulb and the bulb injection port.
The intra-peritoneal portion of the catheter is fenestrated and
the entire Foley catheter is inserted into a fenestrated halfinch Penrose drain. The penrose drain is sutured at each end
of the Foley catheter with two sutures of non-absorbable material. The sump-Penrose drain is placed into the peritoneal
cavity and exited through a dependent portion of the abdominal wall. All intra-peritoneal drains should be kept covered by a sterile bandage to help prevent contamination of
the drain and allow monitoring of the amount and character
of the drainage. Bandages should be changed several times
daily depending on the amount of drainage. Remember that
drainage will not cease completely even if the peritoneal infection has resolved, since the presence of a drain will incite
the production of up to 50-100 mls of fluid per day. In my
experience, most intra-peritoneal sump-penrose drains can
be removed 4-8 days postoperatively. The most common
complication associated with drains is an ascending infec-

4th European FECAVA SCIVAC Congress

tion. This problem can be minimized by maintaining a sterile absorbent bandage over the exposed portion of the drain
until removal. The complications associated with these
drains include incomplete drainage, intestinal or omental
herniation at the drain exit site, and retraction of the drain into the peritoneal cavity. Inadvertent removal of the drain by
the patient can be reduced by bandaging the drain exit site,
and placement of an Elizabethan collar on the patient.

391

excessive discomfort even during bandage changes. They


move around freely and return to food and water consumption during the period of treatment. Most common clinical
complications reported with open peritoneal drainage include hypoproteinemia, hypoalbuminemia, and nosocomial
infections of the peritoneal cavity.

Open peritoneal drainage


Open peritoneal drainage means that the whole peritoneal cavity is left as an open wound. This method of peritoneal drainage has been shown to result in more rapid and
complete drainage of intra-peritoneal radiographic contrast
medium than sump-penrose drainage in normal dogs. Open
drainage technique allows easy abdominal re-exploration
with repeated peritoneal debridement which is beneficial
particularly in open peritoneal drainage of pancreatic abscesses. The technique requires thorough surgical exploration, debridement, and exploration of the peritoneal cavity
first. The linea alba is sutured the full length of the incision
in a loose simple continuous pattern with a monofilament
nonabsorbable suture such as polypropylene or nylon. A gap
of approximately 2 to 2.5 cm is left between the edges of the
linea alba. Subcutaneous tissue and skin are not closed and
a sterile absorbent bandage is placed over the incision. When
attempting opem drainage of the abdomen in male dogs, the
portion of the abdominal incision at the prepuce is closed
primarily in three layers. Only the cranial portion of the abdominal incision is loosely approximated. The open portion
of the incision is planned in the most dependent portion of
the abdomen to promote drainage. Sterile absorbent dressings are placed over the incision using aseptic technique to
prevent contamination. Some surgeons have found that gas
sterilized disposable infant diapers are convenient and a
practical bandage material for open abdominal incisions. A
nonadherent contact layer such as petrolatum impregnated
gauze is used to prevent visceral adhesions to the bandage. I
prefer to use sterile laparotomy sponges as the second layer
with a sterile diaper placed over the sponges when fluid
drainage is excessive. In the male dog an indwelling urinary
catheter may be necessary to prevent urine soilage of the
bandage. Change bandages aseptically when fluid material
strikes through the bandage. Bandage changes are normally
performed without sedation of the standing patient. If the patient appears painful or resistant to bandage changes, a low
dose narcotic analgesic can be used. If the abdominal
drainage appears purulent or the patient shows signs of sepsis, the abdomen is easily re-explored. The abdomen is
closed once drainage is minimal and serosanguineous in nature, and the patients condition has improved. This usually
takes at least three to five days in my experience. The open
abdomen treatment potentially allows drainage from the
whole peritoneal cavity and this provides an unfavorable environment for anaerobic bacteria. It also provides an easy access for re-exploration and assessment of the intra-abdominal problem. Clinical experience has shown that dogs and
cats tolerate this treatment well and do not appear to be in

The selection of the drainage method to be used in the


peritonitis patient should be based on the severity of peritonitis, the source and degree of peritoneal contamination,
and the experience of the surgeon. In the patient with mild
chemical peritonitis (such as that occuring secondary to urinary bladder rupture in the absence of urinary tract infection), post-operative peritoneal drainage may be unnecessary. Management of these patients requires correction of
the cause of peritonitis together with thorough intra-operative peritoneal irrigation with warm, sterile saline. Patients
with localized peritonitis such as that occuring secondary to
a prostatic abscess or patients with generalized peritonitis
of mild severity should be managed surgically by correction
of the cause of peritonitis, intra-operative irrigation, with or
without placement of an intra-peritoneal sump drain. Patients with severe generalized peritonitis or extensive contamination of peritoneal cavity should have open peritoneal
drainage. Abdominal closure can be performed usually
within a week. Open peritoneal drainage is more labor intensive and more costly than sump- penrose drainage and
this may limit its application to patients with severe generalized peritonitis.

Post-operative peritoneal lavage


Some surgeons recommend the use of post-operative
peritoneal lavage in patients with generalized peritonitis;
however, clinical results with this method of treatment are
inconclusive. Lavage aids in continual mechanical removal
of bacteria and substances that enhance bacterial proliferation. The fluid movement is reported to reduce adhesion formation however, small areas of localized fluid accumulations have been reported in human patients after four to five
days of vigorous lavage. Lavage also has been reported to
slow the speed of peritoneal healing possibly because of the
mechanical disruption of the wound or removal of free-floating macrophages.

Post-operative care and supportive


therapy
Mangement of ileus
Ileus is a pathophysiological response to peritonitis. Treatment of ileus has obvious beneficial effects of decompression
of the bowel to reduce intra-abdominal pressure which will in
turn enhance respiration, and venous return from the abdomen. Physical closure of the abdomen is easier and return

MAIN PROGRAMME

Selection of drainage method (Donner)

392

of appetite is promoted which is important in the catabolic patient. Decompression of the stomach can be performed with
the use of nasogastric tubes or, alternately, a jejunostomy tube
can be placed at the time of celiotomy. This will allow bowel
decompression as well as enteral nutrition. The correction of
electrolyte imbalance, particularly hypokalemia, is important
for return of gastrointestinal function.

Nutritional support
Nutritional support has in the past been often overlooked, but it is an important component in the management
of the peritonitis patient. The septic patient has a metabolic
rate up to four times above normal and is catabolic. Surgery
further increases the patients energy expenditure. Anorexia
which is common in the peritonitis patient also contributes
to the negative nitrogen balance. This malnutrition results in
the impaired cell mediated and humoral immunity, increased
suseptibility to infection, delayed wound healing, and increased incidence of wound dehiscence. Enteral hyperalimentation has been used successfully in the dog; however,
the technique is expensive and requires intensive patient
monitoring. Enteral hyperalimentation is the preferred route
of nutritional support in the small animal patient if the bowel is functional. Liquid food products can be administered by
oral-gastric tube, nasogastric tube, pharyngostomy, gastrostomy, or jejunal tube feeding. Feeding methods should use

4th European FECAVA SCIVAC Congress

as much of the patients functional gastrointestinal tract as


possible. A variety of diets can be used for enteral hyperalimentation but my preference is to use gruelled canned dog
food mixed with water or liquid nutritional supplement.

Complications and prognosis


Peritonitis is a complex disease condition. It may be associated with many potentially life-threatening complications. End stage septic shock is the usual cause of death.
Based on reports on mortality from septic peritonitis, up to
70% of dogs will eventually die from complications related
to the condition. With early diagnosis, aggressive supportive
therapy, effective peritoneal drainage, and appropriate antibiotic therapy, the prognosis may be improved.

References
Hosgood G, Salisbury S, (1988), Generalized peritonitis in dogs: 50 cases
(1975-1986). J Am Vet Med Assoc, 193:1448-1450.
Kolata R (1976) Diagnostic abdominal paracentesis and lavage: Experimental and clinical evaluations in the dog. J Am Vet Med Assoc,
168:697-699.
Greenfield C, Washaw R, (1987), Open peritoneal drainage for treatment of
the contaminated peritoneal cavity and septic peritonitis in dogs and
cats: 24 cases (1980-1986). J Am Vet Med Assoc, 191:100-105.
Donner G, Ellison G, (1986), The use and misuse of abdominal drains in
small animal surgery. Compend Contin Educ Pract Vet, 8:705-712.

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393

Clinical update: gastric dilatation-volvulus in dogs


Daniel D. Smeak

Summary
Major advances have been made in the medical and surgical management of gastric dilatation-volvulus syndrome
(GDV) in the dog in the past 10 to 15 years. Hypovolemic
shock, ventricular arrhythmias, and sepsis related to gastric
wall necrosis are common problems associated with this disease syndrome. The morbidity and mortality from these complications have dramatically decreased because of improved
clinical awareness, new anesthetic regimens, the advent of
new surgical techniques, improved perioperative management, and a better understanding of the pathophysiology of
this syndrome. The purpose of this seminar is to update
practitioners to these recent advances and to review current
treatment recommendations.

Introduction
Major advances have been made in the medical and surgical management of gastric dilatation-volvulus syndrome
(GDV) in the dog in the past 10 to 15 years. Hypovolemic
shock, ventricular arrhythmias, and sepsis related to gastric
wall necrosis are common problems associated with this disease syndrome. The morbidity and mortality from these
problems have dramatically decreased because of improved
clinical awareness, new anesthetic regimens, the advent of
new surgical techniques, improved perioperative management, and a better understanding of the pathophysiology of
this syndrome. The purpose of this seminar is to update practitioners to these recent advances and to review current treatment recommendations.

tial studies showed that gastrin concentrations are increased


in dogs afflicted with GDV. However, the cause and effect of
increased gastrin concentrations have not been explained.
Recent studies have shown that gastrin levels in dogs that
have had GDV surgically corrected are not different that of
clinically normal dogs. Plasma concentrations do not increase in clinically normal dogs in response to inflation of an
intragastric balloon. Therefore, the role of gastrin in this disease remains unproven.

Myoelectric dysfunction
It has been difficult to determine if changes in myoelectric activity seen in dogs after GDV correction actually are
the cause of the initiating problem or are secondary to the
event. It appears that surgical manipulation alone disrupts
activity as much or more than experimental creation of
GDV. Clinical use of percutaneous electrogastrography may
be required to determine the role of myoelectric abnormalities in GDV and any changes induced by gastropexy.

Esophageal motility
Abnormal esophageal motility has been documented in
dogs with recurrent GDV. In this study aerophagia was seen
mainly when primary esophageal peristalsis failed to transport
a food bolus into the stomach. In many cases the ingestion of
air elicited secondary peristaltic waves that were strong
enough to transport esophageal contents to the stomach.

Dietary factors
Proposed etiologic mechanisms (Hosgood)
Gastrin
Gastrin has a trophic effect on gastric mucosa, and it has
been proposed that gastrin could play a role in the development of GDV by causing delayed gastric emptying secondary to pyloric obstruction and hypertrophy. Also, increased gastrin concentrations could directly delay gastric
emptying and could increase gastroesophageal sphincter
pressure, thereby inducing esophageal spasm, initiating
aerophagia, and decreasing the possibility of vomiting. Ini-

Diet and feeding have long been implicated in the


etiopathogenesis of GDV. Dogs fed a commercial diet once
daily instead of three times have higher gastrin levels and
more stomach distention. It was proposed that once daily
feeding of a commercial dog food could predispose to GDV
by causing a heavy, chronically distended stomach that
could easily undergo volvulus. More recent studies have
failed to show any difference in gastric motility in dogs that
had distended stomachs from dietary manipulations and
those that did not. Gastric emptying times did not vary between clinically normal dogs and dogs previously fed diets

MAIN PROGRAMME

DVM, Dipl ACVS


Professor, Head of Small Animal Surgery
The Ohio State University, College of Veterinary Medicine,Columbus, Ohio - USA

394

of various volumes, some of which caused massive gastric


distention. Gastric emptying times in dogs that have had surgical correction are not different from clinically normal dogs
when liquid test meals are used. Despite these findings,
feeding small, frequent meals may still be prudent in dogs of
predisposed breeds.

Predisposing factors (Glickman)


A study conducted of 101 dogs that had acute episodes of
GDV were compared to the same number of dogs that had
no GDV history. Control dogs were matched individually to
case dogs by breed or size and age. Predisposing factors that
significantly increased a dogs risk for GDV were male gender, being underweight, eating one meal daily, eating rapidly, and a fearful temperment. The only factor that appeared
to precipitate an acute episode of GDV was stress. Perhaps
stress precipitates GDV by changing hormone levels which
regulate gastric function and motility.

Pyloric surgery - Is it necessary?


Pyloromyotomy and pyloroplasty have been routinely
performed during GDV correction at some institutions despite the absence of evidence that delayed gastric emptying
or pyloric lesions are causal factors in the disease. Gastric
emptying in dogs that previously had GDV without pyloric
surgery was no different than clinically normal dogs in one
study. In addition, the long-term outcome for dogs that underwent surgical treatment for GDV and pyloroplasty was
not different from that for dogs that underwent surgical treatment without pyloric surgery. The rate of complications,
however, was higher in dogs undergoing pyloric surgery.
Complications observed included: vomiting, cardiac arrhythmias, and death. Pyloric surgeries such as the pyloromyotomy and plasty do not significantly alter gastric
emptying time and may, in fact, prolong this time. The relationship between outflow diameter and gastric emptying is
still uncertain. These findings strongly suggest that pyloric
surgery is contraindicated unless a pyloric lesion causing
outflow obstruction is demonstrated. Inclusion of pyloric
surgical techniques with the surgical protocol for treatment
of GDV may have contributed to the high postoperative
complication and mortality rates reported in earlier studies.

4th European FECAVA SCIVAC Congress

tropexy techniques became popular and reported complication rates were dramatically reduced. Recurrence of GDV
ranges between three and 6% with these new techniques. A
rapid gastropexy technique method has been recently developed to prevent recurrence of GDV (Meyer-Lindenberg et
al). It involves including the seromuscular layer of the pyloric antrum in the closure of the cranial portion of the linea
alba. Seven percent of 84 dogs treated with this method had
gastric dilatation without volvulus within six months of
surgery. None of the dogs had GDV recur. In comparison,
76% had recurrence of GDV after orogastric intubation and
gastric decompression alone. This technique is quick but has
the obvious disadvantage of creating difficulties during subsequent laparotomy. It appears that a properly performed
right-sided gastropexy is critical for reducing the risk of recurrent GDV. The tube gastrostomy technique is associated
with more complications but I still prefer this technique if
stomach resection is required. This permits a small tube to be
placed down the foley catheter and into the intestine to bypass an atonic stomach during early postoperative feeding.
The focus in surgery currently is the development of less
invasive methods of gastropexy. Recently, a study was performed to evaluate right-sided percutaneous endoscopic
gastrostomy as a method for creation of permanent gastropexy. The percutaneous method resulted in inferior adhesion formation when compared to incisional gastropexy
(Waschak). Since assessment of gastric wall and splenic viability is important for prognosis and treatment decisions,
early exploratory laparotomy remains the preferred approach. Percutaneous methods may have value for prophylactic gastropexy.

Adjunct treatment modalities update


(Hosgood)
Lipid peroxidation inhibitors
Use of a lipid peroxidation inhibitor could prevent death
in dogs with experimentally induced GDV. Lipid peroxidation activity in the small intestine and colon, pancreas, and
liver was significantly reduced after correction of GDV (after reperfusion) in dogs treated with an inhibitor than in dogs
treated with saline. The results of using these drugs in clinical trials have not yet been published.

Prostaglandin inhibitors
Gastropexy techniques update
Until the mid 1980s, tube gastrostomy was the gastropexy technique of choice. The recurrence rate following
tube gastrostomy for treatment of GDV is from five to 11%.
Complications such as leakage around the tube exit site from
the stomach, cellulitis around the tube exit site in the skin,
premature tube removal, and permanent stoma development
caused mortality in up to 30% of cases so treated. Surgical
techniques that do not require an opening in the stomach and
an external tube were developed after these complications
were reported. Circumcostal gastropexy and belt loop gas-

Plasma endotoxin concentration is high in dogs with experimentally induced GDV. Plasma concentration of prostacyclin, a prostaglandin produced when cyclooxygenase acts
on arachidonic acid released from lipid cell membranes, also is elevated suggesting that the increase in prostacyclin
concentration may be a result of endotoxin-induced cell
damage. Administration of flunixin meglumine, a NSAID
with antiprostaglandin activity, after GDV did not result in
appreciable improvement in hemodynamics but plasma concentrations of prostacyclin did not increase further. It is now
accepted that endotoxemia plays a critical role in pathologic

alternations associated with GDV and that flunixin administration after the onset of GDV may prevent further rise in
plasma prostacyclin and, therefore, attenuate the effects of
endotoxemia.

Hypertonic saline solution


Intravenous administration of hypertonic saline (7% NaCl) solution in 6% dextran (5 ml/kg body weight infused
over five minutes) followed by 0.9% NaCl solution (60
ml/kg/hr) has been demonstrated to be superior to IV administration of normal saline solution alone for initial treatment of shock associated with experimentally induced GDV.
The addition of dextran appears to sustain the effects of hypertonic saline solution, compared with the short-term effects of hypertonic saline solution alone. Slowing fluid administration in dogs receiving normal saline solution resulted in deterioration in hemodynamic values in dogs receiving
normal saline alone; hemodynamic values of dogs receiving
hypertonic saline in dextran followed by normal saline were
maintained.

Brief clinical report updates


Dogs that require gastric wall resection at the time of
correction of GDV have a high complication and mortality
rate. Of 30 dogs with GDV that required partial gastrectomy,
90% developed complications and over 50% died. Although
unavoidable, if partial gastrectomy is required, the prognosis for survival after surgery is poor. Another study showed
that coagulation abnormalities develop in most dogs with
GDV and may contribute to the high mortality rate associated with the disease. Mesenteric volvulus may occur with
GDV and this carries a grave prognosis. A syndrome characterized by intermittent mild bloating, vomiting, regurgitation, and excessive borborygmi has been documented recently. Radiographically, a displaced pyloric antrum is seen
with or without mild gastric distention. Delayed gastric
emptying is not a factor in this syndrome. My experience
with the chronic form of GDV is good. A right-sided gastropexy resolves the clinical signs in most dogs. If spontaneous pneumoperitoneum is seen after surgical treatment of
GDV, splenic infarction, or gastric perforation should be
considered. Recurrent gastric dilatation after GDV correction has been attributed to displacement (kinking) of the pyloric antrum causing partial obstruction. If delayed gastric
emptying can be demonstrated, correction of the kink often
eliminates further dilatation.

Current treatment recommendations


Although exceptions do occur, I believe there is a direct
correlation between mortality and duration of GDV. Improved
client education regarding clinical signs and the importance
of early emergency treatment, especially to owners and breeders of predisposed breeds, cannot be overemphasized.

395

I prefer to perform exploration and gastropexy in any


large or giant breed dog presenting with bloat, regardless
of whether there is radiographic evidence of volvulus. This
opinion is based on 1) the high recurrence rates of dogs that
do not receive prophylactic gastropexy; 2) dogs may spontaneously resolve their volvulus alone or after emergency
decompression and lavage; 3) clinical experience with dogs
that were not operated because of marked clinical improvement after temporary stabilization and normal post-decompression radiographs, and subsequently died followed by
unexpected gastric rupture. In addition, it does not make
sense to delay resuscitation and decompression by taking
radiographs to confirm the diagnosis of GDV unless the dog
is stable.
When possible, early exploratory laparotomy for ongoing
gastric necrosis and prophylactic gastropexy should be performed after clinical stabilization and before the high incidence period of ventricular dysrhythmias. If decompression
is not possible, emergency laparotomy is recommended.
Surgery may be delayed until fluid, electrolyte and acid-base
status is improved provided decompression is possible. Recent experimental studies indicate that 360 degree gastric
volvulus does alter gastric blood flow in decompressed patients. Although most cases of GDV are usually not malpositioned 360 degrees and the effects of lesser degrees of volvulus are not known, decreased perfusion to sections of the
malpositioned stomach may be present despite decompression. Ventricular arrhythmias commonly have a delayed onset (75% occur with 12-36 hours of presentation). Early surgical intervention often allows anesthesia and surgery to be
performed well before the onset of dysrhythmias (Whitney).

Treatment outline for acute GDV


Priority #1 Treatment of hypovolemia, and decompression
A minimum of two large bore catheters in the cephalic or
jugular vein are placed; hypertonic saline (7% NaCl) solution in 6% dextran (5 ml/kg body weight infused over five
minutes) followed by 0.9% NaCl solution (60 ml/kg/hr) is
administered. Pressure bag systems are helpful in increasing
the delivery rate of administration. Do not place catheters in
the saphenous veins- venous return is reduced due to the dilated stomach obstructing caudal vena cava flow. Sedate the
unruly patient with Ketamine and Valium or Oxymorphone
to pass the stomach tube. Tape the mouth closed over a roll
of tape to help prevent tube chewing and fighting. Premeasure a pre-lubricated large-bore orogastric tube to the level
of the last rib and insert until resistance is met or until the
measured spot is reached. If you meet resistance, try blowing in the tube while rotating it 180 degrees. When this is unsuccessful, trocar (use 16 - 18 gauge needle) the most tympanic area of the abdomen (usually right side just caudal to
costal arch; away from the spleen) and remove as much gastric pressure as possible. This maneuver usually unlocks the
cardia area and allows the stomach tube to pass without difficulty. Remember easy tube passage does not mean that the
patient does not have volvulus.
Priority #2 Treat for endotoxic shock
Intravenous corticosteroids and antibiotics are indicated.

MAIN PROGRAMME

4th European FECAVA SCIVAC Congress

396

I administer 20 mg/kg of prednisolone sodium succinate and


Kefzol (20 mg/kg) after the intravenous line is placed. A single IV dose of flunixin meglumine (0.5 mg/kg) may be given if the hemodynamic status of the patient remains unstable
despite adequate volume replacement.
Priority #3 Confirmation of gastric volvulus; rule out
other disease
A right lateral view has been shown to be the most helpful in determining gastric malposition. A thorough radiographic examination should be routinely employed to rule
out gastric perforation, other causes of aerophagia such as
obstruction, intestinal volvulus, and respiratory disease, especially in smaller breeds or those with peculiar histories.
Submit a cell blood count and serum chemistry profile to
evaluate for concurrent disease.
Priority #4 Ensure patient is stable as possible
About 50% of all dogs presenting with GDV have arrhythmias. Treatment with lidocaine is initiated when strings
of VPCs, multifocal VPCs, rapid unfocal VPCs with poor
cardiac output are present. Ensure that hemodynamic status
of patient is stable. Continuously monitor for arrhythmias
throughout perioperative period. Be sure the magnesium and
potassium concentrations are adequate since deficiencies of
these electrolytes in particular will reduce the effectiveness
of lidocaine treatment of arrhythmias.
Priority #5 Anesthetize patient carefully
Arrhythmogenic drugs such as the ultrashort barbituates
and hypotensive agents such as Acepromazine are avoided.
Induce anesthesia with Oxymorphone/Diazepam, Diazepam/ketamine combinations, or mask with Isofluorane.
Nitrous oxide is contraindicated. Assist ventilation especially if the stomach has not been fully evacuated.
Priority #6 Reposition stomach, assess stomach and
spleen viability
Decompress the stomach if it remains distended. Pass an
orogastric tube or use a needle to trocar the stomach. Reach
toward the esophageal hiatus and grasp the pylorus. Move
the fundus caudally and pull the pylorus toward the right
side. Untwist the spleen unless it is necrotic or the hilus is
thrombosed. After the stomach and spleen are repositioned
they should be assessed for viability. The viable spleen will
become smaller and return to a more normal color within
minutes of repositioning. If the spleen is grossly necrotic or
thrombosed, perform splenectomy without fully untwisting
the hilus. Occasionally the short gastric vessels become
avulsed and may require ligation to stop hemorrhage. Observe the fundic area for signs of gastric necrosis. There are
no reliable ways to determine gastric wall viability; serosal
coloration and wall texture are used most. Give the stomach
wall 5-10 minutes after repositioning before making a final
judgement about viability. Larger grey-green, purple, or
black areas with a thin or torn appearance should be resected. Approximately 10% of all GDVs require partial stomach
wall resection. About 30-60% of patients that require partial
gastrectomy will die after surgery. Therefore, the stomach
viability should be assessed carefully; aggressive resection
of questionable areas is not warranted and may increase the
mortality rate needlessly. If perforation and peritonitis are
present, a grave prognosis is given to the owners before proceeding. I prefer to use the partial invagination technique

4th European FECAVA SCIVAC Congress

rather than resection for questionable areas of stomach wall.


The TA autostapling devise or conventional suture techniques are used to resect necrotic areas.
Priority #7 Perform a permanent right-sided gastropexy
The tube gastrostomy technique is usually preferred in
cases requiring gastric wall resection. Continuous decompression and enteral nutritional support can be offered with
this technique. A pyloric outflow surgery is not performed
unless abnormalities are found. The ideal gastropexy technique is simple and quick to perform, permanently adheres
the stomach to the abdominal wall in an anatomic position to
prevent recurrence, does not interfere with gastric emptying,
has minimal complications, and require minimal postoperative care. The belt-loop gastropexy and circumcostal gastropexy are the most practiced techniques in the United
States. To achieve a permanent adhesion, both the abdominal wall and stomach must not have a serosal covering, and
raw muscle surfaces must be in contact until wound strength
is adequate.
Priority #8 Carefully monitor the patient for complications postoperatively
Most postoperative mortality occurs within the first four
days. The two most common problems resulting in death include 1) peritonitis, sepsis and shock associated with gastric
wall necrosis and 2) cardiac dysrhythmias.
Persistent vomiting, anorexia, fever, or depression following surgery should signal to the clinician that an underlying problem exists. Aspiration pneumonia is occasionally
seen after surgery following orogastric intubation. Signs of
shock or sepsis in the early postoperative period may be the
result of cardiac dysrhythmias or stomach necrosis. Since
pneumoperitoneum is present after laparotomy, free air in the
peritoneal space on abdominal films does not necessarily indicate gastric leakage. If gastric perforation is suspected, abdominocentesis and cytologic evaluation or contrast gastrogram studies usually confirm the diagnosis. Constant ECG
monitoring and treatment of severe arrhythmias are essential.

Postoperative Management Goals


1. Maintain normal fluid, electrolyte, and acid-base status
after surgery. Aggressive intravenous fluid administration
is continued after surgery. Watch for hypokalemia, the
most common electrolyte abnormality seen after GDV
surgery. I prefer to supplement of maintenance fluids with
20 mEq/L of potassium chloride during the first few days
after surgery until normal appetite is observed.
2. Monitor for ventricular arrhythmias; treat with lidocaine
if focal VPCs occur greater than 15/min., rapid multifocal
VPCS or runs of ventricular tachycardia are present. Intravenous 2% lidocaine is given as a bolus up to three
times at a minimum of 15 min between injections. A constant rate infusion of lidocaine is begun (50-70
ug/kg/min). I prefer to piggyback intramuscular procainamide (15 mg/kg QID) at the onset of constant lidocaine infusion. Gradual withdrawal of the lidocaine infusion over the next 24 hours and continued procainamide
administration is easier to maintain after surgery since not
drip rates need to be monitored. Watch for signs of lido-

4th European FECAVA SCIVAC Congress

Treatment of recurrent gastric distention


Following gastropexy, or
Chronic Bloaters
Priority #1 Differentiate simple dilation from recurrent
volvulus
Special radiographic studies may be indicated if the right
lateral and ventro-dorsal view do not reveal a problem.
Priority #2 Evaluate for gastric emptying problem
Perform upper GI series and fluoroscopic studies to evaluate gastric emptying times. If the gastropexy site is intact,
use of motility modifiers such as metoclopramide (0.4

mg/kg, TID) and multiple feedings may be beneficial. When


gastric emptying is delayed and medical therapy is unsuccessful, surgical exploratory is performed to rule out underlying pyloric abnormalities. If kinking is seen at the previous
gastropexy site, remove the original adhesion area and
reperform a gastropexy in a more functional area. In my experience, problems with kinking of the pylorus following
gastropexy is usually due to creating a gastropexy more toward the body of the stomach rather than the pylorus.

References
Hosgood G,(1994), Gastric dilatation-volvulus in dogs. J Am Vet Med Assoc, 204:1742-1747.
Glickman L, Glickman N, Schellenberg D, Simpson K, Lantz G, (1997),
Multiple risk factors for the gastric dilatation-volvulus syndrome in
dogs: a practitioner/owner case control study. J Am Anim Hosp Assoc, 33:197-204.
Meyer-Lindenberg A, Harder A, Fehr M, Luerssen D, Brunnberg L, (1993),
Treatment of gastric dilatation-volvulus and a repid method for prevention of relapse in dogs: 134 cases (1988-1991). J Am Vet Med Assoc, 203:1303-1307.
Waschak M, Payne J, Pope E, Jones B, Wagner-Mann C, (1997), Evaluation
of percutaneous gastropexy as a technique for permanent gastropexy.
Vet Surg, 26:235-241.
Whitney W, (1989), Complications associated with the medical and surgical management of gastric dilatation-volvulus in the dog. Prob Vet
Med, 1:268-280.

MAIN PROGRAMME

caine toxicity such as seizures, depression, and vomiting.


3. Observe for gastric dilatation after surgery; monitor for
persistent vomiting.
Postoperative vomiting is usually self-limiting, provided
the patient is not fed in the early postoperative period. Decreased gastric motility is common after surgery and may result in gastric distention and vomiting. The use of a motility
stimulant such as metoclopramide (10 mg IM, TID) may be
beneficial. Another cause of postoperative vomiting is reflux
esophagitis. H-2 blockers such as Ranitidine, or Cimetadine
is recommended for suspected esophagitis or gastric ulceration from mucosal sloughing.

397

4th European FECAVA SCIVAC Congress

399

Treatment of feline otitis media


and inflammatory polyps
Feline sinusitis: surgical management
Daniel D. Smeak

Summary
Middle ear infections and chronic sinusitis are common
disease conditions affecting cats. These conditions are initiated by a variety of causes. A thorough diagnostic workup is
critical since successful therapy depends upon elimination
of the cause of the problem and identification of predisposing factors. This seminar will outline a diagnostic plan for
these diseases to help practitioners identify causal disorders. Indications for medical and surgical treatment, and detailed surgical techniques will be discussed.

Polyps that grow into the nasopharynx cause upper respiratory signs such as sneezing, nasal discharge, and, in late
stages, dysphagia.

Etiopathogenesis

Otitis media is an inflammation within the middle ear


structures, which include the tympanic membrane, tympanic cavity, auditory tube, ossicles, and tympanic nerve (a
small branch of the facial nerve). Otitis media is thought to
occur most often as a sequela to otitis externa in dogs (up
to 50% of dogs with chronic otitis externa have concurrent
otitis media). Another route of infection of the middle ear
is through the auditory tube. Cats are thought to commonly develop otitis media through this route as a sequela to
upper respiratory disease. Although otitis media can be
caused by trauma, foreign bodies, neoplasms, parasites,
and bacterial invasion, many cats presented with middle
ear disease have inflammatory polyps. The purpose of this
seminar is to review middle ear disease in cats with focus
on the surgical treatment of inflammatory polyps and bacterial otitis media.

Although the etiology of inflammatory polyps remains a


mystery, there is some suggestion that they may be congenital or secondary to viral or bacterial infections. A congenital etiology has been proposed because inflammatory polyps
occur predominately in young cats and also because they
have been seen in sibling kittens and in kittens from the
same cattery (Stanton). A viral etiology is suspected because
feline calicivirus has been recovered from the nasopharynx
in two cats and the polyp from another cat (Parker).
Whether otitis media is a primary or secondary factor in
the etiopathogenesis of nasopharygeal polyps is unknown.
Obstruction of the auditory tube causes negative pressure
within the tympanic cavity. The negative pressure gradient
causes vessel transudation and serous otitis media. Potential
causes of auditory tube obstruction include inflammation of
the tubal mucosa (viral, bacterial, or allergic reaction),
anatomical structural abnormalities, and obstructive masses
(such as nasopharyngeal polyps).
The structure of the narrow eustachian tube is a factor in
development of otitis media in infants and young children
(Fireman).
This relationship has not been proven in cats. As a general rule, polyps occur mostly in young cats, otitis media in
middle-aged cats, and neoplasia in old cats.

Feline inflammatory polyps

Diagnosis

Inflammatory polyps or nasopharyngeal polyps may


originate from the pharyngeal mucosa or auditory tube, but,
in the authors experience and others, most arise from the
middle ear region (Pope, Kapatkin). These slowly growing
benign fibrous polypoid masses are composed of myxomatous to dense fibrous connective tissue covered by epithelium. They have been reported to extend externally out the external ear canal or through the auditory tube into the nasopharynx (Faulkner). Depending on the route of growth,
clinical signs vary. External ear extension results in clinical
signs of otitis externa such as otic discharge and head tilt.

A diagnosis of inflammatory polyp is based on otoscopic, radiographic, and histologic information. Heavy sedation
or anesthesia is necessary in most cases to thoroughly examine the external ear canal, tympanic membrane, and nasopharynx. Remove debris in the external ear canal by
lavage with warm saline solution. Avoid antiseptic agents for
lavage if possible because most have been incriminated in
causing inner ear damage if the tympanic membrane is ruptured. Swabs of the debris can be obtained prior to cleaning
if culture or cytology is indicated. Once the debris is cleared
from the canal, look to see if the tympanic membrane is per-

Introduction

MAIN PROGRAMME

DVM, Dipl ACVS


Professor, Head of Small Animal Surgery
The Ohio State University, College of Veterinary Medicine,Columbus, Ohio - USA

400

forated, or bulging, cloudy, or discolored if it is intact. These


changes are consistent with otitis media. Polyps extending
into the ear canal appear smooth, pedunculated, and pink.
Multilobulated masses that bleed when manipulated should
be biopsied since these characteristics suggest another disease process such as ceruminous adenocarcinoma. Try to determine whether the mass appears to originate in the middle
ear or external ear canal. Retract the soft palate forward to
explore the eustachian tube openings. Generally, when clinical signs occur from nasopharyngeal polyps, the masses are
easily seen once the palate has been pulled forward. The ear
and pharynx should be viewed since polyps occasionally extend in both directions. Failure to determine the full extent
of the disease will result in a poor surgical outcome. Oblique
lateral, open-mouth, and ventrodorsal views of the skull are
recommended for adequate evaluation of the tympanic bullae; general anesthesia is required to obtain good quality
films. Oblique lateral and open-mouth views are particularly useful for evaluating the air-filled tympanic cavity. Softtissue density within the cavity suggests either fluid or a
mass within the middle ear. In chronic otitis media, the tympanic bulla become thickened and sclerotic.
Destruction of the bulla may be observed with severe infection or neoplasia. Thickness of the bullae bone is noted
by the surgeon to determine the extent of the surgical approach and the instruments needed to expose the tympanic
cavity. Positive radiographic findings are highly sensitive in
the diagnosis of otitis media, but negative findings do not
rule it out. Nasopharyngeal polyps can be seen best on lateral skull radiographs. The normally air-filled nasopharynx
is obscured by a soft-tissue dense mass.

Treatment
The recommended treatment for long-standing otitis media, or for removal of inflammatory polyps regardless of
where they extend, is ventral bulla osteotomy. Acute otitis
media can be treated with antibiotics with or without
myringotomy (Shell). More than 50% of polyps removed by
traction-avulsion recur within one year. Some surgeons recommend traction when there is no evidence of otitis media
on skull films, while the author and others (Kapatkin)
strongly recommend that the bulla should be explored in all
cats with middle ear polyps.
The author has consistently found remnants within the
tympanic cavity after polyps have been removed by traction
just prior to bulla exploration.

4th European FECAVA SCIVAC Congress

4. A paramedian skin incision is made from the angle of


the mandible to the hyoid apparatus on the affected side.
Avoid the linguofacial vein at the caudal aspect of the
incision.
5. The bulla is located by blunt dissection between the digastric and hyoglossal muscles in a rostral and medial direction. The hypoglossal nerve can be seen on the medial
side of the hyoglossal muscle. The digastric muscle and,
the more dorsal located, external carotid artery are lateral
to the bulla.
6. A periosteal elevator is used to remove the soft tissues
from the ventral surface of the bulla. The bulla is penetrated with a 1/8 Steinmann pin and the opening is enlarged
with a Lempert rongeur. Alternately, when the bulla is very
thick, an air-drill can be used to burr-away the bone.
7. Appropriate culture samples are taken (be sure to submit
a sample specifically for Mycoplasma culture also) and
the ventral compartment of the bulla is inspected. A small
amount of clear serous fluid is normal. An incomplete
septum of the bulla divides the aforementioned area from
the dorsal compartment. This septum is opened with the
Steinman pin and enlarged with rongeurs. The base of the
polyp should become visible when the septum is removed. While traction is placed on the polyp, a small
curette is used to dislodge the base of the polyp stalk. The
remainder of the abnormal tissue and material within the
bulla is removed with gentle curettage and irrigation with
sterile saline (submit tissue for culture and sensitivity, and
biopsy). With primary bacterial otitis media, a rim of
granulation tissue is seen lining the pus-filled inner tympanic cavity. This tissue is gently teased out with elevators and curettes.
8. A Penrose drain is sutured to the periosteum surrounding
the bulla and is exited through the ventral skin incision.
The tubing is secured to the skin with suture. The skin incision is partially sutured closed on the rostral and caudal
borders. Be sure to scope the ear and nasopharynx after
surgery to ensure that all polyp tissue has been removed.

Postoperative care
An Elizabethan collar is placed immediately following
surgery. Drains are usually removed by 3-5 days, when
wound discharge is minimal. Appropriate antibiotics are given for a minimum of 21 days. The external ear is lavaged
and cleaned as needed.

Technique-ventral bulla osteotomy (Ader)

Complications

1. The cat is placed in dorsal recumbency after being intubated and maintained with gas anesthesia.
2. The head and neck is extended and the ventral neck area
is prepared for aseptic surgery.
3. The tympanic bulla is located caudomedial to the muscular process of the mandible and rostromedial to the tympanohyoid bone. The ventral wall of the bulla can be palpated externally in most cats.

Complications associated with ventral bulla osteotomy


include damage to the hypoglossal nerve, auditory ossicles,
oculo-sympathetic trunk, boney labyrinth of the inner ear, facial nerve, and vascular structures in the region. Over 80% of
cats undergoing this procedure will have Horners syndrome;
most resolve within one month (Kapatkin). Iatrogenic inner
ear damage may be permanent. Most cats with polyps or bacterial otitis media will have long-term resolution.

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401

Patient evaluation

Ader P, Boothe H, (1979), Ventral bulla osteotomy in the cat. J Am Anim


Hosp Assoc 15: 757-762.
Pope E, (1990), Feline inflammatory polyps. Friskies Veterinary J,
Sept/Oct, 18-20.
Kapatkin A, Matthieson D, Noone K, Church E, Scavelli T, Patnaik A,
(1990), Results of surgery and long-term follow-up in 31 cats with
nasopharyngeal polyps. J Am Anim Hosp Assoc 26: 387-392.
Faulkner J, Budsberg S, (1990), Results of ventral bulla osteotomy for treatment of middle ear polyps in cats. J Am Anim Hosp Assoc 26: 496-499.
Stanton M, Wheaton L, Render J, Blevins W, (1985), Pharyngeal polyps in
two feline siblings. J Am Vet Med Assoc 186: 1311-1313.
Parker N, Binnington A, (1985), Nasopharyngeal polyps in cats: three case
reports and a review of the literature. J Am Anim Hosp Assoc 21:
473-478.
Fireman P, (1985), Eustachian tube obstruction and allergy: a role in otitis
media with effusion? J Allergy Clin Immunol, 76: 137-140.
Shell L, (1995), Otitis media and interna. WB Saunders Co., Philadelphia,
1128-1132.

A thorough history is important especially with cats affected with chronic nasal disease. Direct your attention toward the
vaccination and environmental history since viral rhinitis is
much more common in catteries, immunocompromised cats
and multi-cat households. Sneezing and nasal discharge are
the most common primary presenting complaints. Gagging
may be noticed if discharge drains into the nasopharynx or a
nasopharyngeal mass is present. Dysphagia and severe gagging are commonly reported complaints from owners of cats
with nasopharyngeal polyps (nasal discharge is also commonly present in these cats). Owners should be questioned about
the presence of gastrointestinal signs, because occasionally ingesta enters the caudal nasal passage and results in rhinitis.
Duration and progression of signs, medications and response
to these treatments should be noted. Characterize the volume
and character of the nasal discharge and whether it is bilateral
or unilateral, acute or chronic. Mucoid discharge is usually
present if the condition is chronic, serous discharge is seem
with more acute disorders. Hemorrhage may be seen with
trauma, coagulopathies, hypertension, erosive or invasive disease, or with severe prolonged sneezing induced by any cause.
Food or water from the nares usually indicates communication
of the nasal and oral cavities. Unilateral nasal disease is more
typical of nasal foreign body, tumor, oronasal fistula, or tooth
root abscess. Physical examination of the cat with nasal disease should include thorough examination of the oral and
nasal cavities and a complete examination of the remaining
body systems to rule out underlying systemic disease. Dyspnea if present, more often is from lower versus upper respiratory conditions in the cat. Palpate the nose to detect defects or
swellings. Facial deformity and lymphadenopathy is most often seen with fungal diseases and neoplasia. Inspect the oral
cavity for oronasal fistulae or severe dental disease. Oral or
corneal ulcers are seen more often with calicivirus than herpesvirus infections. Nasal ulceration or mass in the nostril may
be associated with Cryptococcus or neoplasia. A bulging soft
palate could signal the presence of a nasopharyngeal polyp.
Facial symmetry and nostril patency should be noted. Examine the eyes for discharge or exophthalmia. Fundic examination may provide evidence of systemic disease associated with
Cryptococcus, coronavirus, or Toxoplasma. Otic examination
may reveal signs consistent with otitis media. Horners syndrome may be associated with otitis media.

Feline Rhinitis/Sinusitis: surgical


management
Introduction
Evaluation of a feline patient with rhinitis and nasal discharge may be a frustrating situation for the veterinarian. Although the relative frequency of various causes of rhinitis/sinusitis varies in dogs and cats, many of the same etiologies
that cause rhinitis in dogs are seen in cats (see Table-Van
Pelt). Due to the high incidence of viral induced upper respiratory infections in the cat population, the diagnostic
workup for cats with nasal discharge often is focused on
these etiologies. The anatomic structure of the nasal cavity
and sinuses in cats is different than dogs, and this may at
least partially explain why viral induced upper airway infections become chronic unresponsive sinusitis conditions. The
purpose of this seminar is to review the pathogenesis, diagnostic approach, and treatment of surgical disorders related
to feline rhinitis/sinusitis.

Anatomy and physiology


Significant differences are found when the turbinate and
sinus anatomy is compared in the dog and cat. The attachments of the ventral and dorsal turbinate bones are more
widely separated from each other in the cat than the dog, and
the turbinated portion of the ethmoid is more extensive. The
cat lacks the maxillary recess that is part of the paranasal sinus system in the dog. This recess is believed by some to be
one of the regions of early nasal cancer growth in the dog.
The nasal cavity can only respond in a limited number of
ways, regardless of the cause, so the patients history and
clinical signs are often similar (Van Pelt). The nasal lining is
limited to glandular hyperactivity in response to many different stimuli. As glandular secretions become stagnant, secondary bacterial infection occurs. Therefore most chronic
processes involving the nasal and sinus regions have a bacterial infection component.

Diagnostic workup
Perform a diagnostic workup to rule out nonsurgical disorders. When the diagnosis of a chronic nasal discharge is
not possible with the regimen below, surgical exploration is
warranted. Other tests may be obtained depending on the individual case (see Table).
Diagnostic workup
History and physical examination
CBC, Serum chemistry profile, Felv & FIV tests
Nasal cytology, culture, india ink preparation
Skull radiography, including frontal sinus views
Rhinoscopy and retroflexed nasopharyngeal scoping

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References

402

Surgical Procedures (Nasal exploratory, sinus drainage,


turbinectomy, intranasal mass excision, nasopharyngeal
polyp excision) Cats with chronic sinusitis are candidates for
surgery if medical therapy does not control the clinical signs.
Owners must understand that if the chronic sinusitis is due
to recurrent herpesvirus infection, surgery is attempted to
help CONTROL the secondary bacterial infection by providing drainage and removal of necrotic turbinates. Surgery
should not be considered curative since many cats are improved but most require intermittent treatment throughout
their lives.

Dorsal nasal exploratory


A dorsal midline skin incision is made through the periosteum to bone from the top of the sinus to just behind the
nasal cartilage. A Steinman pin is introduced just off-midline
at the medial canthus level. The bone is removed over the sinus or nasal cavities depending on the extent of the disease
and the need for exposure. Take samples of the abnormal tissue for bacterial and/or fungal culture, and histopathology.
Remove abnormal tissue and be sure to excise enough obstructing ethmoturbinates to allow drainage of the frontal sinuses. Fenestrated 8 French feeding tubes are introduced into both frontal sinuses and the fenestrated portion is passed
to the affected area. Hemorrhage is controlled with gauze
stripping. Periosteum is closed in a simple continuous pattern to form an airtight seal. Skin closure is routine. Fix irrigation tubes to the skin exit sites. An Elizabethan collar is
worn by the patient until suture and tube removal. Antibiotics at recommended systemic dosages (based on the intraoperative culture and susceptibility results) are used for at
least 4 to 6 weeks. Bacteria commonly isolated from affected cats include staphylococci, streptococci, coliforms, and
Pasteurella (Cape). Clavulenic acid/amoxicillin or
cephalosporin antibiotics are recommended for empirical
therapy. Irrigation tubes are flushed with 5 ml of antibiotic
solution (at systemic dosages). I prefer to use Tris EDTA solution with aminoglycosides to irrigate sinuses of cats with

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resistent Gram negative bacteria. Fat obliteration of the


frontal sinuses is considered if persistent signs of infection
occur despite appropriate drainage (Anderson). In a series of
six cats with idiopathic rhinosinusitis treated with this procedure, improvement was seen in all cats. About 65% of cats
treated this way had long-term resolution of sneezing and
purulent nasal discharge without long-term medical therapy.

Staphylotomy
The cat is positioned in dorsal recumbency and the endotracheal tube is checked to be sure there is no evidence of
air leakage. A mouth-gag is used to keep the mandible extended and provide exposure to the caudal pharyngeal area.
If the nasopharyngeal polyp is obstructing the airway, grasp
the mass with a towel forceps or Allis tissue forceps and pull
it out. If the mass cannot be grasped intubate the patient first
and perform a staphylotomy. A midline incision is made in
the soft palate from the hard palate junction to about 0.5 cm
from the caudal aspect of the palate. Preserving this edge reduces the risk of breakdown of the palate incision closure.
Remove the mass and close the incision in two layers; nasal
mucosa and oral mucosal sides. Perform a ventral bulla osteotomy to remove remnants of the polyp within the tympanic cavity.

References
Van Pelt D, Lappin M, (1994), Pathogenesis and treatment of feline rhinitis. Vet Clin N Am [Small Anim Prac] 24: 807-823.
Cape L, (1992), Feline idiopathic chronic rhinosinusitis: A retrospective
study of 30 cases. J Am Anim Hosp Assoc 28:149155.
Bradley R, (1984), Selected oral, pharyngeal, and upper respiratory conditions in the cat. Oral tumors, nasopharyngeal and middle ear polyps,
and chronic rhinitis and sinusitis. Vet Clin N Am [Small Anim Prac]
14: 1173-1184.
Anderson G, (1987), The treatment of chronic sinusitis in six cats by ethmoid conchal curettage and autogenous fat graft sinus ablation. Vet
Surg 16: 131-134.

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403

Dental emergencies
Frank Verstraete

Summary
Emergencies occur in all fields of dentistry and have traditionally been classified as emergencies in periodontics,
endodontics, orthodontics, oral medicine and maxillofacial
surgery. Alternatively, dental emergencies may be classified
according to clinical syndromes, an approach which will be
followed in this paper. The most commonly encountered dental emergencies in small animal clinical practice include the
puppy with the abnormal bite, the loose tooth, acute oral
pain, the fractured tooth, the suspected tooth abscess and
maxillofacial trauma.

THE PUPPY WITH THE ABNORMAL BITE


Persistent deciduous teeth
The exfoliation of deciduous teeth may be delayed (for a
variety of reasons) and, in the extreme form, deciduous teeth
may persist after the eruption of the permanent teeth. This is
most commonly seen with the canines and incisors, especially in toy breeds. In most cases the permanent tooth develops normally, although the time and direction of eruption
are influenced by the persistent deciduous tooth. Permanent
incisors erupt immediately caudal to the persistent deciduous incisors. Persistent deciduous canines cause linguoversion of the erupting mandibular canines, and facial deviation
of the maxillary canines.
Furthermore, persistent deciduous teeth alter the gingival
contour, which results in plaque and dbris accumulating between the deciduous and permanent teeth.

Rostral (anterior) crossbite


The terms rostral crossbite and anterior crossbite are
commonly used for a malocclusion whereby the normal incisor relationship is reversed while the rest of the occlusion
is normal. This usually involves all six incisors but can be
more limited. In most cases a palatoversion of the maxillary
incisors in present.
When a crossbite is evident in the deciduous dentition, or
when there is reason to anticipate that a crossbite will be present in the permanent dentition, the early extraction of the deciduous maxillary incisors is indicated. This is called inter-

ceptive orthodontics and is performed at 6 - 8 weeks. Similarly, the deciduous mandibular incisors can be removed if
there is an indication that an overshot dentition may develop.
The extraction does not stimulate jaw growth but just removes a potential mechanical barrier to normal development.

Linguoversion of the mandibular canines


This syndrome is commonly also referred to as base-narrow canines. In this condition the mandibular canines stand
in a more upright position than normal, thereby impinging
on the gingiva between the maxillary third incisor and maxillary canine, or even the palatal mucosa. This is usually a
dental malocclusion caused by a delayed exfoliation of the
deciduous mandibular canines. The condition should be differentiated from an underdeveloped mandible (mandibular
micrognathia), which is a skeletal malocclusion; the condition is characterized by a mandible that is too narrow and too
short. The condition may also result in the mandibular canines traumatizing the soft tissues of the maxilla. Deciduous
canines traumatizing the soft tissues of the maxilla should be
removed as a matter of urgency, not only because of the associated pain and discomfort, but also to remove a potential
mechanical barrier to normal development.

Wry bite
Wry bite is a descriptive term used for a variety of malocclusion syndromes characterized by asymmetry of the
head. These are skeletal malocclusions of genetic or traumatic origin. Severe maxillofacial trauma in puppies with
disruption of the periosteum is a common cause of skeletal
malocclusion, which often times is very difficult if not impossible to correct. As a general rule, maxillofacial trauma in
puppies should be treated as conservatively as possible in order to avoid further trauma to the periosteum.

THE LOOSE TOOTH


Increased mobility of teeth is most commonly caused by
advanced periodontitis, associated with extensive loss of attachment. Occasionally, cases presenting with increased
tooth mobility have an underlying neoplastic etiology.

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University of California, Davis - USA

404

Acutely increased mobility, however, generally is associated


with periodontal trauma. The following injuries to the periodontal tissues have been recognized:
Concussion
Subluxation
Intrusive luxation
Extrusive luxation
Lateral luxation
Exarticulation (or avulsion)
Concussion and subluxation are very discrete injuries to
the periodontal ligament that are rarely diagnosed in veterinary dentistry. Malocclusion and excessive orthodontic
forces also result in this type of periodontal trauma. An intrusive luxation occurs when the tooth is forced into its alveolus. This is virtually only possible in the maxilla where a
tooth can be pushed into the nasal cavity. In an extrusive luxation the tooth has loosened and come slightly out of the
alveolus. The injury causing the tooth to come out completely is called an exarticulation (also often referred to as
an avulsion). The most common type of periodontal trauma
is a lateral luxation. This is a displacement of a tooth in a direction other than axially and is accompanied by comminution or fracture of the alveolar socket. Most cases of severe
periodontal trauma are associated with disruption of the
pulpal blood supply at the apex, resulting in pulpal necrosis. Luxated and exarticulated teeth can be repositioned and
splinted. The prognosis is guarded because of the high incidence of root resorption. The success of reimplantation depends on the length of time the tooth has been out of the
alveolus, the status of development of the apex and the viability of the periodontal ligament on the root surface.

ACUTE ORAL PAIN


Acute oral pain may be due to a variety of conditions. An
in depth discussion of these is beyond the scope of this lecture. In general, acute stomatitis is relatively uncommon, but
acute exacerbations of chronic stomatitis, e.g. in the cat, are
often seen. The immediate considerations in the management
of these cases is pain and food intake. Hospitalizing and
feeding these patients by means of a nasogastric, pharyngostomy or PEG tube for the first few days may be indicated. A
patient should not be discharged until it can feed itself.
The therapeutic plan may further include the following:
steroidal or non-steroidal anti-inflammatory agents
appropriate antibiotics
antiseptic oral rinses (e.g. chlorhexidine 0.05%) or gels
toothbrushing, if tolerated
dietary measures

THE FRACTURED TOOTH


Classification
Dental fractures are common in the dog and cat. The following classification, derived from the World Health Organization classification of dental fractures in man, has been
proposed:

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Classification of dental fractures


Enamel infraction or fracture

A chip fracture or crack of the


enamel only

Uncomplicated crown fracture A fracture involving enamel


and dentine, but not exposing
the pulp
Complicated crown fracture

A fracture involving enamel


and dentine, and exposing the
pulp

Uncomplicated crown-root
fracture

A fracture involving
enamel, dentine and cementum,
but not exposing the pulp

Complicated crown-root
fracture

A fracture involving enamel,


dentine and cementum, and
exposing the pulp

Root fracture

A fracture involving dentine,


cementum and the pulp

Pathophysiology
Enamel fractures and uncomplicated crown fractures are
of little clinical importance in small animals. The dog is
largely resistant to caries. The exposed dentine is initially
sensitive, but this disappears after sclerosis of the dentinal
tubules and formation of tertiary dentine in the pulp chamber. Dentine is somewhat rougher than enamel and thus facilitates plaque and calculus accumulation. Sharp fracture
edges may cause soft tissue trauma and can be rounded-off
if necessary.
Crown-root fractures involve the periodontal ligament
and may lead to periodontitis because of the altered gingival
contour. A small fracture fragment and the overlying unsupported gingiva can be removed to restore a physiological
contour. Many deep crown-root fractures lead to an irreversible periodontitis and are an indication for extraction.
Complicated fractures cause pulp exposure. The pathophysiology associated with pulp exposure and subsequent
pulp necrosis and periapical pathology will be described later.
Root fractures of traumatic origin are occasionally seen;
iatrogenic fractures are also common. A root tip left behind
may become covered by bone and gingiva in the absence of
infection. Alternatively pulp necrosis may take place and
lead to sequestration. Pathological root fractures are common in the cat because of external odontoclastic resorption
lesions associated with periodontitis. In most root fractures
the coronal fragment is lost; however, traumatic root fracture
with retention of the coronal fragment may occur. Clinical
signs may include increased mobility and crown discolouration. The diagnosis is confirmed radiologically. The prognosis for the tooth depends on the level of the fracture: fractures in the coronal third of the root will not heal. Fractures
further apically can heal by means of a dentino-cemental
callus, a fibrous union or a fibro-osseous union.

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405

THE SUSPECTED TOOTH ABSCESS

Lip lacerations

A so-called tooth abscess usually refers to a periapical abscess or a periodontal abscess. A periodontal abscess is relatively rare. This condition may occur if pus accumulates in a
deep periodontal pocket with a relatively healthy and tight
gingival margin. Periapical pathology is more common. A
wide variety of conditions may cause pulpitis, pulp necrosis
and associated periapical pathology. One of the most common conditions is direct pulp exposure due to a complicated
tooth fracture. Complicated dental fractures cause pulp exposure. Haemorrhage occurs and an acute pulpitis ensues which
is very painful. Soon thereafter, bacterial invasion and obliteration of the blood vessels cause pulp necrosis.
Blood vessel obliteration occurs because the narrow root
canal does not allow for the swelling associated with an inflammatory reaction. A plug of desiccated dbris forms at
the coronal opening of the pulp chamber. At this stage the
condition is no longer painful (because the nerve is necrotic) and it can go unnoticed for a considerable period of time.
The end result of acute pulpitis is generally pulp necrosis. The combination of necrotic pulp and (a usually anaerobic) bacterial infection spreading through the apical delta
gives rise to periapical pathology. Acute periapical periodontitis and abscessation appear to occur infrequently in
animals. This condition is very painful and facial soft tissue
swelling is evident. More commonly, a periapical granuloma
develops. A periapical granuloma may remain quiescent for
a considerable period of time. This lesion has the potential
however, to give rise to a periapical abscess and associated
severe pain and swelling. The acute flare-up of pain and
swelling associated with chronic and thus far asymptomatic
pulp necrosis and periapical pathology, is also known as a
phoenix abscess. Periapical abscessation may also result in
osteomyelitis of the surrounding jaw bone.
In the dog and cat, a complicated fracture of the maxillary fourth premolar causes the occurrence of a typical syndrome. After the formation of the periapical granuloma, a sinus tract forms and breaks open ventral to the medial canthus of the eye. Whether this sinus tract involves the maxillary recess needs further investigation. Haematogenous pulpitis and complicated fractures involving other teeth in the
region can cause the same syndrome. Sinus tracts originating from periapical granulomas involving other teeth may
open into the nasal cavity and can cause a chronic nasal discharge, or they may break out in the oral cavity. A periapical
granuloma is visible on radiograph as a well-circumscribed
round radiolucent area, while a periapical abscess is poorly
circumscribed. A periapical cyst is very radiolucent, wellcircumscribed and often has a mineralized lining. A very
low-grade chronic response may give rise to an increase in
periapical bone density, known as condensing osteitis.

Lip lacerations are commonly seen. Primary closure or


early delayed primary closure, combined with careful
dbridement, is indicated. Closure is effected in two or three
layers. The suture material of choice is fine atraumatic
monofilament nylon or polypropylene for the skin, and synthetic absorbable material for the deeper layers and mucous
membrane. An irregular defect may be converted to a
wedge-shaped defect to facilitate a more aesthetic closure,
especially a smooth mucocutaneous line. More involved
techniques utilizing mucosa and skin flaps have been described for correcting extensive lip defects.

MAXILLOFACIAL TRAUMA
Maxillofacial trauma in small animals commonly arises
as a result of road traffic accidents or fighting. In some parts
of the world gunshot wounds involving the head are also
seen relatively frequently.

Avulsion of the lower lip is a common condition in the dog


and cat, caused by a degloving injury. Bone exposure occurs
and there is usually not enough soft tissue left on the mandible
to allow conventional wound closure. After cleaning and
dbridement the soft tissue flap should be replaced and kept in
contact with the bone using large horizontal mattress suture
which are passed around the canine or incisor teeth.
These are tied fairly loosely, avoiding further compromising the blood supply to the tissue flap, whilst still achieving approximation of the tissues. If the entire mandible is denuded more elaborate fixation techniques should be used.

Trauma to the tongue


Trauma to the tongue is occasionally seen in small animals. Lingual trauma includes bite wounds, sharp penetrating foreign bodies, electric burns and elastic foreign bodies
trapped at the root of the tongue.
Lacerations are managed by primary closure or early delayed primary closure. In all instances the maximum amount
of tongue tissue should be preserved. Healing is rapid because of the abundant blood supply.

MANDIBULAR FRACTURES
Initial management
The patient should be fully examined in accordance with
accepted clinical practice regarding trauma cases.
A mandibular fracture is usually an obvious lesion; a potential pitfall exists in that other less obvious but equally serious problems may go unnoticed. The pathophysiology of
trauma to the head and its anaesthetic implications should be
borne in mind when planning surgical repair of mandibular
fractures.
The diagnosis of a fracture of the mandible can usually
be made by inspection and palpation. The ventral borders of
both mandibles should be gently palpated for asymmetry
and discontinuity. Some patients will permit gentle opening
of the mouth. As most fractures are open to the oral cavity,
the discontinuity in the dental row, gingival laceration and

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Avulsion of the lower lip

406

even the fracture line are usually easily visible. The nature
and extent of the fracture can be further assessed by gentle
palpation once the patient is under anaesthesia prior to surgical treatment.
Radiological examination is indicated to visualize the
fracture site and to diagnose concomitant dental trauma.
This should be done when the patient is anaesthetized and
care should be taken to avoid causing additional soft tissue
trauma.
Fracture of the mandible is a most painful condition because of the inherent sensitivity of facial tissues in general;
in addition, concurrent trauma to the mandibular alveolar
nerve in the mandibular canal makes the condition particularly painful. The mandible is, contrary to many other bones
in the body, a bone which can hardly be spared when traumatized; drinking, eating, swallowing and panting cause
continuous movement at the fracture site. To lessen the patients discomfort and to prevent further damage to the soft
tissues, the fracture should be temporarily reduced and immobilized as soon as possible. Gross reduction can be obtained by gentle palpation using the occlusion of the canine
teeth as a guide. A simple tape muzzle is then applied to
maintain reduction.

Principles
The management of fractures of the mandible body
should be aimed at the restoration of normal occlusion.
It is therefore imperative that the occlusion is inspected
and used to guide the surgical repair of mandibular fractures.
Malalignment of the fracture fragments leads to malocclusion, which is of great clinical importance. Malocclusion
with faulty interdigitation of teeth leads to abrasion of the
teeth involved, periodontal trauma and loss of function, preventing normal mastication.
The mandible is subject to continuous movement under

4th European FECAVA SCIVAC Congress

normal circumstances and the rapid restoration of this function is an important goal in the management of mandibular
fractures.
Most mandible fractures in the dog are open to the oral
cavity and inevitably contaminated. Removing devitalized
tissue will enhance healing and may to a large extent prevent
later complications. The surgical dbridement of soft tissues
is usually limited to trimming irregular and frayed edges of
the torn gingiva and oral mucosa. The dbridement of oral
soft tissues should be very conservative as their blood supply
and healing capacity are excellent. Small, loose pieces of
bone should be removed if they do not contribute to the stability of the repaired fracture. If they are retained, it is important to preserve their soft tissue attachments and to ensure
that they are rigidly fixed. In the presence of infection these
small, loose pieces of bone may cause sequestration and necessitate subsequent surgical exploration and removal.
It is common for an alveolus to be involved in the fracture line. If the tooth involved is luxated, it should be removed. If there is still enough healthy periodontal attachment, evidenced by the fact that the tooth is non-mobile, retention of the tooth is usually indicated as it will contribute
to the stability of the fracture fixation. The presence of a
tooth in the fracture line increases the incidence of infectious
complications;
however, the immediate removal of the tooth cannot reverse these effects. If a tooth involved in the fracture line is
retained, it should be carefully monitored subsequently for
any evidence of periodontal or endodontal pathology; appropriate treatment should be instituted as soon as either is
recognized.

Key words
Dental emergencies, emergency treatment, dentistry,
dog, cat.

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407

An update on feline dentistry


Frank Verstraete

Summary
In addition to the dental diseases that affect all species,
the oral pathology of cats includes some unique conditions.
The pathogenesis of feline odontoclastic resorption lesions
and oral inflammatory diseases, chronic gingivo-stomatitis
in particular, is poorly understood. These diseases cause
considerable pain and discomfort to the patient and the therapeutic options are limited.

ANATOMY
The incisors in the cat are very small single-rooted teeth;
their size increases from the first to the third incisor. The
maxillary third incisor has a triangular cross-section and its
apex is situated adjacent to the nasal cavity. The roots of the
mandibular incisors are mesiodistally flattened. The canines
are the largest teeth. The apex of the mandibular canine
tooth is located lingual to the mental foramen. Only a thin
bone plate is present between the root of the maxillary canine and the nasal cavity.
The premolars in the cat are reduced in number and the
numbering system may be confusing. The first premolar
seen on the maxilla is actually the second premolar, a very
small tooth which is usually single-rooted; double or two
fused roots are occasionally seen. The next premolar is the
third premolar; this tooth is usually two-rooted but a small
third root on the palatal aspect is occasionally present.
The large maxillary fourth premolar is similar to the dog,
except that the distal root is considerably larger than the two
mesial roots.
Only two premolars are present on the mandible, namely the third and fourth. The mandibular first molar has two
similar, large and sharp cusps. The mesial root of the
mandibular first molar and, to a lesser extent, the third and
fourth premolars lie in close proximity to the mandibular
canal. The cat has one very small and largely non-functional two-rooted molar on the maxilla, placed transversely, distal and palatal to the fourth premolar.

MALOCCLUSION IN THE CAT


Malocclusion in the cat used to be extremely rare. This
can largely be attributed to the fact that a cat has a very pre-

cise centric anisognathic occlusion, allowing very little deviation from the normal. Recently however, the incidence of
malocclusion in the cat has increased and this has been associated with the selective breeding of cats with more extreme skull types (e.g. Persian).
The most common abnormality seen is a syndrome characterized by the presence of the mandibular canine tooth on
the outside of the upper lip when the mouth is closed; usually only one tooth is involved. This occurs in extremely flatnosed brachycephalic breeds. This skeletal malocclusion is
characterized by head asymmetry (wry bite) and exaggerated brachycephalism. The canine tooth rubbing against the
upper lip causes the clinical problem.

PERIODONTAL DISEASE IN THE CAT


Pathophysiology
Periodontal disease in the cat is characterized by a number of unique features, compared to other species.
Typical periodontal disease associated with plaque and
calculus, similar to that found in other species, also occurs in
the cat. In addition, inflammatory diseases of infectious origin would appear to play an important role in the pathogenesis of periodontal disease in the cat. Periodontal disease in
the cat is also often associated with the occurrence of external odontoclastic resorption lesions. The nature of this association, if any, is unclear. The radiological signs of periodontitis in the cat may include expansion of the buccal
bone plate overlying the canine teeth, which is not seen in
other species.

Maintenance of oral health


Daily toothbrushing is currently the best way to prevent
periodontal disease. In order to be helpful, toothbrushing
must be performed every day. Patient and owner compliance
with toothbrushing is very limited in the cat. If daily brushing is not feasible, a few options are available.
Treats coated with hexametaphosphate have been shown
to reduce calculus accumulation on teeth by sequestering calcium in dogs. Similar products may be developed for cats. It
should be noted that these products were shown to reduce calculus, not plaque. Cats may enjoy CET Forte Chews, made

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University of California, Davis - USA

408

from freeze-dried fish. Be aware that the edible products may


add a significant amount of calories to the pets diet, and regular feedings should be decreased to avoid obesity.
Hills t/d diet is available for cats and can have a substantial effect on plaque and calculus accumulation.
In cats t/d reduced plaque by 42% and calculus by 47%
compared to Purina Cat Chow. Both diets were shown to be
more effective than once weekly toothbrushing in reducing
plaque and calculus.
Chlorhexidine is a commonly utilized oral antiseptic
rinse. Chlorhexidine gluconate is preferred to the diacetate
form due to its higher residual activity and decreased tissue
irritation. Chlorhexidine is an effective and non-irritating
antiseptic at a concentration of 0.05%; higher concentrations, such as 0.12-0.20% used in most commercial preparations, may be irritating for cats. Alcohol-containing solutions should be avoided.

EXTERNAL AND INTERNAL


ODONTOCLASTIC RESORPTION LESIONS

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Clinical presentation
External and internal odontoclastic resorption lesions can
be difficult to evaluate, both clinically and radiologically. Externally, lesions may be seen as the localized absence of dental substance. The lesions are usually filled with granulation
tissue. The severity of the concomitant gingivitis is variable.
Lesions can be diagnosed using a dental explorer. The lesions
are usually very painful and even under anesthesia, jaw chattering often occurs when probing external FORL. Clinical
examination alone tends to underestimate the incidence and
severity of FORL compared to radiographic examination.
Survey radiographs are indicated if there is any clinical suspicion of FORL, and for diagnosing internal odontoclastic resorption lesions. Lesions are visible as sharply defined radiolucent areas, externally most often at the cemento-enamel
junction, and internally around the root canal or pulp chamber. The extent of FORL varies from superficial to deep; pulp
involvement may occur in the latter. In an attempt at classification the following stages were proposed:

Classification of feline odontoclastic


Resorption lesions

Pathophysiology
Periodontitis in the cat is characterized by the occurrence
of feline odontoclastic resorption lesions (FORL). The lesions mainly occur at or below the cemento-enamel junction, usually on the buccal aspect, on the mesial and distal
edges or at the furcation; lesions may also develop further
apically on the periodontal ligament. The exact pathogenesis
of FORL has not been determined, but they are not carious
lesions. Internal odontoclastic resorption lesions result from
inflammation within the pulp. The lesions appear to occur
most commonly in the canine teeth and may lead to disruption of all organized root structure.
The etiology of odontoclastic resorption lesions is unclear. A local immune response and the release of biochemical components (e.g. cytokines) which attract odontoclasts
offer a plausible explanation. An abnormal local and systemic calcium metabolism, e.g. a calcium-poor diet, may also play a role. Other dietary factors have not yet been identified, except that two studies showed that the acidic coating
of dry cat food did not predispose the teeth to the development of FORL.
Histopathologically, two stages are identifiable in the
pathogenesis of FORL: an acute stage, with many odontoclasts on the surface of the excavated lacunae, and a reparative stage, with few odontoclasts on the dentinal surface and
the deposition of bone-like or cementum-like material in the
defects.
External odontoclastic resorption lesions appear to be a
recent phenomenon, with very few lesions found in skull
collections dating prior to 1950. The current incidence in
cats presented for veterinary or dental care can be as high as
67 %. The prevalence and number of affected teeth increase
with increasing age.
In most studies, the most commonly affected teeth were
the maxillary fourth premolar and the mandibular premolars
and molars.

Stage 1

Shallow cementum or enamel defects

Stage 2

Defects involving cementum or enamel, as well as


dentin

Stage 3

Defects involving cementum or enamel,


dentin and pulp

Stage 4

Severe loss of tooth structure, complete root


resorption or root ankylosis

Treatment
Properly performed periodontal treatment is indicated in
all cases of external odontoclastic lesions associated with
periodontitis. All the principles of periodontal treatment are
applicable. In addition, particular attention should be paid to
the dental examination in order to detect FORL. The treatment for these lesions remains highly controversial. Restoration using various materials such as glass-ionomer and fluoride treatment are currently practiced and advocated by
some veterinary dentists. The rationale for the use of fluoride is to desensitize the exposed dentin and to strengthen
the remaining tooth substance; this is extrapolated from the
use of fluoride in man. There are no studies as to the effectiveness of this treatment in the cat. One author reported a 33
% success rate for glass-ionomer -restoration while others
results were even more disappointing. Failure occurs as a result of progressive resorption alongside the restoration or
new FORL. Restoration of subgingival lesions is technically very difficult even for experienced dentists.
It may be scientifically more justifiable to treat very
shallow lesions by subgingival curettage and root planing,
and to extract teeth affected by deeper lesions. Extraction is

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ORAL INFLAMMATORY DISEASES


Feline stomatitis
Inflammatory conditions affecting the oral mucosa and
gingiva of cats are commonly seen in practice.
Feline stomatitis consists of a number of syndromes
with a common presenting clinical symptom: inflammation
of the gingiva and/or varying parts of the oral mucosa. This
may result from abnormalities in local or systemic immunity. The pathways involved in regulation of the immune response are complex, and poorly understood in cats. Cats infected with the feline immunodeficiency virus (FIV) are
commonly afflicted with severe periodontitis, gingivitis, and
oral ulceration, suggesting that systemic and local immunity
are vital to the maintenance of oral health. However, local
immune responses may contribute to the development of feline lymphocytic-plasmacytic gingivitis-stomatitis complex,
evidenced by the fact that affected cats often respond to immunosuppressive doses of corticosteroid.

Infectious agents in the oral cavity


Many of the bacteria present in a normal feline oral cavity are pathogenic in other circumstances, such as Pasteurella multocida, the most common bacterium present in cat bite
abscesses, but do not cause disease in a healthy mouth. Also, while non-resident bacteria may be present as secondary
invaders following a primary insult, there are few instances
of oral disease initiated by bacteria.
Feline immunodeficiency virus (FIV) and feline calicivirus (FCV) are the most common infectious agents associated with oral inflammatory conditions in cats. These
viruses may be shed in the saliva of infected cats, including
asymptomatic carriers. Severe periodontal disease and gingivitis are commonly noted in FIV-infected cats, and chronic oral ulcerative conditions are also diagnosed in a higher
percentage of FIV-infected cats than in non-infected cats.
Feline calicivirus causes acute faucitis, and persistent oral
carriage has been linked to chronic ulcerative-proliferative
faucitis-stomatitis.
Infection with feline herpesvirus (FHV) may result in ulcers of the tongue, palate, or nasal philtrum in addition to
upper respiratory or ocular symptoms. Stress may precipi-

tate intermittent bouts of virus shedding into saliva and may


lead to recurrent oral ulceration, though this has not been
documented.
The feline leukemia virus, though actively shed in saliva,
is less often associated with oral disease than is FIV. Unlike
FIV, a strong relationship between oral disease and infection
with FeLV has not been demonstrated in clinical studies.
However, FeLV-infected cats may have secondary oral infections as a result of generalized immunosuppression.

Feline lymphocytic-plasmacytic
gingivitis-stomatitis complex
The use of the non-specific term stomatitis suggests a
single clinical presentation and a single cause, and should
therefore be avoided. It is preferred to define lesions according to duration (acute or chronic), severity (mild, moderate, severe), physical characteristics (i.e., erythematous,
edematous, ulcerative, proliferative, suppurative, fibrinous,
vesicular, haemorrhagic), and location (gingivitis, buccal
mucositis, faucitis, pharyngitis, glossitis, palatitis).
The following clinical syndromes are commonly
identified:
(1) acute marginal gingivitis:
inflammation mainly affecting the free gingiva, clinically evident as a red line, occurring most commonly in
young cats.
(2) Severe gingivitis with stomatitis:
grossly obvious gingivitis extending across the mucogingival junction.
(3) Severe stomatitis with gingivitis:
severe inflammation of the glossopalatine folds (fauces),
gingivitis present but less obvious.
(4) Severe oropharyngitis (faucitis):
severe inflammation of the caudal oral cavity and
oropharynx, with ulceration or granulation.
Affected cats may exhibit halitosis, ptyalism, dysphagia,
pawing at the mouth, poor grooming, and weight loss. Lesions may be localized (e.g. to the marginal gingiva, fauces,
or buccal mucosa), or generalized.
Tissues may appear hyperaemic, edematous, proliferative, or ulcerated. Regardless of initiating cause, histopathology of these lesions often reveals deep infiltrates of lymphocytes, plasma cells, and monocytes, suggestive of chronic antigenic stimulation and resulting in the use of the term
lymphocytic-plasmacytic stomatitis. A superficial layer of
neutrophils is often present as well, indicative of ulceration
and secondary infection.
It is often difficult or impossible to identify the cause of
these inflammatory lesions. Contributing factors may include infection with feline calicivirus (FCV), feline herpesvirus (FHV), feline immunodeficiency virus (FIV), and
feline leukemia virus (FeLV). Purebred cats, especially
Abyssinians, Siamese, Persians, Himalayans, and Burmese,
may be predisposed. Periodontal disease and odontoclastic
resorptive lesions are often present concomitantly. A complete diagnostic database should consist of a detailed history, thorough physical examination, dental examination (under anaesthesia if necessary), complete blood count, serum

MAIN PROGRAMME

complicated by root resorption, which make the teeth prone


to iatrogenic root fractures. Leaving fractured root tips behind was found to be acceptable in one recent study but is
thought by others to perpetuate the problem.
External odontoclastic resorption lesions in the reparative stage may result in ankylosis when located apical to the
cemento-enamel junction. This makes an extraction procedure considerably more difficult.
Asymptomatic ankylosis by itself is not an indication for
extraction.
Early internal odontoclastic resorption lesions can be
treated endodontically. However, the lesions typically seen
in the cat are usually advanced and are treated by extraction.

409

410

biochemistry profile, urinalysis, systemic viral serology and


local viral isolation, oral radiography, and histopathology of
affected areas. Hyperglobulinemia is a common biochemical
abnormality identified in cats with chronic gingivitis-stomatitis complex.
Systemic diseases may present with primary oral signs
and must be ruled out prior to initiating therapy.
Uraemia is a common cause of painful oral ulcers in cats
with renal failure. Although auto-immune diseases are less
common in cats than in dogs, it is important to consider them
when a feline patient presents with oral ulceration.
Medical therapy has had limited success in the treatment
of these conditions. Long-acting injectable corticosteroid
(methylprednisolone acetate) is given every four to eight
weeks and may result in significant improvement. However,
benefits may be transient, and adverse side effects may occur (iatrogenic hyperadrenocorticism or diabetes mellitus).
Orally administered corticosteroids (prednisone, prednisolone) are more difficult to administer but may have fewer adverse side effects.
Antibiotics are often administered concurrently with corticosteroid therapy. Amoxycillin-clavulanic acid has an excellent spectrum against oral pathogens. It is available in a
liquid form to improve patient acceptance. Clindamycin has
a narrower spectrum but is also commonly used in practice
for oral diseases.
Surgical therapy is, at this time, the most consistently
successful therapeutic approach to these cases.
Extraction of premolar and molar teeth resulted in substantial improvement in 80% of treated cases in a recently
published study. Refractory cases may respond to extraction
of the remaining canines and incisors.
Supportive treatment, ensuring adequate nutrition and
hydration, and pain management are extremely important in
these cases.

EXODONTICS IN THE CAT


Because of the small size of the roots, root tip elevators
should be used as dental elevators in the cat. These instruments should however, be used with great care, as they are
very sharp and the bone plate between the nasal and oral
cavity is very thin. Oronasal fistula formation is a possible
sequel to the overzealous use of these instruments.
External odontoclastic resorption lesions make dental

4th European FECAVA SCIVAC Congress

extraction in the cat particularly difficult because of the high


risk of root fractures. Root fractures with retention of the
apical fragment may result in persistent pain and complications such as osteomyelitis of the alveolar bone. Leaving
root tips behind may be acceptable in certain circumstances:
e.g. half-resorbed root tips deeply embedded in bone or
anaesthetic-risk patients. Leaving fractured root tips behind,
in the absence of periodontal and endodontic pathology, was
found to be acceptable in one recent study.
Root tip fragments can be loosened and lifted out using
root tip elevators or root tip picks (e.g. Heidbrink # 13/14 or
Davis # 11 root tip elevator). Good lighting, irrigation and
suction are essential for good visibility. If necessary, a
mucogingival flap can be created and an alveolotomy performed in order to get access to and obtain good visualization of a root fragment. Alternatively small root tips can be
drilled out under constant irrigation (pulverization, atomization); however, this technique can result in considerable
iatrogenic trauma and is not recommended.

Key words
Dentistry, oral disease, oral pathology, feline odontoclastic resorption lesion, chronic stomatitis, cat.

References
HARVEY CE (1991) Oral inflammatory diseases in cats. Journal of the
American Animal Hospital Association 27:585-591.
HARVEY CE (1995) Feline oral pathology, diagnosis and management. In:
Manual of Small Animal Dentistry (Eds. DA Crossley & S Penman)
2nd edn. British Small Animal Veterinary Association, Cheltenham:
129-138.
HENNET P (1997) Chronic gingivo-stomatitis in cats: long-term follow-up
of 30 cases treated by dental extractions. Journal of Veterinary Dentistry 14(1):15-21.
LYON KF (1992) Subgingival odontoclastic resorptive lesions. Veterinary
Clinics of North America: Small Animal Practice. 22(6):1417-1432.
OKUDA A, HARVEY CE (1992) Etiopathogenesis of feline dental resorption lesions. Veterinary Clinics of North America: Small Animal
Practice. 22(6):1385-1432.
PEDERSEN NC (1992) Inflammatory oral cavity diseases of the cat. Veterinary Clinics of North America: Small Animal Practice 22(6):13231345.
REUBEL GH, HOFFMAN DE, PEDERSEN NC (1992) Acute and chronic faucitis of domestic cats. Veterinary Clinics of North America:
Small Animal Practice 22(6):1347-1360.

4th European FECAVA SCIVAC Congress

411

Radiology: enhanced visualization of dental problems


Frank Verstraete

Summary
Dental radiographic equipment is easy to use and the
techniques easy to master. Dental radiographs form an essential part of a comprehensive oral examination and may be
taken as part of a full-mouth survey or as indicated by the
clinical findings. The radiological findings are a key element
in diagnostic and therapeutic decision-making. Furthermore
radiography is indispensable to assess the quality of endodontic treatment.

technique of choice but it is difficult to obtain due to the


shape of the oral cavity. When it is not possible to place the
film parallel to the tooth and perpendicular to the X-ray
beam, the bisecting angle technique is used. The X-ray beam
is directed perpendicular to the line that bisects the angle
formed by the film and the long axis of the tooth. In doing so
the image obtained is neither elongated nor foreshortened.

Radiographic technique
The use of proper dental radiographic equipment, films
and technique is strongly recommended. Although diagnostic
radiographs of dental conditions can be made using conventional radiographic equipment, the inconvenience of having
to transport a patient to a separate radiography room may be
an important factor influencing the decision whether to take
radiographs or not. The radiological signs of early periodontal or periapical disease are subtle and can be missed if the
positioning, exposure and developing are not optimal.
Two main techniques are in use in dental radiography: the
paralleling technique and the bisecting angle technique. In
the paralleling technique the long axis of the tooth is parallel
to the film and perpendicular to the X-ray beam. This is the

Figure 1 - The paralleling technique (left) and the bisecting angle technique
(right).

DOG

CAT

The following table summarizes a recommended system


for standardizing radiographic positioning, views
and technique, suitable for full-mouth radiographic evaluation in the dog and cat:

View

Position

Technique

View

Position

Technique

maxillary I and C
(occlusal)

intra-oral

bisecting angle

maxillary I and C

intra-oral
(occlusal)

bisecting angle

caudal maxilla: P4 - M2

intra-oral

bisecting angle

maxilla: P2 - M1

extra-oral

parallel

rostral maxilla: P1 - P3

intra-oral

bisecting angle

mandibular I and C

intra-oral
(occlusal)

bisecting angle

mandibular I and C

intra-oral
(occlusal)

bisecting angle

mandible: P3 - M1

intra-oral

parallel

caudal mandible: P4 - M3

intra-oral

parallel

rostral mandible: P1 - P4

intra-oral

parallel

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Med Vet, DVM, Dipl AVDC


University of California, Davis - USA

412

Additional intra-oral bisecting angle views for the evaluation of the canine teeth are occasionally indicated.
Slightly oblique views of the caudal maxilla are indicated to visualize the two mesial roots of the maxillary fourth
premolars separately.

Indications
Dental radiographs form an essential part of a comprehensive oral examination and radiological findings are a key
element in dental decision-making.
Full-mouth radiographs may be taken when the patient is
first presented for dental treatment.
Full-mouth radiographs of small animal patients presented for dental treatment are not routinely taken in practice,
mainly because it is considered cost-prohibitive, and because it is not established practice to do so. An alternative
approach is to radiograph those areas where one expects to
find pathology, based on the visual oral examination and periodontal probing.
The indications for elective dental radiography can be
summarized as follows: (1) clinical signs of periodontal or
endodontic disease; (2) prior to extraction, and post-extraction, if there is any suspicion of root fracture; (3) before,
during and after endodontic procedures; (4) clinical staging
of oral tumours; (5) maxillofacial trauma (root fractures,
maxillofacial fractures, TMJ-problems); and (6) diagnosis of
missing teeth.

Systematic evaluation of dental


radiographs
The following system is recommended for evaluating
dental radiographs:
(1) Technical quality: Are the films diagnostic? Errors in exposure or processing? Elongation or foreshortening? All
teeth included? All apices included?
(2) Normal anatomy: Deciduous or permanent dentition?
Any teeth missing? Unerupted teeth? Anatomical variations (root dilaceration, fused roots, supernumerary
roots, etc.)? Examples of normal anatomical structures
which should not be mistaken for pathological changes
include: the mandibular canal, mental foramen, infraorbital foramen, palatine fissure.
(3) Periodontal evaluation: Follow the outline of each
tooth and examine the periodontal ligament space for
uniformity (space between the lamina dura of the alveolus and the cementum). Evaluate the alveolar bone
crest and the trabecular bone interproximally and in the
root furcations.
(4) Endodontic evaluation: Compare the diameter of the
pulp chambers and root canals.
Examine the periapical region of each tooth for uniformity of bone density.
(5) Other conditions: Presence of metabolic bone disease,
ankylosis/resorption, tumours, root fractures, etc.

4th European FECAVA SCIVAC Congress

Radiological signs of common dental


problems
Radiology is of great practical value for the early diagnosis of missing teeth in prospective show dogs. This can already be done in 9-12 week-old puppies. The absence of permanent tooth buds underneath the deciduous teeth indicate
that these teeth will be missing in the permanent dentition.
Adult patients with missing teeth are occasionally presented for certification that the tooth loss is due to trauma or
periodontitis, and not to hypodontia. This is only possible
shortly after the tooth loss has occurred when the empty
alveolus has not yet been replaced by bone, or if a root fragment is visible.
Although the diagnosis of periodontitis is primarily a
clinical diagnosis, radiology can be used to document and
assess the extent of the lesions. Radiological signs of periodontitis may include: (1) rounding of the cemento-enamel
junction; (2) widening of the periodontal space; (3) loss of
integrity of the lamina dura; (4) osteolysis of the supporting
bone; and (5) resorption of the alveolar crest. If the alveolar
crest over a number of teeth has receded parallel to the level of the cemento-enamel junctions, the term horizontal
bone loss is used. When the bone loss is irregular and the
alveolar crest is no longer parallel to the cemento-enamel
junctions, the condition is referred to as vertical bone loss;
this condition is usually confined to one or two roots. Resorption of the alveolar crest at the furcation occurs with furcation involvement and is an important finding.
Periodontitis in the cat is characterized by the occurrence
of odontoclastic resorption lesions. These lesions present radiologically as radiolucent areas, most often at the cementoenamel junction. Radiographs are useful for determining the
depth of the lesions and for demonstrating lesions in the furcation area.
Pulpal pathology will usually be clinically evident because of obvious pulp exposure or crown discolouration. Radiology is used to prior to endodontic therapy (1) to assess
the morphology of the pulp chamber and root canal, and (2)
to determine the presence of periapical pathology. Furthermore radiology is indispensable to assess the quality of a
root canal treatment.
Periapical pathology starts as a periapical periodontitis,
evidenced by a discrete widening of the periodontal space
around the apex. Eventually a periapical granuloma or abscess forms which is seen as a round radiolucent area around
the root tip. This is the lesion that may give rise to a dental
sinus tract.
The injuries to the periodontal tissues that have been recognized and that can be radiographically demonstrated, include: (1) concussion; (2) subluxation; (3) intrusive luxation; (4) extrusive luxation; (5) lateral luxation; and (6) exarticulation. Dental fractures are diagnosed on a clinical basis,
but radiology is useful in determining the extent of the subgingival fracture line in crown-root fractures and the diagnosis of root fractures. The extent of the subgingival fracture
line in crown-root fractures is clinically very important and
can be assessed radiographically. A root fracture is a fracture
involving dentine and cementum. Traumatic root fractures
with the coronal fragment still in place are occasionally

4th European FECAVA SCIVAC Congress

Radiology should be used if there is any indication that this


complication might have taken place during the extraction
procedure.

Key words
Dental radiography, dental radiology, intra-oral radiography, intra-oral radiology, dog, cat.

MAIN PROGRAMME

seen. Root fractures can occur in the cat as a result of extensive odontoclastic resorption lesions.
Pre-extraction radiographs of teeth to be removed are indicated to confirm the diagnosis, to allow visualization of
the root morphology and to ascertain the presence of root resorption or root ankylosis.
Post-extraction radiographs are recommended to confirm that no root tips were left behind and to document possible alveolar bone injury due to the extraction procedure.

413

4th European FECAVA SCIVAC Congress

415

Early diagnosis of canine hip dysplasia (CHD)


Aldo Vezzoni
Med Vet, Dipl ECVS
Private Practitioner, Cremona - Italy

Canine Hip Dysplasia is an inherited, developmental


condition that involves a lack of conformity between the
femoral head and acetabulum and invariably leads to osteoarthritis.2 Laxity of the hip joint has been recognized as a
constant feature of CHD and it appears to have an hereditary
basis too.2,3 CHD, in contrast to a similar disease in human
beings, cannot be diagnosed at birth as it develops during the
growth phase as a consequence of several factors leading to
joint laxity and incongruity like collagen disease, imbalance
between hip adductor and abductor muscles, sloped orientation of the acetabular roof, overweight. 2,3 Hip dysplasia is a
dynamic process and all the aspects of the disease depend on
the time in which it is evaluated. Generally it is possible to
separate acetabular hip dyplasia from femoral hip dysplasia,
both leading to hip laxity and joint degeneration.7
Most cases of CHD involve acetabular hip dysplasia
which is characterized by excessive slope of the dorsal rim of
the acetabulum and its secondary osteoarthritic changes.7 This
excessive slope could be caused during growth by an insufficient magnitude or incorrect direction of forces pushing the
femoral head into the developing acetabulum which becomes
shallow.7 During weight bearing the femoral head is laterally
deviated by the inclined plane of the sloped dorsal acetabular
rim stretching the joint capsule which becomes inflammed
and causing microfractures of the cartilagineous labium.
Femoral hip dysplasia is characterized by abnormalities
in the femoral neck length, inclination and anteversion
which lead to uneven loading of the articular surfaces, joint
incongruency and joint capsule stretching.5,7
Clinical signs of CHD can be seen as early as at 5 to 6
months of age in severe cases or in the mature age according to the physical activity and to the degree of degenerative
joint disease developed.2,7 In dogs the disease can be detected radiographically when they are between 4 and 8 months
old although in some individuals the disease is not evident
radiographically until they are 12 to 24 months old2,7,12 Combining a physical orthopaedic evaluation and a dynamic radiographic study it is possible to anticipate the diagnosis of
CHD in every susceptible dog at the age of 6 months which
is very useful for dog selection in controlled breeding programs; it is also a good opportunity to assess the patient for
future hip problems according to the owners expectations
for performance and to provide the possible more appropriate conservative or surgical treatments.

Physical orthopaedic hip evaluation


at 6 months
Gait observation
The dog is observed from behind while walking, looking at the distance between the hind paws; in the base normal walking the paws are touching the ground perpendicularly to the hips, while the dysplastic dog walks passing
from base narrow to base wide.7 With base wide the hips are
reduced by the active contraction of the abductor and rotators muscles and the dog must walk base wide to maintain
the hips reduced, particularly when climbing stairs or before jumping, but with their fatigue the hips reluxates causing the dog to walk base narrow.7 When walking base narrow the dog is showing discomfort and to reduce it the dog
loads more the front legs and flexes the back. While running, the dysplastic dog needs to distribute the hind loading
on both legs simoultaneously for better comfort and thereafter the hind feet are placed close and are used toghether,
with a bunny hopping gait.7 The stand test is performed to
evaluate the ability of the dog to stand on its hind legs only
and to ascertain the possibility of the hip joints to fully extend in loading position without pain; the normal dog has no
difficulty to stand in an erect position while its owner is
holding its front legs; the dysplastic dog will refuse this position or will stand up with discomfort keeping the back and
hips in flexion and staying away with the pelvis, as the
standing position is stressing the inflammed and streched
joint capsule.7
Physical examination without anaesthesia
The physical examination should demonstrate pain in the
hip joint and that lameness is caused by hip problems. Passive movements of the hind legs that would stretch the hip
joint capsule will elicit a positive response from the patient
when inflammation is present; with repeated tearing of the
joint capsule when the femoral head subluxates during
weight bearing, inflammation and synovitis will develop. To
stress the joint capsule the hip is abducted, externally rotated, and extended simultaneously.7 Negative response from
the patient is indifference, while positive response is pain
and discomfort manifested by vocalization or aggressive behaviour. The same type of reactions can be elicited by testing the hip for subluxation pushing the proximal femur laterally and the ilium medially.7

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Introduction

416

Physical examination with anaesthesia


In the anesthetized dog it is possible to evaluate the stability of the femoral head in the acetabulum, the amount of
joint laxity and the features of head subluxation if present.
When the joint is stable it is possible to perform passive
movements in full range without causing any feeling of subluxation. When joint laxity is present, the femoral head is allowed to translate dorsally with axial compression and hip
abduction will cause the Ortolani sign, a characteristic
clunk caused by the femoral head returning into the acetabulum, while hip adduction will cause the Barlow sign
created by the femoral head slipping out of the acetabulum.4,7
It is possible to measure and evaluate the angles at which
subluxation and reduction occur to obtain reference values.
The dog is positioned in dorsal recumbency, with the pelvis
parallel to the table and the sagittal plane being vertical; the
stifle of the leg being examined is brought in vertical position
without hip flexion and extension.4,7 Then slight axial
femoral compression will cause hip subluxation if joint laxity is present and the operator will notice a positive Barlow
sign feeling the femoral head slipping outside the acetabulum
for a certain amount proportional to the amount of joint laxity.4,7 The hip is then abducted slowly until the femoral head
returns into the acetabulum, and the characteristic clunk is
perceived producing the Ortolani sign; the inclination of the
femur relative to the sagittal plane when the reduction occurs
is measured as the angle of reduction (AR).4,7 The hip is then
slowly adducted until the femoral head begins to subluxate

4th European FECAVA SCIVAC Congress

producing the Barlow sign; the inclination of the femur relative to the sagittal plane when the subluxation occurs is measured as the angle of subluxation (AS).4,7 The AS has a negative value if subluxation occurs when the distal femur is medial to the sagittal plane, and positive value if subluxation occurs when the distal femur is lateral to the sagittal plane
These measurements are repeated until consistent results are
obtained. The same procedure is followed in the other hip.
Two angles, AR/AS, are measured and recorded for each hip.
To measure these angles it is possible to use a standard
arthrogoniometer or the Canine Eletronic Goniometer designed by Slocum for this purpose.7 The AR is indicative of
joint capsule laxity: the greater the laxity, more the femoral
head subluxates, higher the AR.7 Higher the AR, greater the
clunk that is perceived, greater the stretching of the capsule. In normal hips, without any joint laxity, the AR is not
detectable, as it isnt in cronic hip dysplasia with thickened
joint capsule. In tolerable joint laxity as it is present in several dogs that will not develop hip dysplasia, the AR range between 10 to 25. AR higher than 25 is indicative of excessive joint laxity that could lead to degenerative joint disease.
The AS is indicative of the dorsal acetabular rim (DAR)
slope and of acetabular filling: the DAR slope is the inclination of the weight bearing dorsal part of the acetabulum.7 It
should be almost perpendicular to the direction of the weight
bearing forces to be perfectly functional; in normal dogs the
slope is no more than 7.5 from a line perpendicular to the
long axis of the pelvis.7 If the DAR slope is more than 7.5 it
will act as an inclined plane dividing the loading forces in two
components, one vertical against the acetabular roof and one
lateral stretching the joint capsule. Higher the DAR slope,
higher the AS at which the femoral head can translate laterally to rest in the joint capsule. Acetabular filling by osteophytes and thickened round ligament also cause an increase
of the AS.7 In normal dogs, without any joint laxity, the AS is
not detectable. In tolerable joint laxity the AS should have a
negative to 5 positive value. DAR slope between 8 to 10
and AS between 5 and 10 are predictive of light hip dysplasia. DAR slope higher than 10 and AS higher than 10 are
predictive of moderate to severe hip dysplasia.
In some normal puppies undergoing rapid growth between 4 and 6 months of age, the adductor muscle mass
overpowers the abductor muscles and the axial femoral force
is directed lateral to the DAR, against the joint capsule
which stretches and became lax.7 As a result of this temporary muscular imbalance the AR is increased as it is the radiographic measurable joint laxity, while the DAR slope is
normal and the AS is 0 or negative. Such joints can be lax
without being pathologic and without any arthrotic changes
and if not damaged by excessive exercise during the growing time will appear normal at 12-18 months of age.7

Static and dynamic radiographic hip study


at 6 months
Using orthogonal views, lateral, ventrodorsal and anteroposterior, a three dimensional study of the hip can be done
to evaluate the bone morphology of both pelvis and femur;
using a distraction device to push the femoral heads apart, a

dynamic evaluation of joint laxity is performed. Because


correct positioning and muscle relaxation are essential to run
this study, the dog is anesthetized.
Standard ventrodorsal view.
To evaluate the joint congruity the pelvis positioning
should be simmetric and the femurs should be parallel, well
extended and inward rotated to have the patella in the center
of the femoral troclea. The center of the femoral heads
should be medial to the dorsal acetabular rim indicating at
least 50% coverage.8 Any tilting of the pelvis would alter the
percentage of head appearing covered by the acetabulum.
The congruency between the craniolateral acetabular rim
and the femoral head is evaluated to identify any flattening
or cranial curvature of the craniolateral acetabular rim.8 The
Norberg angle should be at least 105. In this position any
valgus or varus deviation of the femoral neck is recognized,
according the femoral positioning is correct. Any sign of osteoarthritis is identified examining the craniolateral acetabular rim, the dorsal acetabular rim, the femoral head and neck.
Standard frog view.
In this position the femurs are flexed and slightly abducted and the femoral heads are pushed in the acetabula. In
a normal joint the articular rim should be uniform and thin;
any filling of the acetabular fossa caused by a permanently
displaced femoral head or hypertrophied teres ligament will
widen the articular rim.8 In this position the first osteophyte
formation can be seen on the femoral neck as a spur between
the head and the greater trochanter.
Lateral view.
This position is useful to evaluate the lumbo-sacral joint
to differentiate other problems like diskospondilitis, spondilarthosis, cauda equina compression, OCD of the sacral
proximal endplate; it is also useful to evaluate the femoral
neck anteversion.
Dorsal Acetabular Rim view (DAR).
Described by B.Slocum in 1990 this radiographic view is
the most informative to evaluate the integrity and the slope
of the dorsal acetabular rim. 6 The dog is placed in sternal recumbency with the hind legs pulled cranially to rest along
the thorax. 6,8 A circumferential belt holds the stifles against
the torso and 10 cm elevation of the hocks provides hamstring tension that causes enough rotation of the pelvis to allow the x-ray beam to pass through its longitudinal axis.6,8
With this view it is possible to see and evaluate the weight
bearing portion of the acetabulum in cross section. In normal

417

dogs the lateral aspect of the DAR is pointed and its slope is
no more than 7.5 from a line perpendicular to the long axis
of the pelvis.8 The femoral head is well seated in the acetabulum and is well covered by the DAR. In the dysplastic dog
the slope of the DAR is increased to 20 or more and its lateral aspect is rounded to blunted, the femoral head moves
dorsally and laterally along the inclined plane of the sloped
DAR and osteophyte formation can be seen on the lateral aspect of DAR and filling the acetabulum.8
Distraction view.
Several Authors suggested the usefulness of stress radiographs of the hip to evaluate the joint laxity, but G.Smith
and colleagues at the University of Pennsilvania in 1990 described an improved method both to distract the joint and to
calculate its laxity. 12 With this distraction technique the hip
is held in neutral position to avoid the twisting of joint capsule that would limit the distraction effect; to calculate the
joint laxity he described the distraction index (DI) which is
calculated by dividing the measured distance between the
femoral head center and acetabular center by the radius of
the femoral head.12 This yields a unitless variable that ranges
from 0 to approximately 1.12 A hip having an index of 0 is
tightly compressed in its congruent position, and a hip having an index of 1 has little to no acetabular coverage of the
femoral head (ie, joint luxation). 12 A DI of 0.30 is considered
to be the dividing line between normal hips and hips predisposed to hip dysplasia.2,12,13 Some dogs with a DI greater
than 0.3 could not develop hip dysplasia if the joint laxity is
caused by a muscular imbalance between the abductors and
adductors only and it is not dependant by an excessive slope

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4th European FECAVA SCIVAC Congress

418

of DAR.2,8 Some dogs with hip dysplasia have a DI less than


0.3 because capsular fibrosis, following the inflammatory
arthritis, limits femoral head luxation.
In a study conducted by R. Badertscher at the University
of Georgia in 1977 using the half-axial position to improve the
radiographic visualization of subluxation in canine hip dysplasia, results similar to the ones described later by G.Smith
were found.1 As this procedure was simplest and quicker providing reliable results, we adopted his method since 1994, only improving the device used to distract the hips. The dog is
positioned ventrodorsally with the femurs at approximately
45 to the table top and the tibiae parallel to the plane of the
table surface.1 A teflon table-device 2 cm thick, 5 to 12 cm
width and 50 cm long, with a S shape to better adapt to the pubis area, with an hinged base to keep it in contact and parallel
to the table was placed on the ventral surface of the pelvis; applying pressure to the medial aspects of the proximal femurs
through the hand held tibiae resulted in the fulcrum subluxating the femoral heads from the acatabula.1 To compensate for
the superimposed muscle mass an increase of 10 KvP was
necessary for adequate tissue penetration.1 In our experience
the 45 of hip flexion doesnt cause hip joint capsule twisting
in such an extent to limit the complete hip distraction that is
obtained with the hip in neutral position, as consistent results
were obtained in the same dogs with both positions.

Dog selection in controlled breeding


programmes
With the physical orthopaedic evaluation and the radiographic findings at 6 months of age it is possible to detect
an already established CHD and to advise the breeder not to

4th European FECAVA SCIVAC Congress

select that dog. But the most important result is to predict the
probability that a dog without clinical signs and without radiographic evidence of CHD in the standard ventrodorsal
view at 6 months of age would have normal or dysplastic hip
joint at 1 year of age and later. The key points to predict the
evolution of an apparently normal hip joint at 6 months of
age are the evaluation of the reduction and subluxation angles measured in the anesthetized dog, the distraction index
measured in the distracted ventrodorsal radiographic view
and the slope of the DAR view.
- In all breeds, if the reduction and subluxation angles are
not detectable, the DI is < 0.3 and the DAR is < 7.5 the
probability that the dog will not develop hip dysplasia is
very high.
- In all breeds, if the reduction angle (AR) is < 20, the subluxation angle (AS) is < 5, the DI is between 0.3 and 0.4
and the DAR slope is 8 to 10 the probability that the dog
will develop borderline or light hip dysplasia is high.
- In all breeds, if the reduction angle (AR) is > 20, the subluxation angle (AS) is > 5, the DI is between 0.3 and 0.7
and the DAR slope is > 10 the probability that the dog will
develop moderate to severe hip dysplasia is high.
- In rapid growth breeds if the reduction angle (AR) is up to
30, the subluxation angle (AS) is up to 5, the DI is between
0.3 and 0.6 and the DAR slope is < 7.5 (normal) the probability that the dog will not develop hip dysplasia is good,
but that dog needs a strict nutrition and exercise control.

Treatment planning
When hip dyplasia is diagnosed at an early age it is possible to alter the progression of the disease with appropriate
treatments, before osteoarthrosis prevents successful results.
The window of opportunity to correct the developing hip
dysplasia by surgical treatments is limited and it is lost if
cartilage damage, dorsal acetabular rim microfractures and
acetabular filling occurs.7 Under these circumstances the attending veterinarian that underestimates the problem would
loose the opportunity to have the dog treated and his hip salvaged before arthrosis will develop.7 Particularly when the
expectations by the owner on the functional aptitude of the
dog are high it is essential to consider and to advise a prophylactic treatment.
The surgical options that are available to correct or to
limit the developing hip dysplasia in the growing dog are:
- triple pelvic osteotomy;
the acetabular segment of the ilium is outward rotated
along its longitudinal axis to increase the coverage of the
femoral head and hip joint congruity. The technique described by Slocum is the most reliable;10 this surgical treatment is indicated in dogs 5 to 12 months old, with no or
minimal signs of osteoarthosis, joint subluxation, AR between 20 and 40, AS between 10 and 20, DAR slope
between 10 and 30.7 The degree of acetabular rotation,
i.e. the degree of torsion of the canine pelvic ostotomy
plate (CPOP), is determined according to the DAR slope,
avoiding excessive correction that would limit the abduction of the leg.7 After correction the DAR slope shoul be 0.
With proper indication, the most successful degree of cor-

rection is 20; with this correction there is no impingement


between the dorsal acetabular rim and the femoral neck.
The maximum possible correction without excessively altering the relationship between the femoral neck and the
dorsal acetabular rim is 30. When subluxation is still possible after a 20 or 30 correction, then a femoral neck
lenghtening procedure in adjunct should be performed.7,9

419

mation of the proximal femur with anteversion and valgus


deviation of the femoral neck, being the DAR slope normal.5
In the mature dog, when the degenerative joint disease
has already established, beside the conservative treatment
with NSAID drugs, weight and exercise control, the surgical
options that are available are:
- total hip replacement;
both the acetabulum and the femoral head are substituted
with implants to allow a free and painless joint motion.
Several techniques are used in dogs, with cemented and
not-cemented prosthesis, with excellent functional results
reported.
- head and neck ostectomy;
the femoral head and neck are excised to eliminate the
contact between the bone surfaces of the diseased joint
components and to allow formation of a fibrous pseudoarthrosis with a synovial membrane. This technique is
considered a salvage procedure14 with limited functional
results and it could be indicated when other techniques are
not possible and when functional demand is limited.

References
- femoral neck lenghtening
the femoral neck length is increased by a diverging osteotomy of the proximal femoral methaphysis, to increase
the proximal femoral lever arm and the medially directed
force produced by the internal and external hip rotators
muscles; this procedure is aimed at eliminating the
amount of joint laxity evidenced by the distraction index
in the stressed radiographic view. This technique was described by Slocum and it is indicated as a sole procedure
in dogs with excessive joint laxity (DI between 30 and
70) and a DAR slope less than 10, in dogs with a short
femoral neck like Akita, Chow and several molossoid
breeds;9 it is also indicated in adjunct to triple pelvic osteotomy when an excessive joint laxity is evidenced by the
DI (between 40 and 75) to allow the application of a
lesser degree of acetabular torsion; this avoids the necessity of overrotatong the acetabular segment in patients
with excessive joint capsule laxity.7,9
- dorsal rim acetabuloplasty;
the dorsal acetabular rim is increased by a bone graft harvested from the ilium wings with a bone guage and applied between the joint capsule and the deep gluteal muscle, activating the osteointegration of the graft by drilling
several holes in the dorsal acetabular rim. This technique
was described by Slocum and it is indicated in severly
subluxated and arthosic hips, when the TPO is no more indicated, with DI up to 1.0, AS up to 20-30, DAR slope
between 20 and 40, acetabular filling, ostephytes on the
dorsolateral acetabular rim and on the femoral neck, and
cartilage eburneation.11
- intertrochanteric ostectomy:
the direction of the femoral neck is modified from valgus to
varus and from anteversion to normoversion with and intertrochanteric osteotomy and the removal of a wedge of
bone. This technique was described by Prieur and it is indicated in dogs with hip joint subluxation caused by a malfor-

1.

2.
3.
4.

5.

6.
7.

8.

9.

10.

11.

12.

13.

14.

Badertscher RR: The half-axial position: improved radiographic visualization of subluxation in canine hip dysplasia, MS Thesys,
Athens, Georgia, 1977.
Lust G: An overview of the pathogenesis of canine hip dysplasia, J
Am Vet Med Ass 210- 10:1443, 1997.
Madsen JS: The joint capsule and joint laxity in dogs with hip dysplasia. J Am Vet Med Ass 210- 10:1463, 1997.
Piermattei DL, Flo GL: Brinker, Piermattei, and Flos Handbook of
Small Animal Orthopedics and Fracture Repair, Philadelphia, 1997,
WB Saunders, 441.
Prieur WD: Intertrochanteric Osteotomy. In Bojrab MJ, Ellison GW,
Slocum B, editors: Current Techniques in Small Animal Surgery,
Philadelphia, 1998, WB Saunders, pp 1165-1168.
Slocum B, Devine TM: Dorsal acetabular rim radiographic view for
the evaluation of the canine hip. J Am An Hosp Assoc 26:289, 1990.
Slocum B & Devine Slocum T: Hip: Diagnostic Tests. In Bojrab MJ,
Ellison GW, Slocum B, editors: Current Techniques in Small Animal
Surgery, Philadelphia, 1998, WB Saunders, pp 1127-1145.
Slocum B & Devine Slocum T: Radiographic Characteristics of Hip
Dysplasia. In Bojrab MJ, Ellison GW, Slocum B, editors: Current
Techniques in Small Animal Surgery, Philadelphia, 1998, WB Saunders, pp 1145-1151.
Slocum B & Devine Slocum T: Femoral Neck Lengthening. In Bojrab MJ, Ellison GW, Slocum B, editors: Current Techniques in Small
Animal Surgery, Philadelphia, 1998, WB Saunders, pp 1154-1159
Slocum B & Devine Slocum T: Pelvic Osteotomy. In Bojrab MJ, Ellison GW, Slocum B, editors: Current Techniques in Small Animal
Surgery, Philadelphia, 1998, WB Saunders, pp 1159-1165.
Slocum B & Devine Slocum T: DARthroplasty. In Bojrab MJ, Ellison GW, Slocum B, editors: Current Techniques in Small Animal
Surgery, Philadelphia, 1998, WB Saunders, pp 1168-1170.
Smith GK, Biery DN, Gregor TP: New concepts of coxofemoral joint
stability and the development of a clinical stress-radiographic method
for quantitating hip joint laxity in the dog. J Am Vet Med Ass 196:5970, 1990.
Smith GK, Gregor TP, Rhodes WH, et al.: Coxofemoral joint laxity
from distraction radiography and its contemporaneous and prospective correlation with laxity, subjective score, and evidence for degenerative joint disease from conventional hip-extended radiography in
dogs. Am J Vet Res 54:1021, 1993.
Vasseur PB: Femoral Head and Neck Ostectomy. In Bojrab MJ, Ellison GW, Slocum B, editors: Current Techniques in Small Animal
Surgery, Philadelphia, 1998, WB Saunders, pp 1170-1175.

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4th European FECAVA SCIVAC Congress

4th European FECAVA SCIVAC Congress

421

New material and new implants in bone internal fixation


Tubular external fixator, Pc-Fix, Maxillofacial mini plate

C. Von Werthern
DVM, Dipl ECVS
Veterinar-Chirurgische Klinik der Universitat Zurich - Switzerland

Four new implants for internal fracture fixation are presented. All implants except the external fixator are developed by the AO Davos, Switzerland. These implants were
applied on the cats and dogs at the small animal surgery department of the University of Zurich.
The PC-fix (point contact) is a new bone plate, which has
only point contact with the bone and is fixed with monocortical selftapping screws. The 3,5 mm plate has used for fracture fixation of 47 long bone fractures in dogs. The plate is
easy to apply and reduces operation time. Compared to a dynamic compression plate bone healing time is reduced to
38% and fracture healing is superior.
The tubular external fixator has been developed for
fracture fixation of distal extremities in humans. This fixator was applied to 28 fractures of small animals less than 5
kg body weight.
Advantages compared to other external fixator systems is
its low weight and price and the possibility of placing several Kirschner wires in very close proximity to each other. A
special indication was therefore distal radius /ulnar fractures in toy breed dogs.
A mini titanium maxillofacial plate, smaller than the AO
mini plate, was used for fixation of mandibular fractures in
cats and phalangeal fractures in cats and dogs. With the
cutable mini plate and the selftapping 1 mm screws osteosynthesis of smallest bone fragments is now possible.
A human titanium arthrodesis plate is introduced. It has
been used for panarthrodesis of the carpus and the tarsus
with dorsal application in dogs. It is a LC-DC plate with a
special design that allows insertion of 2,7 mm screws at the
distal end and 3,5 mm screws at the proximal end. The special developed profile of the plate is reinforced at the stress
site over the joint.

erated with this new bone plate and were retrospectively investigated.

Material and methods


The PC-fix is a bone plate which has only a point contact
with the bone (Fig. 1). This is achieved by a special design
of the contact area of the plate with the bone. Multiple arches leave space under the plate for vascularity and callus formation during fracture healing. The PC-fix is fixed to the
bone with monocortical screws. Special screws with a conical head which locks into a complementary hole of the plate
are used (Fig.1). Deformation of the holes is avoided during
contouring using a hole to hole bending. The screws are selftapping and there is only one standard lenght. In contrast to
a dynamic compression plate (DCP) these screws can only
be inserted in a predeterminated 90o angle to the axis of the
plate. The fixed angle between the screw and the plate adds
stability to the plate-bone unit. Because external fixator have
the same mechanical principle, the PC-fix can be regarded
as an internal fixator.
At the small animal surgery department of the University of Zurich the 3.5 mm PC-fix was applied to 47 long bone
fractures in dogs.
Median weight of the dogs was 28.4 kg bodyweight, the
average age was 38 months. The 47 longbone diaphyseal
fractures were classified as transvers (n = 11), oblique (n =
21), spiral (n = 5) and mildly comminuted (n = 4) or severly comminuted (n = 4). Two revisions had been treated with

1. The PC-fix
Introduction
The name PC-fix stands for point contact internal fixator
and is a new bone plate for fracture fixation. It has been developed by the AO Davos, Switzerland (TEPIC et al., 1997).
At the small animal surgery department of the University of Zrich 47 dogs with long bone fractures have been op-

Figure 1 - Design of the PC-fix plate.

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Summary

422

a PC-fix (1 malunion, 1 osteomyelitis). 18 patients had open


fractures. An average plate length of 10 holes with an average screw number of 6 screws were used.
While in the beginning of this study the PC-Fix was used
only in neutralisation function, during the last 18 months we
applied the PC-fix also in higher comminuted fractures with
buttress function. This was achieved by means of double
bone plating (n = 5).

4th European FECAVA SCIVAC Congress

2. Tubular external fixator (F.E.S.S.A.):


Application in small dogs and cats1
The tubular external fixator was designed by the french
military for temporary and permanent fixation of fractures of
the extremities in humans. At the small animal surgery department of the University of Zurich we applied the tubular
external fixator especially in the fracture stabilisation of dogs
less than 5 kg body weight and cats (REICHLER et al., 1997).

Results
Material and methods
All fractures except three healed without complications.
Two fracture fixation collapsed due pull out of the screws.
One fracture repair collaps because the plate broke. Time of
implant removal was on average 3.5 months.

Discussion
Atraumatic soft tissues handling in fracture treatment is
a basic principle for biological osteosynthesis. Healing of a
fractured bone relies on the soft tissue surrounding the fracture which initiates callus formation. Internal fixation of the
fracture should add as little soft tissue damage as possible to
achieve an umcomplicated and fast bone healing.
The design of the new PC-fix plate is based on this concept. The plate is layed only with point contact on the periost
of the bone. This leaves space under the plate for vascularity and callus formation.
The PC-fix is hold in place by the threads of the screws
and the stable 900 angle determinated between the screws and
the plate (Fig. 1). The screws do not press the plate on the
bone, as in DC-plate application, which prevents the development of implant-related cortical necrosis under the plate.
A complete different screw design allows beside monocortical application a smaller number of screws for fracture
fixation (6 average). Selftapping screws reduce the operation
time and the instrumental equipment. Monocortical application minimises damage to peri- and endosteal bloodsupply.
This biological concept of the PC-fix resulted in a 38%
shorter healing time (SAVOLDELLI, 1995) and a superior
healing of fractured bone compared to conventional DCplate application (TEPIC, 1997).
The PC-fix concept is promissing, but smaller plate sizes
for application in cats and smaller dogs would be appreciable. Different shapes of PC-fix plates for fixation of metaphyseal and periarticular fractures could be developed.
Longer screws for metaphyseal application are needed. The
price of the implants should be reduced for their use in veterinary medicine.

References
Tepic S, AR Remiger, K Morikawa, SM Perren (1997). Strength recovery
in fractured sheep tibia treated with a plate or an internal fixator: an
experimental study with two year follow up. J Ortho Trauma 11(1):
14 - 23.
Savoldelli D, PM Montavon (1995). Clinical handling:small animals. Injury
26: 47 - 50.

The tubular external fixator (Fig. 2) consists of a stainless steel tube that is available in different sizes (6, 8, 10 mm
diameter). Six and 8 mm tubes were applied. The tube has
two axial aligned rows of predrilled holes perpendicular to
each other (Fig. 2). One line of holes is for introduction of
the Kirschner wires (K-wires), the holes perpendicular to
these are threaded and provided with little screws for fixation of the K-wires. In the 6 mm tube K-wires of 2 mm or
smaller diameter, in the 8 mm tube wires of 2,5 mm or
smaller can be inserted. Only threaded K-wires were used
and inserted by a low speed power drill.

Figure 2 - Tubular external fixator (FESSA).

The tubular external fixator has been applied to 6 toy


breed dogs with distal radius-/ulna fractures and 20 cats with
various fractures. All patients were less than 5 kg body
weight. The average weight of the dogs was 2,7 kg and that
of the cats 3,2 kg.

COVELY-SMV, Z.I. Lyon-Nord, 69730 Genay, France.

4th European FECAVA SCIVAC Congress

423

Eleven out of 20 fractures in cats were open fractures,


most of them severely comminuted. All fractures were reduced closed or with a minimal approach to the fracture
site. In all cases a Typ I unilateral, uniplanar configuration
was applied.

Fracture healing was radiologically diagnosed after an


average time of 93 days with a range of 21 to 201 days. Out
of 28 fractures fixed with the tubular external fixator 26
healed. One dog was euthanasied for unrelated reasons, a cat
was treated conservatively after premature removal of the
fixator and relaps of the fracture.
Minor complications as pin tract infection or breakage of
K-wires were seen but did not interfere with the fracture
healing.

Discussion
Fracture fixation with an external fixateur is a optimal
way to perform a biologic osteosynthesis. Compared to
bone plating, there is no implant present at the fracture site
and the fracture can be reduced either in closed fashion or
with a mini approach. Additional soft tissue trauma is therefore reduced.
Fracture fixation with the tubular external fixator is easier as with other systems.
Others have a connecting bar and several clamps for fixation of the K-wires. The steel tube of the tubular external
fixateur is one functional unit that combines both the connecting bar and multiple clamps. Beside a simplifed application, its weight is only 14% of other systems (AO,
Kirschner and Menard).
The diameter of the K-wires used with the tubular fixator are equal or smaller than the diameter of the gliding
holes. The diameter of the K-wires is therefore not determinated by the fixator system and can be adapted to the size of
the bone.
Distal metaphyseal radius-/ulna fractures of toy breed
dogs were a special indication for the tubular external fixator. These type of fractures are often very close to the joint.
Even using a AO-miniplate it is often difficult to place two
proper screws in the distal part of the radius. With the tubular external fixator 4 K-wires can be placed on the same distance as 2 screw holes of a AO miniplate. This results in a
better fracture stablity.
Transarticular application is also possible by use of a
connecting joint between 2 tubes. This allows stabilisation
and optimal wound treatment of transarticular shearing injuries.

References
Reichler IM, CJ von Werthern, PM Montavon (1997). Der tubulre Fixateur
externe (FESSA): Klinische Anwendung zur Frakturversorgung bei 6
Zwerghunden und 20 Katzen. Kleintierpraxis 42: 407 - 419.

Figure 3 - Application of the tubular external fixator to a distal tibia.

Craniofacial adaptation plate


(Compact 1,0)2
A craniofacial titanium miniplate system (Compact 1,0)
was developed by the AO, Switzerland for fixation of craniofacial fractures in humans (PREIN und RAHN, 1998).
At the small animal surgery department of the University of Zurich the adaptation plate of the Compact 1,0 has been
successfully used for fixation of manibular fractures in cats,
metacarpal and metatarsal fractures in cats and phalangeal
fractures in small dogs. 12 cases were treated with this plate.

Material and methods


For economical reasons we put together a partial Compact 1,0 craniofacial set which is listed below:
A craniofacial titanium adaption plate (34 holes, thickness 0.7 mm, length 100 mm).
Selftapping screws (core diameter 0.7 mm, outer diameter 1.0 mm, length of 6 or 8 mm).
Emergency screws (core diameter 0.9 mm, outer diameter 1.2 mm, length 6 or 8 mm).
Special screwdriver, two 0.7 mm drills, the handpice of
the screwdriver and the drill were the ones of the AO mini set.

Figure 4 - Mini maxillo facial titanium plate with one screw (1.0 Compact).

Synthes, Mathys Medizinal Technik AG, Bettlach Schweiz.

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Results

424

During the last 6 months 12 cases had been operated with


the titanium craniofacial plates in our small animal surgery
department.
The patients were 6 cats with mandibuar fractures, 2 cats
with metatarsal fractures, 1 cat with metacarpal fractures
and 1 dog with multiple phalangeal fractures. Furthermore 2
avulsion fractures were fixed with single screws of the Compact 1,0 system: One avulsion of the short part of the medial collateral ligament in a cat, one avulsion of the collateral
ligament of a phalangeal joint in a dog.
Ten cases accomplished fracture healing. The follow up
of the other patients is not yet completed.

4th European FECAVA SCIVAC Congress

been started at our departement to evaluate its application


for carpal- and tarsalarthrodesis in dogs. Preliminary results
are very promising.

Material and methods


This 9 holes straight titanium plate is basically a LC-DC
plate. The plate has a distal and a proximal end. The four
screw holes at the distal end are assigned for 2,7 mm screws.
Those of the proximal end have a larger diameter for the use
of 3,5 mm screws. The profile of the plate becomes progressively smaller from the middle to the distal end of the plate.
Two tarsal panarthrodesis and one carpal panarthrodesis
using dorsal plating have so far been performed in dogs
weigthing 28 - 33,5 kg.

Results
Till deadline of this abstract only one tarsal arthrodesis
has been radiologically diagnosed as fused 3 months after
the operation.The other two showed uncomplicated fast fusion of the joint.

Figure 5 - Fracture fixation with the miniplate between vertical and horizontal ramus of the mandibula of a cat.

Discussion
Fracture treatment in cats and small dogs can be challenging regarding the relation between the size of the bones
and available implants. Most of smaller bone fractures can be
repaired with the AO mini instrument and implant set (MONTAVON et al., 1988). Especially in cats and toy breed dogs
some of the bone fragments are too small for the AO mini implants. They can now be stabilized with the AO mini craniofacial plate system. Successful application in mandibular and
phalangeal fractures have been accomplished.

References
Montavon PM, OE Pohler, ML Olmstead, KL Wendelburg (1988). The mini
instrument and implant set and its clinical application. VCOT 1: 44-51.
Prein J, BA Rahn (1998). Scientific and technical bachground. In: Manual
of internal fixation in the cranio-facial skeleton. Editor: J. Prein,
Springer Verlag; 1-50.

Carpal- and tarsal-arthrodesis titanium plate3

Introduction
A special titanium plate for wrist arthrodesis in humans
has been developed by the AO, Switzerland. A study has

Synthes, Mathys Medizinal Technik AG, Bettlach/Schweiz

Figure 6 - Pantarsal arthrodesis in a dog with the titanium arthrodesis


plate.

Discussion
This implant has an advantageous design for panarthrodesis of carpal and tarsal joints in dogs. The LC-DC
principle provides a fast bone healing. The major complication in conventional panarthrodesis is a fracture at the distal
screw hole. Using screws with smaller diameter, as possible
with this plate, reduces this risk. The tappered profile at the
distal end also reduces the probability of suture dehiscence.
Price of this plate should be adjusted by the AO for veterinary use. A steel version from an an American company
is now available in two different sizes (2.7 mm screws and
2.0 mm screws, 3.5 mm screws and 2.7 mm).These are less
expensive.

4th European FECAVA SCIVAC Congress

425

Patellar luxation: techniques for optimal


reestablishment of the articular biomechanics
Cranialization of the tuberositas of patellar luxations in dogs and cats

C. Von Werthern

Summary
A new surgical technique had been developed for the correction of patellar luxation in small animals. This technique
combines the conventional transposition of the tuberositas
tibiae with its additional cranialisation. A broad oblique performed osteotomy of the tuberositas tibiae allows its deplacement in cranial direction. This results in a quicker healing, a reduction of the retropatellar pressure and therefore
an earlier use of the operated limb postoperatively.

Introduction
Patellar luxation is often observed in small breed dogs,
but can also be diagnosed in larger breeds. Medial patellar
luxation predominate in every breed and size of dogs. Lateral patellar luxation are uncommon however more often seen
in large breed dogs.
To classify the severity of a patellar luxation a grading
system from grad I - IV (PUTNAM, 1968) is used. In grad I
and II luxations the patella is located in the trochlear groove
but can be manually dislodged. In grad I luxations the patella repositions back spontaneously, whereas in grad II luxationthis has to be supported manually. Grad III and IV luxations are permanently luxated, whereas grad IV luxated
patellar can not be brought back into the normal position.
The standard surgical technique to correct a patealla luxation is a sulcoplasty of the trochlea femoris combined with
transposition of the tuberositas tibiae. With the conventional
technique the osteotomised fragment of the tuberositas tibae
is very small. It will is transposed and fixed with a K-wire
slightly caudally to its original position. This results in an increased retropatellar pressure (Fig. 1).
By performing a different osteotomy of the tuberositas
tibiae (Fig. 2) it can be transposed medially or laterally and
in a more cranial position. This results in a reduced
retropatellar pressure and the patient uses its leg sooner postoperatively. The technique was applied to over 50 cats and
dogs with all different grades of patella luxation.

dorsal recumbency at the end of the operation table. The leg


is draped proximally and the tarsus is left undraped for better intraoperative manipulation.
A lateral and medial arthrotomy to the stifle is performed
before the tuberositas tibiae is osteomised. To achieve a cranialisation effect of the tuberositas tibae and the straight
patella ligament, a vertical cut must be performed slightly
oblique (Fig. 2). It is directed to the distal end of the
tuberositas tibiae.
The cranial aspect of the medial meniscus and the sulcus
extensorius should be visualized in order to prevent damage.
The short distal osteotomy is then performed horizontally
(Fig. 2).

Figure 1 - Schematic diagramm of retropatellar pressure:


a) normal position, b) cranialisation, c) caudalisation of the tuberositas tibiae.
R represents the resulting pressure between patella and femur.

Material and methods


The affected leg is aseptically prepared for surgery from
the thight distal to the tarsus. The patient is positioned in

Figure 2 - Direction of the osteomies for correction of a medial patellar


luxation.

MAIN PROGRAMME

DVM, Dipl ECVS


Veterinar-Chirurgische Klinik der Universitat Zurich - Switzerland

426

Next the tuberositas tibiae is flipped dorsally and a


wedge osteotomy (SLOCUM, 1982) of the trochlear
femoris is performed with a saw. In dogs younger than 5
months the trochlea femoris in deepened with a chondroplasty (FLO, 1969). The joint is inspected for cranial
cruciate rupture.
The tuberositas tibae is now transposed medial or lateral
and in a more cranial position and fixed with a K-wire. The
transposed position is acceptable, if the patella does not luxate when the leg is rotated externally or internally with the
stifle extended and the tarsus flexed. If you are satisfied with
the result, the tension band wire is completed with an additional K-wire and a cerclage wire.
Soft tissue techniques can be applied if there is still a
trend for a patellar luxation. These can be the imbrication of
fascia lata, the release of the fascia on the opposite side or a
partial myotomie of a severly contracted part of the quadriceps muscle.

Results
Four cats and 16 dogs operated with this technique have
been retrospectively evaluated in our department (Koch,
1997). Fifteen cases showed a medial, 5 a lateral patellar
luxation. Fifteen months after surgery 63% were free of lamness and 27% intermittent lame. Radiologicaly diagnosed

4th European FECAVA SCIVAC Congress

slow progression of arthrosis did not correlate with clinical


findings. All owners except one were satisfied with the results of surgery.

Discussion
The cranialisation of the tuberositas tibiae for treatment
of patellar luxation is a safe and easy surgical technique. The
broad osteotomy provides a fast bone healing. The postoperatively reduced retropatellar pressure allows an early use of
the limb. It has been successfully applied to all degrees of
patellar luxation in dogs and cats.

References
Putnam R. W.(1968):Patellar luxation in the dog. MS Thesis, University of
Guelph, Ontario.
Koch D. A., P.M. Montavon (1997): Klinsche Erfahrungen bei der Therapie
der Patellaluxation des Kleintieres mittels Sulkoplastie und seitlicher
und kranialer Versetzung der Tuberositas tibiae. Schweizer. Arch.
Tierheil. 139, 259 - 264.
Slocum B., D. Slocum, T. Devine (1982): Wedge recession for treatment of
recurrent luxation of the patella. Clin. Orthop. 164, 48.
Flo G. L. (1969): Surgical correction of a deficient trochlear groove in dogs
with severe congenital patellar luxations utilizing a cartilage flap and
subchondral grooving. MS Thesis, Michigan State University, East
Lansing, Michigan.

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427

Identification of lesions the spine


Simon J. Wheeler
BVSc, PhD, MRCVS Dipl ECVN, RCVS Specialist in Veterinary Neurology
The Royal Veterinary College, University of London - United Kingdom

The clinical syndromes seen in animals with spinal disease are generally well recognised. It is usually apparent if
an animal has spinal disease, either from the history or the
physical findings. Lesion localisation depends on the performance and interpretation of the neurological examination, and the use of appropriate ancillary tests. Only then
can a realistic differential diagnosis be determined, and appropriate therapy considered.

The clinical syndromes seen in animals with spinal disease are generally well recognized. It is usually apparent if
an animal has spinal disease, either from the history or the
physical findings. Less obvious circumstances where spinal
disease should be suspected include non-specific pain and
lameness that is not orthopaedic in origin.
Taking a history and making a full clinical examination
are prerequisites to a more detailed neurological examination. The history taken from the owner will often assist in
reaching a provisional diagnosis. Items of particular note are
any history of trauma; whether the condition is progressive,
static or episodic; other episodes of disease; the vaccination
status; current or previous episodes of pain and the patients
urinary status.
A general physical examination should be performed on
all animals where spinal disease could be present. If there has
been trauma or if anaesthesia is contemplated, evidence of
other concurrent problems must be determined. Also, some
patients where spinal disease is suspected are in fact suffering from problems of other systems. It is not unusual for orthopaedic disorders to mimic neurological conditions. Careful clinical examination should identify such problems. Particular note should be made of joint pain or enlargement as
these are present in many dogs misdiagnosed as having neurological disorders. The presence of any spinal pain or deformity also should be noted. The quality of the femoral pulse
must be determined, particularly in acutely paralysed cats.

the animal upright in the first instance and later placed in lateral recumbency.

Assess attitude, posture and gait


Watch the patient as it relaxes in the examination room.
Let it move to the best of its ability, unless it has an acute
spinal injury where movement should be restricted. Note
the degree of function, the gait and general demeanor. In
cats, this part of the examination is particularly important as
later parts may be difficult to perform. It is useful to listen
to dogs as they walk on a hard surface; if conscious proprioceptive deficits are present, the examiner may hear the
claws scuff.

Determine the locomotor status


The animal is encouraged to move, except where an
acute spinal injury has occurred or if there is severe pain.
Dogs that appear paraplegic at rest may show some voluntary movement if supported by a sling or by the tail. Unilateral weaknesses may be revealed by hopping, hemistanding
and hemiwalking tests.
Assess muscle strength, if the dog is able to stand, by
pressing down on the shoulders and hips. The patient may
then be classified according to its locomotor status, for example, paraplegic, hemiparetic, etc.

Assess conscious proprioception


This is evaluated in the standing animal by the paw position test. Animals with deficits of conscious proprioception
that can walk often wear the dorsum of the claws abnormally; this can be appreciated on examination.

Palpate the abdomen


Examination
The neurological examination is carried out with the aim
of determining the location of the spinal lesion. The neurological examination described here is readily performed with

Determine the degree of bladder filling and the ease with


which urine is expressed by palpating the abdomen. Urinary
incontinence is often a feature of spinal disorders, and some
assessment of urinary function should be gleaned from the
history.

MAIN PROGRAMME

Summary

428

4th European FECAVA SCIVAC Congress

Panniculus reflex

Muscle palpation

This is tested by pinching the skin along the dorsal surface of the trunk with fine forceps and observing the twitch
of the cutaneous trunci muscle on both the ipsilateral and, to
a lesser extent, the contralateral side. The arrangement of the
reflex is illustrated in.

Muscle atrophy is assessed by observing and palpating


muscle masses. This is best assessed in muscles with a definite bony border, such as the cranial tibial, infraspinatus and
supraspinatus muscles in the limbs, and the temporal muscles of the head.
Muscle tone is evaluated by gently flexing and extending
the joints. In a normal animal, there is a degree of resistance
to such manipulation. Care must be taken in interpreting
findings in excitable or fractious animals, or where painful
orthopaedic conditions exist, as an incorrect impression of
increased tone may be gained. Increased tone in the forelimbs is seen in the Schiff-Sherrington sign.

Palpate the spine


Determine the presence of spinal hyperaesthesia by palpating the vertebral column and evaluating the patients response. This is an important step in the examination.

Cranial nerve examination


Even though abnormal cranial nerve findings may not be
expected in spinal disorders, it is good practice to perform
such an examination. Some animals with multifocal neurological diseases present as apparent spinal cases. Also, it
adds little time to the routine clinical examination to examine the cranial nerves.
Particular note should be made of the presence of
Horners syndrome (ptosis, miosis, enophthalmos and third
eyelid protrusion), which occurs because of interference
with the sympathetic nerve supply to the eye originating in
the T1-T3 spinal cord segment. This may be a feature of
spinal disease if the cervical or cranial thoracic cord segments, or nerve roots are involved. An ophthalmoscopic examination also should be carried out in a complete neurological examination.
The patient is then placed in lateral recumbency, and
each limb evaluated with the aim of placing it into one of the
following categories:
NORMAL
LOWER MOTOR NEURON TYPE ABNORMALITY
UPPER MOTOR NEURON TYPE ABNORMALITY
Some explanation of the functional anatomy is required
to appreciate the difference between the types of deficit
(See above).
The effect of lesions on the LMN and UMN systems can
be considered in terms of motor function, muscle atrophy,
muscle tone and local reflexes. The clinical signs that allow
differentiation between UMN and LMN abnormalities are
summarized in Table. Lower motor neuron deficits are characterized by flaccid paralysis; severe (neurogenic) muscle
atrophy; reduced muscle tone; and reflex loss. Upper motor
neuron deficits show paresis or paralysis; mild (disuse) muscle atrophy; normal or increased muscle tone and intact or
hyperactive reflexes. There are some variations in mild cases, but from the neurological examination, it should be possible to categorize each limb as being normal, UMN, or
LMN type abnormality.
Motor function has been evaluated previously. With the
animal in lateral recumbency, the examination proceeds as
follows.

Reflex testing
There are a number of local spinal reflexes available for
examination, but it is usual to evaluate the patellar reflex and
the flexor (withdrawal) reflexes. Other reflexes such as the
triceps, biceps, cranial tibial, and extensor carpi radialis may
be tested. However, they are found inconsistently in normal
animals, and their main significance is in finding hyperactive responses in UMN disorders.

Localization
On the basis of the findings, it is possible to identify the
location of the lesion in the cord. Functionally, the cord may
be divided into four regions.
A BRAIN - C5
B C6 - T1/2
BRACHIAL OUTFLOW
C T2/3 - L3
D L4 - S3
LUMBOSACRAL OUTFLOW
For clinical purposes, areas A and C, the cervical and
thoracolumbar cord, may be considered as UMN carrying
areas. Part of the LMN lies within the spinal cord; thus, lesions in certain areas of the cord will produce LMN signs in
the limbs. Area B of the cord provides the LMN to the forelimbs and area D the LMN to the hindlimbs, bladder and
perineum.
Lesions in the various areas will produce different combinations or neurological signs.
Lesions in the cervical cord (A) produce UMN signs in the
fore and/or hindlimbs.
Lesions of the brachial outflow segments (B) produce
LMN deficits in the forelimbs and UMN signs in the
hindlimbs. However, asymmetrical lesions in this area may
produce LMN signs in one forelimb only, with UMN signs
in both the hindlimbs and the other forelimb.
Lesions in the thoracolumbar cord produce UMN signs in
the hindlimbs only, with normal forelimbs (although the
Schiff-Sherrington sign may be present).
Lesions in the lumbosacral outflow segments (D) produce
LMN signs in the hindlimbs, tail and perineum, but the
forelimbs are normal.
There are variations possible, for example, in some
Dobermans with caudal cervical spondylomyelopathy,

4th European FECAVA SCIVAC Congress

Assessing the severity or extent


of the lesion
Assessing the severity of a lesion plays a major part in
the diagnostic procedure. In certain patients, the severity of
the lesion has as much bearing on the prognosis as the aetiology; if a poor prognosis is suggested, further investigations may be deemed unnecessary.
In general, patients with spinal disease showing LMN
deficits have a worse prognosis for a return to function than
cases showing UMN deficits, because of destruction of the
cell body in LMN spinal cord diseases. Patients with major
LMN deficits have a poor prognosis for return of that particular function, although associated UMN signs may recover.
In UMN injuries, the rate of onset, the duration and the
degree of the spinal cord damage all have a bearing on the
clinical signs. The degree of dysfunction can be graded from
mild ataxia, through paresis, to paralysis (or -plegia) with
loss of deep pain perception.
The degree of severity of signs is based on two anatomical features. These are the position in the spinal cord where
the tracts lie that carry the respective function, and the size
of the fibbers transmitting that function. Superficial tracts
are more susceptible to damage, and larger myelinated fibbers are more easily damaged than small nonmyelinated fibbers. Conscious proprioception loss, which is the one of the
earliest neurological deficits seen in mild spinal cord damage, is transmitted by large myelinated fibbers in superficial
tracts. Deep pain sensation is transmitted throughout a large
area of the cord in small, nonmyelinated fibbers. Thus, by
inference, loss of this function indicates a major degree of
cord damage.
The prognosis worsens with the increasing neurological
deficit, which reflects increasing degrees of spinal cord damage. The prognosis for patients without deep pain sensation is
poor, especially if the situation has been so for over 48 hours.
Animals that have lost deep pain sensation following trauma
carry a poor prognosis whatever the duration of the signs.
In patients with similar deficits, the prognosis is dependent on the aetiology. For example, a dachshund with paraparesis may be suffering either from a thoracolumbar disc
protrusion or possibly a spinal tumour. Clearly the prognosis

for such cases would differ greatly.


The further course of action and some assessment of the
prognosis depends on the information gained from the neurological examination. It must be remembered that the radiological appearance of the spine bears no direct relationship
to the neurological status, and the neurological findings
must be considered when assessing the prognosis.
Once the location of the lesion has been established, a
list of likely differential diagnoses can be made. Many components go into making this list, including breed and age of
the patient, history, presenting signs, progression, physical
and neurological findings. Ancillary diagnostic aids are employed to provide the diagnosis.

DIAGNOSTIC AIDS
Routine laboratory evaluations
Serum biochemistry and haematology are unlikely to
provide definitive diagnostic information, but they have an
important role to play in the diagnostic process. Certain
metabolic disorders will effect the nervous system, and the
value of these tests is in identifying or ruling out such conditions. Also, they have an important role in evaluating the
general health of the animal. In selected circumstances, the
evaluation of blood parameters will be virtually diagnostic,
for example, where creatine kinase (CK) concentrations are
raised in myopathy or bile acid concentrations elevated in
hepatic dysfunction.

Cerebrospinal fluid
Cerebrospinal fluid (CSF) analysis plays a significant
role in the investigation of nervous system diseases and
forms a part of the diagnostic protocol in many cases. Cerebrospinal fluid is collected routinely from the cisterna
magna, a straightforward procedure in the majority of dogs.
While the technique is safe in experienced hands, practice
on cadavers is recommended prior to attempting collection
in clinical cases to allow the clinician to become familiar
with the procedure. Cerebrospinal fluid collection is indicated in a number of situations:
Where there is evidence on the neurological examination
of a structural brain lesion except in suspicion of raised intracranial pressure.
In spinal cord diseases, where the diagnosis is not apparent by other means, particularly radiology. As the radiological investigation of spinal diseases often involves
myelography, CSF should be collected before contrast media is injected.
In multifocal neurological diseases.
Where signs of generalized peripheral polyneuropathy are
present, as such signs may be due to nerve root diseases.
In dogs with epilepsy, where seizures are proving difficult
to control with adequate anticonvulsant therapy or where
there are neurological signs indicating the presence of a focal lesion.

MAIN PROGRAMME

UMN signs in the hindlimbs predominate even though the


lesion is in the cervical cord. The possibility of a thoracolumbar lesion in such patients should not be overlooked.
The type of urinary incontinence also indicates the site of
the lesion. The LMN to the bladder are in the sacral segments. Lesions of these segments produce a LMN incontinence with a flaccid, easily expressed bladder. Lesions cranial to the sacral segments produce an UMN incontinence
where the bladder is full and difficult to express.
On the basis of the neurological examination, the location of the lesion can be identified to a particular area of
spinal cord. It must be remembered that the cord segments
are not all located anatomically within the vertebra of the
same name; This is especially so in the lumbar region. This
is important when the actual anatomical location of the lesion is being considered.

429

430

Collection of CSF requires general anaesthesia, thus the


major contraindication to CSF collection is any situation
where general anaesthesia is not considered safe. Performance of a spinal tap, either at the cisterna magna or lumbar
cistern, is dangerous where there is raised intracranial pressure. There is a tendency for the brain to herniate where increased intracranial pressure exists and the procedure should
not be performed. The methods of collection and laboratory
evaluation of CSF are covered elsewhere (Further Reading).

Serology

4th European FECAVA SCIVAC Congress

and has a role in other areas, for example, in evaluating the


tympanic bullae. Plain films are not particularly useful in the
evaluation of brain lesions, other than those that involve the
nasal cavity or the skull.
Myelography is required for the full evaluation of many
spinal lesions. Other contrast techniques such as epidurography or discography may be useful in selected cases.

Computed tomography and magnetic


resonance imaging

The evaluation of blood and CSF for viral antibodies has


some application in canine neurology. It is most useful in attempting to confirm a diagnosis of viral infection of the central nervous system.

The diagnosis of brain lesions has been transformed by


the use of central nervous system imaging. While the equipment required for computed tomography is limited in availability, its use is becoming more widespread in veterinary
medicine.

Microbiology

Electrodiagnostic testing

It can be difficult to culture organisms from the CSF even


in the face of fulminating infections, but attempts should be
made to isolate pathogens and determine antibiotic sensitivity in such cases. Failure to obtain a positive result does not
eliminate the possibility of CNS infection being present.
Blood cultures are useful in dogs with discospondylitis.

The various electrodiagnostic procedures, which are


used in dogs, are limited in their availability due to the requirement for expensive equipment. The indications for performance of the various techniques and the findings have
been reviewed (Further Reading). It is important to remember that none of these methods is a substitute for thorough
neurological evaluation, and the information that they provide only enhances the clinical data. Electromyography and
nerve conduction studies are most useful in peripheral neuropathies and some spinal diseases.

Radiology
Radiology is the major diagnostic tool utilized in neurology, particularly in the identification of spinal and brain lesions. The subject of neuroradiology is ever expanding as
new technology is employed. The reader is directed to other
sources for information regarding technique and interpretation (Further reading). There are certain particular points regarding radiology that warrant emphasis. Plain radiography
will provide the diagnosis in the majority of spinal disorders

Further reading
Wheeler SJ (Ed). Manual of Small Animal Neurology, 2nd edn, BSAVA
Publications, Cheltenham, UK. 1995.
Wheeler, SJ & Sharp, NJH. Small Animal Spinal Disorders: Diahnosis and
Surgery. Mosby, London 1994.

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431

Seizure: diagnosis and management


Simon J. Wheeler
BVSc, PhD, MRCVS Dipl ECVN, RCVS Specialist in Veterinary Neurology
The Royal Veterinary College, University of London - United Kingdom

DIAGNOSIS IN EPILEPSY

Seizures are a frequently encountered clinical sign in canine medicine. The diagnosis and management of the underlying disease process and the control of the clinical signs are
of prime importance. Most dogs with seizures are suffering
from idiopathic epilepsy, but there is no specific test fro this
condition and the diagnosis can only be reached by eliminating other causes. Appropriate therapy can bring good results in many patients.

The presentation of a dog with a history of recurrent


seizures requires a painstaking approach from the clinician.
The fundamental elements of the process are taking a careful history, performing a thorough clinical examination, including laboratory evaluations of blood and urine, and a
complete neurological examination.
The aim in any case is to reach a diagnosis both in terms
of the neurological localization and the underlying pathological process. It is a significant mistake to assume that all
dogs with recurrent seizures are idiopathic epileptics. In fact,
it is not particularly difficult to rule out physical causes of
seizures in most dogs by the judicious use of laboratory tests
and the performance of a careful neurological examination.
A sensible approach in a case is to attempt to rule out structural brain disease by the neurological examination and extracranial causes by the laboratory evaluations.
The breed and age of the patient may have a bearing on
the origin of the presenting problem. Idiopathic epilepsy
usually commences in dogs between six months and five
years old. The occurrence of a first seizure in a dog outside
this age range should alert the clinician to the possibility of
other diseases being present. Certain breeds are predisposed
to idiopathic epilepsy and in some others an inherited pattern
is evident.
Similarly, the brachycephalic breeds are relatively more
frequently affected by brain tumours than other types of
dogs. Other conditions that may cause seizures also may
have breed associations, for example, pug encephalitis. In
cats, idiopathic epilepsy is less common than in dogs.
Seizures in cats are more likely to be the result of structural
brain disease. In considering the history, the owner should
be questioned carefully with regard to the nature of the
episodes. It may be evident that some other body system is
involved. It should be possible to determine whether the
seizures match the typical pattern:
The prodromal phase where there is abnormal behaviour for a period of hours or more prior to the episode. Many
owners recognize this phenomenon. The aura which is usually a very short period of behavioral alteration immediately
prior to the episode. The ictus or fit, which usually consists
of typical rhythmic movements of the limbs, salivation,
chewing, defaecation and urination. This usually lasts for one
to two minutes. The post ictus where the dog again shows a
period of altered behaviour lasting a number of hours.

Seizures are a frequently encountered clinical sign in canine medicine. The diagnosis and management of the underlying disease process and the control of the clinical signs are
of prime importance. A seizure is the physical manifestation
of a paroxysmal electrical disturbance within the brain. It is
important to recognize that a seizure is not a disease entity
in itself. Rather, it is a clinical sign generally indicative of
cerebral dysfunction. The state of recurrent seizures is
termed epilepsy, but similarly this is not a specific disease
condition. The most frequently encountered situation in
which the clinician will see a dog with seizures is in idiopathic epilepsy. Where recurrent seizures become continuous seizures, status epilepticus exists.
The clinician may be presented with a dog in status
epilepticus, or may see an epileptic dog have a seizure. More
frequently, the owners will report a perceived seizure-like
episode although no abnormalities will be evident on evaluation of the patient. Causes of seizures may be classified as
being intracranial or extracranial in origin. Intracranial causes are further subdivided into those where a structural lesion
is identified, for example, encephalitis, tumour or traumatic
injury, and those where no such lesion is present, that is, idiopathic epilepsy. Extracranial causes of seizures include
toxicity, hepatic encephalopathy, hypoglycaemia or other
metabolic derangement.

Classification of causes of seizures


Intracranial

Structural lesion
No lesion - idiopathic

Extracranial

Toxic (Extra-dog)
Metabolic (Intra-dog)

MAIN PROGRAMME

Summary

432

Not all seizures follow this typical pattern and any deviation from it should be noted. The owner should be questioned whether there are any consistent features of the
seizure, particularly if any part of the body shows abnormal
activity as a precursor to the ictus, for example, muzzle
twitching or single limb movement. Such signs are strongly
suggestive of the presence of a focal origin of the seizure,
which indicates structural disease.
The neurological examination must be meticulous with
particular emphasis on cranial nerve function and conscious
proprioception. Neurological deficits that persist in the interictal period are indicative of a focal lesion being present, although the absence of any neurological abnormalities does
not rule out the possibility of structural brain disease being
present. A very small proportion of dogs with brain tumours
will have a normal interictal examination on first presentation. However, the disease usually progresses, leading to abnormal findings on subsequent evaluations.
Caution must be exercised in the interpretation of a neurological examination performed during the postictal phase,
as the findings are likely to be most unreliable. Transient
deficits may be present the day after a seizure in some dogs.
Following the neurological examination, all cases should
have a full blood and urine evaluation. This will help to identify any extracranial causes of the seizures. The collection of
cerebrospinal fluid (CSF) probably should be restricted to
cases where structural brain disease is suspected, although
here some discretion should be exercised if increased intracranial pressure could be present. Also, CSF should be collected where seizures are not controlled by anticonvulsant
medication at normal therapeutic concentrations.

4th European FECAVA SCIVAC Congress

ease, the acute crisis being triggered by some additional insult, for example, anaesthesia.
Hepatic encephalopathy results when blood is diverted
past the intrahepatic circulation via either an acquired or
congenital portosystemic shunt. The diagnosis is based on
laboratory evaluations, particularly the blood ammonia concentration and the sulphobromophthalein (BSP) test, and radiography.
Hypoglycaemia may cause seizures and may be seen in
a number of circumstances. Liver disease, sepsis and insulin
overdose may cause a decline in blood glucose, but the most
common cause is the presence of an insulin-secreting pancreatic tumour (insulinoma). The brain depends on a continuous supply of glucose for normal function as energy stores
are severely limited. Various clinical signs may be seen associated with hypoglycaemia, particularly seizures, weakness, depression, disorientation, visual disturbances and
ataxia. The signs are of a distinctly episodic nature.
The diagnosis is based on demonstrating low fasting
blood glucose concentrations, and the presence of clinical
signs related to these low glucose concentrations that are relieved by glucose administration. The measurement of blood
insulin, with calculation of the glucose:insulin ratio and the
glucagon tolerance test also are useful. If an insulinoma is
suspected, exploratory laparotomy and excision of the mass
is indicated. Surgical removal of the tumour may provide relief from signs for a number of years.
Various electrolyte disturbances also may cause seizures,
for example, hypocalcaemia.

Intracranial structural disorders


Causes of seizures
Extracranial disorders
Toxic insults and metabolic derangements are the most
frequent extracranial causes of seizures.
Many toxins cause seizures, for example, ethylene glycol, various insecticides and herbicides. The identification of
a toxic origin depends largely on historical information and
other physical manifestations of the toxicity, for example,
gastrointestinal upset. Laboratory evaluations may be useful
in some circumstances. Whilst dogs of any age may be poisoned, puppies seem particularly prone. Treatment is aimed
at removing and neutralizing the poison, and controlling the
seizures.
Hepatic encephalopathy is the primary metabolic disturbance causing neurological signs. The signs are often
episodic in nature, although the overall clinical impression is
of a forebrain disorder. The clinical signs include abnormal
behaviour, disorientation, head pressing, seizures, ataxia and
collapse. The episodes may be related to feeding and affected dogs may be in poor body condition. The neurological
disturbance arises due to the presence of toxins in the circulation, which are normally cleared by the liver. Occasional
cases of hepatic coma will be seen where there is a relatively acute picture of profound neurological deterioration. This
usually occurs in dogs where there is underlying hepatic dis-

It is highly unusual for seizures to be the lone manifestation of structural brain disease. In virtually all cases persistent interictal neurological deficits will be present, although
these may be relatively subtle. In forebrain tumours the neurological deficits may be restricted to mild deficits of conscious proprioception in the hindlimbs or a relative loss of
facial sensation. In cases of inflammatory CNS disease,
there often will be spinal hyperaesthesia or multifocal neurological deficits. Also, retinal lesions may be evident on
fundoscopic examination.
Various intracranial disease processes may lead to signs
of forebrain dysfunction in dogs. The most important are
neoplasia, inflammation and trauma. Less common causes
are degenerative conditions, for example, the lysosomal
storage diseases. Hydrocephalus is often implicated in causing forebrain signs, but this is unusual. Investigation of
such cases may reveal an inflammatory process that underlies the hydrocephalus.

Neoplasia
Tumours involving the brain may be primary or secondary, the latter being either metastatic or locally invasive, for example nasal adenocarcinoma. Confirmation of
the diagnosis depends largely on the use of computed tomography. The collection of CSF samples is somewhat

hazardous where there is raised intracranial pressure - a situation often encountered where a tumour is present - due to
the potential for brain herniation. Also, whilst abnormal
CSF findings correlate well with the presence of parenchymal CNS disease, they are relatively nonspecific and rarely
solely diagnostic.
Brain tumours have a primary effect on the nervous system by infiltrating and compressing neural structures. Also,
they have secondary effects, oedema and herniation, due to
the response of the brain to the presence of the tumour. The
secondary effects can be dramatic and account for the acute
signs seen in some cases as well as the early response to
treatment that also may occur.
Brain tumours have long been considered to be candidates only for symptomatic therapy, and until recently there
has been relatively little consideration of more aggressive
treatment in the veterinary literature. However, many centres now are adopting a more radical approach, employing
combinations of chemotherapy, surgery and radiotherapy.
Treatment of the animal with a brain tumour has two aims.
First, to control the potentially life-threatening situation
caused by raised intracranial pressure and seizures, and secondly, the removal or reduction in size of the tumour mass.
The prognosis for dogs with brain tumours is variable and
depends on a number of factors. These include the tumour
type and location, the severity of the secondary effects and
the neurological status of the animal at presentation. Animals
which have severe secondary effects that result in brain herniation carry a grim prognosis. This contrasts with those cases with mild neurological deficits that have a readily accessible tumour, which may be treated with a reasonable expectation of a good recovery. Following surgical removal and radiation therapy, some cases may live for several years.

Inflammatory brain diseases


Inflammatory disease of the CNS are prevalent in the
dog and various aetiological agent are incriminated. The
clinical signs are variable, dependent on the parts of the nervous system involved. The presence of multifocal signs is
strongly suggestive of inflammatory disease being present,
particularly where hyperaesthesia is a feature. The predominant clinical signs vary; there may be forebrain signs with
depression and seizures or cervical signs may be present,
particularly hyperaesthesia. Confirmation of a diagnosis of
inflammatory CNS disease may be problematical. Cerebrospinal fluid evaluation is the most useful test, although
this may be normal between bouts of what often is a episodic disease course. Electroencephalography and CT scanning
also may be useful.
Canine distemper virus infection of the CNS is an important cause of neurological disease in dogs. Seizures are a
frequent finding and are often of the chewing-gum type,
suggestive of involvement of the temporal cortex. The other
common sign is myoclonus where there are rhythmic, involuntary contractions of muscles. The prognosis for dogs with
canine distemper virus infections is poor. Acute forms of the
disease are terminal in many cases. The persistent neurological deficits seen in chronic encephalitis, particularly

433

seizures and myoclonus, may be tolerated for some time, although recovery does not occur.
Rabies causes various neurological signs, including behavioural changes in the early stages, pupillary dilation, hyperaesthesia, photophobia, disorientation, incoordination,
seizures and paralysis. The possibility of rabies infection being present must be considered in any dog with obscure neurological signs and the course of action is well defined.
Toxoplasma gondii infection may cause neurological
signs in dogs, most often spastic paralysis, ataxia and
seizures. Puppies are usually affected, although milder
forms of the disease may be seen in adult dogs.
Steroid responsive meningitis is relatively prevalent in
dogs. Clinical signs suggestive of cervical spinal disease often predominate, although depression and seizures feature.
The condition occurs in young dogs, often less than 2 years
old. Similar clinical signs are caused by a vasculitis of the
CNS. Specific syndromes have been recognised in the
Bernese mountain dog and the beagle, with other breeds occasionally affected. The prognosis for this condition is
guarded, despite some early response to treatment.
Granulomatous meningoencephalitis or reticulosis is a
frequent cause of multifocal CNS signs in dogs. Small and
toy breeds primarily are affected and the condition is most
often seen in dogs of 3 - 7 years old. The most common syndromes are suggestive of cerebral, brain stem or vestibular
involvement. Certain features such a seizures, blindness,
ataxia and cranial nerve deficits may be seen in isolation and
spinal cord involvement occurs. The course is usually chronic, but some dogs show a relatively rapid decline. Treatment
with corticosteroids may lead to a temporary remission, although the long term prognosis is poor.
Pug encephalitis, a syndrome similar to granulomatous
meningoencephalitis has been recognised in the pug breed.
Signs of forebrain involvement predominate although
brain-stem signs also occur. Typically, cases show seizures,
behavioural change, particularly aggression, circling and
depression.
Traumatic injury to the skull has the potential to cause
neurological damage either in association with or independent of skull fractures. Road accidents are the most common
inciting injury in dogs, although kicks or falls may be implicated. Trauma may lead to seizures in the acute phase following the injury. Alternatively, the dog may recover from the
acute episode, but seizures may occur several months later.

Idiopathic epilepsy
If the dog fits into the expected age range, and no cause
for the seizures and no persistent neurological deficits are
identified, the working diagnosis of idiopathic epilepsy is
established.
When to commence anticonvulsant therapy is a matter of
some controversy. Certainly, any dog which has more than
one seizure every three months, or which experiences clusters of seizures, should be treated. Seizures themselves precipitate more episodes via the mechanism of kindling. Thus,
it may be argued that all cases that suffer more than one
seizure should be treated.

MAIN PROGRAMME

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434

The anticonvulsant of choice in the dog is phenobarbitone


(2mg/kg per os, b.i.d.). After 10 days, the serum phenobarbitone concentration must be checked to ensure that it is within the therapeutic range of 15-45 g/ml. If it falls outwith this
range, the dose is adjusted accordingly. It is usual to aim for
a serum concentration of 25-35 g/ml in the first instance.
The serum concentrations should be monitored periodically
as alterations in drug metabolism occur with time and the
dogs response to a particular concentration will change.
Should the dog fail to be controlled, the phenobarbitone
concentration should be checked and the dose increased to
take it to the upper part of the therapeutic range, or even
above. Such therapy will control approximately 60-75% of
canine epileptics to an adequate degree. The prognosis for
the remainder is less good, as other anticonvulsant drugs
alone do not offer increased rates of control.
Primidone is the most frequently used alternative, but
very few dogs that have not been controlled by a therapeutic
dose of phenobarbitone will benefit from primidone, and it
carries a significant risk of liver toxicity. Thus, there is little
merit in the use of primidone in dogs either as the first choice
anticonvulsant or as a subsequent adjunct to phenobarbitone.
Dogs which fail to response to phenobarbitone therapy
alone may be given another drug in combination. Phenytoin
(which, due to its short half life is not suitable as a primary
anticonvulsant), valproic acid and chlorazepam all have been
tried although the clinical efficacy of any of these drugs is
unproven in dogs. These combinations also carry a significant
risk of hepatotoxicity, and thus should be avoided. Recently,
potassium bromide has reappeared as an adjunct anticonvulsant in dogs. Its use in combination with phenobarbitone reduces seizure frequency in some dogs that are resistant to
phenobarbitone alone. The recommended dose is 30-40
mg/kg given once daily. The half-life of KBr is prolonged in
dogs and it takes approximately four months to reach a steady
serum concentration. The therapeutic range is 700-2300 mg/l.
Owner education is an important aspect of the management of the idiopathic epileptic dog. Careful noting of the
frequency of occurrence and severity of the seizures will enable the clinician to discuss reasonable expectations for the
therapy and document the response. Control in idiopathic
epilepsy is often defined as being the doubling of the interictal period, that is, halving the frequency of seizures, and
eliminating clusters. This target should be defined for the
owner early in the discussions of the case, as over-ambitious
expectations are a common cause of owner dissatisfaction.
The importance of regular drug administration must be emphasised to the owner. An abrupt cessation of therapy may
lead to a precipitation of status epilepticus.
Where control is not achieved, repeated neurological
evaluations should be made. If there is any suspicion of a
structural brain lesion being present, further investigative
procedures such as computed tomography scanning and CSF
collection should be performed.
Attempts to wean dogs off therapy may be made if there
have been no seizures for a number of years, although this
process must be extremely gradual.

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Management of status epilepticus


The presentation of a dog in status epilepticus is an
emergency and the priority is to arrest the seizures rather
than to determine the aetiological diagnosis. This is best
achieved by the use of intravenous diazepam, which may be
given in relatively large doses (up to 1mg/kg i/v). If this fails
to control the situation, the use of phenobarbitone (2mg/kg
i/v) or pentobarbitone (4-20mg/kg i/v) is indicated. The patency of the airway should be ensured, if necessary by inserting an endotracheal tube. Hypoxia due to seizure activity and compromise of the airway will lead to cytotoxic brain
oedema and possibly raised intracranial pressure. Blood
should be collected for haematology and biochemistry and
the serum glucose concentration determined. Intravenous
fluids and dextrose, if appropriate, are administered. If the
cause of the seizures is believed to be toxic, the source
should be removed. Seizure control via parenteral agents
should continue until oral medication can be administered.
Only when the seizures are controlled and the postictal
phase has passed can any meaningful neurological evaluation be made.

Further reading
BIRCHARD, S.J. (1984) Surgical management of portosystemic shunts in
dogs and cats. Comp. Cont. Ed. Pract. Vet., 6, 795.
BUNCH, S.E., CASTLEMAN, W.L., BALDWIN, B.H., HORNBUCKLE,
W.E. & TENNANT, B.C. (1985) Effects of long term primidone and
phenytoin administration on canine hepatic function and morphology
Am J Vet Res 4-6, 105.
CHRISMAN, C.L. (1980) Postoperative results and complications of insulinomas in dogs. J Am Anim Hosp Assn, 16, 677.
CUDDON, P.A. & SMITH-MAXIE, L. (1984) Retciulosis of the central
nervous system in the dog. Compendium on Continuinq Education, 6,
223.
DRAZNER, F.H. (1983) Hepatic encephalopathy in the dog. In Current
Veterinary Therapy VIII (ed R.W. Kirk) W.B. Saunders Co.,
Philadelphia.
FARNBACH, G.C. (1984) Serum concentrations and efficacy of phenytoin,
phenobarbitone and primidone in canine epilepsy. JAVMA 184, 1117.
FREY, H.-H. & LOSCHER, W. (1985) Pharmokinetics of anti-epileptic
drugs in the dog: a review J vet Pharmacol Therap 8, 219.
JOHNSON, C.A., ARMSTRONG, P.J. & HAUPTMAN, J.G. (1987) Congenital portosystemic shunts in dogs: 46 cases (1979-1986). JAVMA
191, 1478-1483.
LECOUTUER, R.A. (1995) Seizures and Epilepsy. In Manual of Small Animal Neurology, 2nd edn. (Ed. S.J. Wheeler) BSAVA Publications, 95.
MERIC, S.M. (1988) Canine meningitis. J. Vet. Int. Med., 2, 2635.
OLIVER, J.E., HOERLEIN, B.F. & MAYHEW, I.G., eds. (1987) Veterinary Neurology. W.B.Saunders Co., Philadelphia.
SCHWARTZ-PORSCHE, D (1992) Management of refractory seizures. In
Current Veterinary Therapy Xi (eds R.W. Kirk & J. D Bonagura)
W.B. Saunders Co., Philadelphia.
SKERRITT, G.C. (1988) Canine epilepsy In Practice 10 (1), 27.
TURREL, J.M., FIKE, J.R., LeCOUTEUR, R.A. & HIGGINS, R.A. (1986)
Computed tomographic characteristics of primary brain tumours in
50 dogs. JAVMA 188, 851.
WHEELER, S.J. (1990) Seizures in dogs: Diagnosis and managment. Vet
International 1, 2.

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435

Cervical disc disease


Simon J. Wheeler

Summary
Cervical disc disease is a frequent disorder of dogs. Most
animals present with neck pain or mild neurological deficits.
Other conditions should be considered in differential diagnosis, particularly in young dogs. In view of the high number of patients with significant cord compression, many consider surgical therapy to be the treatment of choice.

creasing caudally. The C6/7 disc is rarely affected, with the


exception of Dobermans and other large breeds as part of
caudal cervical spondylomyelopathy. The C7/T1 disc occasionally herniates. It may be possible to determine the approximate location of the lesion in the cervical spine by
identifying the site of most pain on palpation.

DIAGNOSIS
Cervical disc disease is a frequent disorder of dogs.
Small breeds, particularly those with chondrodystrophoid
characteristics, are commonly affected, but the condition can
occur in any dog. Dachshunds, Beagles, Poodles, Spaniels,
Shih Tzus, Pekinese and Chihuahuas are most often affected. Dobermans suffer from cervical disc disease as part of
the syndrome of caudal cervical spondylomyelopathy. Most
patients are two years old or more, with a mean of six years.
Disc disease is so rare in dogs less than one year old that
other conditions must be considered first, for example, inflammatory CNS disease, atlantoaxial subluxation or discospondylitis. There is no sex predilection. (Denny 1978;
Dallman, Palettas & Bojrab 1992)

CLINICAL SIGNS
The predominant clinical sign is severe neck pain, which
may be acute or chronic. Often this is unremitting and unresponsive to medication. This is one of very few conditions
that causes dogs to scream spontaneously. Affected dogs
may be reluctant to eat unless the food is raised off the floor.
When examining the patient, it is usually not necessary to
flex and extend the neck to demonstrate pain. Generally, it is
adequate to palpate the spine and muscles of the neck where
the tension and pain are evident.
Neurological deficits related to cervical spinal cord compression may be seen; paresis or lameness in a thoracic limb
is the most frequent. However, any signs related to cervical
spinal cord compression can be seen, including hemiparesis
and tetraparesis. Nerve root signature (pain apparent on
palpation or traction of the limb) is another frequent finding.
Disc herniation follows degeneration of the disc. Most
occurrences are Hansen Type I extrusions. Hansen Type II
protrusions do occur, generally in larger breed dogs. The C2/3
disc is the most frequently involved, with the incidence de-

Radiography
The diagnosis is based on the clinical signs described
above. Confirmation is by radiographic demonstration of
narrowing of the intervertebral space and dorsal displacement of mineralised disc material.

Myelography
Myelography is required if the diagnosis is not apparent
on survey films or if there are multiple discs potentially involved. In some lateral or intraforaminal extrusions, lateral
and ventrodorsal projections of the myelogram may be normal; oblique views may reveal the offending disc. They are
also useful in locating on which side an asymmetrical extrusion lies.

CSF analysis
Analysis of CSF is useful to eliminate inflammatory disease. Results of CSF analysis may be abnormal in disc disease, but elevations of protein and cells are usually mild
(Thomson, Kornegay & Stevens 1989).
The differential diagnosis of cervical disc disease is given below. Be particularly cautious in diagnosing cervical
disc disease in dogs less than 2 years old or in aged animals.

DIFFERENTIAL DIAGNOSIS OF CERVICAL


DISC DISEASE
Young dogs with neck pain
Atlantoaxial subluxation
Inflammatory CNS disease

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436

Discospondylitis
Congenital disorders
Trauma
Neoplasia
Dogs without neck pain
Ischaemic myelopathy (generally large breeds)
Neoplasia (intramedullary)
Adult dogs with neck pain
Atlantoaxial subluxation
Discospondylitis
Neoplasia
Trauma
Inflammatory CNS disease

TREATMENT OPTIONS
Treatment may be non-surgical or surgical.

Non-surgical treatment
This entails cage rest and use of anti-inflammatory medications. It is appropriate to try this course with any patient,
unless marked neurological deficits are present. Generally,
NSAIDs are used. Diazepam or methocarbamol may also be
of benefit. Catastrophic worsening of the neurological status
with medical treatment, which is often seen in thoracolumbar disc disease, is rare in cervical discs. Neck pain in cervical disc disease seems to be less responsive to non-surgical
treatment than does pain from thoracolumbar disc disease.
Progression of signs or lack of response in one or two weeks
indicate treatment failure. A dog that is responding well to
non-surgical treatment should be kept rested for at least two
weeks after clinical signs have resolved. Recurrence of clinical signs after non-surgical treatment occurs in 36 per cent
of patients (Russell & Griffiths 1968).

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SURGERY
Fenestration
It is usual to fenestrate the discs from C2/3 to C5/6 as a routine. C6/7 is fenestrated if there is evidence of disease. Some
surgeons have questioned the value and desirability of such
widespread fenestration (Fingeroth 1989), but others believe
it is useful in treatment and prophylaxis. Some dogs will experience very rapid improve-ment following fenestration,
and some dogs with profound neurological disabilities recover after this procedure. A well-executed fenestration
should prevent further herniation of disc material into the
vertebral canal.

Ventral decompression
Accurate identification of the disc involved is necessary
before performing a ventral slot. Removal of the disc material from the vertebral canal provides the most rapid resolution of clinical signs. The best method of performing a ventral slot is by using powered instruments (Swaim 1974). It is
possible to perform the operation using a trephine and
rongeurs, but this is a poor alternative. Fenestration is a useful prophylactic procedure and can be performed on the other cervical discs at the time of the decompression (Russell &
Griffiths 1968).

Hemilaminectomy
Hemilaminectomy via a dorsolateral approach is indicated in a few patients. If there is a markedly asymmetrical
myelographic compression, there may be some doubt about
the diagnosis. Intraforaminal extrusions occur occasionally,
and these are best approached in this way (Felts & Prata
1983).

Surgical treatment
Indications for surgical treatment are:
Failure of non-surgical treatment.
Marked neurological deficits.
Progressive neurological deficits.
Unremitting pain.
Ventral fenestration or ventral decompression (ventral
slot) are the most frequently performed procedures. Rare
cases may require dorsal laminectomy or hemilaminectomy.
The choice between ventral fenestration and decompression
must be made on an individual patient basis. There are advantages and disadvantages to both procedures. General indications for ventral decompression are:
Presence of neurological deficits.
Myelographic evidence of spinal cord compression.
Failure of fenestration.
Clinicians who routinely perform myelography find that
most cervical disc patients come into one of the first two categories. Current opinion is that ventral decompression is the
optimal method of treatment.

COMPLICATIONS
The ventral surgical approach should have few complications if proper care is exercised. It is possible to damage
vital structures, particularly the recurrent laryngeal nerve.
Spinal cord damage during fenestration can occur if the
intervertebral space is explored recklessly. Neurological deterioration after fenestration may occur, probably where incorrect fenestration technique leads to disc material being
forced into the vertebral canal (Tomlinson 1985). Ventral decompression is more prone to complications than fenestration. Inaccurate identification of the disc involved, either on
radiographs or at surgery, is a mistake. Haemorrhage can be
problematical at various stages. Concurrent use of aspirin or
the presence of coagulopathy (particularly VW disease in
Dobermanns) increases the danger of severe haemorrhage.
One study reported death in 3 of 50 dogs undergoing
ventral decompression for cervical disc herniation (Clark
1986). One of the dogs died following uncontrollable haemorrhage from the venous plexus. The other two dogs experi-

4th European FECAVA SCIVAC Congress

PROGNOSIS
The prognosis for dogs with cervical disc herniations is
generally good. Non-surgically treated dogs may have a prolonged convalescent period (several weeks to months) and
have an approximately 36 per cent chance of recurrence of
signs (Russell 1968).

Fenestration
Following fenestration, recovery times vary. Denny
(1978) reported that 11 of 12 dogs with neck pain recovered,
although 30 per cent of these took an average of two weeks
for pain to subside. Of dogs with mild neurological deficits
(thoracic limb paresis), 12 of 17 (70 per cent) recovered in
an average of 3.6 weeks (maximum 8 weeks). Of those with
severe deficits (hemiparesis, tetraparesis, or tetraplegia), 6
of 10 (60 per cent) recovered in an average of 6 weeks.

Decompression
The results of ventral decompression have also been
analysed in a series of 54 patients (Seim & Prata 1982). In
dogs with neck pain and root signature (n=33), all dogs were
normal or improved within 48 hours of surgery, and all were
normal at 12 months after surgery. In dogs with moderate
deficits, but still able to walk (n=14), 12 were improved at 48

hours and all were normal at 12 months. Interestingly, two of


these dogs were worse (more severe pain or worse neurological status, or both) at 48 hours. Of dogs that were unable to
walk before surgery (n=7), 6 were improved at 48 hours and
6 were normal at 12 months, the remaining dog having some
residual deficits but being able to walk and free of pain.
In a comparison of dogs with cervical disc disease that
were able to walk prior to surgery, ventral decompression
provided superior results to fenestration in all neurological
parameters. Dogs recovered more rapidly and recovery rates
were higher following ventral decompression. Surgical complications was fewer in fenestration (Fry et al. 1991).
Thus, ventral decompression carries a more favourable
prognosis, both in terms of rate of recovery and time of convalescence. It is on this basis that we recommend ventral decompression for most dogs with cervical disc herniations.

CERVICAL DISC DISEASE IN CATS


Disc herniation is quite common in cats, particularly in the
cervical region, but clinical signs related to these lesions are
rare (Heavner 1971; Littlewood, Herrtage & Palmer 1984;
Wheeler, Clayton Jones & Wright 1985). Type II protrusions
are more frequent than Type I extrusions (King & Smith
1960). Diagnosis and treatment are as discussed above.

References
Clark, D.M. (1986) An analysis of intraoperative and early postoperative
mortality associated with cervical spinal decompressive surgery in
the dog. Journal of the American Animal Hospital Association 22,
739-744.
Dallman, M.J., Palettas, P. & Bojrab, M.J. (1992) Characteristics of dogs
admitted for treatment of cervical intervertebral disc disease: 105 cases. Journal of the American Veterinary Medical Association 200,
2009-2011.
Denny, H.R. (1978) The surgical treatment of cervical disc disease in the
dog: a review of 40 cases. Journal of Small Animal Practice 19, 251297.
Felts, J.F. & Prata, R.G. (1983) Cervical disc disease in the dog: intraforaminal and lateral extrusions. Journal of the American Animal
Hospital Association 19, 755-760.
Fingeroth, J.M. (1989) Fenestration: Pros and Cons. Problems in Veterinary
Medicine 1(3), 445-466.
Fry, T.R., Johnson, A.L., Hungerford, L. & Toombs, J. (1991) Surgical
treatment of cervical disc herniations in ambulatory dogs. Progress in
Veterinary Neurology 2, 165-173.
Heavner, J.E. (1971) Intervertebral disc syndrome in the cat. Journal of the
American Veterinary Medical Association 159, 425-427.
King, A.S. & Smith, R.N. (1960) Disc protrusions in the cat: distribution of
dorsal protrusions along the vertebral column. Veterinary Record 72,
335-337.
Littlewood, J.D., Herrtage, M.E. & Palmer, A.C. (1984) Intervertebral disc
protrusion in a cat. Journal of Small Animal Practice 25, 119-127.
Russell. S.W. & Griffiths, R.C. (1968) Recurrence of cervical disc syndrome in surgically and conservatively treated dogs. Journal of the
American Veterinary Medical Association 153, 1412-1416.
Seim, H.B. & Prata, R.G. (1982) Ventral decompression for the treatment
of cervical disk disease in the dog: a review of 54 cases. Journal of
the American Animal Hospital Association 18, 233-240.
Stauffer, J-L, Gleed, R.D., Short, C.E., Erb, H.N. & Schukken, Y.H. (1988)
Cardiac arrhythmias during anaesthesia for cervical decompression
in the dog. American Journal of Veterinary Research 49, 1143-1146.
Swaim, S.F. (1974) Ventral decompression of the cervical spinal cord in the

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enced acute bradycardia and hypotension and died during


the surgery. It is suggested that a syndrome of acute sympathetic blockade was responsible for these deaths. Anaesthetic complications are also seen following surgery for cervical disc disease (Stauffer et al. 1988). Arrhythmias (bradycardia and ventricular premature contractions) were seen in
31% of dogs; these were 2.5 times more common in cervical
disc surgery than thoracolumbar disc surgery. Two of 48
dogs died following cervical disc surgery in this study.
Neurological worsening occurs in some patients following ventral decompression. Extensive spinal cord manipulation may account for this, but it is not always clear why deterioration occurs, particularly in dogs with Type II disc
protrusions. Fortunately, this situation usually improves.
Vertebral instability may result if the slot is made too wide,
leading to subluxation and possible nerve root compression.
This will lead to marked deterioration in the condition of
the patient. If this does occur, the lesion should be managed
by distraction and fixation, as for a traumatic fracture or
subluxation.
Infection of the intervertebral space (discospondylitis)
can occur following either procedure if strict asepsis is not
observed. Swelling or oedema may be seen in the ventral
neck. Care with haemostasis and wound closure helps to
avoid this. Use of drains may be occasionally necessary.
Persistent neck pain occurs in many dogs that undergo fenestration, and may take up to a month to resolve. Following
ventral decompression, neck pain usually resolves within a
few days.

437

438
dog. Journal of the American Veterinary Medical Association 164,
491-495.
Tomlinson, J. (1985) Tetraparesis following cervical disk fenestration in
two dogs. Journal of the American Veterinary Medical Association
187, 76-77.

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Thomson, C.E., Kornegay, J.N. & Stevens, J.B. (1989) Canine intervertebral disc disease: Changes in the cerebrospinal fluid. Journal of Small
Animal Practice 30, 685-688.
Wheeler, S.J., Clayton Jones, D.G. & Wright, J.A. (1985) Myelography in
the cat. Journal of Small Animal Practice 26, 143-152.

4th European FECAVA SCIVAC Congress

439

Treatment of caudal cervical spondylomyelopathy


(Wobblers syndrome)
Simon J. Wheeler

Summary
The decision on the best way to treat each patient with
caudal cervical spondylomyelopathy (CCSM) is based on
the presenting history, neurological status, radiological
findings, and the owners expectations and their ability to undertake any necessary aftercare. Most dogs that show neurological deficits are surgical candidates. Many aspects of
surgery make this a difficult problem to deal with, and patients tend to have concurrent diseases. The surgical procedures are difficult and challenging, and the prognosis can be
uncertain.

The decision on the best way to treat each patient with


caudal cervical spondylomyelopathy (CCSM) is based on
the presenting history, neurological status, radiological findings, and the owners expectations and their ability to undertake any necessary aftercare. Most dogs that show neurological deficits are surgical candidates, but consideration will be
given here to non-surgical treatment.

The main factor governing the choice of surgical procedure is the appearance of the spinal cord on myelography,
particularly the traction view. Many lesions, when evaluated
by traction, show a combination of both static and dynamic
compression. A judgement must then be made as to which is
the major component. All of the surgical techniques are technically challenging.

Operative considerations
Because some dogs with CCSM deteriorate postoperatively for obscure reasons, methylprednisolone given prior
to dorsal or ventral decompression may be useful. It should
also be remembered that prolonged excessive extension of
the neck during surgery is undesirable. In addition, overzealous retraction of soft tissues during a ventral approach to the
neck can damage any of the nerves in the cervical region.
This can induce arrhythmia, Horners syndrome, or laryngeal paralysis, and retraction may also exacerbate bleeding
from the internal vertebral venous plexus (vertebral sinuses) by compressing the jugular veins.

NON-SURGICAL TREATMENT
Ventral decompression
Dogs that develop mild neurological deficits following
minor trauma may respond favourably to non-surgical
treatment. However, surgery should be considered as most
dogs will undergo a slow but steady deterioration (Denny,
Gibbs & Gaskell 1977). As surgery is elective for the majority of dogs with CCSM, a two to four week course of severe exercise reduction and use of a chest harness can usually be justified.

SURGERY
A large number of different surgical techniques have
been proposed for CCSM, with many of the authors claiming a 70 to 80 per cent success rate. The way to obtain the
best overall results is to consider three basic types of surgery
and to perform these for certain, relatively well defined indications. The three types of surgery are:
Ventral decompression.
Vertebral distraction/fusion.
Dorsal decompression.

Ventral decompression (ventral slot) is indicated primarily for the relief of static ventral lesions such as herniated disc material, although some surgeons also use it for dynamic lesions. In CCSM it may be complicated by ventral
osteophytosis or a misshapen C7 vertebra. Access to the
C6/7 site may be restricted, but this problem is minimized by
taking particular care with patient positioning.
In general, ventral decompression can only be considered to have been completed satisfactorily when the dura is
clearly visible in the depths of the slot. In CCSM, it is uncommon to identify an obvious mass of herniated disc material as seen with a classic type I disc extrusion in a chondrodystrophoid dog. Rather, the compression often appears
to be comprised of fibres of the anulus fibrosus infiltrated by
degenerate nuclear material.
To promote vertebral fusion at the surgical site, cancellous bone may be packed around the slot. Cancellous bone
enhances fusion, which usually occurs within eight weeks.
Without grafting, osseous fusion is delayed and occurs in
only about 50% of dogs, with the others presumably un-

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440

dergoing fibrous union. Thus some range of motion may be


preserved by not using a graft. This could be advantageous
in a dog where only one of two adjacent lesions is operated on with this technique, to try and lessen the potential for
the domino effect (Chambers et al. 1982; VanGundy 1988,
1989).

Vertebral distraction and fusion


The primary indication for distraction and fusion is the
presence of a dynamic component to the spinal cord compression. This can affect either the dorsal, the ventral, or
both aspects of the vertebral canal. Distraction has been attempted in the past using a number of different techniques,
but the two methods described here are by use of metal implants and bone cement, and a screw and washer technique.
An advantage of both of these distraction methods is that
they often provide rapid relief of cervical hyperaesthesia,
probably because of decompression of nerve roots at the distracted interspace. Both techniques have the potential for
implant failure, which can be catastrophic (Ellison, Seim &
Clemmons 1988; Bruecker, Seim & Blass 1989; McKee et
al. 1990). Other methods have been described, for example
the use of harrington rods (Walker 1989).

Metal implant and bone cement method


In the metal implant and bone cement technique, the cement renders revision of a surgical failure difficult, and also
raises the risk of implant infection. The dog should receive
an intravenous intraoperative antibiotic effective against
staphylococci (such as cephazolin 20 mg/kg, repeated every
1 to 2 hours during surgery). Despite potential disadvantages, metal implant and bone cement distraction is a well
tested technique with good long term follow up results. The
metal implants can either be Steinmann pins or bone screws,
but neither are suitable for distraction at more than one interspace (Ellison et al. 1988; VanGundy 1988).

4th European FECAVA SCIVAC Congress

treated (McKee et al. 1990).


The use of bone screws without washers may also reduce instability and so relieve dynamic spinal cord compression (Denny et al. 1977). It often results in fusion and
can also be used at multiple sites. The screw and washer
technique is preferable because the washer shares the load
of distraction, which should lower the risk of implant failure and enhance fusion.
Ventral fusion performed in horses with Wobbler syndrome, an equivalent condition to CCSM in dogs, can
cause new bone around the articular processes to regress
(Grant et al. 1985). Similarly, ventral fusion in dogs might
also relieve compression caused by dorsally located osteophytes, especially as ligamentum flavum has been shown to
atrophy in dogs following fusion (Bruecker, Seim & Blass
1989; McKee et al. 1990). Using a ventral approach in these
patients may avoid the morbidity problems sometimes associated with dorsal laminectomy in dogs.

Dorsal decompression
This technique would seem to be the logical treatment
for dogs with multiple sites of vertebral canal stenosis, and
for those with osteophytes in the region of the dorsal articular processes. It also provides an option in dogs with ventral
lesions at two or more intervertebral spaces.
Long term results of dorsal laminectomy appear to be
favourable (Lyman & Seim 1991), but several authors have
reported significant postoperative morbidity and deterioration in neurological status (Trotter et al. 1976; DeLahunta
1983; Trotter 1985; Walker et al. 1985). In a survey of perioperative mortality associated with cervical decompressive
surgery, dorsal laminectomy was associated with three times
the mortality rate of ventral decompression (Clark 1986).
Another potential complication is constrictive fibrosis at the
surgical site by so called laminectomy membranes. Dorsal
decompression should not cause the domino effect, as the
vertebrae do not usually fuse together. Fusion can be encouraged, if necessary, by screwing and then bone grafting
the dorsal articular processes.

Screw and washer


The screw and washer technique will probably benefit
from further modification to overcome its main problem of
vertebral endplate resorption, with subsequent collapse of
the distracted interspace. The collapse appears to be caused
by suboptimal washer design, so that all of the force resulting from distraction is concentrated on relatively small areas
of contact between the endplate and washer. However, the
temporary stability provided by the implants seems to allow
fusion to occur. This provides long term relief of spinal cord
compression, despite the subsequent collapse of the distracted site. The reported results are very good. A major advantage is that, unlike metal implant and cement distraction, the
screw and washer technique can be applied to more than one
site. The surgeon can therefore be more aggressive in dealing with a dog that has two adjacent lesions, one of which
could go on to cause a domino problem in the future if not

Ventral fenestration
Fenestration is not a suitable treatment for adult dogs
with CCSM. It has been proposed as an effective treatment
for young Dobermanns with this condition, although others
have reported mixed results (Mason 1979; Lincoln & Pettit
1985).

Dogs with multiple lesions


Between 15 and 50 per cent of Dobermanns present with
compression at both C5/6 and C6/7 intervertebral spaces
(Bruecker, Seim & Withrow 1989; McKee, Lavelle & Mason 1989). Dogs with more than one lesion may be treated
in one of several ways:

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PROGNOSIS
The seriousness of this condition is illustrated by the fact
that a quarter of dogs with CCSM in one series were euthanatized within six weeks of surgery for neurological problems (Seim 1986).
Dogs with more than one lesion generally have a worse
prognosis than dogs with single lesions, and dogs with
chronic tetraparesis have a very guarded prognosis. In contrast, dogs with a sudden onset of tetraparesis often respond
well to surgery if treated promptly. Most severely tetraparetic dogs that are going to recover will do so within six weeks
(Trotter 1985).
A useful general estimate of the likely outcome in this
condition has been provided by Seim (1986). For dogs with
single lesions, about 80 per cent of those that are walking
prior to surgery will have a favourable outcome. However,
but only about 40 per cent of those that cannot walk will recover. These success rates are some 20 per cent lower for
dogs with two lesions.
It is hoped that careful tailoring of the surgical procedure to the type of lesion may be able to improve on these
figures.

References
Bruecker, K.A., Seim, H.B. & Blass, C.E. (1989). Caudal cervical spondylomyelopathy: Decompression by linear traction and stabilization
with Steinmann pins and polymethylmethacrylate. Journal of the
American Animal Hospital Association 25, 677-683.
Chambers, J.N., Oliver, J.E. & Bjorling, D.E. (1986). Update on ventral decompression for caudal cervical disk herniation in Dobermann pinschers. Journal of the American Animal Hospital Association 22, 775-778.
Clark, D.M. (1986). An analysis of intraoperative and early postoperative
mortality associated with cervical spinal decompressive surgery in the
dog. Journal of the American Animal Hospital Association 22, 739-744.
DeLahunta, A. (1983) Veterinary Neuroanatomy and Clinical Neurology,
2nd edn. W.B. Saunders Co., Philadelphia, p204
Denny, H.R., Gibbs, C. & Gaskell, C.J. (1977). Cervical spondylopathy in
the dog - a review of thirty-five cases. Journal of Small Animal Practice 18, 117-132.
Ellison, G.W., Seim, H.B. & Clemmons, R.M. (1988). Distracted cervical
spinal fusion for management of caudal cervical spondylomyelopathy in large-breed dogs. Journal of the American Veterinary Medical
Association 193, 447-453.
Grant, B.D., Hoskinson, J.J., Barbee, D.D., Gavin, P.R., Sande, R.D. &
Bayly, W.M. (1985). Ventral stabilization for decompression of caudal cervical spinal cord compression in the horse. Proceedings of the
31st Annual Convention of the American Association of Equine Practitioners. pp75-103.
Lincoln, J.D. & Pettit, G.D. (1985). Evaluation of fenestration for treatment
of degenerative disc disease in the caudal cervical region of large
dogs. Veterinary Surgery 14, 240-246.
Lyman, R. & Seim, H.B. (1991). Viewpoint: Wobbler syndrome. Progress
in Veterinary Neurology, 2, 143-150.
Mason, T.A. (1979) Cervical vertebral instability (wobbler syndrome) in the
dog. Veterinary Record 104, 142-145.
McKee, W.M., Lavelle, R.B. & Mason, T.A. (1989). Vertebral stabilisation
for cervical spondylopathy using a screw and washer technique. Journal of Small Animal Practice 30, 337-342.
Seim, H.B. (1986). Caudocervical spondylomyelopathy. Proceedings of the
14th Annual Veterinary Surgical Forum. pp.72-78.
Trotter, E.J., deLahunta, A., Geary, J.C. & Brasmer, T.H. (1976). Caudal
cervical vertebral malformation-malarticulation in Great Danes and
Dobermann pinschers. Journal of the American Veterinary Medical
Association 168, 917-930.
Trotter, E.J. (1985). Canine wobbler syndrome. In Textbook of Small Animal Orthopaedics. (Eds. C. D. Newton & D. M. Nunamaker). J.B.
Lippincott Co., Philadelphia. pp.765-790.
Van Gundy, T.E. (1988) Disc-associated wobbler syndrome in the Dobermann pinscher. Veterinary Clinics of North America, Small Animal
Practice 18, 667-696.
Van Gundy, T.E. (1989). Canine wobbler syndrome. Part II. Treatment.
Compendium on Continuing Education for the Practicing Veterinarian 11, 269-284.
Walker, T.L. (1989) Use of Harrington rods in caudal cervical spondylomyelopathy. In Current Techniques in Small Animal Surgery (Ed.
M. J. Bojrab). Lea & Febiger, Philadelphia, 584-586.

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Perform surgery at both sites. This increases the overall


complication rate, and is contraindicated for the metal implant and bone cement technique of distraction because of
the high risk of implant failure. Screw and washer distraction can be used on two adjacent lesions without increasing the complication rate.
Try to determine which lesion is more significant, perhaps
with the help of an extension view during myelography,
and then correct this lesion in isolation. Correcting the
worst lesion might be successful with ventral decompression, but distraction at only one site may well exacerbate
the adjacent lesion (domino effect), and should be undertaken with great circumspection. If only one of two lesions is corrected, dogs that deteriorate or do not respond
after surgery should undergo repeat myelography within
seven days.
Perform a continuous dorsal decompression over both
sites. This approach avoids the risk of a domino lesion, but
can cause significant morbidity.

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4th European FECAVA SCIVAC Congress

443

Surgery of the spine


Simon J. Wheeler

Summary
Surgical treatment is required for many diseases of the
spine in dogs and cats. The surgeon must possess basic surgical skills, and must be familiar with the special techniques
and instrumentation required for neurosurgery. Diseases
best treated by surgical means include disc herniation, atlantoaxial subluxation, trauma, lumbosacral disease, neoplasia and Wobbler syndrome. The presence of neural structures complicates the surgical procedures and surgeons must
be fully aware of these structures when performing surgery.
It is the authors view that neurosurgery is best performed by
persons specifically trained in this regard, and not be considered an extension of orthopaedic surgery.

Ventral fenestration or ventral decompression (ventral


slot) are the most frequently performed procedures.
The choice between ventral fenestration and decompression is made on an individual patient basis. There are advantages and disadvantages to both procedure. General indications for ventral decompression are:
Presence of neurological deficits.
Myelographic evidence of spinal cord compression.
Failure of fenestration.
Clinicians who routinely perform myelography find that
most cervical disc patients come into one of the first two categories. Current opinion is that ventral decompression is the
optimal method of treatment.

Thoracolumbar disc herniation


Surgical treatment is required for many diseases of the
spine in dogs and cats. The surgeon must possess basic surgical skills, and must be familiar with the special techniques
and instrumentation required for neurosurgery. Further details of the techniques are found in Small Animal Spinal Disorders: Diagnosis and Surgery, by S. J. Wheeler & N. J. H.
Sharp, Mosby-Wolfe, London.

INTERVERTEBRAL DISC DISEASE


Intervertebral disc disease is a frequent disorder of dogs
(but is rarely a cause of clinical signs in cats). Most clinicians
are familiar with the diagnosis of the condition, but there is
some confusion about the most appropriate methods of treatment. While there is some controversy regarding certain
regimes, particularly involving unconventional methods,
there is a large amount of data in the veterinary literature concerning the disease. Analysis of these data allows certain
guidelines to be drawn, which can be used in selecting the
most appropriate method of treatment for individual patients.

Cervical Disc Herniation


Indications for surgical treatment are:
Failure of non-surgical treatment
Marked neurological deficits
Progressive neurological deficits
Unremitting pain.

Hemilaminectomy is the treatment of choice for most


dogs with neurological deficits of grade 2 or more. Decompression should be performed as soon as possible after the
onset of neurological signs, especially for dogs with severe
deficits. This is crucial in animals with depressed or absent
deep pain sensation. Those with grade 5 neurological deficits
should be regarded as emergencies, requiring surgery within
24 hours to have the best chance for a successful outcome.
Reasonable results can still be obtained if surgery is performed within 48 hours, but after three days the results are
dismal. The rate of recovery is also faster after hemilaminectomy than after the other two methods of treatment, and there
is less likelihood of any residual neurological deficits after
surgical decompression of the spinal cord.
Specific recommendations for hemilaminectomy include:
Grade 5 lesions of less than 48 hours duration.
Deterioration or lack of response to other types of therapy.
Recurrence after previous treatment.
Myelographic evidence of spinal cord compression.
Presence of LMN deficits.
Hemilaminectomy without fenestration can result in a recurrence rate as high as 27 per cent, so concomitant disc fenestration is recommended. The ideal treatment for disc herniation is to combine decompression of the spinal cord with fenestration of all high risk discs (T11/12 to L4/5 inclusive). This
would require considerable dissection if undertaken from a
dorsolateral approach, and so a compromise is usually
reached entailing fenestration of the affected disc and the one
on either side (where possible including T12/13, T13/L1 and L1/2).

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BVSc, PhD, MRCVS Dipl ECVN, RCVS Specialist in Veterinary Neurology


The Royal Veterinary College, University of London - United Kingdom

4th European FECAVA SCIVAC Congress

445

External and middle ear surgery


Richard A.S. White

Summary
This lecture looks at the common causes of external ear
diseases in both the dog and the cat and emphasises the role
of medical management in the first instance. The indications
for surgical intervention are reviewed, the various techniques for external ear surgery are explained and some of
the common causes of failure are presented.
The aetiology of middle ear problems in the dog differs
considerably to that in the cat and the disease is compared
in the two species. Middle ear surgery in the dog is predominantly the result of extension from external ear disease and
can often be managed medically. Failing which total ear
canal ablation with bulla curettage or lateral osteotomy of
the bulla is indicated and for the dog carries an excellent
prognosis. In the cat, middle ear disease is more likely to result from ascending infection or neoplastic disease. Ventral
bulla osteotomy is more frequently practiced for the cat and
the prognosis tends to be more guared because of neoplastic
disease.
This presentation will cover all of the common surgical
procedures for external and middle ear disease.

Introduction
The ear is composed of structures at three levels - the
outer, middle and inner ear. Most surgically-related conditions are a consequence of disease that involves the outer ear
which is formed around the auricular and scutiform cartilages most distally. The auricular cartilage is subdivided into several components (scapha, helix, anthelix, tragus, antitragus) and forms the pinna dorsally and the cone-shaped
vertical canal below. Below the auricular cartilage the horizontal component of the external ear is formed by the annular cartilage which is attached to the external auditory
prominence.

Aetiologies of ear disease


The concept of initiating, predisposing and perpetuating
aetiologies has been applied to ear disease for more than
decade and has provided a useful basis for analysing the
causes of otitis externa.
Initiating causes: include such causes as foreign bodies

and parasites which are capable of promoting a response


even within the normal ear. Particularly important in this
category are generalised dermatoses since the ear is simply
a specialised part of the skin are a frequent underlying cause
of otitis externa.
Predisposing causes: these can add the the problem
without actually being responsible for starting it. The conformational anomalies of the Spaniel ear is good example of
such a cause. The shape of the ear reduces the efficiency of
the normal ventilatory system and whilst this rarely, if ever,
actually causes the original problem it will exacerbate the inflammatory changes once established.
Perpetuating causes: this category includes the presence
of micro-organisms such as bacteria and yeasts which are capable of prolonging and maintaining the disease process once
an inflammatory change is under way. Once again, they are
unlikely to initiate the problem in the first instance.

Diagnosis
When investigating the chronic ear patient to identify the
underlying aetiology the clinician should always try to consider the patient as a whole and not the ears in isolation. It
should always be borne in mind that the ears are simply part
of the integument - albeit a very specialised part. The external meatus provides the most frictional, most humid and
most enclosed dermal environment possible (others include
the interdigital spaces, the groin and the axillae). Initial inspection should take note of the condition of the pinna, the
external auditory meatus and the tympanic membrane by
means of otoscopy, microbiology. Where disease involving
the middle ear is supected myringotomy may be complemented with radiography although this imaging technique is
useful only in advanced cases. Modern scanning techniques
(CT, MRI) are far more sensitive in determining if disease
exists within the middle ear chamber.. More sophisticated
electrodiagnostic techniques such as brain stem auditory
evoked potential should be reserved for investigation of inner ear disease.

Medical management
Where specific initiating causes can be directly identified (eg: parasites) appropriate therapy can be instigated. In

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B Vet Med, PhD, DSAS, DVR, FRCVS, Dipl ACVS, Dipl ECVS
University of Cambridge - United Kingdom

446

many instances, however, it may not be possible to identify


a specific initiator and treatment follows an empirical path
using cerumen-dissolving agents, anti-inflammatories and
topical antibiotic therapy to manage symptoms rather than
causes. Often with less than satisfactory results. In very high
proportion of chronic otitis externa cases the initiating aetiology will be found to be associated with a dermatosis and it
is not surprising that the ears will be the first indicators of
skin disease. Identification and management of an underlying dermatological problem should therefore be a primary
aim when investigating and managing the chronic ear.

THE EAR - SURGERY FOR CHRONIC


OTITIS
Introduction
The value of surgical intervention to improve ventilation
/ drainage in the management of chronic ear disease has long
been recognised. More than 150 years ago cutting off the
pinna was recommended for dogs that suffered with otitis
externa. Improving the ventilation of the outer ear by incising the lateral wall of the vertical canal was described in
1853 whilst this concept was later improved by removing a
section of cartilage from the lateral wall to prevent the opening from closing over. The lateral wall resection procedure
which later include a ventrally reflected drainage board
was described in the 1930s and provides the basis for the
widely practised lateral wall resection. More recent innovations include the total ear canal ablation which has revolutionised the management of the end stage ear.

4th European FECAVA SCIVAC Congress

the circumferenceis removed in a strip which is folded ventrally. The incisions are continued as far ventrally as the scutiform cartilage (horizontal canal opening). The reflected
cartilage is anchored in position with simple interrupted
monofilament sutures. The edges of the skin are sutured in a
similar pattern to the remaining portion of the vertical canal.
Any excess reflected tragus is amputated.

Prognosis
Despite the widespread use of the LWR for otitis externa
there is no doubt that this procedure alone does not provide
a complete solution to all chronic ear diseases. Some reviews have indicated that as many as 40% of LWRs end in
failure or continuing ear disease. The reasons for LWR failure include: poor surgical technique, poor patient selection,
failure to control the underlying cause of the otitis externa
(usually a dermatological problem) and unremiting middle
ear disease.

Vertical canal ablation


Several other surgical procedures have been developed
in an effort to resolve the nonresponsive cases including vertical canal ablation (VCA) designed to remove the entire
vertical canal to manage irreversible changes which are not
amenable to LWR. VCA was later modified to include a ventral drainage board.

Indications
Lateral wall resection
Indications
LWR is indicated where improved ventilation and / or
drainage will reduce for the need for repeated medical management of persistent otitis externa. Removal of the auricular cartilage will in some cases also minimise the opportunity for frictional dermatoses. It cannot be stressed strongly
enough that many persistent cases of otitis externa are the result of an underlying dermatological problem and attention
should be paid to this aspect of the problem before surgical
management is considered.

Technique
The patient is positioned in lateral recumbency and two
parallel incisions made over the vertical canal from the auditory meatus as far as the level of the horizontal canal. This
strip of skin is reflected dorsally but usually left attached to
the dorsal aspect of the tragus. The auricular cartilage is dissected free of the overlying muscle on its lateral aspect. Any
blood vessels are ligated or dealt with using diathermy. Two
vertical incisions are made through the tragus (ie: lateral aspect of the vertical canal) such that approximately 40% of

VCA is indicated in the management of diseases of the


external ear which are confined to the vertical canal - ie: the
horizontal canal is normal and unaffected by the disease. In
fact this is a rather unusual situation. In most instances of external ear disease the changes are not limited solely to the
vertical canal in which case total ear canal ablation may be
a more suitable alternative.

Technique
The approach is similar to that for LWR however, the
whole circumference of the vertical canal is dissected free of
the surrounding soft tissues. The auricular cartilage is amputated from the base of the scapha to the level of the horizontal canal. A portion of the tragus is preserved to create a
drainage board as for LWR below the opening to the horizontal canal. The resulting dead space above the canal is
closed.

Total ear canal ablation


The need for a procedure to deal with changes that involved the entire aural canal (ie: vertical and horizontal) was
perceived by Youatt as early as 1871 but received little at-

4th European FECAVA SCIVAC Congress

Indications
1. Chronic proliferative changes in the ear canal.
2. Complete ear canal stenosis / para-aural abscessation.
3. Unremiting middle ear disease.
4. Neoplastic disease of the ear canal or bulla.
Most of the dogs requiring this type of surgery will
have undergone prolonged treatment previously and many
will have had unsuccessful surgical interventions. The
most frequently presented breeds include Spaniels, German Shepherds, Labradors and Old English Sheepdogs.
Often the ear disease represents the tip of a dermatological iceberg and ablation may be considered as a salvage
procedure in such cases.

Technique
The procedure includes the following steps:
Mobilisation of the canal by incising around the opening
of the vertical canal and then bluntly dissecting the auricular
muscles away from the ear canal until the lateral aspect of
the bulla is reached. The facial nerve emerging from the stylomastoid foramen and running ventrally to the canal is isolated and retracted from the field of dissection. The ear canal
is amputated at the OEAP. The integumental residue lining
the OEAP and bulla is carefully stripped away until a clean
boney surface is left. In some cases of extensive middle ear
disease lateral bulla osteotomy may be performed to improve access to the tympanic cavity. The lateral aspect of the
bulla is removed with rongeurs and debris within the bulla
gently irrigated away. The soft tissues are closed over the

bulla placing taking care to minimise the potential for dead


space.If indicated, a Penrose drain is placed from the bulla
medial to the parotid salivary gland and exiting
ventrally.The skin is closed in T or inverted L shape.

Complications
A number of complications of TECA (LBO) have been
reported including facial nerve injury - neuropraxia - paralysis, wound dehiscion, haemorrhage from the retroglenoid
vein, vestibular signs and chronic sinus tract development.
Some early reports indicated levels of complication of
80+%. However with careful dissection the incidence of serious complications should be less than 10%.

Prognosis
With care the procedure can be extremely sucessful in resolving the most recalcitrant of chronic ear diseases and
greater than 90% success rates have been reported.

General management of ear surgeries


Whatever the surgical procedure contemplated there are
several important general principles that can be applied:
Surgical asepsis: it is extremely difficult if not impossible to ensure that the surgical site can be prepared to a surgically-aseptic standard. Rather than pursue endless lavage of
the external ear it is probably preferrable to accept that aural
surgery is a contaminated procedure. Hence, there is a strong
rationale for perioperative antibiotic therapy. The postoperative stategy for ongoing therapy should be determined once
the degree of surgical contamination has been assessed.
Analgesia: surgery involving the ear is frequently a
painful procedure and consideration should always be given
to appropriate (often opioid analgesia) in cobination with extended non-sterodial anti-inflammatory therapy.
Self trauma: because ear surgery may be uncomfortable
there is a high risk of self trauma and premature wound disruption. Bandages should be avoided since there is a possibility of airway obstruction and suitable collars should be
used to protect the wounds.

MAIN PROGRAMME

tention until this century. Initially workers advocated removal of the auricular and annular cartilages up to the osseous external auditory prominence (OEAP). This failed to
resolve any middle ear disease andresulted in an integumental residue being left in the bulla and sinus tracts frequently
developed subsequently. Other procedures included the ventral approach to the bulla for the management of middle ear
disease. The classical ventral approach did not meet with
consistent success and long term relief of the infection. Most
recently the concept of total ear canal ablation has been
combined with lateral bulla osteotomy [TECA / LBO].

447

4th European FECAVA SCIVAC Congress

451

Guided transcutaneous fine needle biopsy (FNB)


in abdominal and pelvic disorders
Mario Caniatti
Med Vet, Istituto di Anatomia Patologica Veterinaria e Patologia Aviare, Universit di Milano - Italy

Skill and experience with the technique are important


owing to the fact that cellular material is a prerequisite for
diagnosis. A minimum amount of gel should be used during
ultrasound-guided FNB because it can contaminate the sample and cause cytological artifacts. At least two ot three
smears should be collected.
Unsuitable specimens are commonly caused by the failure to reach the lesion (obese patient, deep seated lesion, single and small-sized lesion...), or because of the firmness of
the lesion (e.g. inflammatory fibrotic reaction, well differentiated spindle-cell tumors, desmoplastic epithelial tumors...).
Hence, the operator must become familiar with the macroscopic appearance of an adequate cellular slide. A rapid microscopic assessment of the sample can also be attained using Romanowsky-type fast stains (e.g.: Hemacolor, DiffQuik, DipStat...). If the cellularity of the sample appears
too scanty for cytodiagnosis, the procedure should be immediately repeated.

Necrosis, hemorrhage or inflammation that may accompany malignancy, can cause false negative diagnosis of tumors in spite of good quality specimens. In these cases, multiple aspirations can help to make the right diagnosis.
Based on the above mentioned causes of inadequacy or
false negative specimens, the rate of false negative aspirate may vary, and an open biopsy via laparotomy may be
necessary for definitve diagnosis. Impression smears or
FNB can be made during surgery, although in this istance
an incisional or excisional biopsy should be always preferred.
The pitfalls in cytomorphologic interpretation, which in
a percentage of neoplastic lesions can cause negative or
suspicious reports of FNB, can be avoided with increased
practical experience of cytopathologists.
The increasing use of the sonographic guidance should
help in this task.
The main purposes of FNB of abdominal and pelvic organs are:
1) Identification of space-occupying lesions (benign-malignant; primary-metastatic)
2) Staging cancer
3) Treating benign cystic lesions. FNA biopsy can be
therapeutic in cases of benign cystic lesions, which are often
completely collapsed by aspiration. In these cases, both diagnosis and treatment are ensured by the aspiration.
4) Evaluation of diffuse disorders of the liver, spleen and
prostate. In some cases of inflammatory process or metabolic disorder, particularly in liver pathology, histologic specimens are best suitable for accurate diagnosis
The main contraindication to transcutaneous abdominal
and pelvic FNB are:
1) Uncorrectable bleeding disorder
2) Lack of a safe biopsy path to the target (e.g. through a
large vessel such as the aorta or the vena cava). Occasionally it is not possible to avoid passing a thin-gauge needle (21to 22- gauge) through a variety of viscera such as the bowel
loops, stomac, liver; however it does not appear that this
procedure increases the risk of infection or hemorrhage. In
fact we should consider that the size of the needle is smaller
than surgical sutures used in these organs.

SPECIALIST/INTERACTIVE PROGRAMME

Clinical signs associated with abdominal, pelvic and


retroperitoneal disorders are often vague and related to the
location, type and size of the lesion. In some cases (e.g neoplasia, infection...), extra-abdominal abnormalities such as
periferal lymphadenopathy can help to reach the diagnosis,
while in many other instances only a bioptic procedure can
lead to a definitve diagnosis.
Fine needle biopsy (FNB) is a well established diagnostic method, which has expanded in recent years to include
sampling of organs and masses in virtually any body site,
whether superficial or deep, palpable or nonpalpable. The
success of FNB is in part due to percutaneous needle biopsy
under sonographic guidance, which has emerged as one of
the most important recent advance in veterinary diagnostic
imaging. It gives the opportunity to assess and biopsy deep
seated organs and tissues without the need of surgery and at
a very low cost.
FNB can be obtained by conventional fine needle aspiration technique (FNA) or by nonaspiration technique termed
cytopuncture or fine needle capillary (FNC) sampling. In
human beings, some reports indicate FNA superior to FNC,
some reports indicate FNC superior to FNA and some others
indicate that there are no differences, suggesting that the technique of FNB (aspiration/nonaspiration) employed for cytodiagnosis can be left to the personal preference of the operator.

452

Fine needle-track seeding of neoplasia is considered a


very rare complication (1 out of 20.000 patients in a study in
human beings)
Many neoplastic (primary or metastatic) and non-neoplastic (inflammatory or degenerative) conditions of the abdomen can cause effusion. Cancer is a common cause of effusion, although not all the patients with abdominal cancer
develop effusion and not all the effusions in patients with
cancer are caused by cancer. It is very easy to collect abdominal fluid, much easier and safe than collect an adequate
specimen from an abdominal mass. Therefore, the patient
with an abdominal disorder should be thoroughly examined
to identify an even mild effusion that must be sampled and
cytologically examined. In this way, many inflammatory and
neoplastic conditions can be diagnosed and useful information for prognosis and treatment can be recorded.
We must be aware that cytology can not replace histopathologic examination, although, very often, a good cyto-

4th European FECAVA SCIVAC Congress

logic sample can help to determine the inflammatory or neoplastic nature of the lesion. Inflammatory lesions can be subclassified as neutrophilic, eosinophilic, macrophagic, lymphocytic or mixed (e.g. mixed neutrophilic-macrophagic),
and a specific etiology can often be determined. Neoplasia
can be classified by cytology as epithelial, spindle-cell
(mostly mesenchymal) and round-cell tumor. Based on these
criteria, most tumors can be easily classified or sublclassified (e.g lymphomas), while others do not exhibit enough
characteristics to be classified by cell type. Based on criteria of malignancy, tumors can be defined as benign or malignant, although some malignant tumors show little criteria
of malignancy.
False positive diagnosis of neoplasia must be avoided
by cytology, therefore extreme caution should be used in
making a cytological diagnosis of neoplasia in cases where
the smear is characterized by a mixed population of inflammatory and non-inflammatory (reactive or neoplastic)
cells.

Ways to approach to selected abdominal diseases


Roberto A. Santilli
Med Vet, Private Practitioner, Samarate, Varese - Italy

Introduction
Percutaneous ultrasound-guided biopsy have a particular
importance in the diagnostic work-up of abdominal diseases.
Ultrasound permits to discover the abdominal organ with
disease particularly when focal lesions are present due to the
difference in acoustic impedance. Ultrasound does not permit to exclude diseases with diffuse infiltration of abdominal organs that could appear with normal echotexture. Ultrasound has a very low specificity in the differentiation of inflammatory vs. neoplastic processes, and in the evaluation of
malignancy of a particular neoplasm.
Percutaneous biopsy include fine needle aspiration biopsy (21 - 22 gauge) for citological examination, and tissue
core biopsy with tru-cut of 18 gauge, for histological examination.
Contraindications for biopsy include coagulation disorders, hypoalbuminemia, and ascitis, although human reports
demonstrated no increases in complications with peritoneal
fluid.
Different opinions exist as for the local tumour seeding
secondary to percutaneous biopsy. A human medicine study
demonstrated, on a sample of 800 biopsy in 19 years, no local tumour seeding following percutaneous biopsy; another

study showed malignant cells in peritoneal lavage fluid in


75% of patients with pancreatic adenocarcinoma that underwent a pre-surgical percutaneous biopsy, while only in 19%
of patients with the same disease that did not underwent the
biopsy. S.J. Withrow has some reserves about local tumour
seeding and he does suggest to perform percutaneous biopsy only for abdominal mass in which citological diagnosis
will permit a palliative treatment, if surgery is an option he
suggests to obtain post-surgical histological samples.
Complications during percutaneous biopsy include minor parenchimal haemorrhages, major cavitary of retroperitoneal haemorrhages, and biliary peritonitis or death. The incidence of these complication varies between 0% for fine
needle aspiration and 2,7-5,6% for core biopsy.
Fine needle aspiration technique is less expensive, easier, quicker with less complications than tissue core biopsy
one. Fine needle citological samples can be obtain throughout aspiration or infissione with spine needle or special
needle prepared for ultrasound-guided biopsy. Tissue core
needle biopsy is performed throughout tru-cut set on a biopsy device (Biopty, Pro-mag or disposable), these devices
permit an automated and pre-set shot which reduces
parenchimal damages. Tissue core samples are about 1 cm
long with a diameter of 2 mm. They must be prepared de-

4th European FECAVA SCIVAC Congress

453

the inability to follow the needle tip since the beginning, so


it is suggested to expertise operators.
Needle guided technique is easier particularly for inexpert because it permit the visualisation of the tip all during
its course, and therefore it limits complications.
Following biopsy the underlining area must be carefully
scanned for 10 minutes and 4 - 6 hours later to look for minor or major haemorrhages. If haemorrhages occur compressive bandage, transfusion or reparative laparatomy are
indicated. A remote possibility of biliary peritonitis does exist, particularly after liver biopsy in patients with cholangitis
or post-hepatic icterus, in case of gallbladder or major biliary tract perforations. Clinical signs of biliary peritonitis
include vomiting, icterus and abdominal pain 24 to 36 hours
post-biopsy. Treatment of biliary peritonitis is surgical peritoneal lavage.

Technique

Personal experience

Before any tissue-core biopsy the coagulation profile, the


packed cells volume and total solids must be obtained from
the patient. The latter two parameters must be repeated 4 to
6 hours later to evaluate haemorrhage occurrence.
Sedation is rarely needed during fine needle aspiration
technique, while it is always indicate during tissue-core
biopsy to prevent movements of the animal during the procedure that could cause laceration of the organ. Anesthesiological protocols more utilised both for cats and dogs include the association of diazepam (0,5 mg/kg) and ketamine
chloridrate (10 mg/kg) I.V.
The animal must be shaved and scrub with alcohol and
betadine, a complete ultrasound examination must be repeated before the biopsy particularly to find the right area
for the sampling, avoiding vascolarized areas and vital structures. Focal lesions apart, liver biopsy must be done at the
left subcostal region, kidney biopsy at the cortical zone of
caudal pole of the left kidney.
There are two way to perform ultrasound-guided percutaneous biopsy: free hand and with needle guided. With the
former the operator has free movement with less risks of laceration of the tissues, he can obtain different angle between
the transducers and the needle to better visualised the tip
(45 angle). The major problem with this technique is often

During 1996 and 1997 the author performed 59 tissue


core biopsy (28 liver, 12 kidney, 7 prostate, 4 digiunal linfonodes, 1 uterus, 6 mediastinal mass) and 172 fine needle
biopsy (78 liver, 31 abdominal nodes, 24 spleen, 17 prostate,
12 stomach or small intestine, and 10 kidney)
Accuracy of citological diagnosis with fine needle biopsy was 77%, while histological diagnosis with tissue core 96%.
Complications with fine needle aspiration were around
0,58% with one case of biliary peritonitis in a suppurative
cholangitis resolved with immediate peritoneal lavage. The
incidence of complications during tissue core biopsy was
around 3,38% with one case of major retroperitoneal haemorrhages resolved with compressive bandage and transfusion and one case of bladder haemorrhage self-limiting.

Conclusions
Ultrasound-guided percutaneous biopsy is an important
diagnostic tool, its use and performing by expertise operators permit to limit complications and to obtain diagnostic
samples both for citological and histological examination
that allow to establish a correct treatment and to formulate a
precise prognosis.

SPECIALIST/INTERACTIVE PROGRAMME

pending on the type of histological examination in 10%


buffered formalin for light microscopy, 2% buffered glutaraldehyde for ultra-structural electron microscopy and
with Michels fixative for immunocytochemistry or immunofluorescence. It is particularly important to include a
coltural examination both for aerobes and anaerobes if a septic process is suspected.
The choice between the two types of biopsy depend on
the organ, and on the disease suspected. Tissue core biopsy
are indicated in liver, kidney, prostate, linfonodes or mediastinal diseases; fine needle biopsy is indicated in spleen,
pancreas, lung, prostate and liver diseases. Citological examination of the kidney is rarely diagnostic.
Accuracy of percutaneous biopsy is about 84% for fine
needle technique, while about 97% for tissue core with some
variations depending on the organ.

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455

Intramedullary interlocking nailing:


a new technique in small animal orthopedics
Daniele Cotto
Med Vet, Private Practitioner, Torino - Italy

Gian Luca Rovesti

Summary
Intramedullary interlocking nailing expanded for a terrific extent the indications for classic intramedullary nailing. In the past few decades different kinds of nails were developed for human orthopedic surgery, whereas the systems
available for veterinary orthopedics are few and they need
further experimental and clinical trials. The common feature
of all these nails is to be locked in the medullary canal. The
most common interlocking technique is to put screws
through some holes in the nail perpendicular to its longer
axis. When the interlocking is performed both proximally
and distally to the fracture site it is referred to as static,
whereas if it is done only on one side of the fracture it is referred to as dynamic. The technical modalities of application
differ if an open or closed osteosynthesis is to be performed.
The more demanding procedure of the technique is getting
the distal holes with the screws. Tolerance of the implant is
usually excellent and the results are very encouraging, even
if in our experience healing times are longer than those commonly seen with external fixation techniques on average. It
is possible to allow free weightbearing very early in the
course of recovery, preferably in case of static interlocking,
also if the osseous callus is still immature. Complications
are grouped in intraoperative, postoperative and late.
Among the operative ones the most frequent is the missing of
the distal holes in the nail by the screws, and among the
postoperative the most severe is the development of a nonunion. Complications related to the removal of the implant
are negligible.

Intramedullary nailing was one of the first techniques


used in both human and veterinary orthopedics.1 From the
mechanical point of view the intramedullary nail is the device of choice for fixation of tubular bones, because it is
coaxial with the bone, and the axis of loading of the nail and
of the bone is the same.2-4 On a bone segment can be exerted bending, torsion, compression and distraction forces. A

cylindrically shaped nail can counterbalance only bending


forces that are exerted on a fracture.5 In an attempt to counteract rotational forces, Kuntscher introduced a nail with a
clover-leaf cross-section and a longitudinal slot, so that it
could exert a strong friction on the inner cortex by means of
a spring effect. An other technique suggested to neutralize
torsional forces is the stack pinning.6,7 None of these techniques, however, can counterbalance axial compression and
distraction forces. For this reason the selection of the fractures amenable with these techniques was limited to those
not comminuted, transverse or short oblique of the shaft, so
that their anatomical features could hinder the fracture collapse and the eventual proximal extrusion of the nail.8 Intramedullary interlocking nailing effectively solved these
problems, extending the selection of cases in which intramedullary nails may be used.9 Many different interlocking nails have been developed in the past few decades in human orthopedics5,9 and they all have the common feature to
be interlocked in the medullary canal, even when they differ
for shape and technical modalities of application. The most
common device used for interlocking is a screw positioned
through a hole in the nail perpendicular to its longer axis.
This can be done in two different ways: if the nail is locked
both proximally and distally to the fracture site this is referred to as a static lock, whereas when is locked only proximally or distally is referred to as a dynamic lock. In the first
configuration the forces exerted on the fracture are completely bypassed by the nail, while in the dynamic configuration an axial shearing along the major axis of the bone is
allowed. The interfragmentary compression obtained with
the dynamic locking can be intended as a mean to stabilize a
fracture already quite stable, for example a transverse one,
or be used to accelerate the maturation of the osseous callus
when, coming from a static lock, this is dynamized by removing the screws, proximally or distally, once a primary
bony callus is present.5 Intramedullary locking nailing may
be performed with reamed or unreamed nails. Reaming has
been proposed with the aim to adapt to the maximum degree
the diameter of the medullary canal with the one of the nail,

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Med Vet, Dipl ECVS, Private Practitioner, Reggio Emilia - Italy

456

increasing in this way the contact surface, and to use nails of


bigger size. Furthermore, some authors have emphasized the
role of the reaming products as osteoinductive material,
even if the procedure was heavily debated when first suggested.5 As a matter of fact, however, reaming is very harmful for the endosteal vascularization that, as shown by
Rhinelander in his studies, supplies the medullary canal and
at least the 2/3 of the cortex.10 If the physiological responses to the fracture are impaired by the medullary vascular
damage the outcome may be a non-union. Some authors disagree with this hypothesis, and they suggest that the periosteal vascular system is more important, and it can supply
the tissues formerly supported by the medullary vascularization.11 Unreamed unlocked nails, for example the Ender or
Rush ones, and some unreamed locked nails used in human
orthopedics have not been widely used in veterinary orthopedics. Only the Kirschner and Steinman pins used for the
stack pinning technique have been applied in veterinary orthopedics. The intramedullary locked nail proposed by dr.
Dueland12 has a full round section, and is not intended to fill
completely the medullary canal with the purpose not to severely damage the medullary vascularization. Reaming may
be done by means of rigid reamers if the fracture is surgically exposed, or it must be done by means of cannulated
flexible reamers if the surgery is going to be performed
without opening the fracture site. In this latter case the image intensifier is also needed. These requirements make this
modality of nailing applicable in only few veterinary institutions. For closed nailing a preliminary reduction of the fracture by means of a transcheletal traction technique is required. Once the correct alignement of the bone segments is
obtained, the guide wire is inserted until it bypasses the fracture area (Fig. 1) and then seated in the distal portion of the
distal bone segment. Next the cannulated flexible reamers
are inserted in the medullary canal following the guide wire
(Fig. 2), starting with the smallest diameter and then increasing the diameter of the reamer of 0,5 mm until the desired size. Our protocol is to stop at that reamer that first
reams the inner cortex, and to use a nail whose diameter is
0,5 to 1 mm smaller. Manual reamers are available, but it is
better to use the motorized ones, at 300 to 600 rpm based on
the bone characteristics. When the reamer bypasses the fracture site it is better to push it along the guide wire without
reaming, to avoid both damaging the soft tissues and spreading apart the bony fragments when present. The guide wire
has a distal olive that hinder the reamer to escape distally,
avoiding in this way unplanned perforations; furthermore, it
is useful in retrieving reamers broken in the medullary canal.
It is very important its use during closed osteosynthesis, because it keeps the reamer along the longer axis of the bone
without damaging the cortex. Using an open technique and
rigid reamers is simpler, because usually reaming of the bone
segments is performed starting from the fracture site and can
be visually checked, even if it is easier to damage the cortex
during the procedure. Unreamed nails are inserted directly or
with a previous directional drilling. They have a point to proceed in the cancellous bone, and they are usually inserted by
means of rotation movements or by hammering.
Once the nail has been inserted in the medullary canal
and the axis of the bone has been checked, locking is done

4th European FECAVA SCIVAC Congress

next. Conceptually the interlocking may be performed in a


static or dynamic way, as already told. Static interlocking is
usually performed in unstable fractures, for example comminuted, long oblique, fragmented or with loss of substance.
Static interlocking produces a great stability at the fracture
site, and allows the maintaining of the bone segment length
even when its anatomical reconstruction has not been done.
Dynamic interlocking is performed only proximally or distally to the fracture site. Usually the interlocking is done on
the smaller bone fragment, and is used when the fracture is
quite stable, for example the transverse or short oblique
without comminution and the impacted ones. In the absence
of specific technical reasons, in our experience is preferable
to interlock the nail proximally, to avoid it may slightly protrude from the hole of insertion causing seroma formation
and local pain. It is possible to convert a static interlocking
in a dynamic one when the local conditions of the fracture
are ready to allow more loading.
The positioning of the screws for interlocking is one of
the most difficult parts of the technique. The proximal interlocking is usually the simpler to perform, because the proximal holes of the nail are closer to the targeting device, and
therefore the drilling and the insertion of the screws are quite
easily performed. For the distal screws the problems are
many more. During the insertion of the nail in the medullary
canal, in fact, the nail is subjected to bending and torsion
forces that make the finding of the holes with an external targeting device very difficult, because it was set on a not deformed nail. This problem is bigger in human5 than in veterinary orthopedic, because the length of veterinary nails is
much shorter, and for this reason the mistakes in targeting
are less likely. Nevertheless, a system capable to get the distal holes with a percentage close to the 100% of attempts has
not been proposed to date. Now the distal interlocking is feasible with different techniques. In human orthopedics is
available the Brooker-Wills nail, that gains distal fixation by
means of two flanges that are extruded from the nail. Quite
commonly targeting devices applied on the image intensifier are used; when the hole in the nail is seen perfectly round
through the targeting device, it is possible to drill and put the
screw through it.5 Two techniques used both in human and
in veterinary orthopedics are the free hand positioning of the
screws and the use of external targeting devices to be connected with the nail. The free hand positioning needs the use
of the image intensifier, and is done by positioning the limb
of the patient so that the hole in the nail is seen perfectly
round, that means the X-ray beam and the hole have the
same axis (Fig. 3). A drill bit or a Kirschner wire are moved
on a plane parallel to that of the limb until their point is seen
at the center of the hole, and then the drill bit or the wire are
tilted so that they are positioned perpendicular to the limb,
without moving the point. If the point has not been translated during the maneuver the hole should be centered. Once
the drill bit is removed, a self-tapping screw is inserted (Fig.
4). An other option is using a cannulated screw, that can be
advanced along the Kirschner wire positioned through the
hole and then removed after the screw is tightened. Now
many efforts are put in developing an external targeting device that does not require the use of an image intensifier. If
such a device could be developed, it would have the double

4th European FECAVA SCIVAC Congress

457

tramedullary nail with section similar to the Kuntscher nail


(Fig. 5). Once secured the nail to the targeting device, the
centering bushings are set to get the holes in the nail, and
they are fastened in that position. The nail is disconnected
from the targeting device and inserted in the medullary canal
by means of the handler that can be hammered, and then the

Figure 1 Intraoperative image of the guide wire while it is pushed through


the fracture site in the distal bone segment.

Figure 2 Intraoperative image of a flexible cannulated reamer while it is


advanced along the guide wire in the medullary canal.

Figure 3 Intraoperative image of the distal holes in the nail. When they
are seen perfectly round this means that the radiographic beam and the
holes are on the same axis.

Figure 4 Intraoperative image of the screws inserted through the distal


holes in the nail.

Figure 5 The targeting device proposed by dr. Cotto.

Figure 6 The targeting device derived from the Grosse & Kempf system
by dr. Rovesti.

SPECIALIST/INTERACTIVE PROGRAMME

result to reduce the X-ray exposition of the operating room


personnel and to allow a bigger diffusion of the technique in
veterinary medicine, because the availability of an image intensifier is not common in veterinary institutions. Our experience has been done mostly with an adjustable targeting device proposed by dr. Cotto, which is connected to an in-

458

4th European FECAVA SCIVAC Congress

Figure 7 X-ray film showing a screw that broke the near cortex and went
inside the medullary canal, seating directly on the nail.

Figure 8 X-ray film showing a non-union whose development was attributed to an excessive reaming of the medullary canal and to the use of a too
big nail.

handler is removed and the targeting device is connected to


the nail again. The bushings are now the guides for getting
the holes. This targeting device can be used for nails customized for a specific patient, creating new holes in the nail
and setting the bushings to get the new holes. The first experiences are encouraging, but more experimental and clinical work are needed to make the procedure more precise and
repeatable. An other system is available in veterinary medicine, adapted from the Huckstep human nail for veterinary
use by dr. Dueland, with an external targeting device with a
series of holes. I used a personal system, derived from the
human Grosse & Kempf one, with an handler can be hammered for insertion of the nail and targeting device specific
for each size of nail (Fig. 6). These systems have good results but they do not have solved the problem of positioning
the distal screws easily to date.
In the postoperative period the patient is allowed full
weightbearing, but with a restricted physical activity. In our
experience the fracture healing took longer times if compared with external fixation techniques. Tolerance of the implant is usually excellent and the patient can have a quite
normal life before the complete healing is achieved. Once a
primary bone callus is present, if the interlocking was static
it can be changed in dynamic to further stimulate the fracture
healing. The nail may be removed when a complete healing
has been achieved as judged radiographycally. In our expe-

rience the removal has been done between 4 and 14 months


after the surgery. The removal of the nail is usually uneventful. For the procedure to be done correctly it is necessary an
extractor; it should be performed cautiously, to avoid iatrogenic fractures. Complications can be classified as surgical,
postsurgical or relating to the recovery period, and late or relating to the extraction of the implants. The most frequent
surgical complication is the missing of the distal holes by the
screws.13 As already anticipated, this is one of the major
drawbacks for the application of the technique. If bent tibial
nails are used, particular attention should be paid not to damage the posterior cortex, particularly when using rigid reamers. The damage to the posterior tibial cortex can cause a iatrogenic metaphyseal proximal fracture or a more severe lesion of the popliteal vessels.5 A surgical problem that has
consequences on the removal of the nail is the breaking of
the near cortex when the screw is tightened, so that it is anchored only on the far cortex and the screw head sits on the
nail inside the medullary canal (Fig. 7). In the postsurgical
period the most severe complication we had was a nonunion (Fig. 8). The cause of this problem has been attributed
to the excessive reaming of the medullary canal and the use
of a nail of too big size, with potential damage to the endosteal and medullary vascularization. In this case has been
used a different technique. If a delayed consolidation is present with a static interlocking the dynamization of the con-

4th European FECAVA SCIVAC Congress

References
1.
2.
3.
4.
5.

6.
7.

8.

9.
10.
11.
12.

13.

Brinker WO, Hohn RB, Prieur WD et al., (1983), Manual of internal


fixation in small animals, Springer-Verlag, Berlin, 5.
Roe SC, (1995), Biomechanics of interlocking nail fixation., Am Coll
Vet Surg Sympos, Chicago, IL, 280-281.
Tarr RR, Wiss DA, (1986), The mechanics and biology of intramedullary fracture fixation, Clin Orthop Rel Res, 212: 10-17.
Kinast C, Freigg R, Perren SM, (1990), Biomechanics of the interlocking nail, Arch Orthop Trauma Surg, 109: 197-204.
Fontanesi G, Costa P, Giancecchi F, (1991), Inchiodamento endomidollare bloccato dellarto inferiore, Aulo Gaggi, Bologna, 37-38, 1319, 5, 35, 45-47, 107-110.
Kagan KG, (983), Multiple intramedullary pin fixation of the femur
of dogs and cats, J Am Vet Med Assoc, 182: 1251-5.
Vasseur PB, Paul HA, Crumley L, (1984), Evaluation of fixation devices for prevention of rotation in transverse fractures of the canine
femoral shaft: an in vitro study, Am J Vet Res, 45: 1504-7.
Brinker WO, Piermattei DL, Flo GL, (1990), Handbook of small animal orthopedics and fracture treatment, 2nd ed., W.B. Saunders Company, Philadelphia, 29.
Court-Brown CM, (1991), An atlas of closed nailing of the tibia and
femur, Martin Dunitz Ltd, London, 11-12, 1-7.
Rhinelander FW, (1968), The normal microcirculation of diaphyseal
cortex and its response to fracture, J Bone Joint Surg, 50(4): 784-800.
Strachan RK, McCarthy I, Fleming R et al., (1990), The role of the
tibial nutrient artery, J Bone Joint Surg, 72-B: 391-4.
Dueland RT, Berglund L, Vanderby R et al., (1996), Structural properties of interlocking nails, canine femora, and femur-interlocking
nail constructs, Vet Surg, 25: 386-396.
Durall I, Diaz MC, Morales I, (1994), Interlocking nail stabilization
of humeral fractures. Initial experience in seven clinical cases, Vet
Comp Orthop Trauma, 7: 3-8.

SPECIALIST/INTERACTIVE PROGRAMME

figuration is usually enough to accelerate the callus formation. Infections were not a problem in our experience. The
dynamization of the nail gave some problem when performed proximally, because even a slightly protrusion of the
nail through the insertion hole may result in seroma formation and local pain. For this reason dynamization was done
almost exclusively distally, except for specific technical reasons. In the late complications we found the difficult finding
of the heads of the screws because covered by fibrous tissue.
If the head of the screw broke the near cortex during the
surgery, when it is to be removed is necessary to drill the
cortex, to find the screw inside the medullary canal and then
to remove it. A minor problem was the presence of fibrous
or osseous tissue in the proximal part of the nail, so that it is
not possible to introduce the extractor. This tissue is usually
easily removable, and this problem could be solved by positioning a plug on the top of nail when its insertion is completed. Iatrogenic fractures are reported as consequences of
brutal maneuvers during the extraction of the nail. We did
not see any complication following the removal of the implants.

459

4th European FECAVA SCIVAC Congress

461

Leukemias in the dog


C. Guillermo Couto

Summary
Leukemias are malignant hemolymphatic neoplasms that
originate in the bone marrow. Although they are not as common as lymphomas, they should be recognized clinically.
This lecture will discuss the diagnostic and therapeutic approach to acute and chronic leukemias in dogs.

Epidemiology and classification


Leukemias are malignant neoplasms that originate from
hematopoietic precursor cells in the bone marrow. These
cells have the inability to undergo terminal differentiation,
thus self-replicating as a clone of usually immature (and
nonfunctional) cells. The neoplastic cells may or may not
appear in peripheral circulation, thus the confusing terms
aleukemic or subleukemic leukemia are used when neoplastic cells proliferate within the bone marrow but are absent or
scarce in circulation.
Leukemias can be classified philogenetically according
to the cell line they originate from into two broad categories:
myeloid (or nonlymphoid) and lymphoid. The term myeloproliferative disease or disorder has also been used to refer
to myeloid leukemias. According to their clinical course and
the cytologic features of the leukemic cell population,
leukemias can be classified as acute or chronic. Acute
leukemias are characterized by an aggressive biologic behavior (i.e., death ensues shortly after diagnosis if untreated)
and by the presence of immature (blast) cells in bone marrow and/or blood; chronic leukemias have a protracted, often indolent course, and the predominant cell is a well-differentiated, late precursor (i.e., lymphocyte in chronic lymphocytic leukemia and neutrophil in chronic myelogenous
leukemia). In dogs, chronic myelogenous leukemia (CML)
can undergo blast transformation (blast crisis), during which
stage the disease behaves as an acute leukemia and is usually refractory to therapy. Blast crises do not appear to occur
in dogs or cats with chronic lymphocytic leukemia (CLL).
Acute leukemias may be difficult to classify morphologically based on evaluation of Giemsa- or Wrights-stained
blood or bone marrow smears as myeloid or lymphoid because poorly differentiated blasts look similar under light
microscopy. In veterinary medicine, cytochemical stains are
used routinely in several diagnostic laboratories to establish
whether the blasts are lymphoid or myeloid, and also to sub-

classify myeloid leukemias as described below (i.e., myeloid


vs. monocytic vs. myelomonocytic). These cytochemical
stains reveal the presence of different enzymes in the cytoplasm of the blasts, which aid in establishing their origin.
A classification scheme for acute leukemia in people was
devised by a group of French, American, and British investigators (the FAB scheme) based on the morphologic features of the cells in blood and bone marrow Giemsa-stained
smears. So far, this scheme has no prognostic or therapeutic
implications in cats or dogs; thus it is not discussed.
In the dog, leukemias represent less than 10% of all hemolymphatic neoplasms and are therefore considered to be
rare. In our hospital, the leukemia-to-lymphoma ratio is approximately 1:5 to 1:7. This ratio is artificially high, since
most dogs with lymphoma are usually treated by the local
veterinarians, whereas most dogs with leukemia are referred
for treatment. Most leukemias in dogs are considered to be
spontaneous, although radiation exposure and viral particles have been identified as possible etiologic factors in dogs
with this disease.

Acute leukemias
In the dog, acute myeloid leukemias are more common
than acute lymphoid leukemias, representing approximately
three fourths of the cases of acute leukemia. It should be remembered, however, that morphologically (i.e., by evaluation of a Wrights- or Giemsa- stained blood or bone marrow
smear) most acute leukemias are initially classified as lymphoid. After performing cytochemical staining of the
smears, approximately one third to one half of them are reclassified as myeloid. Approximately half of the dogs with
myeloid leukemia have myelomonocytic differentiation
when cytochemical stains are used.
The clinical signs and physical examination findings in
dogs with acute leukemia are usually vague and nonspecific. Briefly, most owners seek veterinary care when their
dogs develop lethargy, anorexia, persistent or recurrent
fever, weight loss, shifting limb lameness, and other nonspecific signs; neurologic signs occur occasionally.
Splenomegaly, hepatomegaly, pallor, fever, and mild generalized lymphadenopathy are commonly detected during routine physical examination. The spleen in these dogs is usually markedly enlarged, and it has a smooth surface on palpation. Careful inspection of the mucous membranes in dogs

SPECIALIST/INTERACTIVE PROGRAMME

DVM, Dipl ACVIM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine
The Ohio State University - Columbus - USA

462

with acute leukemia often reveals petechiae and/or ecchymoses in addition to pallor; icterus may also be detected if
marked leukemic infiltration of the liver or hemolysis is present. The generalized lymphadenopathy in dogs with acute
leukemia is usually mild, in contrast with dogs with lymphoma, in which the lymph nodes are massively enlarged.
Also, the majority of dogs with leukemia display constitutional signs (i.e., they are clinically ill), whereas over half of
the dogs with lymphoma are asymptomatic.
The treatment of dogs with acute leukemias is usually
unrewarding. Most dogs with these diseases respond poorly
to therapy, and prolonged remissions are rarely obtained.
Treatment failure is usually because of one or more of the
following factors:
1. Failure to induce remission (more common in AML
than in ALL)
2. Failure to maintain remission
3. Presence or development of organ failure resulting
from leukemic cell infiltration does not allow for the use of
aggressive combination chemotherapy (i.e., because of enhanced toxicity)
4. Development of fatal sepsis and/or bleeding caused by
already existing or treatment-induced cytopenias
Prolonged remissions in dogs with AMLs treated with
chemotherapy are extremely rare. In most dogs with AML
remissions are rarely observed. If they do so, the remission
is usually extremely short-lived, and survivals rarely exceed
3 months. Also, over half of the dogs die during induction
because of overwhelming sepsis or bleeding. The supportive
treatment required in these patients (e.g., chemotherapeutic
agents, blood component therapy, intensive care monitoring)
is financially unacceptable to most owners (the cost of treatment for a 70-pound dog with acute leukemia ranges from
$1500 to $3000 for the first month of treatment), and the
emotional strain placed on the owner is also quite high.
Therefore, the owners should be aware of all these facts before deciding to treat their dogs with chemotherapy.
In dogs with ALL, the prognosis may be better; however, responses to treatment and survival times are considerably lower than in dogs with lymphoma. The remission rates
in dogs with ALL are approximately 20% to 40%, in contrast
with those in lymphomas, in which they approach 90%; survival times are also shorter than those in dogs with lymphoma, averaging 1 to 3 months, when appropriate
chemotherapy protocols are used. Untreated dogs usually
live less than 2 weeks.

Chronic leukemias
In dogs, CLL is more common than CML; the latter is a
poorly characterized entity. In our hospital, we evaluate approximately 6 to 8 dogs with CLL a year, whereas we evaluate approximately one dog with CML every 3 to 5 years.
Chronic lymphocytic leukemia is one of the most commonly diagnosed leukemias in most diagnostic referral laboratories.
As with their acute counterparts, clinical signs in dogs
with CLL or CML are vague and nonspecific; however, a
chronic history of vague clinical signs precedes the diagno-

4th European FECAVA SCIVAC Congress

sis of chronic leukemia in approximately half of the dogs. A


large number of cases of chronic leukemia are diagnosed incidentally during routine physical examination and laboratory evaluation (i.e., dogs are asymptomatic). Clinical signs
are present in approximately half of the dogs with CLL and
include lethargy, anorexia, vomiting, polyuria/polydipsia,
detection of enlarged lymph nodes by the owners, intermittent lameness, intermittent diarrhea and/or vomiting, and
weight loss. Physical examination findings in these dogs include mild generalized lymphadenopathy, splenomegaly, hepatomegaly, pallor, and pyrexia. The clinical signs and physical examination findings in dogs with CML appear to be
similar to those of dogs with CLL.
A terminal event in dogs with CLL is the development of
a diffuse large cell lymphoma termed Richters syndrome,
characterized by massive generalized lymphadenopathy and
hepatosplenomegaly. Once this multicentric lymphoma develops, chemotherapy-induced long- lasting remissions are
difficult to obtain, and survival times are short.
Blast crisis, characterized by the appearance of immature
blast cells in blood and bone marrow, occurs in humans and
dogs with CML months to years after the initial diagnosis. In
humans, these blasts are either myeloid or lymphoid; the origin of the blast cell in dogs with blast crises has not been determined. Five of 11 dogs with CML reported in the literature for which sufficient clinical and hematologic information is available developed blast crises. Blast crises do not
appear to occur in dogs with CLL.
The clinician usually faces the dilemma of whether or
not to treat a dog with chronic leukemia. If the dog is symptomatic, or has organomegaly or concurrent hematologic abnormalities, treatment with an alkylator (with or without corticosteroids) is indicated. If paraneoplastic syndromes (i.e.,
immune hemolysis or thrombocytopenia, monoclonal gammopathies) are absent, we recommend using single-agent
chlorambucil (Leukeran) at a dose of 20 mg/m2 PO once
every 2 weeks. If paraneoplastic syndromes are present, the
addition of corticosteroids (prednisone, 50 to 75 mg/m2 PO
sid for 1 week; then 25 mg/m2 PO qod) may be beneficial.
Because the growth fraction of neoplastic lymphocytes
in CLL appears to be low, a delayed response to therapy is
common. In a high proportion of dogs with CLL treated with
chlorambucil or chlorambucil/prednisone, resolution of the
hematologic and physical examination abnormalities may
take over 1 month (and as long as 6 months). This is in contrast to dogs with lymphoma and acute leukemias, in which
remission is usually induced in 2 to 7 days.
The survival times of dogs with CLL are quite long. Indeed, even without treatment, survival times of over 2 years
are common. Over two thirds of the dogs with CLL treated
with chlorambucil (with or without prednisone) in our clinic have survived in excess of 2 years. Most dogs with CLL
do not die from leukemia-related causes, but rather from
other geriatric disorders.
Treatment of dogs with CML using hydroxyurea may
result in prolonged remission, provided blast crisis does
not occur. However, the prognosis does not appear to be as
good as for dogs with CLL (i.e., survivals of 4 to 15
months with treatment). Treatment of blast crises is usually unrewarding.

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463

Extranodal lymphomas
C. Guillermo Couto
DVM, Dipl ACVIM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine
The Ohio State University - Columbus - USA

Extranodal lymphomas are relatively common in both


dogs and cats. In the former they occur in the alimentary
tract, skin, and other areas, while in cats they are common
in the alimentary tract, upper respiratory system, and central nervous system. This lecture will discuss the clinical
recognition and treatment of this neoplasm.

Epidemiology
Lymphoma (malignant lymphoma, lymphosarcoma
[LSA]) is defined as a lymphoid malignancy that originates
from solid organs (e.g., lymph nodes, liver, spleen). This differentiates lymphomas from lymphoid leukemias, which
originate in the bone marrow.
Previous reports document that approximately 70% of
cats with lymphoma are feline leukemia virus (FeLV)-positive. The prevalence of viremia in cats with lymphoma
varies with the anatomic form of presentation (see below);
but, in general, young cats with lymphoma are FeLV-positive, whereas older cats are negative. Over the past few
years, the prevalence of FeLV infection in cats with lymphoma in our clinic appears to be decreasing. The role of feline immunodeficiency virus (FIV) in the pathogenesis of feline lymphoma is still unclear, although it has been documented that FIV-positive cats appear to have a higher risk of
developing lymphoma.
In dogs, lymphomas are considered to be multifactorial
in nature, since no single etiologic agent has been identified.
However, a genetic component is evident, since the prevalence of this neoplasm is high in certain blood lines. There is
also a distinct breed predisposition for lymphoma in dogs,
with some breeds such as Boxer, Basset Hound, Rottweiler,
Cocker Spaniel, St. Bernard, Scottish Terrier, Airedale Terrier, English Bulldog, and Golden Retriever being at high risk;
the breeds most commonly affected in our clinic are Golden
Retrievers, Cocker Spaniels, and Rottweilers.
The age of presentation in cats with lymphoma is bimodal, with the first peak occuring at approximately 2 years
of age and the second one at approximately 10 to 12 years of
age. The first peak is composed mainly of FeLV-positive
cats, whereas the second one includes predominantly FeLVnegative cats. The mean age of presentation of lymphoma in
FeLV-positive cats is 3 years, whereas in FeLV-negative cats

it is 7 to 8 years. As discussed previously, the prevalence of


lymphomas in FeLV-positive cats appears to be decreasing.
In contrast, most dogs with lymphoma are middle-age or
older (6 to 12 years of age).

Clinical features
The clinical signs and physical examination findings in
cats and dogs with extranodal lymphomas are extremely
variable and depend on the location of the mass(es). In general, the clinical signs are the results of compression or displacement of normal parenchymal cells in the affected organ
(e.g., azotemia in renal lymphoma, variable neurologic signs
in central nervous system [CNS] lymphoma). Common extranodal forms in dogs include cutaneous and ocular, and in
cats they include nasopharyngeal, ocular, renal, and neural.
Cutaneous lymphoma is one of the most common extranodal forms of presentation in dogs, representing the most
common extranodal form of this neoplasm in dogs in our
clinic, but it is rare in cats. Clinical signs and lesions are extremely variable, and they can mimic any primary or secondary skin lesion. Dogs with mycosis fungoides (an epidermotropic T-cell lymphoma) usually present with a chronic history of alopecia, desquamation, pruritus, and erythema,
eventually leading to plaque and tumor formation. Mucocutaneous and mucosal lesions are relatively common, and
generalized lymph node involvement may be absent on first
presentation. A characteristic lesion in dogs with this form of
lymphoma is a circular, raised, erythematous, donut-shaped,
dermoepidermal mass that contains normal skin in the center of the lesion. Most of the cases of cutaneous lymphomas
in cats reported in the literature were in cats with negative
FeLV status.
Renal lymphoma is relatively common in cats, but rare in
dogs. Cats with this anatomic form are presented for evaluation of vague clinical signs, usually secondary to chronic
renal failure. Physical examination reveals an emaciated cat
that is usually anemic and has large, irregular, and firm kidneys; both kidneys are commonly affected. There is a purported association between renal and CNS lymphoma in
cats, to the point that some clinicians recommend using
drugs that achieve high CNS concentrations (i.e., cytosine
arabinoside) in cats with renal involvement in attempts to
prevent secondary CNS dissemination. In our clinic, this association has not been recognized.

SPECIALIST/INTERACTIVE PROGRAMME

Summary

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Table 1: Chemotherapy protocols for dogs and cats with extranodal lymphomas
1) Induction of remission:
COAP protocol1:
- cyclophosphamide (Cytoxan) 50 mg/m2 BSA, PO, 4 days a week (or every other day); in cats, cyclophosphamide is used at 200300 mg/m2, PO, every 3 weeks to decrease prevalence of anorexia.
- vincristine (Oncovin) 0.5 mg/m2 BSA, IV, once a week
- cytosine arabinoside (Cytosar-U) 100 mg/m2 BSA/day, IV drip or SQ, for only 2 days in cats and 4 days in dogs
- prednisone 50 mg/m2 BSA, PO, sid for a week; then 20 mg/m2 BSA PO, every other day
2) Intensification:
DOGS:
l-asparaginase (Elspar) 10,000-20,000 IU/m2 BSA, SQ (one dose) or
vincristine (Oncovin) 0.5-0.75 mg/m2, IV, every 1 to 2 weeks
CATS:
doxorubicin (Adriamycin) 25 mg/m2, IV, every 3 weeks or
mitoxantrone (Novantrone) 4-6 mg/m2, IV, every 3 weeks
3) Maintenance2:
LMP protocol:
- chlorambucil (Leukeran) 20 mg/m2 BSA, PO, every other week
- methotrexate (Methotrexate) 2.5 mg/m2 BSA, PO, 2 to 3 times per week
- prednisone 20 mg/m2, PO, every other day
COAP protocol:
- use as above every other week for 6 treatments, then every third week for additonal 6 treatments, and try to maintain the patient on
one treatment every 4th week.
MAINTENANCE THERAPY IS CONTINUED UNTIL THE TUMOR RELAPSES
4) Rescue:
DOGS:
- D-MAC protocol (14-day cycle)
- dexamethasone 0.5 mg/lb, PO or SQ on days 1 and 8
- actinomycin D (Cosmegen) 0.75 mg/m2, IV push on day 1
- cytosine arabinoside (Cytosar) 200 -300 mg/m2, IV drip over 4 hours OR SQ, on day 1
- melphalan (Alkeran) 20 mg/m2, PO, on day 8*
- AC protocol (21 day cycle)
- doxorubicin (Adriamycin) 30 mg/m2 BSA IV, day 1
- cyclophosphamide (Cytoxan) 100-150 mg/m2, PO, days 15 and 16
- ADIC protocol (cycle is repeated every 21 days)
- doxorubicin (Adriamycin) 30 mg/m2 BSA, IV, on day 1
- dacarbazine (DTIC) 700-1,000 mg/m2 BSA, IV infusion (over 6-8 hours), on day 1
- CHOP protocol (21 day cycle)
- cyclophosphamide (Cytoxan) 100-150 mg/m2, IV, on day 1
- doxorubicin (Adriamycin) 30 mg/m2, IV, on day 1
- vincristine (Oncovin) 0.75 mg/m2, IV, on days 8 and 15
- prednisone 20-25 mg/m2, PO, every other day
CATS:
- MiC protocol (21 day cycle)
- mitoxantrone (Novantrone) 4-6 mg/m2, IV drip over 4-6 hours on day 1
- cyclophosphamide (Cytoxan) 200-300 mg/m2, PO, day 15 or 16
- AC protocol (21 day cycle)
-doxorubicin (Adriamycin) 25 mg/m2, IV, on day 1
-cyclophosphamide (Cytoxan) 200-300 mg/m2, PO, day 15 or 16
- MiCA protocol (21 day cycle)
- mitoxantrone (Novantrone) 4-5 mg/m2, IV drip over 4-6 hours on day 1
- cyclophosphamide (Cytoxan) 200-300 mg/m2, PO, day 15 or 16
- cytosine arabinoside (Cytosar-u) 200 mg/m2, IV drip over 4-6 hours (MIXED IN THE SAME BAG WITH MITOXANTRONE) on day 1
- CHOP protocol (21 day cycle)
-cyclophosphamide (Cytoxan) 200-300 mg/m2, IV, on day 10
-doxorubicin (Adriamycin) 20-25 mg/m2, IV, on day 1
-vincristine (Oncovin) 0.5 mg/m2, IV, on days 8 and 15
-prednisone 20-25 mg/m2, PO, every other day
1

Use for 6 to 10 weeks, then use LMP.


Use until relapse occurs; then go to rescue.
* After 6 doses, substitute Leukeran (20 mg/m2, PO, q/2 weeks) for Alkeran
2

4th European FECAVA SCIVAC Congress

Diagnosis
Before instituting therapy, a confirmatory cytologic or
histopathologic diagnosis should be obtained. In addition, a
minimum data base consisting of a CBC, serum biochemistry profile, and urinalysis should be obtained if the owners
are contemplating treatment.
In most cats and dogs with multicentric, superficial extranodal, mediastinal, or alimentary lymphoma, a diagnosis can
easily be obtained by fine-needle aspiration cytology of the
affected organ(s) or lymph node(s). Lymphomas are characterized by the prevalence of a monomorphic population of immature round lymphoid cells, with prominent nucleoli.
In our practice, lymphomas can be diagnosed cytologically in approximately 90% of dogs and 70% to 75% of cats

evaluated (i.e., usually in only 10% of the dogs and 25% to


30% of the cats is histopathologic evaluation of a surgically
excised lymph node necessary to establish a diagnosis). Until conclusive evidence that the histopathologic classification of canine and feline lymphomas offers prognostic information, the surgical removal of a lymph node or extranodal
mass for histopathologic evaluation in a patient with a cytologic diagnosis of lymphoma is not indicated. Obtaining a
cytologic diagnosis rather than a histopathologic diagnosis
from an excisional lymph node biopsy also offers two major
benefits: it is associated with minimal or no morbidity, and
it is financially acceptable to most owners.

Treatment
The treatment of cats and dogs with lymphoma is divided into several phases or strategies: induction of remission,
intensification, maintenance, and reinduction of remission
or rescue (Table 1). Immediately after diagnosis, a relatively aggressive multiple agent chemotherapy protocol
(COAP) is used to induce remission; during this phase,
which lasts 6 to 8 weeks, the patients are evaluated by a veterinarian weekly, at which time they receive an intravenous
injection of an antimitotic agent (vincristine) in addition to
undergoing a routine physical examination (with or without
a CBC). If at the end of this phase the patient is considered
to be in complete remission (CR) (i.e., complete disappearance of all neoplastic masses), the maintenance phase is initiated. During the maintenance phase, a multiple agent
chemotherapy protocol consisting of three drugs (LMP) administered orally is used, so that the patient requires less intensive monitoring (once every 6 to 8 weeks). This phase
continues until the tumor relapses (i.e., is out of remission),
at which time the reinduction phase begins. This phase is
similar to the induction phase, in that intensive treatments
are used. Once remission is obtained, the patient is placed
again on a maintenance protocol that is usually a modification of the original maintenance protocols (at OSU we typically use the LMP protocol, but we substitute Cytosar for the
methotrexate, at a dose of 200-300 mg/m2, SQ, every other
week). If at the end of the induction phase the patient is not
in CR, intensification with L-asparaginase is recommended
before initiating the maintenance phase. In addition to the
chemotherapeutic approach discussed in this section, a variety of protocols have been used successfully in the treatment
of cats and dogs with lymphoma.

SPECIALIST/INTERACTIVE PROGRAMME

Ocular lymphoma occurs both in cats and dogs, but is


apparently more common in the former. In dogs ocular involvement appears to be commonly associated with the multicentric form, whereas in cats both primary and secondary
ocular involvement are commonly recognized. A variety of
signs and lesions may be present in these patients, including
photophobia, blepharospasm, epiphora, hyphema, hypopyon, ocular masses, third eyelid infiltration, anterior uveitis,
chorioretinal involvement, and retinal detachment.
Nasopharyngeal lymphoma is relatively common in cats
but is extremely rare in dogs. Clinical signs are similar to
those of cats with any upper respiratory disorder and include
sneezing, unilateral or bilateral nasal discharge (from mucopurulent to frankly hemorrhagic), stertorous breathing,
exophthalmus, and facial deformity; this is one of the most
common forms of presentation of extranodal lymphoma in
cats in our clinic.
Cats and dogs with neural lymphoma are presented with
a variety of neurologic signs. Although CNS signs are more
common, peripheral nerve involvement may occur (predominantly in cats). Three forms of presentation are clinically
recognized, including solitary epidural lymphoma, neuropil
(intracranial or intraspinal) lymphoma (also referred to as
true CNS lymphoma), and peripheral nerve lymphoma.
Neurologic signs are usually multifocal, although solitary
intracranial or spinal involvement also occurs. Neural lymphomas can be primary (e.g., epidural lymphoma), or they
may be secondary to the multicentric form; as discussed,
secondary CNS lymphoma may be common in cats with the
renal form.

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467

Follicular dysplasias
Luis Ferrer
Med Vet, Dipl ECVS
Private Practitioner, Cremona - Italy

Common clinicopathologic features

Dysplasia originates from the greek words dys (bad) and


plassein (to give form). In medicine, initially was used to
describe abnormalities in the development, growth or tissue
differentiation and may be this is the most correct definition. We still use the word with this sense in renal dysplasia, retinal dysplasia or hip dysplasia. However, in
1949, Papanicolau used dysplasia in medical lenguage with
another aception: to define pre-malignant lesions or lesions
of borderline malignancy: cervical dysplasia or epithelial dysplasia.
Furthermore, the term dysplasia have a few more minor
aceptions, restricted to some scientific fields. In consequence, some authors have suggested that the term is empty
of meaning and it is useless. The term is very unprecise1 and
should be avoided. For those authors, the term prostatic
dysplasia is so vague that it is equivalent to disease of the
prostate, only seems more technical, more precise. It is true
that dysplasia is a confusing and abused terminology. The
problem is their substitution in the several meanings that
this word has accumulated. Dunstan has suggested to substitute, in dermatopathology, the term dysplasia by dystrophy. However, dystrophy is also very difficult to define and
in pathology textbooks and dictionaries is used with different meanings.
Before a broad consensus is reached, I will continue using the term follicular dysplasia. In veterinary dermatology
the term is used to define a group of diseases of hair follicles, with a strong genetic basis but usually not congenital,
in which there is abnormal development of hair follicles of
non-neoplastic and non- inflammatory origin, which leads to
abnormal follicular architecture.
Although the list of diseases included in this group
changes from one author to the other, a few diseases are almost always included:
colour dilution alopecia, black hair follicular dysplasia and
other dysplasias related to the pigmentary system.
Follicular dysplasia of portuguese water dog and other
curly coated dogs (spanish water dog, irish water
spaniel, ...).
Cyclic dysplasia of Boxers, Airedale Terriers and Staffordshire Terriers (also called cyclic flank dysplasia).
Melanoderma and alopecia of Yorkshire Terriers.

1) Strong breed predilection (reflecting the genetic background).


2) Affect young to middle aged animals (usually between 6
months and 4 years).
3) Clinically, the affected dogs present symmetric alopecia,
with typical regional distribution (trunk, pinnae,
flanks,...). Alopecic areas usually develop hyperpigmentation. There is not pruritus and the general condition of
the patients is otherwise good. Seborrhoea and bacterial
folliculitis are also common in the alopecic areas.
4) The diagnosis based on examination of skin biopsies.
Histologically the hair follicles are abnormally or incompletely formed.
5) There is no effective treatment.

Colour dilution alopecia and related


follicular dysplasias
Cause and pathogenesis: unknown. Several hypothesis
have been proposed. Some authors think that these diseases
are conquence of a defect in the transfer of melanine from
melanocytes to keratinocytes. Other dermatologists2 think
that the key defect is an abnormal degradation of
melanosomes, may be due to abnormal calcium metabolism.
For either reason, there is an abnormal accumulation of
stage III and IV melanosomes inside keratinocytes and hair
cortex cells. Later, these melanosomes rupture and leak
melanine, which is toxic to epithelial cells.
The genetic basis is partially known. The locus D, probably together with others, regulates the dilution of the hair
colour. The alelle d, recessive, leads to the diluted colour.
In consequence, d/d dogs have a blue-gray coat. However,
not all blue-gray animals develop alopecia and an alopecia
of identical clinicopathologic charcteristics have been identified in brown-black dogs. The alopecia/follicular dysplasia
may be is the consequence of another gen, that is most
prevalent between diluted animals or the effects of this gen
are more evident on dogs of diluted coat.
Presentation: blue or gray dogs, males or females without distinction. Any breed or cross. Very common in Doberman Pinschers, Yorkshire Terriers and Great Danes. The disease usually begins between the 6th and 9th month of life. In
less diluted animals the alopecia begins later, between the

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Dysplasia: a confusing term

468

2nd and 3rd year. Beco and coworkers3 have described an


early development of the disease in Teckels (before the third
month).
Clinical signs: symmetric alopecia that usually begins on
the dorse of the patient and progressively extends to all diluted areas. In early stages, occasionally, the disease waxe
and wane (hairs regrow), but the alopecia with time become
permanent. At 2-3 years of age diluted dogs (blue or gray) are
usually completely alopecic (in all diluted areas). Desquamation and folliculitis are common in the alopecic areas.
In black dogs (black and brown) a very similar disease
has beeen described.4 However, in these animals the alopecia begins after the second year of life and is less severe.
Complete truncal hair loss has not been recognized. May be
these animals are recessive for the gen that causes the alopecia or in non-diluted dogs the efects of the gen expression
are less severe. The so-called black hair follicular dysplasia
-the alopecic change only affects black hairs- is considered
to be also a related disease.
Dysplasia, because it is cyclic (reversible).
Clinical signs: the disease is more common in Boxers,
Bulldogs, Airedale Terriers and Staffordshire Terriers, but
can be diagnosed in any breed. Males and females are equally affected. Most animals are older than 2 years and the lesions appear predominantly in spring and autumn. Characteristic signs consist in well-demarcated (geometric)
alopecic and hyperpigmented areas located in both flanks.
The alopecia persist for a few months and then, usually, the.
Mild pigmentary incontinence is also common in early
stages. Later, hair follicles present dysplastic forms and follicular keratosis. Inside hair follicles appear clumps of melanine. In chronic stages hair follicles appear in telogen, dilated, filled with melanine and keratine. Pigmentary incontinence around hair follicles is very prominent. Suppurative
folliculitis is common.
Treatment: there is no known treatment. Some authors
have suggested that retinoids can be useful to stop the development of alopecia but in our experience this treatment is
uneffective. If necessary, topical therapy has to be used to
control seborrhoea and folliculitis.

Follicular dysplasia of portuguese water


dog and other curly coated dogs
Cause: unknown. Probable genetic origin. The authors
that have investigated the disease5 think that there are abnormality in the pigmentary system and in the hair matrix cells.
Clinical signs: the disease affects, probably, all curly
coated breeds although it has been described in portuguese
water dogs, spanish water dogs and irish water spaniels.
Both males and females are equally affected. The clinical
signs appear between the first and the fifth year of life and
consist in symmetric alopecic areas that affect the trunk,
posterior limbs and periocular areas. The hair is brittle, dull.
In some patients the hair loss is permanent and in other patients waxes and wanes.
Diagnosis: histologic. Hair follicles appear dysplastic,
filled with melanine and detritus. Perifollicular pigmentary
incontinence is prominent. There is apoptosis of ker-

4th European FECAVA SCIVAC Congress

atinocytes of the hair sheaths and vacuolization of cells of


the inner root sheath.
Treatment: there is no effective treatment.

Cyclic dysplasia of Boxers,


Airedale terriers and Staffordshire
Terriers (also called cyclic flank dysplasia
and cyclic flank alopecia)
Cause: Unknown. Hormonal imbalances has been discarded.6 May be the alopecia is related to abnormal responses to photoperiod. Many authors consider that this entity should not be considered a dysplasia, because it is
cyclic (reversible).
Clinical signs: the disease is more common in Boxers,
Bulldogs, Airedale Terriers and Staffordshire Terriers, but
can be diagnosed in any breed. Males and females are equally affected. Most animals are older than 2 years and the lesions appear predominantly in spring and autumn. Characteristic signs consist in well-demarcated (geometric)
alopecic and hyperpigmented areas located in both flanks.
The alopecia persist for a few months and then, usually, the
hair grows again. General condition is good and there is no
pruritus.
Diagnosis: clinical picture is very suggestive. However,
deffinitive diagnosis is based on skin biopsy. In early stages,
hair follicles appear in telogen, moderately dilated and with
dysplastic images. Dysplastic follicles usually have an octopus-appearence. Sebaceous glands are melanized.
Treatment: Paradis has treated some patients with melatonine. Prognosis is unpredictable in any given patient.

Alopecia and meloderma


of Yorkshire Terriers
Cause: unknown. Genetic basis suspected (only YT affected, high prevalence in certain families and breederds).
Clinical signs: Yorkshire Terriers, males and females,
between 6 months and 3-4 years are affected. Typical
changes are alopecia and hyperpigmentation over the bridge
of the nose, on the pinnae and occasionally tail and feet. Affected skin is smooth and shiny. There is no pruritus.
Diagnosis: skin biopsies revealed hyperkeratosis, and
telogenic, moderately dysplastic hair follicles.
Treatment: no effective treatment for these entity has
been described.

References
1.
2.
3.

4.
5.

King DF, (1992), Dysplasia. An abused and confusing terminology,


Am J Dermatopatol, 14: 454-461.
Roperto F, Cerundolo R, Restucci et al., (1995), Colour diluton alopecia (CDA) in ten Yorkshire Terriers, Vet Derm, 6: 171-178.
Beco L, Fontaine J, Gross TL et al., (1996), Colour dilution alopecia
in seven dachshunds. A clinical study and the heredity, microscopical
and ultrastructural aspects of the disease, Vet Derm, 7: 91-97.
Miller WH, (1990), Folllicular dysplasia in adult black and red
Doberman pinschers, Vet Dermatol, 1: 181-186.
Miller WH, Scott DW, (1995), Follicular dysplasia of the portuguese

6.

7.

water dog, Vet Derm, 6: 67-74.


Curtis CF, Lloyd DH, Evans H, (1995), An investigation of the reproductive and growth hormone status of dogs affected by cyclical
(seasonal) flank alopecia at both maximu and minimum photoperiod,
Proceedings of the 12th Annual Congresss of the ESVD, pp 230,
Barcelona.
Miller M, Dunstan R (1993), Seasonal flank alopecia in Boxers and
Airedale Terriers: 24 cases (1985-1992), J Am Vet Med Assoc, 203:
1567-1572.

469
8.

9.
10.
11.

Paradis M, (1995) Hereditary skin diseases in dogs and cats: selected


topics, Proceedings of the 12th Annual Congress of the ESVD, pp
138-139.
Carlotti DN, (1993), A propos de alopecies auriculaires. Point Veterinaire, 25: 8-12.
Lampiris D, (1985), Skin condition in Yorkshire Terriers, Canine
Pract, 12:29.
Lampiris D, (1985), Skin condition in Yorkshire Terriers, Canine
Pract, 12:29.

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471

Fracture, nonunion and deformity treatment


with the Ilizarov Method
Antonio Ferretti

The Ilizarov apparatus is a circular type, three-dimensional fixator characterized by wires which can be driven
through the bone in all directions, fixed to the rings at 360.
The only limitation is the anatomy, with certain positions
which have to be avoided to prevent neurovascular damage
or tenomuscular interference which may lead to motory
function failure or alteration. The possibility of inserting
wires at an angle, possibly at 90, opposing wires with stoppers or threaded pins make the Ilizarov apparatus incredibly
stable against shear and rotational forces.

Fracture treatment
It is for these reasons that the Ilizarov system is perfectly indicated for fracture and nonunion treatment. Furthermore, the possibility of correcting bone segment positioning
via wire or ring movement makes the closed reduction of
fractures, as well as fracture site compression and distraction, possible.
The ideal assembly, which produces the highest degree
of stability, is the one with four levels of fixation: a proximal
block with two rings and a distal block with two rings (Fig.
1a). The proximal and the distal rings have to be as far as
possible from the fracture site; the middle rings as close as
possible to the fracture site. This is clearly not always possible. Figure 1b shows the assembly which is necessary when
dealing with an extensive diaphyseal comminuted fracture:
in this case the apparatus has a support function. The assembly in Figure 1c is not correct for fracture or nonunion treatment while it may be used, even if it is not the ideal solution,
for bone lengthening. The stability of the apparatus is increased by the tenomuscular elements and by the regenerated tissue subject to distraction tension. The assembly in Figure 1d is surely not correct because of its instability. Both the
rings of the proximal block and the rings of the distal block
are too close to the fracture site and are consequently unable
to contrast a long lever arm.
To stabilize metaphyseal fracture sites it may be necessary to extend the apparatus to the contiguous bone segment
(Fig. 2a-b). If this is not possible the metaphysis is to be
fixed with two levels of fixation (Fig. 3): at least two wires
on the ring and the third wire on supports or with threaded
pins as in Figure 4b.

The use of threaded pins in the proximall portion of some


segments (femur, humerus, tibia, radius-ulna) proved itself
an extremely valid solution enabling the stable fixation of
segments which cannot be surrounded by the apparatus
(proximal humerus and femur) (Fig. 4a) or when the wires
have to be positioned at an angle inferior to 60 (proximal
tibia and radius). The use of threaded pins in the proximal
tibia resulted extremely valid while problems have arisen in
the proximal radius, due to the limited thickness of the bone.
A hybrid assembly (wires and threaded pins) may easily
be used in the distal radius and tibia. If in the distal stump of
a short radius or tibia two levels of fixation cannot be used
(two rings with 4 wires or one ring with 2 wires and a third
wire on supports) an extremely stable fixation may be
achieved using two wires and a threaded pin, thus avoiding
the need of having to extend the apparatus to the metacarpus
or metatarsus (Fig. 4b).
The stability of the construct and the closed surgical
technique usually enables fracture healing in extremely brief
periods of time: 30-45 days. This is also dependent on the
extent of the vascular damage, the degree of contamination
of open fractures and the age (puppy or adult).

Nonunion treatment
The Ilizarov transosseous osteosynthesis technique
may be used extensively in small animal long bone
nonunion treatment.
The correct therapeutical approach makes it first necessary to analyse and classify the nonunions:
clinical presentation: stiff, mobile
radiographic presentation: hypertrophic, normotrophic,
atrophic
biological presentation: aseptic, septic.
The apparatus has to be assembled so as to guarantee the
maximum stability.
Goal of the approach is to re-establish (directly or subsequently) bone continuity.
That being said, nonunion treatment is as follows:
closed synthesis: the method is usually non invasive,
open synthesis: nonunion site opening is necessary to
- remove foreign bodies (metal implants)

SPECIALIST/INTERACTIVE PROGRAMME

Med Vet, Dipl ECVS


Private Practitioner, Cremona - Italy

472

4th European FECAVA SCIVAC Congress

Figure 1 - Different assembly confgurations of the Ilizarov apparatus.

- bring together stumps with a minimal contact surface


- sequestrectomy
- resection of necrotic or septic stump ends.
In consideration of the already limited viability of atrophic nonunion tissue any invasive intervention has to be as
limited and as precise as possible.
In small animals the nonunion osteosynthesis techniques more commonly being used are:
- distraction monofocal osteosynthesis: indicated in the
treatment of hypertrophic, aseptic, stiff nonunions with sure
stump viability;
- compression monofocal osteosynthesis: indicated in all
cases of nonunions (including the hypertrophic, for which a
simple stabilization would be enough), while it is absolutely
indispensable in the treatment of atrophic nonunions;
- compression and subsequent distraction monofocal osteosynthesis: it may be used for normotrophic or atrophic
nonunions in which the compression has led to an improved
trophism of the nonunion site.
- Distraction and subsequent compression bifocal osteosynthesis, also defined as transportation or internal
lengthening osteosynthesis: it may be used for atrophic
nonunions with spontaneous loss of substance or following
the surgical resection of necrotic or septic bone.

a
Figure 2 - Frame extension to the carpus and tarsus.

In the case of transportation or internal lengthening the


distraction should be of 1/4 mm every 6 hours, the same as
for lengthenings, however in all other cases of nonunion site
distraction it is necessary to go down to 1/4 mm every 12
hours or even every 24 hours. This until the appearance of a
lively and abundant regenerated tissue. At this point the distraction can continue with a faster pace.
Nonunion consolidation takes place in times varying between 50 and 90 days.

Limb deformity treatment


Causes of limb deformity in the dog are various. In the
growing animal they may depen d on metabolic disorders or
on traumas affecting the growth cartilage; the radio-ulnar
segment is the most affected. In both mature animals and
puppies the deformity may present itself as a stiff nonunion,
a malunion or joint stiffness.
Deformity analysis
The deformity may be simple, if it has a single plane of
deviation, or complex if the deviation is on more planes.
Taking the curved radius as an example there are three

b
Figure 3 - Metaphyseal fixation with wires.

4th European FECAVA SCIVAC Congress

473

Figure 4a - Proximal fixation of tibia and femur with half-pins.

Figure 4b - Distal metaphyseal fixation of radius and tibia with wires and
half-pins.

Figure 7 - Hinges application in a complex deformity.

planes of deviation: valgism, forward curvature and external rotation. The first two may be assessed radiographically,
while the external rotation is to be assessed on the patient.
A careful analysis of the deformity helps to plan the procedure and to carefully pre-assemble the apparatus. The intervention is thus easier and faster.

b
a

Figure 5 - Positioning of the rings: the rings have to be perpendicular to


the bone on both a) the frontal plane and b) on the lateral plane.

Assembly of the apparatus


The apparatus is pre-assembled using x-rays as reference. The ring and half ring diameter is selected according
to the patients size: it has to be greater (by at least 2 cm per
side) than the maximum diameter of the segment to be treated. Taking the radius and the tibia as an example the dimension which determines the diameter of the assembly is the

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Figure 6 - Construction of hinges.

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4th European FECAVA SCIVAC Congress

Figure 8 - The type of correction depends on the positioning of the hinges: a) in correspondence with the apex of the convexity; b) beyond me apex of the deformity; c) in an intermediate position between the convex and concave apex of the deformity.

one of the proximal third of the bone.


The rings have to be perpendicular to the longitudinal
axis of the bone segment. To apply the rings correctly it is
therefore fundamental to recognize the various planes of deviation. In a deformity with both valgism and forward curvature the rings have to be perpendicular to the bone on both
the frontal plane (valgism) and on the lateral plane (forward
curvature). The rings are consequently set in an oblique position, downward anteriorly and medially (Fig. 5).
It is not always necessary to correct all the deformities
present. In a deformity with a serious valgism and a slight
forward curvature it may be for example better to treat the
first and not the second, clearly only if this should not lead
to functional disorders.
Hinge positioning
The hinges are the mechanical elements which enable
the dynamic correction of the deformity (Fig. 6). It is thanks
to the invention of the hinges that Ilizarov transformed a
circular external fixator into a real bio-apparatus capable,
via distraction and compression, of progressively altering
the shape of a bone segment.
Hinges
- They have to be positioned at the same level of the deformity with their axis exactly perpendicular to the plane of
deformity (Fig. 7).
If the deformity is characterized by more deviations (as
in the case of the curved radius), the plane of deformity is
not exactly frontal or lateral but is instead an oblique plane
resulting from the combination of the two deviation planes.
Taking the curved radius as an example the plane is oblique
in a postero-anterior and lateral-medial direction with a tendency to being closer to the plane of the more serious deviation; or exactly in-between if the two deviations are of
equal importance.
- They may be positioned in correspondence with the
apex of the convexity (Fig. 8a): by progressively distracting
the opposite side a wedge shaped space is obtained which
will then be filled by regenerated bone (Fig. 9).
- If the correction of the axis together with a bone
lengthening are desired, the hinges have to be positioned be-

yond the apex of the deformity and the amount of lengthening is proportional to the distance between the hinge axis
and the apex of the deformity (Fig. 8b).
- If they are instead set in an intermediate position between the convex and concave apex of the deformity this determines the distraction of the concave part and the compression of the convex part (Fig. 8c).
Site of the deformity
The site of deformity does not always correspond to the
part which is visually deformed. To establish the exact site it
is necessary to trace the axes of the segment. Their point of
intersection corresponds to the real point of deformity, the
point where the hinges have to be positioned with the possible variations presented in Figure 8 a, b, c.
Figure 10 explains this concept in greater detail: in a the
position of the stumps is presented. In b the point of intersection of the segments axes enables to identify the real site
of the deformity. The hinges are positioned in correspondence with such point (Fig. 10c). In Figure 10d the axis is
perfectly correct; while in Figure 10e the hinges have been
positioned in correnspondence with the apex of the malunion area. This enables to correct the angle however a lateral shift of the stumps remains.
Distraction
The correction requires that the cortical bone distraction
on the concave side of the deformity is of 1 mm per day (Fig.

Figure 9 - Radiographic appearance of 23 days regenerate.

4th European FECAVA SCIVAC Congress

475

Figure 10 - Deformity site in a case of malconsolidation: a) position of the stumps. b) The point of intersection of the segament axis enables to identify the real site of the deformity. c) The hinges are positioned in corrispondence with such point. d) The axis has been perfectly corrected. e) The hinges have been positioned in corrispondence with the apex of the malunion area. This enables to correct the angle however a lateral shift of the stump remains.

Figura 11 - Calculation of the distraction rate.

radiographic appearance of a viable regenerated tissue.


Should this take place the usual 1/4 mm every 6 hour distraction may be resumed.
Fixation
The fixation period following deformity correction
(meaning lengthening) is necessary to enable the consolidation of the regenerated tissue and is proportional to the extent of the lengthening. For example: a 3 cm lengthening of
a dog radius-ulna requires about 30 days of fixation. Before
removing the apparatus it is however necessary to confirm
the degree of consolidation with an x-ray examination.

References
Aaron A, Eilert R: Results of the Wagner and Ilizarov methods of limblengthening. J Bone Joint Surg Am 78:20-9, 1996
Aronson J, Johnson E, Harp J: Local bone transportation for treatment of
intercalary defects by the Ilizarov technique. Biomechanical and clinical considerations. Clin Orthop p 71-9 1989
Breur GJ, Zerbe CA, Slocombe RF, et al.: Clinical, radiographic, pathologic, and genetic features of osteochondrodysplasia in Scottish deerhounds. J Am Vet Med Assoc 195:606-612, 1989
Catagni MA, Malzev V, Kirienko A: Correction of angular deformities, in
Bianchi Maiocchi A (ed): Advances in Ilizarov apparatus assembly.
Milan, Italy, Medicalplastic, 1994, pp 98-112
Delloye C, Delefortrie G, Coutelier L, et al.: Bone regenerate formation in
cortical bone during distraction lengthening. An experimental study.
Clin Orthop 250:34-42, 1990
Elkins AD, Morandi M, Zembo M: Distraction osteogenesis in the dog using the Ilizarov external ring fixator. J Am Anim Hosp Assoc 29:419426, 1993
Ferretti A: The application of the Ilizarov technique to veterinary medicine,
in Bianchi Maiocchi A, J Aronson (eds): Operative principles of
Ilizarov. Baltimore, Williams & Wilkins, 1991, pp 563-565, 570
Ferretti A: Small bone fixator, in Bianchi Maiocchi A (ed): Advances in
Ilizarov apparatus assembly. Milan, Italy, Medicalplastic srl, 1994, pp
134-139
Fleming B, Paley D, Kristiansen T, et al.: A biomechanical analysis of the
Ilizarov external fixator. Clin Orthop 241:95-105, 1989
Frierson M, Ibrahim K, Boles M, et al.: Distraction osteogenesis. A comparison of corticotomy techniques. Clin Orthop 301:19-24, 1994
Ilizarov GA: The tension-stress effect on the genesis and growth of tissues.

SPECIALIST/INTERACTIVE PROGRAMME

11A). To achieve this it is necessary to measure (Fig. 11B)


(both on x-rays and on the patient) the distance between the
hinge axis and the distraction rod (C) and between the hinge
axis and the cortical bone on the concave side of the deformity (B). The C:B ratio gives the daily rod distraction which
generates a 1 mm bone distraction per day. These measurements are obviously approximate since both radiographic
and patient measurements are also approximate. To verify if
the amount of distraction is sufficient a radiographic examination is carried out after 7 days.
If a corticotomy or an osteotomy have been carried out,
meaning in all cases of deformity or malunion, the bone distraction rate has to be of 1/4 mm every 6 hours (after a 3-7
day waiting period depending on the damage produced). In
the case of hypertrophic stiff nonunions the bone is not discontinued and is instead directly distracted with the goal of
both correcting the deformity and of inducing, via the distraction tension, the consolidation of the hypertrophic
nonunion site. In this case the distraction rate has to be slower, for example 1/4 mm every 12 hours, continuing until the

476
Part I. The influence of stability of fixation and soft-tissue preservation. Clin Orthop 238:249-281, 1989
Juan J, Prat J, Vera P, et al.: Biomechanical consequences of callus development in Hoffmann, Wagner, Orthofix and Ilizarov external fixators.
J Biomech 25:995-1006, 1992
Latte Y: A specific vet Ilizarov apparatus for the treatment of fractures, delayed union, non union and mal union. Proc Vet Orthop Soc 1991, p
51 (abstr)
Latte Y: Studies of 63 cases treated by Ilizarov apparatus: indications, results, complications. Proc Vet Orthop Soc 1993, p 12 (abstr)
Latte Y: Application de la mthode dIlizarov en chirurgie orthopdique
vtrinaire. Prat Md Chir Anim Comp 29:545-570, 1994
Marcellin-Little DJ, Ferretti A, Roe SC, DeYoung DJ. Hinged Ilizarov external fixation for correction of radial deformities in dogs. Vet Surg
1997, 26:5, 439
Marcellin-Little DJ, Ferretti A, Roe SC, DeYoung DJ. Hinged circular external skeletal fixation for correction of radial deformities. ACVS
Meeting, Orlando, Florida,1997/ ECVS Meeting, Versailles, France,
1997
Marcellin-Little DJ, Ferretti A, Roe SC, et al.: Hinged Ilizarov fixation for
correction of antebrachial deformities. Vet Surg 27:in press, 1998
Orbay J, Frankel V, Finkle J, et al.: Canine leg lengthening by the Ilizarov
technique. A biomechanical, radiologic, and morphologic study. Clin
Orthop 1992, p 265-73

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Paley D: The principles of deformity correction by the Ilizarov technique:
technical aspects. Techniques Orthop 4:15-29, 1989
Paley D, Catagni MA, Argnani F, et al.: Ilizarov treatment of tibial
nonunions with bone loss. Clin Orthop 241:146-165, 1989
Paley D: Problems, obstacles, and complications of limb lengthening by the
Ilizarov technique. Clin Orthop 250:81-104, 1990
Paley D, Fleming B, Catagni M, et al.: Mechanical evaluation of external
fixators used in limb lengthening. Clin Orthop 1990, p 50-7
Stoffelen D, Lammens J, Fabry G: Resection of a periosteal osteosarcoma
and reconstruction using the Ilizarov technique of segmental transport. J Hand Surg [Br] 18:144-6, 1993
Tetsworth K, Krome J, Paley D: Lengthening and deformity correction of
the upper extremity by the Ilizarov technique. Orthop Clin North Am
22:689-713, 1991
Tetsworth KD, Paley D: Accuracy of correction of complex lower-extremity deformities by the Ilizarov method. Clin Orthop 301:10210, 1994
Waanders NA, Herzenberg JE: The theoretical application of inclined
hinges with the Ilizarov external fixator for simultaneous angulation
and rotation correction. Bull Hosp Jt Dis 52:27-35, 1992
Zembo MM, Elkins D, Morandi M, et al.: Radiographic analysis of regenerate bone formation following tibial distraction osteosynthesis by
the method of Ilizarov with a circular external fixator in a canine
model. Trans Orthop Res Soc 1990, 15: p 120 (abstr)

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477

Lymphnode cytology:
normal, inflammatory and neoplastic aspects
Corinne Fournel-Fleury
Laboratoire dImmunopathologie-Hmatologie-Cytologie, Ecole Vtrinaire de Lyon - France

Cytology allows in most cases, the differential diagnosis


between reactive and neoplastic lymphadenopathy.
The different reactive lymphadenopathies may be classified in hyperplasias (plasma cells, follicular, immunoblastic,
T-cells and mixed hyperplasias), adenitis (neutrophilic,
granulomatous and eosinophilic) and mixed patterns.
Neoplastic lymphadenopathies fall into two categories:
the primary tumors of the lymph node i.e. malignant lymphomas and the metastatic lymphadenopathies. The main
cancers which metastasize to the lymph node are mast cell
tumors, carcinomas and malignant melanomas and, occasionally, sarcomas (in particular hemangiosarcomas).
Three main difficulties exist for the diagnosis of metastatic
lymphadenopathy: extensive necrosis, massive lymph node
infiltration and micrometastasis.
Malignant lymphomas can be recognized in most cases
by cytology. They can be classified on the bases of morphological criteria which are closely related, in our experience,
with their immunophenotype. Either in the B-cell or in the Tcell lineage, one can distinguish low-grade lymphomas,
mainly constituted of small differentiated cells and highgrade blastic lymphomas. However, the determination of
the immunophenotype necessitates immunological labellings which are used, either on cytological preparations
or on tissue sections. The main difficulties for differential diagnoses between hyperplasias and malignant lymphomas
are encountered for small-cell lymphomas, mixed lymphomas and lymphomas at early stages. In doubtful cases,
the cytological examination provides the best arguments for
a rapid lymph node excision and histological examination.

Lymph node fine needle aspiration cytology is justified:


- in any case of a lymphadenopathy which constitutes a
major clinical sign and particularly in all cases of generalized lymph node enlargement;
- in any case of a persistent lymphadenopathy even moderate or isolated, whose origin is not apparent.
Cytology allows in most cases:
- the differential diagnosis between reactive and neoplastic lymphadenopathy;
- furthermore, in many cases, the diagnosis or the presomption of the underlying disease.
However, a histological examination of the lymph node

is indispensable in any instance where the diagnosis cannot


be established with certainty by cytological examination
alone.

Normal lymph node cytology


To understand lymph node cytology and so, the possibilities and limits of cytological diagnosis, it is important to understand:
- the histology of the normal lymph node;
- the normal cellular composition of the different lymph
node areas on a morphological and phenotypical point of view;
- the successive stages of the lymphoid differentiation.
On tissue section, the normal lymph node is organized in:
- a dense cortical area
- and medullary cords centred on the hilus.
The cortical area is itself separated into:
- a superficial cortex in which are located the follicles
with the germinal centers;
- a deep cortical area which goes from the interfollicular
region to the medullary cords.
The cellular composition of those different lymph node
areas is constituted by lymphoid cells and non lymphoid accessory cells
- The two categories of lymphoid cells are:
B-cells which produce antibodies via plasma-cells.
They are located in the superficial cortex and the medullary
cords which constitute B-cell areas
T-cells which regulate the humoral response (helpers
or suppressors) or are effector cells (particularly the cytotoxic cells). They are located in the paracortex = T-cell area.
- The three categories of non-lymphoid accessory cells of
the immune response, are:
antigen presentating cells: follicular dendritic cells for
B-cells and interdigitating cells for T-cells;
histiocyte-macrophages;
inflammatory cells, which appear only in reactive conditions.
Cell identification is based on size, nuclear and cytoplasmic criteria:
- cell size, established from the size of the nucleus in comparison with the size of two red blood cells;

SPECIALIST/INTERACTIVE PROGRAMME

Summary

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4th European FECAVA SCIVAC Congress

- nuclear shape and chromatin;


- nucleoli: number, size and location;
- cytoplasm, size and colour.

So, the expected effect of an Ag stimulation is an increase of


the number of blast cells and plasma cells in the lymph node!
It is now easy to understand that:

The different B cells are:


- Small B lymphocytes (mainly in the superficial cortex
and primary follicles)
- Centrofollicular cells in germinal centers of follicles
- B immunoblasts (follicles and interfollicular regions)
- Plasma cells (in the medullary cords)
- An original macronucleolated medium-sized cell (MMC),
particular to the canine species, in perifollicular marginal
zones.
Follicular B cells are also identified by their grouping
with follicular dendritic cells which are recognized by their
highly elongated, sinuous and pink cytoplasm.
By contrast, the T-cell lineage is restricted to two categories of cells:
- small T-lymphocytes,
- T-immunoblasts,
Small T-lymphocytes are very similar to their B-cell
counterpart, except some nuclear irregularities and sometimes a more extended pale cytoplasm which may argue for
their T-cell origin.
T-immunoblasts, are quite similar to the B-immunoblasts
but their cytoplasm may be paler than that of B-immunoblasts.
So, regarding the common pale cytoplasm of T cells,
clear cells, either in reactive lymph node or in lymphomas,
may suggest a T-cell origin.
Finally, T-cell areas are identified by the presence of
their particular antigen-presentating cells named interdigitating cells characterized by their twisted nucleus and
their abundant pale, poorly-outlined cytoplasm which
stands out against the dense mass of surrounding small
lymphocytes.
At last, macrophages and inflammatory cells can be observed in the lymph node, and they are, more numerous, of
course, in inflammatory conditions.
The lymphoid differentiation scheme, established by
Lennert for humans, can probably be applied, in the main
outlines, to dog and cat. In this scheme, the successive stages
of B and T cell differentiation would be the following:
For the T-cell lineage:
After Ag stimulation, small T lymphocyte (T1) gives rise
to a T immunoblast and then to small lymphocytes (T2), regulator, effector of the cellular immune response or memory
cells.
For the B-cell lineage:
After Ag stimulation, small B lymphocyte (B1) gives rise
to a plasma cell via a B immunoblast or enters the follicle for
amplification of the immune response and gives rise to a
centroblast and then centrocytes and small B lymphocytes
(B2), memory cells.

- Normal lymph node cytology is characterized by:


an heterogeneous lymphoid population
a large predominance of small mature lymphocytes (Bor T- cells)
less than 5% of blast cells (centroblasts and immunoblasts)
up to 5% of plasma cells.
- Cytology bases the identification of the different reactive lymphadenopathies on the incidence of the different cell
populations but also on their possible groupings.

REACTIVE LYMPHADENOPATHIES
One can distinguish:
- predominant lymphoid reactions (= hyperplasias), under Ag stimulation
- and predominant inflammatory reactions (= adenitis).
Reactive hyperplasias are characterized by:
-an heterogeneous lymphoid population because of the
mixing of the different cell populations involved in the normal differentiation scheme
- an increasing number of blasts cells even if small lymphocytes remain predominant
- a high number of plasma cells.
However they can be classified on the basis of the predominant increasing cell population in:
- Plasma cell
- Follicular (centroblastic)
- Immunoblastic
hyperplasias.
T-cell, and
- mixed

* Plasma cell hyperplasia:


-indicates a strong, local or systemic, antigenic stimulation
- is very common in veterinary dermatology
- is particularly suggestive of Leishmaniasis and other
chronic dysglobulinemia in case of multiple adenopathies.
* Follicular hyperplasia:
-is suggested by an association of centroblasts, centrocytes, follicular dendritic cells, macrophages (with tingible
bodies), numerous mitoses in dense packed cell agregates
- is mainly encountered in feline retrovirus related persistent lymphadenopathies.
* Immunoblastic hyperplasia
- is characterized by an increasing number of immunoblasts, more numerous than the centroblasts
- is a rare condition which suggests mainly a viral infection

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Adenitis are partial infiltrations of the lymph node by inflammatory cells. They consist of:
- neutrophilic, acute or subacute
- granulomatous (chronic)
adenitis
- eosinophilic
- mixed

* The classification of neutrophilic adenitis is based on cell


morphology:
- The presence of degenerative changes (light staining of
the nucleus, effacement of cytoplasmic outline...) is characteristic of acute suppurative adenitis and suggests sepsis. In
our experience, it is a very rare event in canine and feline
medicine.
- On the other hand, the presence of neutrophils without
degenerative changes is common in subacute non septic
adenitis, mainly encountered in mixed inflammatory
processes (especially associated with chronic skin diseases).
* Granulomatous adenitis
- is recognized on the basis of an increased number of
histiocytes and macrophages
- suggests a chronic process and especially a chronic
bacterial or fungal infection, Leishmaniasis or mycobacterial infection if epithelioid cells are present
- Finally, benign multicentric histiocytosis is a rare multicentric involvement of the skin and the lymph nodes of the
young dog by histiocyte population, that may be classified
like a particular granulomatous adenitis.
* Eosinophilic adenitis
- is easy to recognize due to the numerous eosinophils
and frequently mast cells.
- is a common feature in chronic skin disease associated
with hypersensitivity.
- is especially massive in feline eosinophilic granuloma
complex.

eosinophils
MMC
- Leishmaniasis, if are encountered together:
plasma cell
epithelioid cells
MMC

Neoplastic lymphadenopathies
They fall into two categories:
- The primary tumors of the lymph node: the malignant
lymphomas
- The secondary invasions of the lymph node: the
metastatic lymphadenopathies

METASTATIC LYMPHADENOPATHIES
The main non-hematopoietic cancers with a predilection
for lymphoid tissue are the carcinomas, mast cell tumors and
malignant melanomas. Occasionally, certain sarcomas, and
in particular hemangiosarcomas, may follow the lymphatic
route. Furthermore, with certain malignant, non-lymphoid
hemopathies, such as acute myeloid leukemias (AML) and
malignant histiocytosis, there may be a secondary invasion
of the lymph node.

General principles of diagnosis on the basis of a lymph


node smear
The results given by a lymph node smear depend on the
following factors, in order of importance:
- its technical quality;
- the degree of invasion of the lymph node;
- the degree of morphological difference between the tumor cells and the residual lymph node cell population;
- the possibility of carrying out, in parallel, a cytological
examination of the primary tumor, which considerably facilitates the identification of the same cells in the lymph node
smear.

Metastatic, non-hematopoietic cancers


* In fact, mixed patterns are more commonly encountered in
reactive lymph node cytology. Among these mixed patterns,
three are highly suggestive of a particular aetiology:

Malignant mast cell tumors

- Chronic skin disease lymphadenopathies grouping together:


various inflammatory cells
hemosiderin or melanin-laden macrophages
numerous plasma cells

In dogs, essentially, grade II and grade III mast cell tumors frequently metastasize to the lymph node. The diagnosis is mainly based on:
- the massive involvement
- and the abnormal morphology of the neoplastic cell in
mast cell tumors.

- Systemic lupus erythematosus, suggested on lymph


node smear by the grouping of:
numerous plasma cells

A particular difficulty exists in the differential diagnosis


between adenitis and metastasis due to the possible massive
invasion by the mast cell and eosinophils in the cat, in the

SPECIALIST/INTERACTIVE PROGRAMME

* T-cell hyperplasia is different from other reactive patterns because of the predominance of an homogeneous small
lymphocyte population.
- It can be recognized by the presence of numerous interdigitating cells and sometimes of pale immunoblasts. It is
mainly associated with chronic dermatitis (like in human
medicine).

479

480

Eosinophilic Granuloma complex, but also in the dog in case


of hypersensitivity.

Carcinomas
These metastasize, most frequently, in the form of voluminous emboli which preserve their organization in the form of
characteristic juxtaposed epithelial cell clusters within the
lymph node. The cells, which are often large, and with strong
cytological criteria of malignancy, stand out in the middle of the
residual lymph node cell population, which is often dispersed
and mixed with a large population of inflammatory cells.
A misdiagnosis between granulomatous adenitis and
metastatic carcinoma must be avoided especially when
epithelioid cells are very numerous. But the histiocytic appearance of this population, its frequent association with
neutrophils and the absence of malignancy criteria are the
basis of the diagnosis of reactive granulomatous adenitis.

4th European FECAVA SCIVAC Congress

a residual lymph node population. Hemangiosarcomas, in particular, give highly hemorrhagic lymph node smears, in which
a few cells, or groups of cells, are dispersed. These are cytologically very malignant, and for the most part, distinctly spindle-shaped, what suggests a mesenchymal origin.

Malignant metastatic non-lymphoid hemopathies


Acute myeloid leukemias (AML)
All AMLs can invade lymph nodes secondarily. It is the
recognition of an often partial invasion of the lymph nodes
by poorly-differentiated blast cells, with, occasionally, some
rare, characteristic granules against a background of a reactive lymphoid cell population, which, associated with the result of the blood smear and the bone marrow smear, corroborates the diagnosis.

Malignant histiocytosis
Malignant melanomas
A diagnosis of metastatic invasion of the lymph node by
a malignant melanoma may be very easy, or very difficult.
It is very easy in case of:
- lymphadenopathy associated with a pigmented oral or
digital tumor
- a massive invasion by cells with, frequently, abnormal
nuclei, and characteristic, fine, blackish, dispersed cytoplasmic melanin granules.
It is more difficult in:
- the early detection (which is also the most useful) of
rare, dispersed cells in a dense lymph node smear.
- malignant amelanotic melanomas, which are often
highly atypical, and suggest a metastatic lymphadenopathy
of undifferentiated cancer as the only diagnosis.
- when micrometastases appear against the background
of an inflammatory lymph node with numerous melanophages and granules of melanin dispersed in the smear background.
So, it is important:
- to perform a careful examination of the smears which
can allow the vizualisation of a single malignant cell which
contains some granules of melanin.
- to use the Fontanas stain which can also be a valuable
aid to the revelation of melanin granules.
The identification of authentic melanophages is always
of real diagnostic value in an oncological context, since, by
concentrating melanin granules, they serve as a means to
identify weakly-pigmented melanomas.

Sarcomas
In comparison with the tumors mentioned previously,
sarcomas rarely metastasize to the lymph node.
When they do so, it is often in a massive fashion and with
very aggressive tumors, it is sometimes very difficult to detect

This rare tumor invades lymph nodes and numerous other soft tissue sites (notably the lungs and pleura), and, especially, the hematopoietic bone marrow. The diagnosis is supported by the following histiocytic characteristics:
- the finely reticulated appearance of the chromatin and
- weakly basophilic cytoplasm, with imprecise outlines
and cytophagocytosis capacities. As in the previous cases,
the lymph node smear is no more than a complementary element in the diagnosis.

Finally, three main difficulties remain in the diagnosis of metastatic lymphadenopaties


1) The existence of extensive necrosis in all samples,
without any possible characterization of underlying cells
which poses in itself the problem of a neoplastic necrosis
and often indicates the absolute necessity of doing a control
biopsy.
2) The massive lymph node infiltration without any
residual lymphoid population.
3) The possible existence of micrometastasis.

MALIGNANT LYMPHOMAS
Classifications
Malignant lymphomas are characterized by the progressive invasion of the lymph node by a neoplastic cell clone
that has been more or less arrested at a certain stage of differentiation, destroying little by little the normal histological
lymph node architecture.
The classifications are based on the principle that lymphomatous cells represent the malignant equivalent of the
different normal lymphoid cell types.
In the dog the determination of the immunophenotype allows a classification of canine lymphomas according to the

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B-cell lymphomas
Low-grade malignancy
Small cell
Lymphocytic
Lymphoplasmocytic
Prolymphocytic
Centrocytic
Centroblastic/centrocytic
Macronucleolated medium-sized cell (MMC)
High grade malignancy
Centroblastic
Monomorphic
Polymorphic
Immunoblastic
Small cell, unclassifiable
Burkitt-type
Plasmacytoid
Lymphoblastic
T-cell lymphomas Low-grade malignancy
Small cell
Clear cell
Prolymphocytic
Pleomorphic small cell
Mycosis fungoides
High grade malignancy
Pleomorphic, mixed, small and large cell
Pleomorphic large cell
Immunoblastic
Small cell, unclassifiable, plasmacytoid
Lymphoblastic
According to their frequency, the most common types of
NHL encountered in the dog are of the B-cell phenotype,
mainly centroblastic polymorphic with a mixing of several
cell components.

histological examination
It is true that a cytological examination alone cannot
confirm the follicular or diffuse architecture of a lymphoma,
which requires histology. This is important for a prognosis,
since follicular lymphomas are of lesser malignancy. The
problem, however, remains minor with canine and feline
lymphomas, given the low percentage of follicular lymphomas encountered
In cytology, the diagnosis of the majority of lymphomas
is easy on the basis of a blastic, monomorphous, homogeneous cell population without an associated plasma cell hyperplasia. This population replaces the reactive lymph node
cell population, which is normally heterogeneous and rich in
plasma cells. Cytologically speaking, the more massive the
lymph node invasion is, and the more the lymphomatous
cells differ from the cell populations that are normally dominant in the lymph node, the easier the diagnosis will be.
However, the cytological diagnosis is difficult:
- at the beginning of an invasion, or with an associated
reactive lymphadenopathy (which is a frequent case when a
lymph node smear is done on the mandibular lymph node
that has been the site of repeated antigenic stimulation),
- in small-cell lymphomas whose cells are similar to
small normal lymphocytes,
- in mixed lymphomas.
The main difficulties remain among the small cell proliferations and the differential diagnosis must be established
between:
- T-cell hyperplasias and small cell lymphomas,
- Plasma cell hyperplasias and immunocytomas or multiple myelomas which are two malignant lymphomas with
plasmocytic differentiation.
Among the blastic proliferations, the differential diagnosis will be made between:
-blastic lymphomas and some marked follicular and / or
immunoblastic hyperplasias.

General principles of the cytological characterization


of lymphomas
Cytological analysis of a lymph node smear or lymph
node imprint gives an excellent identification of cell types,
and distinguishes between variants that may escape notice at

- MMC lymphomas and marginal zone hyperplasias.


In doubtful cases, a lymph node smear will settle the
question of carrying out a rapid lymph node excision for
a confirmatory histological examination.

SPECIALIST/INTERACTIVE PROGRAMME

Updated Kiel classification. In this model the various types


of canine lymphomas may be classified in:

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4th European FECAVA SCIVAC Congress

483

Inflammatory diseases of hair follicles


Luca Mechelli
Med Vet
Institute of Veterinary Patology, University of Perugia - Italy

The primary task of the hair follicles is to produce hairs


and this cyclic activity requires a complex structure. The
knowledge of the microanatomy of the hair follicle provides
the basis for the understanding of pathogenetic mechanisms
occuring and to classify follicular inflammation/non-inflammation diseases.

The anagen hair follicle, extending from top to bottom,


can be divided in three major anatomic regions:
1) the superficial segment, or infundibulum, which extends from ostium to the site insertion of the sebaceous
gland duct, lined by an epithelium identical to epidermis;
2) the isthmus which extends from infundibulum to the
insertion of the arrector pili muscle or, better, from the end
of the follicular inner root sheath cornification to the beginning of it in the bulge region. The follicular outer sheath
cells of this segment are small, differentiate and produce
amorphous keratin (trichilemmal keratinization);
3) the inferior segment, which extends from the insertion of the arrector pili muscle to the base of the follicle.
The inferior portion contains a spherical base known as the
hair bulb. Inner and outer root sheath are present during the
anagen phase in the inferior segment. Hair bulb with hair
matrix surround dermal papilla. A hyaline basement membrane and fibrous tissue surround hair follicle (fibrous
sheath).

Inflammatory diseases of the hair follicle


The anatomical classification of folliculitis is based on
the specific region of the hair follicle that is involved by inflammatory reaction and particular importance is placed upon whether there is invasion of the follicular lumen by inflammatory cells.
A. PERIFOLLICULITIS
This term, falled into disuse, is emploied to describe a
perivascular inflammatory cells infiltration of the periadnexal vascular plexus without involment of the outer root
sheath and no destruction of the basal cell layer of the hair
follicle.

B. MURAL FOLLICULITIS
The inflammatory response involves the outer root
sheath of the hair follicle without invasion of the pilar canal.
1. Interface mural folliculitis
The histological hallmarks are:
a) sparse cell necrosis, mainly in the follicular basal layer
and, less frequently, in stratum spinosum of the outer root
sheath;
b) diffuse hydropic change in the follicular basal layer;
c) pigmentary incontinence, free in the dermis or phagocytosed by macrophages;
d) diffuse infiltrates of inflammatory cells restricted to
the middle and upper portions of the hair follicles.
Examples:
erythema multiforme
lupus erythematosus
demodicosis
dermatomyositis
dermatophytosis (some manifestations)
2. Infiltrative mural folliculitis
The inflammatory reaction involves the wall of the hair
follicle mainly at and above the level of isthmus.
Mononuclear cells, for the most part lymphocytes and
histiocytes, are directed against antigens located into the
outer sheath epithelium of the hair follicles.
Interface mural folliculitis and infiltrative mural folliculitis are invariably connected, representing different
phases of the same immunological reaction.
Examples:
Canine and feline sebaceous adenitis
Feline idiopathic mural folliculitis
Idiopathic granulomatous folliculitis of dogs
Equine linear alopecia
3. Necrotizing mural folliculitis
This lesion represent a particular form of mural folliculitis where the necrosis affects the wall of the follicle at and
below isthmus. The cell infiltrate is predominantly
eosinophilic and the lesions are the same as those described
for eosinophilic furunculosis.
Examples:
Canine eosinophilic furunculosis of the face
Feline mosquito bite hypersensitivity

SPECIALIST/INTERACTIVE PROGRAMME

Summary

484

4th European FECAVA SCIVAC Congress

4. Pustular mural folliculitis


The inflammatory process is characterized by pustules
within the wall of the superficial hair follicle, usually at or
above isthmus. The pustules contain neutrophils, rare
eosinophils and acantolytic follicular epithelial cells.
Examples:
Pemphigus erythematosus
Follicular pemphigus foliaceus.
C. LUMINAL FOLLICULITIS
This type represent the most common pattern of folliculitis. The inflammatory cells, usually neutrophils or eosinophils,
migrate into the lumen of the hair follicle and gather in this
side before releasing their inflammatory mediators. Evidently,
all luminal folliculitis must be mural initially.
Examples:
Bacterial or dermatophytic or parasitic folliculitis.

D. BULBITIS
The lesion is characterized by cellular infiltrate that surrounds, invades and damages the inferior segment of the hair
follicle, resulting in telogenization, follicular atrophy or dystrophic hair production.
The infiltrate, often described as like a swarm of bees
around the bulb, is primarily represented by T-lymphocytes
(CD8 +) and handful of macrophages, Langerhans cells and
neutrophils.
Apoptotic cells in bulb and in outer root sheath of the inferior part of the hair follicle are a possible feature.
Example:
Alopecia areata.

References
Caswell, J.L., Yager, J.A., Ferrer, L., Weir, J.A.M. Canine demodicosis: a
re-examination of the histopathologic lesions and description of the
immuno-phenotype of infiltrating cells. Veterinary Dermatology,
1995, 6: 9-19.
Dunstan, R.W. and Credille, K.M. The hair follicle and its diseases. Third
Veterinary Dermatology Residents Pre-Congress Meeting ESVD /
ECVD, Edimburgh, 11 September 1996.
Fondati, A., Fabbrini, F. and Mechelli, L. Due casi di follicolite e foruncolosi eosinofilica facciale nel cane. Veterinaria 1997, 11(6): 99-103.
Gross, T.L., Ihke, P.J., Walder, E.J. Veterinary Dermatopathology: a macroscopic and microscopic evaluation of canine and feline skin disease.
St louis: C.V. Mosby, 1992.
Gross, T.L., Stannard, A.A. and Yager, J.A. An anatomical classification of
folliculitis, Veterinary Dermatology, 1997, 8:147-156.
Mechelli, L. Patologie infiammatorie del follicolo pilifero del cane e del
gatto - Atti del XV Convegno Nazionale Associazione Patologi Italiani Veterinari (A.P.I.V.), 1996.
Olivry, T., Moore, P., Naydan, D. et al. Antifollicular cell-mediated and humoral immunity in canine alopecia areata. Veterinary Dermatology,
1996, 7: 67-69.
Scott, D.W., Miller, W.H., Griffin, C.E. Bacterial skin diseases. Muller and
Kirks Small Animal Dermatology, 5th edn. Philadelphia: W.B. Saunders Co., 1995.
Stannard, A.A., Gross, T.L. Noninfectious folliculitis. Proceeding of the 11th
Annual Congress of the European Society of Veterinary Dermatology,
1994; Bordeaux, France.
Von Tscharner, C. Inflammatory diseases of the follicles. Third Workshop
on Veterinary Dermatopathology (ESVD), 8-12 August 1995 - Royal
Veterinary College, University of London, UK.
Yager, J.A., Wilcock, B.P. Color Atlas and Text of Surgical Pathology of the
Dog and Cat; Volume 1: Dermatopathology and Skin Tumors. London: Wolfe, 1994.
Yager, J.A., Scott, D.W. The skin and appendages. In: Jubb, K.V.F.,
Kennedy, P.C., Palmer, N., eds. Pathology of Domestic Animals, Vol.
1, 4th edn. San Diego: Academic Press, 1993.

4th European FECAVA SCIVAC Congress

485

Approach to the patient with upper airway obstructive


diseases
Richard A. White

Summary
This interactive session gives the audience an opportunity to discuss the common problems encountered in small animal airway obstructive disease.
The first session is dedicated to the management of the
brachycephalic patient and deals with problems such as
stenotic nares, overlarge soft palate, hypertrophied pharyngeal mucosa, everted tonsils, laryngeal collapse and the related conditions which exacerbate the obstructed brachycephalic dog.
The second session deals with laryngeal dysfunction
concentrating on the current opinions on the diagnosis of laryngeal paralysis and reviews the controversies which surround its management. Other less commonly encountered
laryngeal diseases (polyps, tumours, trauma etc) will be discussed.

Brachycephalic obstructive disease


Incidence
Obstructive airway disease is commonly regarded as a
problem of the brachycephalic breeds including Bulldogs,
Pekingese, Pugs and to a lesser extent the less severely-affected breeds such as Mastiffs, Cavalier King Charles
Spaniels. The syndrome has many separate features which
contribute to the overall problem of airway obstruction and
it is important to appreciate that some of these factors are
primary, heritable and congenital as a consequence of deliberate conformational development whilst others are secondary and acquired as a consequence at a later stage in life.
The early recognition and management of the primary features is important to limit the potential for the development
of the more serious and possible fatal secondary changes.
Clinical signs and evaluation
The clinical features of airway obstruction are well established and range from stridorous breathing (pharyngeal
turbulence) in mild cases to intermittent cyanosis and syncopal collapse. Other presenting signs may include noisy
respiration, exercise intolerance, regurgitation and even dysphagia. The age of onset is variable and in some case may be
in puppyhood in some cases whilst others only become

symptomatic as the secondary changes become more evident.


Investigation should include auscultation of the entire
upper respiratory area, thoracic radiography, ECG and inspection under general anaesthesia. Anaesthesia for investigation and airway surgery should always be undertaken with
caution because of the difficulty of maintaining an airway
during the period between induction and intubation and during the recovery period. Ideally, procedures should be
planned during cooler weather or in environmentally-controlled circumstances.
Intubation may be problematic due to the narrow size of
the tracheal lumen and the obscured view of the larynx
which may itself be narrowed.
Stenotic nares
The external nose of the brachycephalic dog is, in common with the remainder of the respiratory tract, considerably
foreshortened and as a result the cartilaginous tissue of the
lateral cartilages especially is broader and less rigid than is
found in other breeds. The airway at the level of the nostril
is in some dogs may be virtually obliterated and this problem may be exacerbated during the inspiratory phase during
which the cartilage because of its lack of rigidity may be
drawn into the nasal sinus. Although some authors have considered the problem of stenotic nares to be inconsequential
there is no doubt that airway obstruction at this level is extremely important since in the normal animal the external
nose and nasal sinus represents at least one third of the resistance to the flow of air. Research has shown that not only
does narrowing of the nares contribute to airway obstruction
it also causes significant turbulence in the nasopharyngeal
region which may underlie pharyngeal weakness. Management is directed towards resection of the bulk of the lateral
cartilage to increase the airflow and also towards stabilising
the remaining tissue by anchoring laterally to the integument.
Nasal sinuses
Although there is little that can be considered in terms of
management there is no doubt that the relatively narrow diameter of the brachycephalic nasal sinuses contributes significantly to the overall resistance to airflow patterns in the
upper airway. There is evidence too in favour of the devel-

SPECIALIST/INTERACTIVE PROGRAMME

B Vet Med, PhD, DSAS, DVR, FRCVS - Dipl ACVS , Dipl ECVS
University of Cambridge - United Kingdom

486

opment of the acquired secondary pharyngeal changes resulting from turbulent flow patterns resulting from the narrow nasal airway.
Overlarge soft palate
The brachycephalic soft palate is one of the major contributory features of upper airway obstruction. Although it is
probably of normal dimensions for the mesocephalic dog of
comparable weight its relative oversize in the compressed
nasopharyneal space of the brachycephalic causes obstruction of both nasal and oral airways. In addition, more severely affected patients may be dysphagic and become syncopal whilst eating.
Resection of the caudal aspect of the soft palate is considered the most practical option. The level of resection is
important and generally should not be made cranial to the
level of the tonsils because of the risk of nasopharyngeal reflux. In Bulldogs, however it is difficult to achieve over-resection. Although electrosurgical resection is practised by
some surgeons removal with right-angled clamps followed
by oversewing the pedicle with absorbable suture material is
considered to be a safer option. Haemostatic control is crucial and even mild oozing at the site of surgery represents an
unaceptable risk of postoperative airway obstruction. Relief
immediately after surgery is often marked although this may
deteriorate temporarily due to swelling at the surgical site
and response to implanted suture material.
Tonsilar hypertrophy
Enlargement of the tonsils contributing to the obstruction
of the airway is generally considered to be a secondary
change. It may occur as a consequence of either:
i) the conformation of the brachycephalic pharynx which
tends to evert the tonsilar tissue from the fauces allowing
them to constantly irritated or,
ii) the chronically-reduced airway pressures in the pharynx which tend to induce collapse of the structures in the
pharyngeal wall or,
iii) both of these factors.
Their relative contribution to airflow turbulence and obstruction is uncertain, however most consider their removal
useful in improving airflow dynamics. The tonsils should be
removed clamping the pedicle and oversewing this to control
haemorrhage following sharp excision. Once again the value
of electrocautery in this procedure is open to controvesry.
Pharyngeal hypertrophy
The precise mechanisms whereby the pharyngeal wall
hypertrophies and weakens is not clear but it is thought that
turbulent airflow patterns created by obstructed airways further cranially, chronic negative airway pressures and obesity are important contributing factors. The mucosa of the
pharynx may become thrown up into redundant folds which
due to their inherent weakness permit partial collapse of the
pharyngeal diameter during the respiratory cycle. In severe
cases these folds may even totally obliterate the airway (socalled aryepiglottic entrappment) precipitating severe syncopal episodes. Resection of redundant mucosa may be indicated although improving pharyngeal rigidity is a less attainable goal.

4th European FECAVA SCIVAC Congress

Diseases of the larynx


Anatomic structure
The larynx is a semirigid fibroelastic cyclinder separating the upper and lower respiratory tracts, the structural basis of which are three major and two smaller hyaline cartilages. The larger cartilages include the spoon-shaped
epiglottis positioned most rostrally, behind which are found
the horseshoe-shaped thyroid cartilage and the circular
cricoid cartilage. The thyroid and cricoid cartilages occupy
fixed positions relative to each other by virtue of their firm
attachment at the cricothyroid articulation although the thyroid is capable of some limited movement in a rostrodorsal
plane. This chassis provides the rigid base necessary for
movement of the other cartilages. The epiglottis hinges in a
rostrocaudal plane about its base which is in contact with the
thryoid cartilage. The smaller, paired arytenoid cartilages articulate with the cricoid cartilages on their medial aspect and
are capable of a swinging lateromedial movement about the
cricoarytenoid articulations. Interposed between the arytenoids and lying rostral to the lamina of the cricoid are the
interarytenoid and the sesamoidean cartilages which bind
the arytenoids to the dorsal aspect of the cricoid. The larynx
is supported rostrally by its attachment to the hyoid apparatus - the thyrohyoid membrane and caudally by its attachment to the trachea.
Two paired of ligaments are found within the lumen of
the laryngeal cylinder - the vocal ligaments which extend
from the vocal processes of the arytenoids to the ventral
midline and the vestibular ligaments which extend from the
cuneiform process to the ventral midline. The larynx is lined
with a stratified mucosa, folds of which protrude into the lumen of the cylinder over these ligaments - these are, respectively, the vocal and vestibular folds. The resultant crypts
formed between the two folds are the laryngeal ventricles.
The ventricles are absent in feline species. The diamondshaped opening within the laryngeal lumen delineated by the
arytenoids dorsally and the vocal folds ventrally is termed
the rima glottidis and is the narrowest point separating the
upper and lower airways. The diameter of the rima is determined by the position and length of the vocal folds which in
turn are dependant on the position of the arytenoid cartilages
and to a lesser extent on that of the thyroid cartilage. Dorsolateral movement of the arytenoids about their cricoid articulation pulls the vocal folds apart thereby widening the rima.
Medial movement reduces the diamond-shape of the rima to
a slit-like opening or completely closes it. Cranial to the rima is the wider opening of the larynx the aditus laryngis
which is delineated by the corniculate processes of the arytenoids, the epiglottis and the aryepiglottic folds.
The larynx has both extrinsic and intrinsic muscles. The
extrinsic muscles function in concert with the hyoid apparatus to vary the position and angle of the larynx. The intrinsic
muscles of the larynx are responsible for controlling glottic
diameter and can be broadly divided into the constrictors
and dilators, depending on their primary function. They contain Type I and II fibres providing both rapid and sustained
contractile function. The majority of the intrinsic muscles
are associated with glottic constriction (adduction) of the rima and include the cricothyroid, lateral crico-arytenoid,

4th European FECAVA SCIVAC Congress

Laryngeal function
The larynx performs a valve-like role at the junction of
the upper and lower respiratory tracts and its major functions
can be summarised as:
1. Protection of the lower respiratory tract from inhalation of debris,
2. Control of airway diameter during the respiratory cycle,
3. Phonation.
Airway protection
Prevention of aspiration is the result of a twofold reflex
mechanism. Firstly, during the swallowing phase the
epiglottis hinges abouts its base and is flipped backwards
over the aditus to direct the food upwards and over the larynx into the lateral food channels, thereby preventing aspiration. The epiglottis provides a tight seal at the level of the
aryepiglottic fold and the whole process occurs in conjunction with rostral movement of the larynx and caudal movement of the tongue. Secondly, glottic protection is also provided by the intrinsic muscles of the larynx which adduct the
vocal folds and arytenoid cartilages sealing off the rima
tightly during swallowing. This may also occur in response
to stimulation of the cranial laryngeal nerves by any food or
liquid debris passing beyond the aditus.
Control of airway diameter
During the resting phase of the respiratory cycle the arytenoids and vocal folds lie in a passive or neutral midline
position such that the rima is a narrow slit. Contraction of
the dorsal cricoarytenoid muscles during inspiration causes
the arytenoids to rotate quickly in a dorsolateral direction dilating the rima to accommodate the inward flow of air. On
expiration, the vocal folds move passively towards the midline slowing the outward air flow. During prolonged or

heavy exercise the rima may remain dilated during both the
inspiratory and expiratory phases to minimise resistance to
continued air flow.
Phonation
Barking or meowing is a glottic function and is the result
of vibration of the vocal folds as air flows over them. The
tone and pitch of the bark or meow are determined by the
speed and amplititude of the vibrations which in turn are
governed by air flow rate and the length of the vocal cords.
Vocal fold characteristics are governed primarily by tone in
the vocalis and cricothyroid muscles.

LARYNGEAL PARALYSIS
Pathophysiology
Laryngeal paralysis is the failure of arytenoid movement
during the respiratory cycle. The absence of abducting function affecting one or both arytenoids during the inspiratory
phase with consequent narrowing of the rima results in an increased resistance to air flow through the larynx. Air flow becomes turbulent both due to the increased resistance which
necessitates a higher flow rate through the rima and to the
movement of air over the fixed vocal fold(s). The concommittant reduction in intralaryngeal pressure may narrow the
rima still further contributing to additional air flow resistance. This airway obstructive condition is encountered with
some frequency in dogs and is occasionally seen in cats.
Aetiology
Paralysis of the vocal folds through failure of arytenoid
function most often results from disease or damage to the innervation of the intrinsic muscles of the larynx. Much less
frequently it may occur through disease involving the dorsal
cricoarytenoid muscles themselves.
Idiopathic laryngeal paralysis (ILP): by far the majority of dogs with laryngeal paralysis fall into this category.
ILP has a marked predisposition for medium to large breeds
which in the UK includes such breeds as Labrador retrievers, Afghan hounds, Irish setters, Pointers and some giant
dogs. The male is affected two or three times more frequently than the female and the average age of the affected
dog is usually greater than 10 years. The underlying cause
of ILP still remains unclear. The suggestion that the condition may arise more frequently in hypothyroid dogs remains
largely unsubstantiated. The condition has also been reported as part of a laryngeal paralysis-polyneuropathy (LPP)
complex in which affected dogs manifest signs of a generalised neuropathy including motor deficits involving the rear
limbs. Demyelination and remyelination and also axonal degeneration involving the intrinsic laryngeal and appendicular peripheral nerves has been recorded in these dogs.
Congenital: laryngeal paralysis has been reported as an
inherited congenital disease in the Bouvier des Flandres and
the Siberian Husky. The disease is transmitted as autosomally dominant trait in the Bouvier affecting the male more
frequently and may be unilateral or bilateral. Degenerative
changes are found both peripherally in the laryngeal nerves

SPECIALIST/INTERACTIVE PROGRAMME

transverse arytenoid ventricular and thyroarytenoid muscles.


The latter of these being the most important in terms of constricting function. Only the dorsal cricoarytenoid muscle is
concerned purely with dilation (abduction) of the rima. This
muscle originates on the dorsal aspect of the cricoid cartilage and inserts on the muscular process of the arytenoid. Its
contraction rotates the arytenoid laterally over the articulation with the cricoid.
The larynx is innervated by the vagus via the cranial and
caudal laryngeal nerves. The cranial laryngeal nerves are
concerned primarily with sensory function and provide innervation to the mucosal lining of the larynx via their internal branches. The sole exception to the sensory function of
the external branches is the motor innervation to the
cricothyroid muscles. The caudal (recurrent) laryngeal
nerves arise from the vagal branches at the thoracic inlet, the
right looping behind the subclavian artery and the left behind the aorta before heading rostrally to lateral surface of
the larynx. They provide motor innervation to all the intrinsic muscles of the larynx with the exception of the cricothryoid muscle.
The vascular supply of the larynx originates from the external carotid artery via the cranial laryngeal artery. The cranial laryngeal vein drains to the external maxillary vein.

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and centrally in the nucleus ambiguus. Selective breeding


has now significantly reduced the incidence of this condition
in Europe. More recently, a LPP complex has been recorded
in the Dalmatian affecting dogs under the age of 6 months
and presenting as a diffuse, generalised polyneuropathy distinct from that found in the Bouvier and Husky. 5,6 Electromyographic abnormalities are present in laryngeal, facial,
oesophageal and distal appendicular muscles and axonal degeneration is found affecting the laryngeal and appendicular
nerves. A significant number of these dogs also have
megaoesophagus. Most dogs with inherited laryngeal paralysis are presented as young pups and are rarely suitable for
treatment.
Traumatic: injuries to the neck or cranial thorax may
bruise, or even sever the laryngeal innervation. Pharyngooesophageal trauma and Big dog / little dog confrontations
resulting in crush injuries to the cervical region are probably
the most important causes in this respect.
Neoplastic: tumour infiltration of the caudal laryngeal
nerve may disrupt normal conduction function. Amongst
the more common tumours causing this presentation are
malignancies of the thyroid gland and cranial mediastinal
masses such as lymphomas and thymomas. Lymphomatous
infiltration of the laryngeal nerve has also been recorded in
the cat.
Iatrogenic: any surgical intervention in the cervical region or rostral thorax which involves dissection of the caudal laryngeal nerves may result in their temporary dysfunction through neuropraxia or more seriously, in permanent
paralysis. Although many surgeries may potentially result in
this complication the most notable procedure in this category is reconstruction of the trachea which necessitates separation of the nerves from their tracheal course and may give
rise to this complication.
Cats: the aetiology of laryngeal paralysis in the cat is unknown although it has been recorded as part of a generalised
neuropathy.
Clinical presentation
ILP typically has a prolonged and insidous onset and the
clinical signs associated with it may predate presentation by
months or even years. Inspiratory stridor is the major and
consistent finding in all patients and results from the accelerated, turbulent air flow over the fixed vocal fold(s).
Exercise intolerance occurs frequently although this
sign is less obvious in some dogs which appear to tailor their
exercise function to the reduction in their respiratory capacity. Severe cases will exhibit degrees of cyanosis and syncopy, possibly progressing to asphyxiation. These signs are
frequently exacerbated by a warm environment and although
dogs may present at any time of the year many are presented during the summer months. Excitement, car travel, anxiety and stress also tend to promote the signs.
Dysphonia, or change in the character of the bark, is a
very useful diagnostic pointer but is only found in approximately half of dogs with ILP. Dysphagia or cough whilst
eating or drinking is occasionally encountered although aspiration leading to lower respiratory infection and coughing
is probably less common than has previously been suggested. The symptoms of some patients may be exacerbated or

4th European FECAVA SCIVAC Congress

precipitated by the presence of other coexisting respiratory


disease, for instance, primary lung tumours.
Many of the above features are also common to cases of
laryngeal paralysis caused by non-idiopathic conditions. The
consistent presenting sign in cats with laryngeal paralysis is
a whistling inspiratory stridor.
Diagnosis
In many cases the presenting signalment may help the
clinician to reach a presumptive diagnosis. A ten year old,
male Labrador retriever with a prolonged history of exercise
intolerance and stridorous breathing should raise a significant index of suspicion.
Auscultation over the larynx even in the resting dog
should allow detection of the earliest inspiratory stridor. This
high-pitched, whistling respiratory noise should become
more audible during exercise but care should be taken not to
over-stress the patient and precipitate an obstructive crisis
merely for the purposes of diagnosis.
A complete physical examination should be performed
in all cases and in cases of non-idiopathic paralysis a search
should be made for possible causes (e.g.: thoracic mass).
Thoracic radiographs should be taken at this stage to assess
if any aspiration pneumonia is present which until satisfactorily resolved may temporarily preclude progression to the
next diagnostic step.
Laryngeal paralysis is a failure of dynamic function and
hence a definitive diagnosis can only be made by observing
this function or lack of it. In most instances this is done by
means of laryngoscopy. In some dogs it may be possible to
inspect laryngeal function under sedation but in most a light
plane of anaesthesia is more satisfactory. A deep plane of
anaesthesia will paralyse the intrinsic laryngeal muscles and
remove all laryngeal movement preventing a meaningful assessment of function. Laryngoscopy is best performed,
therefore either during induction of light anaesthesia or in
the recovering patient as the laryngeal reflexes return. Arytenoid abduction is reduced or absent during the inspiratory
phase in dogs with laryngeal paralysis. Most cases of ILP are
affected bilaterally although it is common for one side to be
more severely affected than the other and asymetric abduction may occur. Care should exercised when evaluating arytenoid movement since paralysed vocal folds often show
paradoxical movement (i.e.: move apart passively due to the
expiratory air flow). It is essential, therefore, that each phase
of the respiratory cycle is identified preferrably by an assistant, whilst the larynx is observed. In some dogs the mucosa
overlying the corniculate process of the paralysed arytenoid
cartilage(s) is often hyperaemic due to the turbulent air flow
over the mucosal surface.
The use of ultrasonographic examination of the canine
larynx has recently been described. Movement of the arytenoid and vocal folds during the respiratory cycle could be
identified and this gives rise to the possibility of recognising
laryngeal dysfunction using this technique. The non-invasive nature of ultrasonographic examination of the larynx
coupled with the ability to perform it in unanaesthetised patients are attractive advantages of this approach.
Respiratory function measurement techniques have been
described in the investigation of laryngeal paralysis. The pa-

4th European FECAVA SCIVAC Congress

LARYNGEAL EVERSION / COLLAPSE SYNDROME


Pathophysiology
Chronic respiratory diseases resulting in turbulent airflow
and abnormal negative pressures in the lower respiratory tract
or abnormal cartilage structure can initiate a progressive and
degenerative sequence of events within the upper airway
which eventually result in obstruction of the rima. In the early stages the mucosal lining of the larynx and pharynx become
oedematous and chronically thickened. This process also involves the mucosa within the laryngeal ventricle and the saccules are consequently forced to evert into the ventral rima. As
the condition progresses the laryngeal cartilages begin to
loose their structural rigidity and collapse towards the midline. The leading and lateral edges of the epiglottis roll inward
and the cartilage folds dorsally towards the glottic opening.
The weaker regions of the arytenoids, including the cuneiform
processes, collapse medially drawing the corniculate processes with them. The rima is progressively narrowed by these
processes and in the final stages is completely occluded. The
early changes involving the saccules and pharyngeal tissue are
often reversible and may be resolved by prompt management
of the underlying problem.
Changes involving the cartilages are, however, more permanent and once clinically-evident laryngeal collapse is a
difficult condition to manage.
Aetiology
Airway obstruction syndromes: the development of
LECS is most often associated with concurrent upper airway
obstruction syndrome. It is frequently encountered in the
brachycephalic dogs in which the overlarge soft palate,
stenotic nares and hypoplastic nasal sinuses are responsible
for upper airway turbulence.
It is unclear, however, if it is this airway turbulence during the inspiratory phaseor the presence of abnormally-weak
laryngeal cartilages which are unable to resist deformation
during the expiratory phase which allow the problem to develop. LECS may also be encountered as the sequel to other
ostructive airway conditions such as tracheal collapse and
hypoplasia.
Congenital: laryngeal collapse is seen as an infrequent
presentation in young English Bull Terriers during the first
year of life. There is some indication that a congenital cartilaginous anomaly resulting in a weak, non-rigid larynx
rather than airway may underlie the condition.

Clinical presentation
Laryngeal obstruction due to collapse results in stridorous breathing and severely restricted exercise ability. In
the brachycephalic dog the onset of these signs is insidious
and often difficult to separate from those caused by the remainder of the obstructive airway syndrome. Ongoing exercise intolerance following surgical management of the overlarge soft palate and tonsils and the stenotic nostrils, however, should alert the clinician to the possibility of degenerative laryngeal changes.
Diagnosis
Dogs with laryngeal collapse have severely obstructive
upper airway function. Auscultation directly over the larynx
should enable the stridorous turbulence to be detected but in
brachycephalic dogs it may be difficult to distinguish this
from the accompanying stertor. Laryngeal inspection in
mildly affected dogs will reveal the glistening pea-like,
everted laryngeal saccules immediately in front of the vocal
folds whilst in more advanced cases the rima will be obscured by the inverting epiglottis and arytenoids.

LARYNGEAL TRAUMA
Pathophysiology/Aetiology
Laryngeal trauma is uncommon in small animal species
due to the relatively protected position of the larynx as compared with that of man or the larger species. External trauma
may result from bite wounds, choke chain injuries and occasionally, crush injuries from road accidents. Compressive injuries such as these may fracture or dislocate the laryngeal
cartilages and hyoid bones obstructing the airway. Additionally, there may be neurogenic damage particularly in the
case of cervical bite wounds resulting in paralysis of the vocal folds. Damage directly to the laryngeal mucosa, epiglottis and arytenoids may be seen in stick penetration injuries.
In the acute phase of laryngeal trauma the airway may be obstructed due to haemorrhage, oedema or dislocations and
fractures of the cartilages. More long term complications include fibrosis of the cartilage articulations which prevent
normal arytenoid function and glottic stenosis resulting from
the development of intralaryngeal scar tissue.
Clinical presentation
Injuries involving the larynx are clinically evident due to
the obstruction of the airway. Patients may have laboured
respiratory patterns, stridor, cyanosis and asphyxiating syncope. Occasionally, there may be subcutaneous emphysema
due to air leaking into the perilaryngeal tissues.
Diagnosis
Inspection of the cervical region may reveal obvious
penetrating wounds or cervical swellings may be evident on
palpation. Auscultation will reveal stridorous laryngeal
sounds. Radiography may demonstrate hyoid fractures or
variations in the normal relationship of the laryngeal cartilages. Air may be present in the perilaryngeal tissues. Laryngoscopy should be performed to assess the severity of the
airway obstruction and detect the presence of paralysis.

SPECIALIST/INTERACTIVE PROGRAMME

tients hypoxic (i.e.: low PaO2) status can be quantified by


blood gas analysis. The abnormal air flow versus volume
pattern can be identified by tidal breathing flow volume loop
(TBFVL) studies. It is doubtful if these measurements add
materially to the assessment of an individual clinical case
which can be gained by careful auscultation and laryngoscopy but they do permit a more objective analysis of the
problem for research purposes.
Electromyography, nerve conduction velocity and histological studies have been used to demonstrate abnormalities in the laryngeal nerves and intrisic muscles.

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4th European FECAVA SCIVAC Congress

LARYNGEAL STENOSIS
Pathophysiology/Aetiology
Disease or injury involving the mucosal lining of the larynx may result in the development of either scar tissue or
proliferating granulation tissue which narrows the glottic
opening. Intralaryngeal surgical interventions are particularly implicated in the development of scar tissue and occasionally it may result from traumatic intubation of the larynx. A proliferating granulomatous form of laryngitis has
been recorded as a cause of stenosis.
Clinical presentation
Dogs with laryngeal stenosis will have reduced exercise
tolerance and stridorous breathing.

Diagnosis
Auscultation over the laryngeal region may localise the
source of the respiratory stridor but direct inspection under
general anaesthesia is the only means of confirming the
presence of the lesion. This should be undertaken with great
care since the upper airway may be obstructed to a considerable degree by the tumour and prior preparation should be
made to pass a narrow endotracheal tube or if necessary to
perform tracheostomy intubation. Biopsy should also be performed with caution because of the risk of haemorrhage
which may be aspirated. Radiography plays little role in the
diagnosis of the primary tumour but a search for metastatic
extension should be made.

Surgery for laryngeal paralysis


Diagnosis
Laryngeal auscultation will confirm the presence of stridor. Laryngoscopy will allow inspection of the scar or proliferating tissue within the rima. Surgically-induced lesions
most often involve the vocal fold sites whereas granulomatous lesions may affect the arytenoid cartilages.

LARYNGEAL NEOPLASIA
Epidemiology and incidence
Tumours of the larynx are rare in the dog and cat but a
variety of histological types have been reported including:

Benign:
Malignant:

Dog
oncocytoma
chondroma
squamous cell carcinoma
adenocarcinoma
chondrosarcoma
osteosarcoma

Cat

lymphoma
squamous cell carcinoma

Little is known of the epidemiology of tumours in this


site although lymphoma seems to be common in the cat.
There is no apparent breed predeliction but males may be at
greater risk. Secondary tumours or local extension of other
primary tumours, most notably thyroid carcinomas, are occasionally seen.
Aetiology
The aetiology of most laryngeal tumours is unclear. In
man these tumours are frequently encountered and may be
related to inhalation of the carcinogens associated with
smoking. The oncocytoma in man it is derived from cells of
epithelial origin found in glandular tissue in the head and
neck region.
Clinical presentation
Symptoms are the result of upper airway obstruction and
failure of laryngeal function such as is found in laryngeal
paralysis. Early signs include respiratory stridor, exercise intolerance, dysphonia and hoarseness, dysphagia and cough.
More advanced lesions cause serious respiratory obstruction
with episodes of cyanosis and syncope.

Undoubtedly the most common indication for surgical


intervention involving the larynx of small animals is the relief of laryngeal paralysis. Techniques for the managment
of laryngeal paralysis are intended to enlarge the rima permanently and ameliorate the restricted air flow. It should
be emphasised that a variety of surgical procedures have
been described for the treatment of this condition since it
was first recognised and there is ongoing controversy as to
what are the most appropriate procedures. It is convenient
to categorise these procedures according to whether or not
the surgery disrupts the structures within the lumen of the
larynx.
Extralaryngeal procedures
Procedures which dilate the rima without disrupting the
laryngeal mucosa have significant advantages and in the authors view are to be preferred. In particular, the following
advantages are recognised:
Gaseous anaesthesia can be maintained by routine endotracheal intubation throughout the surgery.
The risk of aspiration during surgery and the postoperative period is minimal.
The requirement for postoperative care, notably temporary tracheostomy management, is substantially reduced.
The incidence of intralaryngeal scarring is extremely
low.
Arytenoid lateralisation
Dilation of the rima by fixing the arytenoid(s) in abduction and attempting to mimic the function of the dorsal
cricoarytenoid muscle has been described by various authors
and is now a well established technique. The procedure may
be performed with a variety of modifications and the following is a description of the basic technique.
The unilateral procedure is performed with the patient in
right lateral recumbency for a right-handed surgeon and
vice-versa for the left. The neck is partially extended and
supported on a pack. An incision is made at a point below
the junction of the maxillary and linguofacial veins and the
fibres of the panniculus muscle split. The dorsal wing of the
thyroid cartilage is palpated through the overlying soft tissue
which is dissected bluntly to expose the thyropharyngeus
muscle. This muscle is transected horizontally or its fibres

split longitudinally to expose the dorsal wing of the thyroid


cartilage. The thyroid cartilage can then be retracted laterally allowing the fascial tissue lying between the thyroid and
the cricoid to be broken down. At this point the firm
cricothyroid articulation may be disrupted if required. Selfretaining retractors are used to retract the dorsal aspect of the
thyroid laterally and the sharp prominence of the muscular
process of the arytenoid cartilage overlying the rostrodorsal
aspect of the cricoid cartilage is located by digital palpation.
The fibres of the dorsal cricoarytenoid muscle fan out from
this to the dorsal midline of the cricoid and are carefully
transected to allow access to the cricoarytenoid articulation
below. In cases of idiopathic paralysis this muscle will be atrophied but in cases of acute onset paralysis (eg: trauma) the
muscle remains substantial. It is very useful to leave part of
the muscle attached to the muscular process to permit manipulation of the arytenoid during the procedure without
tractioning the cartilage itself since it may prove to be friable
in some cases. The arytenoid cartilage is now carefully separated with fine scissors from its underlying cricoarytenoid
articulation without disrupting the laryngeal mucosa medially. The sesamoidean interarytenoid articulation is then cut
which permits free movement of the cartilage.
The arytenoid is now anchored in abduction by means
of a suture prosthesis. A non-absorbable suture material is
essential since this will be required to retain the abducted
arytenoid permanently. Materials such as polypropylene
or monofilament nylon are most suitable since stainless
steel even when coated may tear through a more delicate
cartilage. A swaged-on needle is used to introduce the suture through the thyroid cartilage immediately rostral to
the caudal cornu. The needle is passed through the lateral
aspect of the arytenoid emerging in the centre of its articular face and is then passed back through this surface from
a more medial point. The mattress pattern is completed by
passing the suture through the medial face of the thyroid
cartilage in the region of, but not immediately adjacent to
the original bite. The suture is now tied firmly but without
overtensioning since this may cause it to cheese wire
through the cartilages. The degree of arytenoid abduction
can be inspected at this stage by temporarily removing the
endotracheal tube. The thyropharyngeus muscle is closed
routinely with absorable sutures over the thyroid cartilage
and the potential dead space overlying the larynx is obliterated by meticulous closure of the various layers of overlying soft tissues. If not previously inspected the larynx
should be evaluated at this stage before the patient recovers consciousness to confirm that there is satisfactory dilation of the rima. Any blood which may have accumulated in the laryngeal lumen should the mucosa have been
perforated during the procedure should also be removed
by suction.
Modifications of the above technique include the following:
Bilateral arytenoid lateralisation can be performed by
repeating the above technique contralaterally with the patient in left-sided recumbency has been reported. This has
been recommended for younger, working dogs in which
there may be a need for more glottic dilation to accommodate their greater exercise requirements. Bilateral surgery is

491

reported to be associated with a higher incidence of postoperative dysphagia and aspiration.


A ventral approach has been described with the patient
positioned in dorsal recumbency to permit bilateral surgery.
Access to each arytenoid is achieved by rotating the larynx
laterally about its longitudinal axis and is restricted as compared with that achieved by the lateral approach.
Disarticulation of the cricothyroid junction is an optional step to allow further retraction of the thyroid cartilage
and exposure of the cricoid and arytenoid cartilages. Some
bleeding may occur from small vessels in the region of the
articulation and it is important that this should be dealt with
by careful diathermic cautery. Although omitting this step
restricts access to the arytenoid cartilage it shortens the operative time somewhat and may result in a more stable base
to which the lateralising prosthesis can be anchored. Bilateral disarticulation of the cricothyroid joint is reported to result in dorsoventral collapse of the rima.
Studies in post-mortem specimens suggest that sectioning
the inter-arytenoid band with cricoarytenoid disarticulation allows greater dilation of the rima glottidis. The use of the
cricoid rather than the thyroid cartilage for anchoring the prosthetic suture has been suggested as providing greater dilation
of the rima. It should be emphasised, however, that neither of
these assertions have been supported by clinical studies.
Preoperative workup should include:
Routine haematological and biochemical investigations
since almost all patients will be geriatric.
Thoracic radiographs to rule out co-existing pulmonary disease (e.g.: primary neoplastic masses, aspiration pneumonia).
Investigation of any dysphagic signs.
Postoperative care should include:
A brief period of hospitalisation to permit observation
of the patient for any signs of respiratory distress. In most
cases this should be no more than 24 hours and patients
should be discharged with instructions for limited exercise
and permanent avoidance of collar use.
Perioperative antibiotic therapy since there is potential
for minor disruption of the laryngeal mucosa and perforation
of the airway mucosa. Antibiotic therapy may be extended
postoperatively if any risk of aspiration is perceived.
Complications of arytenoid lateralisation include:
Fragmentation of the arytenoid or thyroid may occcur
during the procedure if either cartilage is handled too vigorously or the prosthetic suture is repeatedly placed through
the cartilage. In the event of this complication the procedure
should be repeated contralaterally.
Oedema may develop within the first 24-48 hours postoperatively in the perilaryngeal tissues causing obstruction
of the rima and severe respiratory distress. Corticosteroids
may be employed following a prolonged dissection to preempt this complication which may otherwise necessitate
temporary tracheostomy intubation. The development of a
seroma or haematoma is a similar possibility which may also necessitate airway by-pass in severe cases.
Prosthetic avulsion is occasionally encountered in the
immediate postoperative period and is normally due to the
inclusion of an inadequate cartilage anchor within the suture. Much less commonly, it may be seen as a chronic de-

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492

velopment several weeks or even months after surgery. A repeat, contralateral procedure is a feasible solution in cases in
which a unilateral procedure has been performed.
Aspiration is in theory at least, a complication of all
procedures which leave the rima permanently dilated. Although this may appear as a potential problem after arytenoid lateralisation workers have reported no increase in the
incidence of this problem after the unilateral procedure.
There appears, however, to be more risk of dysphagia and
aspiration following the bilateral surgery. Providing that the
other glottic protection mechanisms (ie: epiglottic movement, lateral food channels) remain functional after surgery
the risk of aspiration after unilateral procedures should be
acceptably low.
Prognosis
The long term results of unilateral lateralisation for older dogs with ILP are very favourable indeed with rapid return to previous exercise function. In one long term study of
the results of unilateral lateralization more than 90% of dogs
were alive one year postoperatively and had little disernible
stridor or excercise intolerance due to respiratory dysfunction. The technique can be applied to all sizes of dog and is
also feasible in the cat.
Laryngeal re-innervation
Re-innervation of the larynx by both neuromuscular
pedicle grafting and nerve anastomosis has been reported in
dogs. Experimental studies with artificially-created laryngeal paralysis have shown that the dorsal cricoarytenoid m.
can be re-innervated by transplanting a neuromuscular pedicle innervated by the first cervical nerve. Dogs regained abductor function over periods of 9-11 months. The sternothyroid m. was selected for the graft since it is:
not innervated by the recurrent laryngeal nerve,
an inspiratory muscle and therefore provides synchronous abduction of the rima,
has a nerve supply long enough to allow transplantation
without undue tension on the graft.
A number of practical problems complicate this otherwise encouraging approach. Firstly, re-innervation has only
been demonstrated in recently-denervated (ie: nerve-sectioned) muscle and whilst this may be feasible for traumatic
injuries of the laryngeal nerve it may not be effective in
chronic neuropathies such as ILP. Secondly, re-innervation
of the intrinsic laryngeal muscles is indiscriminate such that
simultaneous contraction of both abductors and adductors
(synkinesis) may occur resulting in uncoordinated movement of the arytenoids. Finally, the long interval between
surgery and the clinical result represents an unacceptable delay in the management of the older dog with severe airway
obstruction. Microsurgical repair of the caudal laryngeal
nerve may be feasible in some instances but this only has application for traumatic lesions.
Intralaryngeal procedures
Procedures which necessitate surgery within the lumen
of the larynx are characterised by a number of significant intra- and postoperative considerations. These include:
Endotracheal intubation is precluded during the proce-

4th European FECAVA SCIVAC Congress

dure and hence maintenance of general anaesthesia dictates


either placement of a temporary tracheostomy tube or the
continuous infusion of an intravenous agent.
Blood or tissue debris from the surgical site may aspirated into the lower respiratory tract. The risk of aspiration
during the procedure is further increased in the absence of
endotracheal intubation.
The tracheostomy tube should be maintained in situ beyond the postoperative period to by-pass any upper airway
obstruction resulting from intralaryngeal oedema.
The surgical disruption or removal of the laryngeal mucosa is intermittently associated intermittently with the incidence of intralaryngeal scarring or so-called webbing
which may severely stenose the airway at the level of the rima.
All of the above considerations should be examined
carefully before selecting any intralaryngeal procedure. It
should be emphasised that a description of the intralaryngeal procedures is included here for the sake of completeness rather than the authors confidence in their suitability
or efficacy in the management of laryngeal paralysis.
Partial laryngectomy
Resection of the vocal folds or ventriculocordectomy is
perhaps the oldest approach to creating a permanently-enlarged rima. Several options exist including resection of one
or both folds, and combination of this with partial arytenoidectomy (ie: removal of part of one or both arytenoid
cartilages). Following the induction of anaethesia a midcervical, transverse tracheotomy is performed to permit
gaseous anaesthesia via an endotracheal tube or cuffed tracheostomy tube. Conventional laryngeal intubation with intermittent withdrawal of the endotracheal tube from the
anaesthetised patient to allow access to the surgical site is an
alternate, but less desirable option for maintenance of anaesthesia. The dog is positioned in sternal recumbency with the
mouth held open by means of a gag. The rima is visualised
by simultaneous rostral retraction of the soft palate and ventral depression of the tongue and epiglottis.
Ventriculocordectomy
This is performed by grasping the vocal fold with long
dissecting forceps and tensing it rostrally. Begining at its attachment to the vocal process of the arytenoid the vocal fold
and adjacent vocalis muscle are then resected using either
fine Metzenbaum scissors or crocodile-action cup biting forceps the latter allowing for piecemeal removal of the fold.
The procedure is repeated bilaterally. A small section of mucosa is left at the ventral commissure of the rima between
the resected folds and is said to reduce the risk of postoperative intralaryngeal scarring.
Partial arytenoidectomy
Arytenoid resection is performed in conjunction with
ventriculocordectomy as described above. Cup forceps are
then used to resect additional arytenoid cartilage. Opinion is
divided as to how much of the cartilage should be removed
in order to achieve the desired improvement in airway function. Previously, it has been customary to remove corniculate, cuneiform and vocal processes but more recent reports

4th European FECAVA SCIVAC Congress

Castellated laryngofissure
Ventral bisection and separation of the thyroid cartilage
has been described as an alternative concept for glottic dilation. The technique as originally described for the dog was
a modification of a procedure for the management of cricoid
collapse in humans and involved the creation of a series of
step-like incisions through the base of the thyroid cartilage
following tracheotomy intubation. The castellated thyroid
projections allow the two halves of the cartilage to be abducted ventrally thereby dilating the rima. The basihyoid
bone is then used to anchor the unstable thryoid fragments.
This technique is combined with bilateral ventriculocordectomy and consequently has many of the problems associated with intralaryngeal manipulation. There is only one long
term studies of the results of castellated laryngofissure.
Modified castellated laryngofissure
The subsequent modification of the castellated laryngofissure procedure to include bilateral arytenoid lateralization, underlined the unsatisfactory results achieved by the
original procedure. There must be doubts too as to the ratio-

nale for the modified procedure since it is clear that arytenoid lateralisation alone is extremely successful in alleviating the signs of laryngeal paralysis and there are few
reports of the clinical use of modified castellated laryngofissure.

SURGERY FOR LARYNGEAL COLLAPSE


Conservative management
In many dogs laryngeal eversion/collapse is a progressive process and hence early detection and management of
the underlying disease is essential to limit the ultimate extent
of the condition. Upper airway obstruction in brachycephalic dogs should be relieved at an early age by lateralising the
nares, shortening the soft palate and resecting hyperplastic
tonsils or redundant pharyngeal mucosal folds. This may relieve the turbulence and abnormal airway pressures sufficiently to permit remission of the earliest changes within the
larynx (ie: mucosal oedema and eversion of the saccules)
without additional management. For this reason it is essential that every effort should be made to correct the underlying pathology before any surgical intervention involving the
larynx itself is undertaken. The judicious use of steroidal,
anti-inflammatory drugs may be helpful in promoting resolution of the laryngeal changes after upper airway surgery.
Resection of laryngeal saccules
In cases where the laryngeal changes are limited to chronic eversion of the saccules which does not respond to conservative management resection of the everted tissue may be performed. The patient is prepared for surgery as for partial laryngectomy (see above) and positioned in sternal recumbency.
The everted saccules are identified as small, red pea-like protrusions immediately behind the vocal folds and grasped with
dissecting forceps. The saccules are resected through their
base with fine scissors and haemorrhage is controlled by direct pressure over the site. As is the case for laryngectomy
procedures the risk of postoperative aspiration may be reduced by temporary tracheostomy intubation.
Partial laryngectomy
Resection of the vocal folds and arytenoids has been
used in the management of LECS. The long term results,
however, are poor due to significant postoperative complications and the need for repeated surgeries to maintain the
airway. Major intralaryngeal resection is therefore no longer
recommended in the management of laryngeal collapse.
Permanent tracheostomy
Permanent tracheostomy is effective in the management
of many advanced cases of laryngeal collapse since not only does it provide immediate upper airway by-pass but it also relieves the abnormal airway pressures responsible for the
degenerative changes involving the larynx. Permanent tracheostomas should be managed by careful cleaning during
the initial 2-3 weeks when tenacious tracheal secretions may
tend to occlude the opening. Thereafter, once daily cleaning
is sufficient to maintain its patency. Long term problems include skin fold obstruction and stenosis of the stoma.

SPECIALIST/INTERACTIVE PROGRAMME

indicate that the incidence of postoperative complications,


notably aspiration pneumonia, may be reduced by removal
of only the corniculate process. The procedure is performed
unilaterally and the decision as to which side should be operated is based on preoperative laryngoscopic examination
in the case of unilateral paralysis.
Haemorrhage after partial laryngectomy procedures is
controlled by direct pressure using a small dental sponge on
the excision sites. Any blood clots or mucus which accumulate in the airway should be meticulously suctioned following the completion of surgery. The tracheostomy tube is
maintained postoperatively and periodically occluded over
the next 48 hours to ascertain at what point it may be safely
removed. Antibiotic therapy should be maintained for several days after surgery to reduce the risk of pneumonia resulting from the aspiration of any debris.
Complications of partial laryngectomy include:
Aspiration pneumonia has been reported as a frequent
and potentially fatal postoperative complication after vocal
fold resection and partial arytenoidectomy. Recent reports
suggest that bilateral vocal fold resection alone or alternatively, the use of an inflatable tracheostomy tube during
surgery may result in a significant reduction in the incidence
of this problem.
Glottic stenosis may be encountered as a longer term
problem due to scarring ventrally of the site of the excised
vocal folds. The so-called webbing granulation tissue may
prove difficult to manage and may recurr after resection.
Other techniques include lining the site with mucosal flaps
or the use of a ventral silicone stent to dilate the rima. Tapering doses of prednisolone following surgical resection
has been reported as providing good results.
Oedema may develop within the larynx at the resection
sites necessitating temporary tracheostomy. The perioperative use of dexamethasone sodium phosphate (0.25 - 1.0
mg/kg iv) or methylprednisolone sodium succinate (0.5 - 2.0
mg/kg iv) may reduce the incidence of this problem which
otherwise prolongs the postoperative tracheostomy period.

493

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Tracheostomy must be regarded as a salvage procedure


and the long term prognosis for dogs with advanced laryngeal collapse is very guarded. Techniques such as arytenoid lateralisation, designed to alleviate the signs of laryngeal paralysis by enlarging the rima are notoriously ineffective in the management of LECS since the rigid cartilage chassis essential for the success of the procedure is
no longer present.
Surgery for laryngeal trauma
Animals presented with airway obstruction due to laryngeal trauma frequently require prompt tracheostomy intubation to enable an airway to be maintained pending a more
detailed evaluation of the larynx under general anaesthesia.
Laryngeal trauma resulting from both compressive injuries
and penetrating wounds are prone to perilaryngeal oedema
and bruising. Early surgical intervention may exacerbate this
and immediate management should, therefore, be limited to
the control of any haemorrhage, debridement of non-viable
tissue obstructing the airway and tracheostomy. In the case
of penetrating wounds involving the perilaryngeal tissues
provision should be made for drainage and the removal of
any residual foreign material. Anti-inflammatory and antibiotic therapy should be maintained with upper airway bypass until the oedema resolves, normally 3-5 days, at which
time mucosal tears can be further debrided and repaired.
Dislocations of the arytenoid cartilages or hyoid bones
should also be corrected where possible at this time. Laryngeal function may be more meaningfully evaluated at this
point since laryngeal neuropraxia and paralysis are impossible to differentiate in the initial phases of the injury. In
cases where laryngeal dysfunction is still evident it is more
practical to assume permanent paralysis and perform lateralising surgery (see above) than to continue to manage the
patient in the expectation of possible return of function. Injuries resulting fibrosis around the arytenoid cartilages may
result in the development of glottic stenosis in the longer
term and management of this condition by lateralisation
may prove difficult. In such cases there may be little alternative but to consider an intralaryngeal intervention or permanent tracheostomy.
Glottic stenosis due to intralaryngeal webbing is a possible long term complication of trauma and may be managed
as previously described. The prognosis is guarded for return
to normal laryngeal function in such cases.
Surgery for laryngeal neoplasia
Few laryngeal tumours present as candidates for definitive surgical excision. The single exception to this is the oncocytoma which is usually found as a discrete mass underlying the laryngeal mucosa. The mass can often be removed
by careful submucosal dissection from its position within the
larynx where it obstructs the rima.
Ventral laryngotomy
Some benign tumours, and occasionally polyps, found
within the larynx are less easily accessed via the rima and
are better approached through a ventral laryngotomy
wound. The patient is positioned in dorsal recumbency and
the airway is maintained by either a narrow diameter endo-

4th European FECAVA SCIVAC Congress

tracheal tube or temporary tracheostomy intubation during


the procedure.
An incision is made through the cricothyroid ligament
and continued forward through the ventral keel of the thyroid cartilage. The two halves of the cartilage are separated
by means of retractors to permit access to the mass and other intralaryngeal structures. The thyroid is repaired with simple interrupted sutures in its ventral aspect taking care to
achieve accurate apposition and stability. The cricothryoid
membrane is repaired in a continuous pattern to ensure an
airtight seal.
Laryngectomy
Malignant laryngeal tumours (carcinomas, adenocarcinomas etc) do not lend themselves to dissection from the larynx because of their tendency to local infiltration and their
advanced stage at the time of detection. A variety of fanciful
techniques for their management by partial laryngectomy
have been described but are derived from human surgical literature and significantly, there are no long term reports of
their successful application in small animals. Laryngectomy
combined with permanent total tracheostomy is, in theory,
an option. The dearth of reports of the long term results of
its use in the management of canine tumours should probably be regarded as an indication of its lack of success and
suitability. Experience with this procedure in 10 dogs with
malignant laryngeal tumours shows that the complication
rate is high and few dogs go on to enjoy a normal quality of
life for periods of more than 3 months after the surgery.
Megavoltage radiation therapy using twin oblique portals to spare the adjacent spinal tissue is commonly used in
the treatment of laryngeal malignancy in man. There are no
reports in the veterinary literature of the routine use of radiation in this mode although it is certainly a viable possibility. Cytotoxic therapy is indicated in the management of lymphoma of the larynx in the cat and may achieve dramatic resolution of the clinical signs. The value of chemotherapy for
other histological types is unknown.
The prognosis following surgical excision of the oncocytoma is guardedly good. Its growth is normally slow and
does not appear to metastasise although local recurrence
over periods of many months or years is possible. Palliation
of feline lymphomas is normally short-lived and the outlook
for most malignant laryngeal tumours is poor. Since the
overriding determinant is airway function euthanasia is often
sought by owners at an early stage in the disease.

Tracheotomy and temporary


tracheostomy
Indications
a) Bypass of upper airway obstructions (e.g. laryngeal
injuries/obstruction tracheal trauma, nasomaxillary trauma
electrical/chemical burns, neoplastic lesions, foreign bodies). A major indication in small animal practice is to facilitate anaesthesia during upper airway surgery.
b) Ventilatory management: tracheostomy may be used
as a means of maintaining prolonged postoperative mechanical ventilation.

4th European FECAVA SCIVAC Congress

Technique
Often the procedure is indicated as an emergency step
and may be performed in the sedated animal using local
anaesthesia only and some of the following comments may
not apply. However, under elective circumstances the procedure should be performed as aseptically as possible under
general anaesthesia. The dog is positioned in dorsal recumbency with the neck extended on packs. A standard ventral
midline approach is made to the trachea through a small skin
incision. The tracheotomy would should be located well
away from the thoracic inlet and larynx alike so that it cannot be obstructed by normal flexion movements of the neck.
The 5th-6th tracheal interspace is a suitable site and a variety of techniques may be used to open the trachea.
Surgical techniques include:
i) Transverse splitting of the annular ligament: allows for
anatomic restoration once the tube is removed (65% of circumference cut).
ii) Flap resection: resection of circular or rectangular flap
allows for easy re-intubation and may be very useful where
inexperienced help is available. The flap may be left hinged
for replacement.
iii) Longitudinal ring splitting: allows stenosis during the
healing phase.
Tracheostomy tube design
Tubes may:
- be made of nylon, PVC (or previously silver).
- be cuffed for inflation and the addition of a cuff allows
for a complete seal to prevent aspiration of debris and for the
ability to use positive pressure ventilation.
- have a removable obturator allows the easier introduction of the tube into the wound.
- have a removable cannula to allow the inner sleeve to
be removed for regular cleaning.
Instrumentation
For this procedure should include:
- basic cut down pack
- tubes with a range of sizes
- suction (trap bottle)
- good illumination
- ideally ECG monitor

Immediate complications
These are uncommon but may include:
- apnoea
- haemorrhage
- tracheotomy misplaced
- cardiac arrhythmias
Management
- Cleaning: should be performed regularly. The frequency depends on the rate of secretion production. A removable
cannula is very useful in this respect.
- Position should be frequently inspected and cuff inflated if used.
- Humidification: lack of humidity and air warming depresses cilial function and increases the viscosity of the
secretions as well as predisposing infection. To counter
this the animal can be placed in humidified cage or the
tube should be flushed with 0.5 ml-5.0 saline every1-2
hours.
- Suction: secretions should be removed regularly.
- Wound: the tracheostomy wound is always contaminated and needs constant attention to reduce risk of aspiration.
Short term complications
There are 2 major and important complications during
management:
- tube dislodgement
- tube obstruction
Other complications can include: - subcutaneous emphysema (with pneumomediastinum, and possibly pneumothorax),
- aspiration
- infection
Long-term complications
- Subcutaneous emphysema can develop after the tube
has been removed,
- exhuberant granulation at site of tracheotomy,
- tracheal stenosis,
- tracheomalacia
- tracheobronchial fistula
Tube removal
There is no hard and fast rule for when the tube should
be removed but the obstructive problem should be resolved.
Always check airway function by deflating cuff and obstructing tube temporarily.

SPECIALIST/INTERACTIVE PROGRAMME

c) Access to the lower airway - the production of chronic tracheal debris (e.g. blood, mucus) may require repeated
aspiration. Some foreign bodies may be removed from the
trachea via this route.

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499

THORACOSCOPIC PERICARDIECTOMY FOR RECURRENT PERICARDIAL EFFUSION:


CLINICAL EXPERIENCE IN TWO CASES
F. Acocella Med Vet, F. Addis MedVet
Istituto di Clinica Chirurgica Veterinaria, Facolt di Medicina Veterinaria - Universit degli Studi di Milano, Italy

Pericardiectomy is the surgical choice for recurrent effusive and constrictive pericardial disease. The traditional techniques
need a thoracotomy or sternotomy with high morbidity. The thoracoscopic tecnique it seems to be a satisfactory technique,
with high accuracy and low morbidity and short operating time only for recurrent effusive pericarditis. First case: German
Sheperd dog, male, 8 years old with clinical, radiological and ecocardiografic signs of pericardial disease. The diagnosis was
idiopatic pericarditis after pericardiocentesis. The surgical choice was decided after no results of multiple pericardiocentesis
and conservative treatment. The dog was drained before induction of anaesthesia. No selective ventilation was established and
the dog was positioned in a right lateral recumbence. The first trocar was positioned at the VI i.s. on the superior axillary line.
This port was for the thoracoscope. The other two ancillary ports were positioned at the IV i.s. on the middle axillary line and
at the VII i.s. along an intermediate line between the inferior and the middle axillary lines. The lung was displaced posteriorly
and after visualization of the frenic nerve a subfrenic pericardial window was estabilished starting from the caudo-dorsal border of the pericardium. After a two years follow up the dog did not presented any clinical, radiological and ecocardiographic
signs of pericardial disease. Second case: mix breed female dog, 9 years old with clinical signs of dispnea and ascites. After a
clinical, RX, US and citological examination the diagnosis was effusive malignant pericardial disease. Video assisted partial
pericardiectomy was performed with no complication. The istopathologic response was pericardial mesothelioma. The owner
refused any cancer chemotherapy. The dog was killed after 6 months for multi organ failure.

LUTEOLYTIC PROPERTIES AND SIDE EFFECTS OF ALFAPROSTOL,


A SYNTHETIC PROSTAGLANDIN F2 ALPHA ANALOG, IN THE BITCH: PRELIMINARY RESULTS
S. Romagnoli DVM MS, S. Annarella DVM, I. Vannozzi DVM, R. Ballabio DVM*
Dept of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University of Pisa, Italy
*Centralvet, Agrate Brianza, Milano, Italy

SHORT COMMUNICATIONS

Luteolytic properties and side effects of Alfaprostol (ALF), a synthetic analog of prostaglandin F2 alpha, were evaluated in the
bitch.
Side effects. Four anestrous bitches of different breeds and age were treated SC with 20 mcg/kg diluted 1:1 or 1:2 in saline.
Side effects (increased respiratory frequency, decrease of 1C of rectal temperature, occasional vomiting and diarrhea, some
depression) were short lived, similar in degree to what reported for other PGF2a compunds in the bitch, and were not a cause
of concern.
Luteolytic properties. Three bitches in diestrous were treated SC with ALF diluted 1:2 with saline BID for 5 days starting on
cytological diestrous day 11-12. Serum progesterone (assayed with RIA) was 35.2+13.7 ng/ml on day 1 (prior to onset of
treatment), 0.6+0.5 ng/ml on day 5-6, 0.3+0.2 ng/ml on day 8 (N=2) and 0.0 ng/ml on day 15 (N=2). It is concluded that ALF
can be used as a luteolytic agent to induce abortion in the bitch.

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4th European FECAVA SCIVAC Congress

PROTECTIVE EFFECT OF AN INSECTICIDAL SPRAY AGAINST PHLEBOTOMUS PERNICIOSUS,


A VECTOR OF LEISHMANIASIS
F. Ascher1 DVM, C. Alves-Pires2 DVM, C. Campos3 DVM, M.J. Capela2 DVM, P. Aguiar2 DVM
Virbac S.A., 06511 Carros, France - 2Instituto de Higiene e Medicina Tropical, 1300 Lisboa, Portugal
3
Laboratoire Vtrinaire Dpartemental, R.E.S.F.I.Z., 06902 Sophia Antipolis, France

Phlebotomus perniciosus (P) is a primary vector of Leishmania sp. and the dog in addition to being the victim of the disease is
the main reservoir in Europe. The objective of this study was to evaluate the effect of a long acting spray formulation containing an insect growth regulator (pyriproxyfen 0.02%) and a pyrethroid insecticide (permethrin 2%) on rabbits and dogs exposed
to sandflies, with the purpose to prevent blood sucking and thus reduce Leishmania sp. transmission.
Animals were allocated to two groups, either untreated control or treated (sprayed once with Duowin, Virbac S.A. at day 0).
P were supplied from the Instituto de Higiene e Medicina Tropical of Lisboa in-house colony. Animals were exposed for 30
minutes to male and female unfed P under controlled conditions in mosquito cages (75% RH, 20 to 24C, darkness). The P
were removed from the cages 24 hours later and counted as dead or alive, fed or unfed. Three New Zealand rabbits were used
to check the feasibility of the test, one of them as control. In the treated group only 2.1% P took an incomplete blood meal,
half of them having died. In the control group, 43.1% P were fed and most of these were alive. Three treated (5 ml/kg BDW)
and three untreated Beagle dogs were exposed respectively to a total of 572 and 556 female P at 1, 8 and 15 days post-treatment. P mortality was higher (p < 0.001) in the treated group with 60% vs 7% in the control group. Only 1% of the P took
some blood (incomplete blood meals) in the treated group compared to the 18% fed P in the control group. It is noteworthy
that all but one of the fed sandflies in the treated group died. P were killed by the treatment either before or after having taken
a blood meal, preventing them from searching for another host. As the flying range of P is limited and dogs represent the main
reservoir of infection, control measures could therefore be implemented by collectively spraying dogs with the aim to reduce
disease incidence in highly infected areas. Where 10% of the dogs are infected and 4% of the P are vectors of protozoans, the
percentage of new infections over one year could theoretically be reduced to 0.93% instead of being 6%. This epidemiological
feature deserves to be tested in field conditions.

OESTRUS INDUCTION IN THE BITCH WITH AN ANALOGOUS OF GnRH


S. Belluzzi Med Vet, D. Zambelli Med Vet, G. Mari Med Vet
Veterinary Clinical Department, Obstetric Gynaecology Section, Bologna University, Italy
The aim of this work was to check the real effectiveness of a LH-RH agonist to induce oestrus and ovulation in the bitch. In
the man, the continuous administration of this drug is able to stop the testicular and ovarian production of steroids. The choice
of this drug is due to its property (already tested on other species) to induce oestrus and ovulation, and also to the original depot formulation (the drug persist for 28 days) of small dimension which is easy and practical to administer. Ten bitches of different breeds were treated, anoestrus was defined on the basis of serum P4 < 1 ng/ml and the vaginal smear. The interval between the previous oestrus and the beginning of the treatment was 214.8158.6 days (min. 95 max 510). The analogous used
was goserelin acetate (Zoladex, I.C.I). The bitches up to 25 kg of body weight were treated with 1.8 mg. and bitches higher
weights with 3.6 mg. of goserelin acetate by a single subcutaneous administration. The vaginal smears and serum concentration of E2 and P4 were carried out every other days after the implant. After a mean interval of 5.5 days clinical signs of
proestrus took place clearly in six bitches while in a mild way in two of them and finally were absent in two bitches. The
proestral peak of estradiol occurred in those six bitches after 8.33 days after the treatment and the mean values of E2 were
75.359.3 pg/ml (min. 37,3 max. 143.7), in the other subjects the values of E2 experienced discontinuous growths without
reaching a real peak. Serum levels of P4 increased 10.32.3 days after the treatment. The cytological individuation of dioestrus
allowed to identify the time of ovulation which was observed 120.5 days from the beginning of the proestrus. Four bitches
(66.6%) was diagnosed pregnant by echography and then pupped normal litters. The two bitches which did not respond (absence of proestrus) to the treatment belonged to the German Shepherd breed and to the same breeding. A more careful check
of the minimum quantities of product required will allow to the considerable cost of use.

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HISTOLOGICAL PARAMETERS OF PROGNOSIS IN MALIGNANT MAMMARY TUMOURS OF THE CAT


C. Benazzi* DVM ECVP, M. Galeotti# DVM, G. Sarli DVM, P.S. Marcato* DVM ECVP
Dip.to di Sanit Pubblica Veterinaria e Patologia animale*, Facolt di Medicina Veterinaria - Bologna
Dip.to Scienze Produzione Animale#, Facolt di Agraria, Udine, Italy
Mammary tumours are the most important after the skin tumours and lymphoid tumours in the cat, and have a high malignancy potential (up to 90%). This study shows the prognostic histological results obtained from 52 cats, which resulted M0 at
mastectomy, followed up for two years. Among the histological parameters valued, the grade of invasion was the only one
which resulted significant for the prognosis (P<0.05), while tubular differentiation showed to be not significant (P=0.34). As
for the grade of invasion, significant survival differences were recorded between non-infiltrating and infiltrating tumours, and
within these latter, between those with stromal invasion only and with intravascular emboli. In the subjects showing stromal
invasion, the division into intracapsular and extracapsular stromal invasion was significantly associated with survival (P<0.05).
In the cases with emboli in the lymph and/or blood vessels, useless was the division into massive embolism (s.c. inflammatory carcinoma, indicative of systemic micrometastases) and occasional emboli (P=0.22). The results obtained, analysed in
terms of survival and/or post-surgery relapse, are presented as useful indicators of the need to support or not surgery with an
additional therapy: mastectomy for the non-invasive tumours or for those with intracapsular stromal invasion; mastectomy
eventually associated with an additional therapy for the tumours with extracapsular stromal invasion; additional therapy which
is only a palliative for all the cases with massive embolism and for many of those with occasional emboli. In contrast to
the inflammatory carcinoma of the woman, the ability to discriminate between these last two aspects (cases with diffuse probable micrometastases from those with the involvement of the regional lymph node only) by the histological exam of the tumour and surrounding tissue seems to be low.

EFFICACY OF A HIGH TITRE MLV AGAINST CDV IN PUPPIES WITH MATERNAL ANTIBODIES

Background. Trials carried out in the early eighties indicate that the percentage of puppies at 6 weeks of age that responded to
the CDV component of Nobivac Puppy DP was around 80%1. The average percentage of response to vaccination can differ
between populations of puppies with different average maternal antibody levels, and these levels can change in time. A recent
Swedish survey2 where the percentage of animals that responded to the CDV component of 4 different vaccines was evaluated
demonstrated that not all vaccines were equally reliable. Two field studies were carried out to confirm the efficacy of the CDV
component of Nobivac Puppy DP that was found in earlier studies.
Material and methods. The proportion of responders in both experiments was determined by calculating the percentage of
animals that showed an increase in VN titre between serum samples taken before and 3 weeks after vaccination.
In the first experiment 105 animals from 7 different breeds were included, 52 were vaccinated with Nobivac Puppy DP, 53
served as unvaccinated controls.
In the second experiment 63 animals from 6 different breeds were included, 32 were vaccinated with Nobivac Puppy DP, 31
were vaccinated with a bivalent vaccine against CDV and CAV2a.
Results. The percentage of animals that responded to vaccination in the first experiment was 83%. In the second experiment,
94% of the animals responded to the CDV component of Nobivac Puppy DP, compared to 3% of the animals vaccinated with
the bivalent vaccine.
Conclusion. The results from both trials confirm that the CDV component of Nobivac Puppy DP is suitable for vaccination
of puppies at the age of 6 weeks.
Literature
1) Chalmers W.S.K., and W. Baxendale, (1994), Vet. Record, 135, 349-353.
2) Olsen, P, Klingenborn, B, Bonnet, B, and A. Hekhammar, (1997), Proc. ACVIM forum, 15, 695.
a) Canivax CH, Merial

SHORT COMMUNICATIONS

J.G.H.E. Bergman DVM, G. Paul DVM PhD, R. Jaspers


Intervet International B.V., P.O. Box 31, 5830 AA Boxmeer, the Netherlands

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ATYPICAL BEHAVIOR OF A NASOPHARYNGEAL POLYP CAUSING A VESTIBULAR


SYNDROME IN A CAT
X. Roura* DVM, M. Bernardini# Med Vet ECVN, D. Fondevila# DVM PhD, T. Pea# DVM PhD
Veterinary Teaching Hospital*, and Department of Animal Production and Pathology#, Faculty of Veterinary Medicine,
Universitat Autonoma de Barcelona, Spain
Polyps of the bulla timpanica are a common cause of peripheral vestibular syndrome in cats. This syndrome is due to the compression of the vestibular structures in the inner ear by the mass. The polyps from the middle ear either growth down to the
Eustachian tube into the nasopharynx or, less commonly they growth into the external ear canal. Surgical excision of the
polyps is the treatment of choice in most cases. A two year old female european cat was presented at our hospital due to a
chronic dyspnoic respiratory problem. The owner reported that the first signs of the disease, as sneezing and inspiration noises,
appeared one year ago. The history was lacking of any symptoms related to ear and nervous diseases. At physical examination
the cat was found in good general condition. A stertorous inspiratory breathing was the only clinical sign. Minimum data base
was normal. Under general anesthesia, the exploration of the nasopharynx showed a 1,5 cm non ulcerated polypoid pink mass
attached to the nasopharynx. No alterations were found during the examination of the external ear canal and tympanic membrane. Radiologic examination of the osseous bullae was negative. Differential diagnosis included polyps, neoplasias or granulomatous inflammation. A complete removal of the mass was performed. Post-anesthetic recovery was good and an antibiothic
treatment was instituted. The histological results was an inflammatory polyp. Then, a steroid oral therapy was administered
during three weeks. The cat showed no signs of the disease in the following four months. Then, a steroid non responsive inspiratory distress reappeared, followed after two weeks by a left head tilt. The reevaluation showed a regrowth of the mass in the
nasopharynx, a growth of a mass in the external ear canal and radiological signs of thickening of the left bulla. The owner refused surgery and asked for euthanasia. Post mortem pathological findings were consistent of a polyp occuping the middle ear,
Eustachian tube, part of the external ear canal and the nasopharinx. In conclusion, we believe that the growth of the polyp
started in the nasopharinx up to the middle and external ear throught the Eustachian tube mainly because of the lack of signs
of chronic otitis and the late occurrence of the neurologic syndrome.

PANCREATIC PSEUDOCYST ASSOCIATED WITH PANCREATIC ACINIC CELL CARCINOMA, CHRONIC


PANCREATITIS AND MULTIFOCAL NECROTIZING STEATITIS IN A CAT
A. Boari Med Vet, L. Della Salda* Med Vet, M. Cipone Med Vet, G. Gandini G. Med Vet,
M. Joechler Med Vet, D.A. Williams DVM MSc PhD
G. Sarli DVM, P.S. Marcato DVM ECVP
Dip. Clinico Veterinario, *Dip. Sanit Pubblica Vet. e Patologia Animale, Universit degli Studi di Bologna, Italy
Dept. of Small Animal Medicine and Surgery, Texas A&M University, USA
The purpose of this study is to document clinical, laboratory, histopathological and ultrastructural findings of a rare case of
pancreatic pseudocyst associated with pancreatic carcinoma, chronic pancreatitis and multifocal necrotizing steatitis in a cat.
A 15-year-old neutered male siamese cat was referred for evaluation of vomiting and anorexia of 1 week of duration. In the
last three years the cat had chronic intermittent vomiting. On physical examination, a mass was palpable in the middle-right
cranial abdominal quadrant. Significant laboratory findings included leukocytosis with neutrophilic left shift (30.794 neutrophils/l; reference range 3000-11000/l), mild hyperamylasemia (1540 IU/l; reference range: 450-1400 IU/l), hyperglycemia
(153 mg/dl; reference range: 70-130 mg/dl). The serum fTLI concentration was within normal range (48 ug/l; reference range:
17-49). Loss of detail throughout the entire abdomen mostly apparent in the cranial areas and just to the right of the midline
associated with increased, irregular, soft tissue opacity caudal to the stomach was noted on survey radiographs. Ultrasonographically, in the region of right-pancreatic lobe, between the descending duodenum and right kidney, a well defined cist-like
structure containing anechoic fluid and surrounded by hyperchoic tissue was identify.
A cystic mass in the left lobe of the pancreas associated with severe saponification of mesenteric fat and mild serosanguineous
peritoneal effusion were identified during an exploratory celiotomy. A fine-needle aspirate of the cyst yielded a very clear (water-like) fluid. The fluid amylase, lipase and fTLI were respectively 660 U/l, 6140 U/l and 80 ug/l. The mass was resected but
the cat was euthanized per the owners request before recovery and necropsy was performed. Histopathologic examination revealed pancreatic pseudocyst associated with pancreatic acinic cell carcinoma, chronic pancreatitis and multifocal necrotizing
steatitis.

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ELECTROCARDIOGRAPHIC FEATURES OF DEERHOUNDS


A.R. Bodey, BSc, BVSc, PhD, MRCVS
Centre for Small Animal Studies, Animal Health Trust, P.O. Box 5, Newmarket, Suffolk, CB8 8JH, United Kingdom
Background. Electrocardiographic features differ from breed to breed in dogs on account of differences in chest shape and
size, heart shape and size and spatial relationships between heart and chest.
Method. Six lead electrocardiographs were recorded from 155 Deerhounds in right lateral recumbency using a Nihon Kohden
Cardiofax ECG-6851. Dogs were considered to be normal by their owners at initial examination and ranged in age from 8
months to 13 years. Where possible examinations were repeated at 9 to 12 monthly intervals. In total 281 records were made.
Results. Twenty dogs were electrocardiologically normal and among the normal dogs there was an wide range in heart rate,
amplitude and durations of the various ECG features, and especially of mean electrical axis which often fell outside the previously described canine normal range (+40 to +100). Amplitudes of R waves often exceeded the previously described canine
normal range. Dogs considered to be electrocardiologically abnormal (that is those with non sinus rhythm or extra complexes)
were older and had higher heart rates than normal dogs. Most frequent electrocardiographic abnormalities were ventricular
premature contractions, atrial fibrillation and atrial premature contractions.
Conclusions. Electrocardiographic features of Deerhounds exhibit a large range in apparently normal animals and care must
be taken when interpreting traces in the light of this. However, electrocardiographic abnormalities are often recorded in the absence of any clinical signs.

RADIOLOGY OF ORAL NON ODONTOGENIC TUMOURS IN THE DOG

Primitive tumours of the oral cavity of the dog are classified as benign tumours and malignant tumours. The malignant tumours account for approximately the 6% of all canine tumours, they are locally invasive and rarely metastasise. They are also
classified as odontogenic tumours (arising from dental or periodontal tissues) and non-odontogenic tumours. The non-odontogenic tumours include the most common malignant oral neoplasm: squamous cell carcinoma, malignant melanoma, fibrosarcoma and osteosarcoma. Clinically, dogs affected by malignant oral tumours present symptoms that are common to many other oral pathologies, so to diagnose oral tumours it is mandatory to biopsy. The radiological characteristics of these lesions are
also not specific, but it is possible to associate different images with different tumours types, and radiology is indispensable in
determining their extension, aggressiveness and clinical stage. At least in the 60% of cases the primitive tumour invades the
underlying bone, but often radiology underestimates the real grade of bone infiltration. This because bone lysis becomes evident radiographically when more than 40% of the compact bone has been already demineralized. Other imaging modalities,
such as CT and RMI, give a better estimation of the tumour extension and a better idea of the tumour margins, but they have
now a moderate or low availability in veterinary practice, and higher costs. Today, in veterinary medicine, radiology is probably the most useful imaging modality to study the behaviour of the non-odontogenic oral tumours, because of good quality of
the informations obtained and the relatively low cost, if compared with other imaging techniques.

SHORT COMMUNICATIONS

D. Bonello, Med Vet


Department of Animal Pathology, School of Veterinary Medicine, University of Turin, Italy

504

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EFFICACY OF INJECTABLE MARBOFLOXACIN IN THE TREATMENT


OF LOWER URINARY TRACT INFECTIONS IN THE DOG
C. Brovida* DVM, P. Gruet** DVM, M. Deinert*** DVM, E. Thomas** DVM
*ANUBI Ospedale per Animali da Compagnia - Strada Genova 299/A - I-10027 Moncalieri - Italy
**VETOQUINOL Research Centre - F-70204 Lure Cedex - France
***I. Med. Tierklinik - Veterinrstr. 13 - D-80539 Mnchen - Germany
Background. Marbofloxacin is a third generation fluoroquinolone specifically developed for Veterinary Medicine and available for small animals as tablets in several European countries. Its massive elimination by renal route as the parent compound,
its broad antimicrobial spectrum and excellent tolerance appear especially interesting characteristics. An ex-vivo study in dogs
allowed to show the bactericidal activity of urine after 4 mg/kg-1 marbofloxacin dosage for at least 4 days on Staphylococcus
intermedius and Escherichia coli. A new therapeutic dosage of 4 mg/kg-1 marbofloxacin, 3 subcutaneous (SC) injections at 4day intervals was thus selected and assessed in a previous comparative study, showing excellent efficacy and tolerance results.
Aims. To confirm marbofloxacin injectable solution efficacy and safety in canine lower UTI.
Methods. 55 dogs presenting clinical signs of lower UTI were included in France, Germany and Italy. The clinical diagnosis
was confirmed by urine sampling taken by cystocentesis for complete urinalysis with bacteriology and antibiosusceptibility
testing. The animals received then 3 SC injections at the dosage of 4 mg/kg-1 marbofloxacin, 4 days apart. Antimicrobials and
anti-inflammatory drugs were forbidden but ancillary treatments could be undergone to treat the underlying disorders (Diabetes mellitus, Cushings disease, urolithiasis...). Dogs were clinically assessed on D0, D4, D8, D12 and D21 and urine sampled on D0, D12 and D21. Side effects were systematically sought at each visit.
Results. Escherichia coli was the most frequently isolated pathogen, in 73.0% of the cases. Marbofloxacin provided 85.7%
bacteriological cure rate and 77.3% clinical cure rate on D12. Few side effects were reported during the study but none led the
investigator to stop the therapy.
Conclusion. Marbofloxacin, used according to a new dosage regimen (3 SC injections at 4 mg/kg-1, 4 days apart), was shown
to be a practical treatment for lower urinary tract infections in the dog, with both excellent efficacy and safety.

CLINICAL TRIAL OF PIMOBENDAN: A NEW INOTROPIC/VASODILATOR


DRUG: LONG TERM SURVIVAL TIME STUDY: THE RESULTS
D. Bruyre DVM
Cardiology Department of Brussels Referal Center, Belgium
Material. PIMOBENDAN (Boehringer UD-CG 115) Its mechanism of action is a phosphodiesterase inhibition (which increases the intracellular calcium disponibility) and an improvement of the sensitiveness of myofibrils for calcium.
Protocol. 65 dogs with dilated cardiomyopathy (DCM) received Pimobendan 0.25 mg/kg BID.
Some dogs with severe cardiomyopathy and atrial fibrillation received also digoxin. The heart failure treatment (vasodilators
such Enalapril or Lisinopril and diuretics such Furosemide) was not interrupted.
Results. NYHA class* and contractility (LVSF**) evolution.

Pimobendan
Pimobendan + digoxin

Day 0
3.0/14%
4.0/10%

1 week
2.0/24%
2.4/23%

3-4 weeks
1.4/31%
1.6/31%

2 months
1.2/32%
1.5/30%

*New York Heart Association: (4 = severe, 1 = asymptomatic).


**LVSF: Left ventricule shortening fraction.
Long term study. From 1992 untill 1997.
Breeds. 13 Labradors, 11 Dobermans, 10 Great Danes, 5 Cockers, 4 New Foundlands.
Gender. 75% males.
Age. 8 years (1-13 years).
Median survival time of the dogs who died of cardiac disease: 7 months. (Exclusion of the deaths within the first month of
treatment): 9 months.
Median survival time of the surviving dogs or the dogs died of non cardiac diseases: 15 months (2 to 51 months).

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CARDIOPULMONARY RESPONSES IN NORMAL AND COMPROMISED DOGS


DURING PROPOFOL ANAESTHESIA
A. Bufalari* Med Vet PhD, C.E. Short** DVM MS PhD Dipl ACVA ECVA, R. Gialletti*** Med Vet,
M. Pepe* Med Vet, R. Arcelli* Med Vet
Institute of Surgery*, Faculty of Veterinary Medicine, University of Perugia; Dept. of Clinical Sciences**,
Faculty of Veterinary Medicine, Cornell Univ., Ithaca, NY, USA; Faculty of Veterinary Medicine***, University of Camerino, Italy
The purpose of this study was to determine the safety of propofol anaesthesia in cardiopulmonary compromised propofol
anaesthetized dogs. Anaesthesia was maintained with propofol administered by infusion pump. The study was completed in
adult dogs randomly selected to receive (a) 0.1 mg/kg IM acepromazine followed by propofol induction (4.4 mg/kg IV) and
maintenance by infusion without cardiopulmonary compromise; (b) 0.1 mg/kg IM acepromazine followed by deliberate propofol overdose to cause respiratory depression; the final group (c) 0.1 mg/kg IM acepromazine, 4.4 mg/kg IV propofol with establishment of hypovolemic hypotension (20 ml/kg blood loss) during propofol anaesthetic maintenance. Blood pressure, heart
rate, respiratory rate and arterial blood gas parameters remained in physiologic range in control group (a). In group b, fifty
percent of dogs developed apnea (>60 sec.) to deliberate anaesthetic overdose and slight hypotension. Remaining dogs had
significant respiratory depression as demonstrated by drop in oxygenation. All dogs responded well to oxygen administration
with or without assisted breathing. Cardiopulmonary responses to deliberate haemorrhagic shock were evaluated during propofol anaesthesia along with the effects of fluid therapy, blood replacement and oxygen-enriched ventilation. Blood loss resulted
in significant drop in mean arterial blood pressure (30.1%). Oxygenation remained satisfactory. Propofol reduced the heart
rate (-22.1%) during the hypovolemic state, blocking the normal sympathetic response to increase the heart rate, but did not
interfere with pulmonary sympathetic compensatory mechanism to maintain a normal blood pH, O2 (+12.7%) and CO2 (-6.2%)
level. Treatment of hypovolemia with fluid, blood and oxygen increased heart rate (+57.2%), mean arterial blood pressure
(+81.5%) and PaO2 (+25.3%). The successful management of deliberate respiratory depression and hypotension during propofol anaesthesia in the groups of dogs by oxygenation or fluid therapy has been demonstrated safe and effective patient management during propofol anaesthesia.

INTEGRATION OF CLINICAL AND HISTOLOGICAL PARAMETERS FOR THE PROGNOSIS


OF MAMMARY TUMOURS OF THE DOG AND CAT

Clinical parameters (dimension of the tumour (T) following the TNM system and lymph node involvement confirmed on histological basis) were singularly evaluated using survival analysis in 78 dogs and 31 cats, which were M0 at surgery, and followed up for 2 years. Each group determined according to T was then divided up into 3 levels of neoplastic infiltration as assessed on histological basis (non-infiltrating tumour, tumour with stromal invasion, tumour with emboli in the vessels). In the
3 groups (T1, T2, T3), both in the bitch and in queen, a significant survival difference was detected (P<0.05: T1vsT2 and
T1vsT3 in the bitch, T1vsT3 in the queen); this difference was sligtly associated with survival in other comparisons (P=0.06
T2vsT3 in the queen; P=0.07 T1vsT2 in the bitch) with the only exception of T2vsT3 in the bitch (P=0.37). In both species
lymph node involvement was significantly associated with prognosis (P<0.0001). Integration of T with grade of invasion: in
the T1 group it did not offer additional prognostic information (P=0.37 in the queen; P=0.40 in the bitch); in the T2 group it
evidenced a survival difference statistically significant between tumours with intravascular emboli and those non-infiltrating
or with stromal invasion only (P<0.0001 in the bitch; P<0.05 in the queen); in the T3 group it maintained the same effect
shown for T2 in the bitch (P<0.0001) but not in the queen (P=0.27). The information deriving from the integration of the neoplastic dimension and the grade of invasion would be important to define, in some T groups, 2 different risk classes: the one
including the non-infiltrating tumours and those infiltrating with stromal invasion only, and the other including the cases with
neoplastic emboli in vessels.

SHORT COMMUNICATIONS

O. Capitani* DVM, G. Sarli# DVM, C. Sassetti*, P.S. Marcato# DVM ECVP


Dipartimento Clinico Veterinario*, Dipartimento di Sanit Pubblica Veterinaria e Patologia animale#
Facolt di Medicina Veterinaria - Bologna, Italy

506

4th European FECAVA SCIVAC Congress

NEUROLOGICAL FINDINGS IN COCKER SPANIELS WITH FAMILIAL VITAMIN E DEFICIENCY


AND RETINAL PIGMENT EPITHELIAL DYSTROPHY
R. Cappello* DVM, G. McLellen* DVM, S. J. Wheeler* DVM, K. Chandler* DVM, C. Rusbridge* DVM,
P. Lyabert* DVM, R. Elks* DVM, I.G. Mayhew# DVM, A.P. Bjornson DVM
Departments of Small Animal Medicine* and of Veterinary Pathology, The Royal Veterinary College Universitity of London,
Department of Veterinary Clinical Studies, Royal (Dick) School of Veterinary Medicine,
University of Edinburg, Easter Busch Veterinary Centre#
Background. Vitamin E deficiency has-been described in Cocker Spaniels suffering Retinal Pigment Epithelial Dystrophy
(REPED). A spectrum of neurological disorders has been associated with chronic vitamin E deficiency in a range of species including man.
Aim. To characterise the neurological and neuropathological changes in Cocker Spaniels with RPED and familial vitamin E deficiency.
Methods. A full neurological examination was conducted on Cocker Spaniels which were diagnosed as suffering from RPED by
the ophthalmology service of The Royal Veterinary College, University of London, between March 1996 and October 1997. In all
cases plasma vitamin E deficiency was confirmed by High Performance Liquid Chromatography. In two cases electromyography
(EMG) was performed and motor nerve conduction velocities (MNCV) measured. In 4 cases cerebrospinal fluid (CSF) examination and in 1 case magnetic resonance imaging were also performed. In 2 cases full post mortem examination including neuropathological examination was conducted.
Results. The mean age at presentation was 4 years (range 2-7 years). Six dogs were female and 2 male. Three dog demonstrated
severe ataxia affecting all four limbs, 2 dogs were ataxic in the pelvic limbs and 3 were normal. Proprioceptive deficits were noted in all four limbs in 2 dogs and in the pelvic limbs in 5 dogs. Four dogs manifested whole body tremor. EMG abnormalities
were present in 3 dogs. MNCVs and amplitude were normal. MRI performed in one case was normal. CSF examination was normal in all 4 dogs in which it was performed. The neurohistopathological findings were similar in both dogs. Spinal cord neuronal
fibre degeneration was recognised in most funiculi, being slightly more evident in the gracile, spinocerebellar and ventromedial
tracts. In the medulla oblongata, the lateral cuneate nuclei revealed profound neuroaxonal dystrophy with spheroid formation,
neouronal loss and astrogliosis.
Conclusion. These clinical and neuropathological findings suggest that chronic vitamin E deficiency in Cocker Spaniels results in
a proteiform neurological syndrome. These findings are similar to those associated with familial isolated vitamin E deficiency in
man, and to those of equine degenerative myeloencephalopathy in which vitamin E deficiency has been described.

INCIDENCE OF ATOPIC DISEASES IN DOGS IN SLOVAKIA


P. Chandoga, DVM, M. Kozk, Assoc Prof, DVM, PhD, J. Mojzis ov, DVM, M. Tuckov, Dipl Ing

Department of Internal Diseases of Solipeds, Small Animals and Birds, University of Veterinary Medicine in Kosice, Slovakia

Goals. To observe and evaluate anamnestic and clinical aspects at atopic disease in dogs. To judge the significance of allergendiagnostics for the evidence of environmental allergens at detection of atopy in dogs in the region of Kosice in Slovakia.

Material and Methods. A basic set consisted of 65 patients with atopic symptoms of the disease. Dogs were examined at the
1st Internal Clinic of the University of Veterinary Medicine in Kosice during 1994-1997. Intradermal tests were performed us
ing the Dutch allergens ARTU-BIOLOGICALS for diagnostics of atopy in dogs.
Results. The highest incidence of atopy was found in German Shepherd dogs, then in crossbreds and Poodles. Atopic disease
was recorded also in Slovak long-haired sheep dog. The first symptoms of allergy occurred between the 1st and 3rd year of
life in 37 (56.9%) examined patients. The seasonal dependence of the diseases (spring-autumn) was observed in 30 (46.1%)
cases. Besides pruritus with characteristic distribution of skin lesions, also disorders of gastrointestinal tract and paranal sacs
were recorded. Of the seasonal allergens, the highest number of reactions (13.8%) was found on weed pollen, then grass pollen
(4.6%) and tree pollen (3.1%). Of the non seasonal allergens, Dermatophagoides farinae (67.7%), Tyrophagus putrescentiae
(55.4%), Acarus siro of (36.9%) and human epithelia (35.4%) ahowed the high number of reactions. Multisensitivity was observed in 78.5% cases.
Conclusion. Atopic diseases with wide scale of allergens in dogs have been found to be frequent also in our conditions. Based
upon our experiences at making diagnosis of atopy, it is necessary to map and to have at our disposal a complete set of environmental allergens for a certain geolocality.

4th European FECAVA SCIVAC Congress

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TERMINATION OF PREGNANCY IN THE BITCH BY VAGINAL ADMINISTRATION OF PGF2


M. Cinone* Res, G. Aiudi* DVM, M.E. DellAquila* Tec Biol, A. Zarrilli # Ass Prof, R.L. Sciorsci* Res
Inst. Biol. Reprod. & Obstetr. Dom. Anim.*, University of Bari, Italy
Inst. Physiol. Vet.#, University of Bari, Italy
The wide spreading of small animals and the birth control enlarged the requirements of pregnancy termination in the bitch. A
suitable method to induce abortion is not available up to date and very toxic drugs, such as isochinolina, are currently commercialized. The aim of this work has been the definition of a pharmacological treatment useful to cause the abortion induction by means of PGF2 endovaginal administration. The experiment has been carried out on 10 bitches 2-7 years old and
middle/large size (20-35 kg b.w.) which were between the 355 day of the pregnancy. The pregnancy period was calculated
on the basis of the first day of cytological diestrus. The pregnancy diagnosis was made by ecographical test. All bitches in
healthy conditions were treated with endovaginal administration of syntetic PGF2, luprostiol (Prosolvin-Intervet) every 24h
up to abortion occurred. The dose was of 0.15 mg/kg b.w. adsorbed with a gel made of fumed silice and triacetin (Sigma).
Blood levels of progesterone have been recorded by RIA. The abortion occurred after 4-5 days of treatment with the expulsion
of fetuses and fetal membranes without complications. The subjects had mucoid losses after the first day of treatment. Blood
losses were observed one day before the fetuses expulsion and continuing up to 3-4 days after the abortion. The side effects
such as tachycardia, polypnoea, ipersalivation, contraction of the abdominal muscle with kyphosis, which were of low degree
spontaneusly resolved 30after the treatment. The subsquent clinical control did not show undesidered consequencies, indeed
after 3-4 months the bitches presented natural fertile heat and two of them were coupled and became pregnant. The progesterone, after the second PGF2 administration, presented a fast fall and remained at basal levels till the abortion. The endovaginal administration in abortion induction allowed to use a very low dose of PGF2 and to reduce indesidered side effects.

A CASE OF CANINE CENTRAL DIABETES INSIPIDA CAUSED BY A CHROMOPHOBE


CELL ADENOMA OF THE HYPOPHYSIS

Central diabetes insipidus (CDI) is a rare condition found in small animal practice. Idiopathic CDI is much more frequent than
secondary CDI due to a neoplasm of the neurohypophysis or hypothalamus. The aim of this presentation is to make a differential diagnosis of a 6 year old male Boxer with polidipsia and polyuria without neurological signs.
The first approach to this case was to differentiate the possible CDI from hyperadrenocorticism, diabetes mellitus and renal
failure. This differential was based in clinical signs, history and results of blood and urine tests. Because the urine was hiposthenuric, the next step was to differentiate between central or nephrogenic diabetes insipidus and psicogenic polydipsia.
After a water deprivation test, CDI was diagnosed. As the dog had no neurologic signs and the CSF was normal, a vasopressin
treatment was recommended. In the next month the dog improved the polidipsia and polyuria, but subsequently showed some
visual impairment and a lethargic state. A new neurologic examination revealed clinical signs compatible with a space-occupying lesion located in the cerebrum or diencephalon. CT scan showed a tumour over the hypophysis with a large oedema and
deviation of the right cerebral ventricle. Three days later the dog became very ill and died. Histology and immunohistochemistry identified the tumour as a chromophobe cell adenoma of ACTH-secreting cells, originating from the pars distalis of the
adenohypophysis.
The differential diagnosis in these cases is complex; although the nature of the tumour ought to determine a clinical picture of
Cushings disease, CDI was the presentation, probably due to compression of the hypophysis. CT scan is critical in arriving to
a definite clinical diagnosis. Repeating the neurologic examination is probably the best method to rule out neurological involvement when it is impossible to use CT scan. The CSF sample was normal and, in this case, useless to assess the existence
of the tumour.

SHORT COMMUNICATIONS

J.H.D. Correia*, DVM, PhD, A.J.A. Ferreira*, DVM, PhD, M.M.G.R.E. Niza*, DVM, PhD, J.M.J. Correia, DVM*,
Mulas, J.M.#, DVM, PhD, M.L. Ferreira*, DVM, PhD
*DEMOC, Faculdade de Medicina Veterinria, Universidade Tcnica de Lisboa, Portugal; #Dept. Anatomia y Anatomia
Patologica Comparadas, Fac. Veterinaria, Universidade de Crdoba, Spain

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4th European FECAVA SCIVAC Congress

A CASE OF PRIMARY CILIAR DYSKINESIA IN A DOG


D. De Lorenzi Med Vet
Libero professionista, Forlimpopoli, Italy
Although primary ciliary dyskinesia is an infrequent disease, it should be taken into account with young dogs suffering from
recurrent rhinosinusitis, bronchitis and bronchial pneumonia.
This disease is likely to be connected to a recessive autosomic gene causing ciliar asynchronism and consequently functional
immobilization as well as very little or no mucociliar clearance activity.
Thanks to electron microscopic ultrastructure tests of cilias, it is possible to evaluate which anomaly is affecting cilias and the
percentage of cilias involved.
A 5-month-old English Springer Spaniel, male, regularly vaccinated, has undergone a clinical examination, x-rays and bronchoscopic tests, because it had been underdeveloped, suffering from cough and occasional bilateral nose discharge with no response to previous antibiotic treatments, since the age of two months.
No foreign body accidentally inhaled has been detected by the bronchoscopy. A bronchoalveolar lavage has been performed
showing infectious neutrophilic exudate from which Pasteurella multocida and Staphilococcus intermedius have been isolated,
but no Micoplasma sp. A 30-day antibiotic treatment based on the antibiogram has only ensured temporary results. Therefore
the dog has subsequently undergone one more bronchoscopy even to take some fragments of the tracheobronchial and nose
mucosa and carry out an ultrastructure evaluation of cilias. 300 ciliar structures from trachea, bronchi and nasal mucosa, almost half sectioned, have been examined. Ultrastructure modifications were apparent in 78% of them: loss of one or both central single tubes, partial absence of dineine arms, disarrangement of outer doublets, cilias accidentally arranged. The same test
has been performed on a reference standard from an asymptomatic dog of the same race and age. Only 2.9% of cilias has
shown a modified ultrastructure. As far as the author knows, this is the first case in Italy in which the assumed diagnosis has
been confirmed by ultramicroscopical tests on the structures involved.

PRIMARY CUTANEOUS LYMPHOMATOID GRANULOMATOSIS IN A DOG


M. Baldi Med Vet, L. Della Salda* Med Vet, A. Boari# Med Vet, B. Passarini Med Vet
*Dip. Sanit Pubblica Veterinaria e Patologia Animale, # Dipt. Clinico Veterinario,
Istituto di Clinica Dermatologica, Universit degli Studi di Bologna, Italy
Ist. di Patologia Speciale e Clinica Medica Veterinaria, Universit degli Studi di Teramo, Italy
The purpose of this report is to document clinical, histopathological and ultrastructural findings and therapeutical approach of
a rare case of primary cutaneous lymphomatoid granulomatosis in a dog.
A 5-year-old mixed breed male dog was referred for facial erythematous-erosive cutaneous plaques. Skin examinations were
negative for cutaneous mites, bacteria and fungi. Cytological findings were compatible for a pyogranulomatous dermatitis.
Two months after the initial visit the dog developed a severe erosive to ulcerative skin lesions associated with scaling and nodules over the head and left rear limb. Skin biopsies showed a pleocellular periadnexal and angio-invasive nodular to diffuse
cell infiltration. Cell populations were mainly atypical large lymphohistiocytic cells, plasma cells and occasional neutrophils.
Immunohistochemical examination (Antisera specific for T and B lymphoid markers used: CD3, CD4, CD8, CD21, MAC 387,
and IgG, IgA, IgM) demonstrated an antigen expression referable to an atypical T-cell lymphoma. Ultrastructurally, the large
lymphohistiocytic cells showed irregular cytoplasmic and nuclear contours, abundant heterochromatin and rough endoplasmic
reticulum, some multivesicular bodies but no lysosomes. In the dermal endothelial cells several paracrystalline tubuloreticular
structures were frequently observed. Based on the histopathological diagnosis of lymphomatoid granulomatosis, treatment was
than started with a combination of prednisone and cyclophosphamide as proposed by Woods et al. (1984)1. Ciclophosfamide
treatment was changed to chlorambucil (2 mg//m2/4 consecutive days/week os) when a sterile hemorrhagic cystitis recurred after about 1 year of ciclophosfamide therapy. Over the 16 month follow up, during which the dog was under clinical-laboratory
control, skin lesions (alopecia, nodules and erythema) were still present on the face.
References
1. British Journal of Dermatology 110, 619-625.

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MEDIAL APPROACH FOR TOTAL HIP REPLACEMENT IN DOGS. AN EXPERIMENTAL STUDY


Z. Diszegi DVM, Z.S. Kendik DVM, J. Tth DVM PhD, B. Fenyves DVM
Department and Clinic of Surgery and Ophthalmology, University of Veterinary Science, Budapest, Hungary
Background. Total Hip Replacement is a continuously developing procedure in canine orthopedic surgery.
Aims. To experience the possibility of a new approach to the hip joint for Total Hip Replacement which provides better exposure of the acetabulum, has not negative effect on the gluteal muscle group, and has much better cosmetic appearance.
Methods. In dorsal recumbency the origin of pectineus muscle, and the insertion of iliopsoas muscle is tenotomized. The adductor muscle is partly elevated from the femur, and the femoral head excision is completed. With abduction and caudal traction of the femur the acetabulum is widely exposed.
To prepare the femur for the reaming of prosthetic stem the greater trochanter is lifted into the acetabulum and the leg is ad
maximum abducted. From this point the procedure is similar to other cemented THR. Techniques finally the tenotomies are repaired and the wound is closed.
Results. In the first case we did not repaired the pectineal miotomy, and so a medial luxation occurred.
In two other cases the medial luxation was due to the improper placement of the acetabular component.
One dog was exterminated intraoperatively due to the fracture of the greater trochanter.
The remaining four cases were successful.
Conclusion. We found it possible to do Total Hip Replacement via medial approach. The visibility of the acetabulum was better, the reaming was easier, but we had to learn the correct placement of the acetabular component in dorsal recumbency.
Reaming of the femur was less convenient, even in cases with serious arthrosis with diminished angle of abduction. Avoiding
the operative trauma of the gluteal muscle group, the possibility of lateral luxation is diminished. Last but not least for the
pleasure of the owners in the future the hairclipping and the wound is hardly visible on a standing animal.

EFFICACY OF CIS:TRANS 25/75 MICROINCAPSULATED PERMETRINE IN THE THERAPY


OF OTODECTIC MANGE IN THE DOG AND IN THE CAT

Objective. Clinical evaluation of the efficacy of a dermatologic acaricide cis:trans 25/75 0.3% water suspension permetrine
(Zekout ICF), in the treatment of otodectic mange in small animals.
Material and methods. 20 animals (7 dogs and 13 cats) with otodectic mange (diagnosis obtained with otoscopic examination and/or microscopic examination of the exudate). When presented, none of the pets had been treated with injectable ivermectin (Ivomec), parasitcides and corticosteroids (neither topic medication, nor ear canal medication used) in the previous 15
days. Every patient was submitted to general and dermatologic/otologic examination. All data concerning: presence of parasites and/or exudate in the ear canal, pruritus, erythema, and skin lesions, were recorded on day 0, 7, 14, 21, 31 on a special
clinical record. All the subjects included in the study were submitted to the following therapy: A) ear canal detersion: a single
application, only if the ear canal resulted obstructed with debris, of cerumene and NaCl solution. B) dermatologic acaricide:
application of the acaricide in the ear canal (3-4 drops), on the neck, on the back and on the base of the tail skin, every 7 days
for 4 times (days: 0, 7, 14, 21). Criteria of selection for withdrawal in the therapeutical trial: no positive answer detected or
worsening of the clinical signs, sudden signs of a drug reaction. The clinical evaluation of the efficacy of the acaricide used
was detected by direct and mineral oil microscopic examination of the exudate (presence and number of parasites/eggs detected on 5 fields at 50x magnification) before the treatment (day 0), during the treatment (days: 7, 14, 21) and after 10 days since
the end of the treatment (day 31). The efficacy was classified as: good (no parasites and/or eggs detected), moderate (presence
of dead parasites and no eggs detected), no efficacy (presence of vital parasites and eggs detected). The clinical evaluation was
done by detection of total absence of the following clinical signs, at the end and during the 10 days of therapeutical trial: 1)
presence of pruritus and pain in the ear canal. 2) presence of erythema in the ear canal. 3) presence of exudate in the ear canal.
The efficacy was classified as: good (no clinical signs detected) moderate to low (50% of clinical signs still detected), no efficacy (persistence of clinical signs detected).
Results. In all the 20 cases presented a good efficacy of the microincapsulated permetrines has been detected. Nor parasites
neither eggs has been found and clinical signs has not been detected too (two weeks since the first day of treatment). No side
effects has been detected.
Conclusions. According to the results obtained in this pilot study it is possible to state that 0.3% suspension of cis-trans 25/75
microincapsulated permetrine are effective in the treatment of otodectic mange in the dog and in the cat.

SHORT COMMUNICATIONS

F. Fabbrini DVM
Clinica Veterinaria Papiniano 50 - 20123, Milano, Italy

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4th European FECAVA SCIVAC Congress

CASE REPORT OF ROCKY MOUNTAIN SPOTTED FEVER IN A DOG FROM NORT-EASTERN ITALY
M. Caldin1 Med Vet, T. Furlanello1 Med Vet, G. Lubas2 Med Vet
San Marco Private Veterinary Clinic, Padua, Italy; 2Veterinary Clinical Medicine Institute, University of Pisa, Italy

The Rocky Mountain Spotted Fever (RMSF) is a rickettsial disease caused by Rickettsia rickettsii. The disease is well known
in North America, but it has been very rarely described in Europe, except in the recent years in Southern Italy.
In April 1997, a referring veterinarian submitted to our Clinic a newfoundland female dog, 3 years old, with an history of
febrile syndrome. The dog used to live in a large courtyard in a semi-urban area close to the city of Padua. At the clinical examination we found pyrexia (40.2 C) and an obvious subcutaneous erythematous swelling, diffuse to the ventral area of the
body. The main abnormalities in the blood works (including bile acids assay) were hypoalbuminemia (2.2 g/dl, normal 2.54.0) and a slight hyponatremia (139 mEq/L, normal 141-154). The coagulation profile was normal, except for a severe hypoantithrombinemia (79.3%, normal 100-148). The most obvious site of albumin and antithrombin loss was the subcutis and a
diagnosis of vasculitis has been proposed. Since one of the most common cause of vasculitis is the acute infection by Rickettsia rickettsii, we tested the dog with a validated semiquantitative test. The serum titer for IgM was positive and comprised
between 1:64 and 1:128. The titer for IgG was similarly beetwen 1:64 and 1:128. The serum titers for Ehrlichia canis and Borrelia burgdorferi were negative. At that point we suspected the RMSF, although no other diagnostic tests had been employed
to support our thought.
The dog has been treated with doxycycline (10 mg/kg q12h PO for 1 month). We experienced a very rapid clinical response to
the treatment, although the hypoalbuminemia needed more than one month to recover.
In summary, the clinical presentation (diffuse skin rush), the haemato-biochemistry findings (hypoalbuminemia, hyponatremia,
no evidence of DIC) and the serum titer suggested us a diagnosis of RMSF. No informations were available about the source
of the infection and the vector.
Further researches are needed for redefining the epidemiology of RMSF, and european veterinarians need to be aware of the
occurence of this infection, taking in account also the zoonotic importance of this tick-borne infection.

HISTOLOGICAL PARAMETERS OF PROGNOSIS IN MALIGNANT MAMMARY TUMOURS OF THE DOG


M. Galeotti* DVM, C. Benazzi# DVM ECVP, G. Sarli# DVM, M. Montagnese* DVM, P.S. Marcato# DVM ECVP
Dip.to Scienze Produzione Animale*, Fac. di Agraria, Udine, Italy
Dip.to di Sanit Pubblica Veterinaria e Patologia Animale# - Fac. di Medicina Veterinaria - Bologna, Italy
Mammary tumours are the most important tumours for their frequency in the dog, with a malignancy ranging from 40% to
60%. This study shows the prognostic histological results obtained from 107 dogs, which resulted M0 at mastectomy, followed
up for two years. Among the histological parameters valued, the grade of invasion (P<0.0001) resulted significantly associated
with prognosis while tubular differentiation (P<0.05) and myoepithelial proliferation (P=0.09) slightly associated with prognosis. As for the grade of invasion, significant survival differences were recorded between non-infiltrating and infiltrating tumours, and within these latter, between those with stromal invasion only and with intravascular emboli. In the subjects showing stromal invasion, the division into intracapsular and extracapsular stromal invasion was not important for the survival
(P=0.35), but significantly associated with the cancer-free interval (P<0.01). In the cases with emboli in the lymph and/or
blood vessels, the division into massive embolism (s.c. inflammatory carcinoma, indicative of systemic micrometastases)
and occasional emboli (P=0.078) was useful. The results obtained, analysed in terms of survival and/or post-surgery relapse,
are presented as useful indicators of the need to support or not surgery with an additional therapy: mastectomy eventually associated with an additional therapy for locally invasive tumours; mastectomy associated with an additional therapy for the tumours with occasional emboli; additional therapy which is only a palliative for all the cases with massive embolism, in
which micrometastases are usually active. The loss of tubular differentiation and absence of myoepithelial proliferation do not
seem important histological data, as the different survival times in these cases do not appear biologically important (1 month
difference in the average value), even though they may influence the prognostic judgement and the therapeutic criteria to be
followed.

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CORRELATION BETWEEN LEFT ATRIAL ENLARGEMENT, BODY WEIGHT


AND ATRIAL FIBRILLATION IN THE DOG
C. Guglielmini* Med Vet, V. Chetboul Med Vet, M. Pietra* Med Vet,
J.L. Pouchelon Med Vet, M. Cipone* Med Vet
Dip. Clinico Veterinario*, Universit di Bologna, Italy
Service Mdcine, E.N.V.A.
Among the population of dogs referred for cardiovascular examinations during the period 1996-97, 164 subjects were selected
with the criteria of cardiovascular diseases associated with left atrial enlargement (i.e. mitral valve endocardiosis, dilated cardiomyopathy, subaortic stenosis, patent ductus arteriosus and mitral valve dysplasia). An electrocardiographic (ECG) and
echocardiographic, two-dimensional real-time and M-mode, examinations were conducted on all subjects. On the basis of
ECG the dogs were divided in: Group A, 40 cases (24.4%) with atrial fibrillation (AF) and Group B, 124 cases (75.6%) without AF. The latter Group (B) was subdivided into Group C, 89 dogs (54.3%) which showed normal sinus rhythm (SR) and
Group D, 35 dogs (21.3%) which showed other types of arrhythmia. The echocardiographic measurement of left atrial sistolic
diameter (LA) and aortic diastolic diameter (Ao) were made and the LA/Ao ratio was calculated as an index of LA enlargement independent of body weight (BW). A statistical analysis (ANOVA) was carried out comparing the dogs of Group A with
those of Group B and C according to the variables BW, LA and the LA/Ao ratio. A significant difference (p<0.001) was found
between dogs of Group A and those of Group B and C for each of the considered variables. The predictive areas of developing
an AF was subsequently calculated comparing to the maintenance of SR or the developing of other types of arrhythmia correlating the BW with the LA and the LA/Ao ratio. For the same degree of LA enlargement (expressed by the LA/Ao ratio) the
probability of developing an AF increases in the same way of BW. Therefore AF is correlated to absolute LA enlargement
rather than to its relative degree of enlargement, explaining the prevalence of this type of arrhythmia in giant dogs.

ATTEMPTS TO CURE FELINE LEUKEMIA VIRUS INFECTION


WITH BIOLOGIC RESPONSE MODIFIER TREATMENT.

It caused a sensation when HRBER and MAYR (1991) published to be able to cure 80 to 100% feline leukemia virus- (FeLV) infected cats from viremia by using a biologic response modifier, because FeLV infection is still considered to account for
most disease-related deaths in pet cats. Different treatment attempts with various drugs were performed in the past but none
resulted in healing or complete virus elimination. HRBER and MAYR (1991) however, used the paramunity inducer PINDORF (Baypamun, Bayer, Leverkusen) consisting of inactivated parapox ovis virus to cure FeLV infection. Since that time,
Baypamun is the most commonly used drug for treatment of FeLV infection in Germany.
Two placebo-controlled double-blind trials were performed to determine the therapeutic efficacy of Baypamun in naturally
FeLV-infected cats under controlled conditions. In the first study, 120 cats were involved. Sixty cats were treated with Baypamun, 60 with a placebo preparation of virus-free cell culture medium. Dosage and administration of the drug over a 7 week
period were performed according to the instructions given by the company. Remission of viremia occurred in 12% and 7% of
the cats treated with Baypamun and placebo, respectively. This difference was not statistically significant. In the second
study, 30 naturally infected cats were treated in a placebo-controlled double-blind trial. In complete, 20 clinical, laboratory,
immunological, and virological parameters were examined, but no statistically significant differences could be demonstrated
between Baypamun and placebo application.
Therefore, FeLV infection was not influenced by Baypamun treatment. The importance of placebo-controlled studies to prevent uncritical misinterpretation was demonstrated.

SHORT COMMUNICATIONS

K. Hartmann* Priv-Doz Dr, A. Block* Dr, G. Ferk* Dr, A. Vollmar# Prof Dr,
H. Lutz Prof Dr
I. Medizinische Tierklinik*, Institut fr Pharmakologie#, Ludwig-MaximiliansUniversitt Mnchen, Germany, Veterinrmedizinisches Labor der Universitt
Zrich, Switzerland

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4th European FECAVA SCIVAC Congress

SAFETY TRIAL IN BITCHES WITH TABLETS CONTAINING OESTRIOL (INCURIN)


S. Hendriks DVM, B. Janszen DVM PhD
Intervet International B.V., P.O. Box 31, 5830 AA Boxmeer, the Netherlands
Background. Incurin is indicated to treat bitches suffering from urinary incontinence due to sphincter mechanism incompetence. Because the active ingredient of Incurin , oestriol, is an oestrogen with a short receptor residence time, it shows only
early oestrogenic effects. Experience in humans for over 30 years has shown that these early effects do not lead to toxicity.
Results from clinical studies indicate that the effective dose is between 0.5 and 2 mg/animal, once daily or every other day. A
safety trial in dogs was carried out to confirm the safety of oestriol when given up to 5 times the maximum clinical dose.
Material and methods. Four groups of intact bitches were treated with 0 (n=5), 2 (n=4), 6 (n=4) or 10 (n=6) mg oestriol/animal for a period of 90 days. Clinical examinations were carried out at regular intervals, and blood samples were taken for
haematology and blood biochemistry. Necropsy including histopathology of the bone marrow was performed after completion
of the study.
Results. All animals remained healthy during the study. Signs of oestrus were seen, mainly in the animals receiving the high
doses. Haematology results and histopathology of the bone marrow indicated that bone marrow suppression did not occur.
Conclusion. Incurin is safe, even at 5 times the maximum clinical dose. This finding is in line with the results from clinical
studies in which animals were treated up to 600 days without significant adverse reactions.

TREATMENT OF URINARY INCONTINENCE IN THE BITCH:


CLINICAL TRIAL WITH TABLETS CONTAINING OESTRIOL (INCURIN)
S. Hendriks DVM, J.G.H.E. Bergman DVM, T. Nell DVM, P.H. van Laar, B. Janszen DVM PhD
Intervet International B.V., P.O. Box 31, 5830 AA Boxmeer, the Netherlands
Background. Sphincter mechanism incompetence (SMI) is an important cause of urinary incontinence (UI) in bitches. A clinical trial was performed with Incurin (containing 1 mg oestriol/tablet) in bitches suffering from UI.
Material and methods. One hundred and thirty-three (133) bitches with UI due to SMI were treated with Incurin . Of these
bitches, 96% was spayed. The starting dose was 2.0 mg/animal once daily. In case of sufficient response after one week the
dose was reduced to 1.0 mg and after two weeks to 0.5 mg/animal. In case of a response to either 0.5, 1.0, or 2.0 mg once daily, this dose was given once every two days. The total trial period was 42 days. Blood parameters were determined before and
after treatment to monitor the influence of treatment on bone-marrow.
Results. Response to treatment was seen in 83% of the bitches, 61% became continent and 22% improved. In 16% the condition was unchanged or worsened or treatment had been discontinued due to a lack of effect.
The final effective dose varied from 0.25 to 3 Incurin tablets per administration. In 65% of the cases tablets were given daily,
in 35% on alternate days. The dose and the treatment frequency were not related to the weight of the animal.
In 12 (9%) dogs, mainly at the 2 mg dose, signs of oestrus were reported. These signs disappeared after lowering the dose. In
12 dogs (9%) mild and transient side effects (vomiting, panting, short of breath) were reported. Treatment did not have any effect on haematological parameters.
Conclusion. From the results of this clinical trial, it can be concluded that treatment with Incurin is efficacious and safe. No
signs of bone marrow suppression were observed.

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CLINICAL EFFICACY OF THE NEW INODILATOR PIMOBENDAN, IN COMPARISON


TO DIGOXIN FOR THE TREATMENT OF CONGESTIVE HEART FAILURE IN DOGS
R. Kleemann* Med Vet, G. Le Bobinnec DVM D ECVIM-CA, D. Bruyere# DVM,
C. Justus* Med Vet, H. Schmidt* Med Vet
Boehringer Ingelheim Vetmedica GmbH, Product Development, D-55216 Ingelheim, Germany*
5, Allee des Tanneurs, F-44000 Nantes, France, Theo Verbeecklaan 25, B-1070 Bruxelles, Belgium#
Introduction. Pimobendan is a novel drug which is currently being developed for the treatment of congestive heart failure in
dogs. Due to its dual mode of action calcium-sensitisation and inhibition of phosphodiesterase-III it exhibits positive inotropic
as well as vasodilatory properties. Compounds with this combined mode of action are often referred to as inodilators.
Aims. To assess the clinical efficacy of Pimobendan (0.4-0.6 mg/kg daily) in comparison to a standard digoxin treatment in
dogs with congestive heart failure.
Methods. A total of 109 dogs with congestive heart failure of which 60 dogs were treated with Pimobendan and 49 subjected
to Digoxin were evaluated. Diagnosis was based on clinical examination, x-ray, ECG and echocardiography. The clinical assessment of heart insufficiency was based on the guide-lines of the New York Heart Association (NYHA-score 1-4). Follow up
examinations were performed after approximately 7 and 28 days of treatment. Digoxin plasma levels were monitored to avoid
Digoxin overdosing. The investigators had the option for a longer follow up.
Results. Prior to initiation of therapy the mean NYHA-score was 3.5 for the Pimobendan and 3.4 for the Digoxin group. At
the final examination it improved to 1.9 for the Pimobendan group but only to 2.6 in the Digoxin group. Overall 56 of 60 Pimobendan treated, but only 30 of 49 Digoxin treated animals improved their NYHA score during the study (p < 0.001). During the study significantly less side-effects were reported in the Pimobendan group (p < 0.05). During the optional follow up
period (up to 524 days) sudden death occured in 20% of the Digoxin treated animals but only in 8% of the Pimobendan treated
dogs.
Conclusion. It is concluded that Pimobendan is superior to Digoxin for the treatment of congestive heart failure in dogs.

ANALYSIS OF MORBIDITY OF DOGS IN THE REGION OF THE CITY KOSICE,


SLOVAKIA DURING 1995-1997
M. Kozk, DVM, PhD, Assoc Prof, M. Tuckov Dipl Ing, P. Chandoga DVM

Department of Internal Diseases of Solipeds, Small Animals and Birds, University of Veterinary Medicine in Kosice, Slovakia

SHORT COMMUNICATIONS

A great interest in breeding of small animals, above all, dogs emphasizes the health problem of these animals and their diseases. Modern veterinary medicine starts from preventive principles of active prevention of animal health.
Goals. Clinical and scientific workers, teachers of veterinary universities have to know to which direction they should orientate their activity within preventive activity and consultation. Our work, evaluating the frequency of the disease incidence and
analysis of morbidity in dogs at the Internal Clinic of the University of Veterinary Medicine in Kosice during 1995-1997, con
tribute to this.
Methods. 28.600 case histories of examinations of the dogs affected with various diseases during three years were evaluated.
Results. During three year observed period, there were 5 most numerous diagnoses: 1. Diseases of digestive (30,6%), 2. Diseases of skin and hair (29.6%), 3. Infectious diseases (10.25%), 4. Diseases of respiratory organs (8.2%), 5. Endoparasitoses
(7.42%). As well, the seasonal dependence of dermal diseases and etiotrophic factors were evaluated.
Conclusion. Our work indicates to the orientation in the practice of small animals. It analyses in detail morbidity of dogs
within individual organ systems.

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EFFECT OF RECOMBINANT HUMAN GRANULOCYTE COLONY-STIMULATING FACTOR


ON HEMATOPOIESIS IN NEUTROPENIC CATS CAUSED BY DIFFERENT DISEASES
M. Kuffer-Frank DVM, W. Kraft DVM
Department of Veterinary Internal Medicine, Ludwig Maximilians University Munich
I. Medizinische Tierklinik, Veterinrstr. 13, 80539 Mnchen, Germany
Background. Colony stimulating factors are glycoproteins that regulate the proliferation and differentiation of hematopoetic
progenitor cells. The recombinant human granulocyte stimulating factor (r-metHuG-CSF) filgrastim raises mainly the amount
of neutrophile granulocytes in the blood (Cancer Res 1988; 48:5624-37). The use of r-metHug-CSF in cats has not been studied intensively. Fulton, et al., administered rhG-CSF to normal cats, demonstrating a significant increase in neutrophile counts
(Exp Hematol 1991; 19:759-67).
Aims. To evaluate the efficacy of r-metHuG-CSF in sick, neutropenic cats.
Methods. 26 cats with severe neutropenia were treated with filgrastim during a two day trial period. WBC count, blood smears,
PCV and the serumparameters AP, -GT, lactic dehydrogenase, cholesterin were monitored during the treatment period in all
cats. Depending on the underlying disease process, the cats were divided into four groups for further evaluation: retrovirus infection (FIV, FeLV), cat flue, panleucopenia and bacterial infection.
Results. A significant overall increase of neutrophile granulocytes was found. There was a more limited raise on monocytes
and eosinophiles. Comparing the four groups, the group with retrovirus infected cats did not show an increase of neutrophile
granulocytes, whereas the patients in the other groups showed a marked increase of this cell population.
Conclusion. Therefore the clinical relevance of using r-metHuG-CSF in neutropenic cats appears beneficial. Filgrastim increases neutrophile granulocyte cell counts in neutropenic cats when neutropenia is caused by cat flue, panleucopenia and bacterial infection. No efficacy of filgrastim was found in the retrovirus group. Reasons therefore are possibly the obstruction of
proliferation and differentiation by the virus itself or by cofactors.

COMPARATIVE STUDIES OF THE EFFICACY OF TWO LEUKAEMIA VIRUS VACCINES


Hans Lutz DVM
Clinical Laboratory - Dept of Internal Veterinary Medecine
University of Zrich, Switzerland
In a study conducted in 1997, we were interested in how well 2 different FeLV vaccines are able to protect against vigorous
FeLV challenge infection. To this end, 45 cats were housed in 3 groups in 3 rooms of a special facility of the Dutch Institute
for Animal Science and Health. Two veterinarians of our laboratory vaccinated the cats of group 1 with Fevaxyn FeLV + Dohycat Tetrafel (containing calici-, herpes-, parvovirus and chlamydia antigens, Solvay), of group 2 with Leucogen + Feligen
(containing calici-, herpes-, parvovirus antigens, Virbac) and of the third group with a placebo (phosphat-buffered saline, PBS)
under blinded conditions. Three weeks after the second vaccination, all 45 cats were challenged with 500 000 ffu of FeLV A
Glasgow by intraperitoneal injection. The course of the infection was monitored by personnel and veterinarians ot the Institute
who were not informed about which cats had received which vaccines. The parameters investigated included daily clinical observation, weekly clinical examination, weekly assays for p27 (by ELISA) and weekly quantification of anti p45 antibodies.
Two months after challenge infection, the cats of groups 1 and 3 became depressed, showed reduced appetite, reduced weight
gain and had enlarged palpable lymphnodes. With the exception of 1 cat where enlarged lymphnodes were palpated, all cats of
group 2 were clinically normal, showed normal appetite and normal weight gains. The rate of viremia -the most important parameter to characterize protection- was 5 of 15 for the Leucogen group, 10 of 15 for the Fevaxyn group and 11 of 15 for the
placebo group. It became clear that Leucogen was able to protect significantly (Fischers exact test, on-sided, p=0.0328)
against viremia while the percentage of viremic cats in the Fevaxyn group was not distinct from that in the placebo group
(p=1.0).
In summary, Leucogen has not only be shown to be highly efficacious to protect cats against long-term FeLV challenge but also to be by far superior than other FeLV vaccines.

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COMPARATIVE DIAGNOSTIC IMAGING OF THE PELVIC CAVITY IN DOGS


D. Malleczek - Dipl- Tzt
Radiology Clinic, University of Veterinary Medicine, Vienna, Austria
Purpose. The pelvic cavity is one of the hardest regions to examine, because of the surrounding pelvic bone. A number of
dogs with lesions in the pelvic area were examined with different imaging methods. The purpose was to find the imaging
method with the best diagnostic results.
Materials and methods. Various cases with signs of obstipation and/or dysuria were referred to the Radiology Clinic. In most
cases an undifferentiated mass was palpated rectally. The caudal abdomen and pelvic region were examined radiographically,
sonographically, followed by computertomography. Surgery and/or a post mortem examination, including patho-histology,
verified the diagnosis.
Results. Lateral x-rays of the abdomen showed gross lesions in the pelvic region. A good indicator is a narrowing of the colon
descendens in this area. The urinary bladder was often not distinguishable from the soft-tissue tumor mass. Exact localization
of the mass was not possible.
Lesions or masses near the apertura pelvis cranialis image well ultrasonographically. The colon descendens or surrounding
bones may cause imaging artefacts. Lesions deeper inside the pelvic cavity are difficult to visualize with ultrasonography.
CT-scans offer the best insight into the pelvic cavity. Bone structures, filled colon descendens, and superimposition do not interfere with axial scans deeper in the pelvic region. The size, origin, and localization of a mass or lesion can be imaged. The
density of every tissue or mass can be measured in Houndsfield-units and allows for a more exact diagnosis.
Conclusions. Computertomography is the imaging method with the highest diagnostic value for structures within the pelvic
cavity. CT examinations should always be preceeded by a good radiographic and/or sonographic work-up.

EVALUATION OF THE LOCAL RELEASE OF CISPLATIN


IN A RODENT MAMMARY CARCINOMA MODEL

The aim of this study was to determine the efficacy of cisplatin against local recurrence (LR) and metastatic spread (MT)
when implanted in the tumor bed after marginal resection in a mammary carcinoma model. Ninety C3H-HeJ mice were injected with MTG-B (murine mammary tumor Gollin-B) tumor cells. Tumors were marginally (histologically incomplete) excised
and the mice were randomly assigned to three treatment groups: 1 Cisplatin administred intraperitoneally (IP), 2 OPLA -Pt
(biodegradable polymer containing cisplatin), and 3 no treatment (control). Fifteen mice (short-term group) chosen randomly
from each of the three treatment groups were sacrificed 14 days after surgery and 30 (long-term group) were sacrificed 60
days after surgery. A complete necropsy was performed in each mouse. The results from the short term group were as follow.
Group 1. Eight of 14 mice had LR. None had MT. Group 2. Ten of 14 mice showed evidence of LR. One had MT. Group 3.
Thirteen of 15 mice had LR. One had MT. Results from the long term group were the following: Group 1. Ten mice of 14 had
LR. Two had MT. Group 2. Five of 15 mice had LR. Two had MT. Group 3. Fifteen of 15 mice had LR. Ten had also MT. Results from long term group were more complete and interesting. Cisplatin and OPLA -Pt groups had significant advantages
over controls in all variables measured (LR, MT, tumor score, survival time and delay to regrowth). OPLA -Pt had significant advantages over cisplatin in LR rate, tumor score, survival time and delay in regrowth.

SHORT COMMUNICATIONS

E. Morello* DVM, W. Dernell # DVM, MS, C. Kuntz # DVM, MS, P. Buracco* DVM, S. Withrow # DVM
Department of Animal Pathology*, School of Veterinary Medicine of Torino, Italy
Comparative Oncology Unit#, Department of Veterinary Clinical, College of Veterinary Medicine and Biomedical Sciences,
Colorado State University, Fort Collins, USA

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RESULTS OF THE TREATMENT OF 56 CANINE ORAL TUMORS


E. Morello* DVM, M. Martano# DVM, C. DellAcqua# DVM, P. Buracco* DVM
From the Department of Animal Pathology*, School of Veterinary Medicine of Torino, Italy
Private Practice#
Oral tumors represent 6-7% of all malignancies in dogs. They can be either benign or malignant and can be localized everywhere in the mouth. A presurgical evaluation (clinical examination, X-rays, biopsy) is necessary to identify the tumor type and
both clinical (TNM) and histological grading. Surgery is generally the first choice of treatment; in selected cases, neoadjuvant
or adjuvant radiation therapy can be used. In this serie 56 dogs are presented (January 1989- November 1997). Nine had an
acanthomatous epulis (AE), 5 an ameloblastoma (AM), 14 a malignant melanoma (MM), 10 a fibrosarcoma (FSA), 7 a squamous cell carcinoma (SCC), 5 an osteosarcoma (OSA), 1 a histiocytic lymphoma (LSA), 3 an undifferenziated sarcomas (US),
1 a chondroma rodens (CR), and 1 a matricial carcinoma (MC). Mandibulectomy and maxillectomy were performed respectively in 31 and 21 dogs. An en bloc resection (tongue, cheek, etc) was performed in 4 dogs. The survival at 1 and 2 years
(with no recurrence and/or progression to metastasis) is respectively for dogs with AE 77.8% and 55.6%, with AM 100%, with
MM 38.5% and 15.4%, with SCC 71.4% and 42.8% and with OSA 60% and 20%. For dogs with FSA the survival at 1 and 2
years is 40% while for those with US is 33%. The MC recurred after 89 days from surgery. The dog with CR is alive after 771
days from surgery. The LSA, despite chemotherapy, recurred after 84 days from surgery. In conclusion, radical surgery can be
considered a valid option for the treatment of oral tumors in dogs. Cosmetic and functional results are encouraging.

GM1-GANGLIOSIDOSIS IN ALASKAN HUSKIES


A. Moritz1 DVM, G. Mller2 DVM, A. Sewell3 DVM, W. Baumgrtner2 DVM
Medizinische und Gerichtliche Veterinrklinik I1, Institut fr Veterinr-Pathologie2, Justus-Liebig-Universitt Giessen
Zentrum der Kinderheilkunde3, Wolfgang-Goethe-Universitt Frankfurt, Germany
GM1-gangliosidosis was diagnosed in a breeding colony of Alaskan Huskies. Clinically, diseased animals exhibited proportional dwarfism and neurological dysfunction. Signs of nervous impairment, characterized by hyper- and dysmetria especially
of the hind legs, intention tremor and nystagmus developed slowly and were most prominent between 4 to 7 months of age. In
one female dog no skeletal abnormalities, in a male dog a prohibited enchondral ossification were noted radiographically.
Blood parameters and CSF were normal, in urinanalysis typical oligosaccharides were found. Histological examination of the
central nervous system revealed that the majority of neurons was enlarged, displayed a foamy cytoplasm, and were frequently
filled with vacuoles that displaced the Nissl substance. Vacuoles were also present in various extracerebral cells including
macrophages and circulating lymphocytes. Biochemical analysis of cultered primary skin fibroblasts and formalin-fixed splenic
and spinal cord tissue revealed marked elevation of GM1-ganglioside, lack of -galaktosidase activity and normal -hexosaminidase activity in affected animals. Pedigree analysis indicated a transmission of the disease through an autosomal recessive pattern of inheritance.

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EVALUATION OF VALTRAC BIOFRAGMENTABLE ANASTOMOSIS RING


ON THORACAL ESOPHAGUS IN THE DOG
T. Kovcs MD, T. Nmeth# DVM, I. Kves MD PhD, J. Tth# DVM PhD
Dept. of Surgery, National Institute of Oncology Budapest, Dept. and Clinic of Surgery and Ophthalmology,
University of Veterinary Science Budapest#, Hungary
The biofragmentable anastomosis ring (BAR) has been using as an alternative to hand-sutured or stapled anastomosis on intestinal tract in human surgery. Regarding its absorbable character, BAR provides with safe, atraumatic and sutureless anastomosis without remaining material. This technique has not been assessed so far in the thoracal esophagus in dogs. The main
purpose of the study was to evaluate the VALTRAC BAR-created thoracal anastomosis (Daevis-Geck) in surgical, postoperative clinical and morphological-histological respect. Two groups of 3-3 experimental dogs were operated performing BAR
anastomosis on the thoracal esophagus. Intraoperative features as surgical handling, expected complications and operation
time were observed. During the follow-up period of 4 (Group I) and 14 (Group II) days, patients were fed with concentration
diet through tube gastrostoma and were under continuous clinical supervision including the assessment of general state and
respiratory signs. At the time of evaluation dogs underwent in vivo endoscopy and positive contrast esophagography. The
anastomosis site was examined by in situ hyperbaric tensile strength measurement. Macroscopic as well as histological evaluation were also done. The surgical technique of BAR anastomosis was found easy to perform within a mean time of 13.6 minutes with no intraoperative difficulties. During the postoperative period neither general nor respiratory disorders were experienced excepting an episode of moderate pleural effusion in one dog of Group I. Either endoscopic or positive contrast esophagographic examination revealed no stricture or leakage in the anastomosis site. Strong adhaesions with the trachea and the
pleura were found via necropsy. The mean tensile strength of the anastomosis was 80 mmHg in Group I and 192.5 mmHg in
Group II. Histological evaluation revealed mild granulation tissue reaction in 2 dog of Group I and 1 dog of Group II, which
did not lead to significant stricture. According to the results of the study, BAR can be a useful alternative surgical technique of
thoracal esophagus anastomosis in dogs.

CLINICOPATHOLOGICAL FEATURES OF MULTIPLE CARTILAGINOUS


EXOSTOSIS IN THREE LITTERMATE DOGS

Background. Multiple cartilaginous exostosis (MCE) is a rare benign proliferative cartilaginous and osseous disease characterized by knobby and protuberances involving endochondral bones during skeletal development. MCE have been occasionally reported in dog, and rarelly in horse and cat. In man, dog and cat, malignant transformation of MCE to chondrosarcoma or
osteosarcoma has been described. An inherited origen, associated with an autosomal dominant gene, has been reported.
Aims. To describe the clinicopathological aspects of MCE in three, 6 months-old, male, cross-breed littermate dogs and a
comparative analysis with previous studies.
Results. Exostosis were bilaterally symmetrical, involving in all cases the humerus, cubitus, radius and metacarpus in the
forelimbs and femur, tibia, and perone of the hindlimbs. Metatarsus, pelvis bones, ribs, thoracic vertebrae and pennis bone
were affected only in one of the three dogs. Radiographic analysis demonstrated exostoses in different stages of evolution,
which arise from the methaphyseal and diaphyseal regions of long bones. In the three dogs premature closure of the distal
cubital physis induced a poorly development of the radius, as well as secondary osteoarthosis of the elbow. Haemogram only revealed moderate hypercalcemia and mild increase of alkaline phosphatase. The urinalysis was normal. Gross pathology
showed proliferative cartilaginous and osseous tissue lesions and areas of atrophy of normal cancellous bone. Microscopically, exostoses consisted on proliferative hialine cartilage tissue cap underlying spongous bone with variable degree of endochondral ossification.
Conclusion. The symmetrical location and the similar stages of the lesions found in the three dogs resemble, more closely,
some cases reported in human beings than that previously described in the dog.

SHORT COMMUNICATIONS

M. Novales* DVM PhD, J. Prez** DVM PhD, E. Hernndez* DVM, E. Mozos** DVM PhD
Depts of Clinical Pathology* and Veterinary Pathology** - University of Crdoba, Spain

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SYSTEMIC RESPONSE OF BLOOD INFLOW OCCLUSION TO THE LIVER IN DOGS


J. Pecar DVM, J. Butinar DVM MSc PhD, D. Podgornik DVM MSc, A. Seliskar DVM MSc

Small Animal Clinic, Veterinary Faculty, University of Ljubljana, Slovenia


Introduction. Liver surgery is relatively common in small animal medicine, including management of abdominal trauma or
liver resection for other problems. Hepatic bleeding presents the problem sometimes difficult to manage. Portal triad clamping
(PTC) which interrupts all the arterial and venous inflow to the liver is recognized and useful technique to arrest hepatic bleeding, well tolerated by human patients for up to 60 minutes. Clinical experiences and results of the study evaluating perihepatic
packing suggest that dog may not resist the PTC for a period listed in veterinary literature, i.e. 15-20 minutes. A clinical trial
was conducted to evaluate the systemic response and determine time of PTC, which is safe and useful when performed to control hepatic bleeding. Preliminary results are presented.
Materials and methods. 5 beagle dogs were used in the clinical trial. Laparatomy was performed, lesser omentum opened
and hepatoduodenal ligament (pedicle) encircled with a tape and PTC performed with Rummel tourniquet to occlude blood inflow to the liver. Blood pressures measurements and samples for blood gas analysis (arterial, mixed venous and portal) were
taken and recorded before PTC, first and second minute after PTC and then in two minutes intervals. Mean arterial blood pressure (MAP) of 35-55 mmHg was considered as minimal safety margin to terminate the experiment and release the PTC.
Results. Total blood inflow interruption (PTC), resulted in rapid deterioration of haemodynamics. The average duration of
PTC was 5,25 (4-7) min. Values of MAP decreased from 128 (120-140) to 48,5 (38-56) mm Hg just prior of releasing PTC.
ETCO2 values decreased from 5,65% (5,3-5,9) to 3,38% (2,9-3,8) before releasing PTC. Values of arterial, mixed venous and
portal blood gas analyses reflect changes in haemodynamics.
Conclusions. Preliminary results suggest that PTC is poorly tolerated in the dog, and therefore might be of limited value as a
mean to minimize hepatic bleeding by establishing control of the major vascular structures.

SPINAL MENINGEAL CYSTS IN THREE DOGS:


LONG TERM OUTCOMES EVALUATION AFTER THERAPY
S. Romussi DVM PhD*, M. Digiancamillo DVM#, L. Carnevale DVM*,
R. Lombardo DVM PhD*, F. Addis DVM Prof*, L. Leonardi DVM Prof#
Istituto di Clinica Chirurgica Veterinaria*, Istituto di Radiologia Veterinaria# - Universit degli Studi di Milano, Italy
Introduction. Meningeal cystic dilation of the spinal cord represents an uncommon pathology with uncertain etiology and
classification reported in dogs as rare isolated cases. The aim of the present work is to present three additional cases and to
discuss the therapeutical results with a long term follow-up.
Materials and Method. Three cases of meningeal cystic dilation were diagnosed at the Institutes of Veterinary Surgery &
Veterinary Radiology - University of Milan from 1995 to 1997. All the patients underwent, after neurological examination,
plain spinal radiographs and myelography under general anaesthesia. Cervical myelography was obtained in one case and lumbar myelography in the other two using a dymeric non ionic water-soluble contrast medium (300 mg/I/ml). Two dogs were
submitted to dorsal laminectomy and complete cyst resection, the other patient underwent conservative treatment. The followup was based either on neurological examinations or telephone interviews. In one case M.R.I. was obtained during the followup period.
Results and Conclusions. Case 1 (Surgical therapy) Pug, male 3 yrs. Two mos hystory of bilateral hind limb ataxia. Subarachnoid dilatation at T12-T13. Complete recovery 4 wks after surgery. Neurological worsening with similar initial clinical
signs 20 mos. after therapy. Case 2 (Surgical therapy) Rottweiler male 5 yrs. Five mos hystory of fore and hind limb ataxia
unresponsive to corticosteroid therapy. Subarachnoid dilatation at C5-C6. M.R.I. 32 wks. after surgery: no signs of local relapse. Significant improvement in neurological status following physical therapy. The dog was standing 6 wks. and walking 42
wks. after surgery. Case 3 (Conservative treatment) Rottweiler male 3.5 yrs. Weakness, hind an fore limbs ataxia, severe hip
dysplasia. Unchanged clinical conditions 28 mos. after diagnosis. Despite the prognosis of meningeal cysts appears, according
to the literature, to be favorable in case of surgical drainage, the long terms outcomes in case of cysts resection seems to indicate a more guarded final prognosis.

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TREATMENT OF FLEXION XONTRACTURE OF THE CARPUS


WITH THE ILIZAROV TECHNIQUE: FOUR CASES
G.L. Rovesti* Med Vet Dipl ECVS, A. Margini* Med Vet
Ambulatorio Veterinario Associato M. E. Miller, Cavriago (Reggio Emilia), Italy
Flexion contracture of the carpus is a severe disease with the unability to extend the carpus, actively and passively, as a common clinical feature, either in the awake patient and under general anesthesia. Its equivalent to the Volkmanns disease in
man, and its pathophysiology is complex. The differentials to be considered are compartimental syndrome of the antebrachii,
peripheric palsy of extensors muscles with predominance of flexors, primary rigidity or ankylosis of the radio-carpal joint, and
sympatethic reflex dystrophy. The purpose of this study is to evaluate the technical feasibility, complications and results of this
diseases treatment using the Ilizarovs technique. Four cases of flexion contracture of the carpus treated at the Ambulatorio
Veterinario Associato M. E. Miller, Cavriago (Reggio Emilia), Italy, have been evaluated. In the first patient the contracture
followed a proximal articular fracture of the ulna with tissue loss, treated with Ilizarov technique as well. In the second case it
developed following some bandages, used to treat a procurvatus posture of the dogs carpus when he was 2-3 months old. The
third and fourth cases had no hystory about the problem, because both of them have been adopted from the present owners
when the disease was already present. One of them had a functional radial nerve, whereas the other one was diagnosed to be
affected by radial palsy. The treatment has been the same for all the patients, and was performed by means of a progressive extension of the carpus, using a frame with hinges centered on the rotation axis of the carpus and a threaded bar for traction on
the cranial part of the device. The treatment lasted from 16 to 63 days, followed by 6 weeks of stabilization for patients with
functional radial nerve or by a pancarpal arthrodesis for the one with radial palsy. All the patient could use the leg at the end of
the treatment, even with some specific problem due to the presenting disease. The extension of the carpus to 20 has been a
technical choise, because we believe that in patients with functional radial nerve this reduces the amount of contracture recurrence, whereas in those who will undergo arthrodesis it gives better posture of digits. We conclude that the Ilizarov technique
has been useful in treating flexion contracture of the carpus.

CANINE LEPTOSPIROSIS, DO WE USE PROPER VACCINATION PROGRAMMES?


D. Salgado DVM, R. Barrera DVM PhD, M.C. Ma DVM PhD, C. Zaragoza DVM, S. Andrs DVM PhD, M. Benito DVM
Dept. of Medicina y Sanidad Animal, Faculty of Veterinary, University of Extremadura, Spain

SHORT COMMUNICATIONS

It is usually considered that a proper immunization against Leptospira interrogans is achieved by 2-3 doses of vaccine (against
serotypes canicola e icterohemorragiae), given at 3-4 weeks intervals and with booster injections each year to get a good IgG
response. The aim of this study is confirm that the above mentioned statement is true. The vaccination programme of 246 dogs
with leptospirosis, from the Veterinary Teaching Hospital of UEX (Spain) was studied. The animals were divided into 3 groups:
I) Not vaccinated; II) Vaccinated in the last 6 months; III) Vaccinated in the last 6-12 months. Each group was divided in 4
subgroups according to age: < 6 months; 6-12 months; 1-6 years; > 6 years. The most remarkable results are: 42.68% of the
affected animals belong to group III. Thus indicates that the yearly vaccination is not adequate. In fact, vaccinal immunity usually lasts at least 6-8 months. The percentage falls to 19.91% in group II. The data of the above mentioned groups, in relation
with the total number of dogs sent to the referral center, show that the most affected population is that of dogs without vaccination (4.47%), followed by groups III (3.53%) and II (1.64%). The incidence of age in the groups with respect to the population studied, shows that in the non-vaccinated animals the risk increases with age, specially from 6 months. In group II there is
a low incidence of the disease, decreasing with age. A higher incidence, although the same distribution, is observed in group
III. Therefore, 3-4 doses of vaccine with 2-3 weeks intervals and booster injections each 6 months are recommended.

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DETECTION OF MICROMETASTASES IN LYMPH NODES


IN MALIGNANT MAMMARY TUMOURS OF THE DOG
G. Sarli DVM, P.S. Marcato DVM ECVP
Dipartimento di Sanit Pubblica Veterinaria e Patologia Animale - Facolt di Medicina Veterinaria - Bologna, Italy
The histological evidence of neoplastic cells in mammary lymph nodes may be difficult in routine sections (stained with
Hematoxylin-Eosin) when these cells do not appear in a large number, but only in microgroups or single cells. This study considers sections of regional lymph nodes (axillary or superficial inguinal) in cases of malignant mammary tumours of the the
bitch at different histological stage: stage 0 (non infiltrating tumour) 20 cases; stage I (stromal invasion) 31 cases; stage II
(presence of emboli in the lymph or blood vessels) 10 cases. All the cases were negative for metastasis in the regional lymph
node with the routine staining method. Section of lymph node, formalin-fixed and paraffin-embedded, were used for immunohistochemical staining with a monoclonal antibody anti-cytokeratin-19. As positive control, for each case, a section of the corresponding mammary neoplasm was used. The immunohistochemical positivity to cytokeratin-19 was evidenced in the cytoplasm of both neoplastic cells of the primitive tumour and lymph node. The micrometastases in the lymph node were revealed
prevalently in the subcapsular sinuses and rarely in the medullary ones. In no stage 0 malignant tumour micrometastases were
present. These were evident in 7 cases out of 31 (22.5%) of the stage I malignant tumours and in 100% of the histological
stage II neoplasms. The results obtained may be considered an estimation of the frequence that cases of mastectomy without
regional lymphadenectomy have to mantain some cells which could give origin to a new neoplasm. The most interesting data
concerns histological stage I, in which it could be possible to correct the gradation of invasion (from I to II for the presence of
micrometastases) assessed on routine preparations.

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DIAGNOSIS OF GLOMERULOPATHY IN THE DOG:


THE QUALITATIVE ASSESSMENT OF PROTEINURIA
P. Scarpa Med Vet PhD, V. Corso Med Vet, O. Pozza Med Vet
*Istituto di Patologia Speciale e Clinica Medica Veterinaria, Universit degli Studi di Milano, Italy

SHORT COMMUNICATIONS

Introduction. Recently, the quantitative assessment (UP/UC) of proteinuria has aroused great interest in veterinary nefrology. On
the contrary, in human medicine, the qualitative assessment and the concept of marker has been developed. The marker is a
proteine that, detected in urine, is used to localise in an early time the seat and the severity of the renal lesion. The aim of this trial is to test the usefulness of the qualitative approach for a more complete diagnosis of glomerulopathy.
Materials and methods. Urine samples from 15 proteinuric and suspected nephropatic dogs were collected. The physical-chemical properties and the sediments were analyzed. The quantitative assessment of proteinuria was performed by the UP/UP ratio.
The qualitative assessment was made by: a) cellulose acetate electrophoresis previous samples concentration (densitometric reading); b) cellulose acetate electrophoresis followed by immunofixation and gold staining (visual interpretation). Immunofixation
was performed using specific antibody in order to reveal the glomerular markers (anti dog -albumin and anti dog-IgG antibodies).
Results. The cellulose acetate immunofixation resulted a valid method to discriminate the glomerular selective proteinuria (only albumin detected in urine) from the unselective form (both albumin and IgG detected). Data are summarized in table 1. Althought performed on a limited number of samples, the results show the limits of the quantitative index (UP/UC ratio), which is
actually considered a good indicator of the glomerular function. As in human medicine, the lack of correlation between the amount
of the proteinuria and its selectivity has been pointed out. A high proteinuria doesnt necessarily correspond to wide bands of IgG,
which instead could be detected in mild proteinuric samples with an UP/UC ratio just in the low side of the doubt range. Because of the different prognosis between the selective and unselective proteinurias and the possibility of achieving different
therapies, further studies on the qualitative assessment of proteinuria should be necessary, in order to obtain better laboratory definitions of the different glomerular patterns.

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PERCUTANEOUS BALLOON VALVULOPLASTY IN DOGS WITH PULMONIC STENOSIS


M. Schneider* Dr, I. Schneider* Med Vet, A. Steinberg* Med Vet, U. Wolf* Med Vet,
K.-J. Hagel# Dr. PrivDoz., H. Neu* Dr. ADir.
Innere Krankheiten der Kleintiere*, Medizinische und Gerichtliche Veterinrklinik I, Justus-Liebig Universitt Gieen
Pdiatrische Kardiologie#, Zentrum fr Kinderheilkunde, University of Gieen, Germany
The purpose of this study was to evaluate the immediate effects of balloon valvuloplasty (BV) of pulmonic stenosis in two different groups of dogs. Eigtheen dogs between 3 and 53 months of age (mean=13) and weighing between 3 and 33 kg
(mean=15,8) were examined. In awake dogs one day before and one week after the BV continuous wave Doppler echocardiography (DE) was performed. Under general anesthesia, pressure was measured in the right ventricle and the pulmonary artery
before and after the BV. Peak to peak pressure gradient was calculated. The pulmonic valve diameter (PVD) was measured in
the right ventricular angiography. The balloon diameter was chosen equal to the PVD for group A (n=6) or 20-30% lager then
the PVD for group B.
The effect of the BV was significantly (p<0,05; p=0,012) different between both groups. In group A the peak pressure gradient
change from an average value of 61 mmHg (sd=37) to 53 mmHg (sd=38) and the percentage of decreasing was not significant. In group B the peak to peak gradient decrease from an average value of 97 mmHg (sd=32) to 47 mmHg (sd=34). The
percentage of decreasing amount to 51% (sd=26%) and was strongly singnificant (p<0,0001). The connection between peak to
peak gradient before BV and percentage of decreasing was not significant. The rate of complication was nearly equal in both
groups.
Because of the better results with lager balloons we prefer this method for the future.

BONE DEFECTS IN DOGS TREATED BY A NEW TISSUE TRANSPLANTATION METHOD


OF ADAPTIVE PERIOSTEAL CAMBIPLASTY
N. Sesic* MD MSc, J.T. Triffitt# BSc PhD, M. Zobundzija & DMV PhD Prof, Z. Bacetic+ DMV MSc
Dept. of Surgery*, University Hospital KBC Rebro, Zagreb, Croatia
MRC Bone Research Laboratory#, Nuffield Orthopaedic Centre, University of Oxford, Oxford, UK
Dept. of Anatomy, Histology and Embryology & Veterinary Faculty, University of Zagreb,
Croatia Veterinarska Klinika Zoe+, Zagreb, Croatia
A new operative procedure has been applied to traumatic bone injuries in dogs and compared with the use of autologous cancellous bone grafts (ACBG), which are currently considered the best materials for use in bone reconstructions. In this method,
which is termed adaptive periosteal cambiplasty (APC), mechanical stimulation of periosteal bone yielded highly active osteogenic tissue which was used for autologous bone grafting in the skeletal defects. Faster healing of these defects by this mechanically-stimulated bone tissue transplant is based on highly increased cellularity and metabolic activity of this graft. Four
weeks before transplantation, specially adapted conical screws were percutaneously applied to the healthy tibial bone shaft and
this induced rapid production of new osteogenic tissue for grafting. The small induced injury to the tibia had no influence on
the normal function and healing at this site was rapidly restored. Healing of the bone defects was assessed by scintigraphic,
histomorphometric, densitometric and mechanical methods and the results of these investigations confirmed that autologous
cambian bone derived by APC possessed greater osteoinductive activity than ACBG. Technecium scintigraphy indicated twice
the osteogenic activity per unit mass and histomorphometry showed higher cellularity and osteoblast/osteoclast activity in the
cambial graft compared with ACBG. By densitometry APC expressed in the healing defects at all phases after transplantation
higher densities than the same bone defects treated with ACBG. In addition, there was a shorter time of immobilisation required and a more rapid healing without the appearance of delayed union. From these results it is concluded that the APC
method is more efficient for curing bone defects in dogs than the use of ACBG.

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SIALADENITIS AND SALIVARY GLAND INFARCTION IN CATS AND DOGS


M. Sozmen* DVM, P. Brown* BVMS PhD Dipl ECVP MRCVS, T. Whitbread** Bsc BVSc MRCVS
Comparative Pathology Lab*, University of Bristol, School of Veterinary Science, Bristol BS18 7DU Abbey Veterinary
Services**, 14 Oak Place, Newton Abbot, Devon, TQ12 2HW, United Kingdom
The histochemical and immunohistochemical aspects of salivary gland necrosis and sialadenitis were studied. Salivary gland
infarction is rare but most commonly affects the submandibular gland of dogs. The aetiology is largely speculative; it has been
postulated that it results from inflammation because of constriction of the enlarged, inflamed gland within its fibrous capsule.
A breed predisposition has also been suggested. The analogous disease in humans is termed necrotizing sialometaplasia; it has
identical histological features but occurs mostly in the palate. It is a benign, self limiting ischaemic disorder of the salivary
glands which has many clinical and histological features of neoplasia. Sialadenitis is a general term used to indicate inflammation within the parenchyma of the salivary gland and is the second most frequent pathologic change in dogs and cats. Males
are more sensitive than females to salivary lesions, in both cats and dogs, and the submandibular gland was most frequently
affected. The parotid gland was seldom affected and neither zygomatic nor sublingual glands were involved.
Histochemical techniques applied included lectin histochemistry, immunochemistry of cytokeratins, a-SMA, S-100 protein and
GFAP.
Changes were detected in binding of lectins, CK14 and cytokeratin MNF116 in salivary gland infarction. Lectin histochemical
changes were also detected in canine sialadenitis with DBA, PNA, SBA and TGP lectins; other lectin staining was unchanged.
Loss of cytokeratin and CK14 expression by myoepithelial cells was a prominent finding in sialadenitis and salivary gland infarction, respectively.

SERUM BILE ACIDS AND FELINE TRYPSIN-LIKE IMMUNOREACTIVITY


AFTER EXOGENOUS PANCREATIC STIMULATION WITH CERULETID IN NORMAL CATS

Objective. To assess the change of serum bile acids and feline trypsin-like immunoreactivity (fTLI) after stimulation of gall
bladder contraction and pancreatic secretion with Ceruletid in normal cats.
Design. Eleven normal cats received a single IM bolus of Ceruletid (0.3 g/kg of body weight) together with 0.1 ml Lidocain
2%. Blood was collected at 0, 10, 20, 30, 40 and 50 minutes (min.). Serum bile acids were determined in 10 and fTLI in 11
cats.
Procedure. Serum bile acid concentration was established by enzymatic measurement using Merckotest (Merck) with the autoanalyser Cobas Mira (Hofmann La Roche) and the fTLI concentration was determined by radioimmunoassay.
Results. The geometric mean of fasting serum bile acid concentration was xg = 8.7 mol/l (5.6 - 13.7). There was a significant
increase in bile acid concentration after Ceruletid application (p< 0.01) with a maximum of xg = 13.7 mol/l (8.9 - 21.1) at 40
min.
The arithmetic mean of fasting serum fTLI was xg = 23.14 g/l ( 4.12). There was a slight but significant rise in fTLI concentration after Ceruletid application (p<0.01) with two maximums of xg = 26.02 ( 6.13) at 10 min. and xg = 26.78 g/l ( 6.72)
at 30 min. after stimulation. Concentrations of fTLI at 10 and 30 min. have a statistically significant difference from the fasting fTLI value (p<0.01).
Conclusion. In normal cats serum bile acids and fTLI concentrations rise significantly after IM administration of Ceruletid but
remain within the reference ranges throughout the test. Whether the determination of postprandial bile acids in cats with suspected hepatic diseases can be replaced by the Ceruletid test needs to be investigated as well as the diagnostic value of the
fTLI stimulation reaction in cats with suspected disorders of the exocrine pancreas.

SHORT COMMUNICATIONS

T. Spillmann* Med Vet, Ines Jacob* Med Vet, E.G. Grnbaum* Med Vet,
K. Failing# Dr rer nat Dipl math, J.M. Steiner+ Med Vet, D.A. Williams+, MA, VetMB, PhD, MRCVS
Department of Small Animal Internal Medicine*, Department of Biomathematics and Data Processing#,
Justus-Liebig-University, Giessen, Germany
College of Veterinary Medicine+, Texas A&M University, Texas, USA

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EXPLANATORY PRINCIPLES CONCERNING THE USE OF FULCRUM-LEVER


IN TEETH EXTRACTION IN DOGS
Paolo Squarzoni Med Vet
Libero professionista, Molinella (BO), Italy
The different techniques in dentals extractions often needs the aid of Beins lever restricted to the fragments of the single tooth
using the neigh bours teeth as lever fulcrum we can induce the luxation of these ones. At the end of a personal study, the author after having misured all the teeth roots in different dogs cadavers (see the tablet enclosed), suggest that only some teeth
can be used as fulcrum without being damaged. The author present different explanatory cases showing the possible techniques.
COEFFICIENTS ESTABILISHED FOR BOTH ARCHES GIVING THE REFERENCE VALUE OF 1 TO THE SINGLE CANINE AREA

RECONSTRUCTION OF A LOWER CANINE IN A BOXER USING A RICHMONDS CROWN


Paolo Squarzoni Med Vet
Libero professionista, Molinella (BO), Italy
Dental rebuilding in human medicine has wide possibilities and techniques, independently on the number of therapeutical session. On the contrary, in veterinary medicine we must use simple and relatively cheap techniques that need only few anaesthesiological session. In this report the author will deal with the application of a Richmonds crown (fusion between crown and
pivot) in a boxer. The therapeutical schedule is based on two anaesthesiological sessions, excluding the cluttered test and the
colour test normally used in human medicine.
The case reported was treated in 95 and, up to now, the reconstruction is still unaltered.

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EXTRACTION OF AN UPPER PARATOPIC CANINE TOOTH IN A DOG


E. Stefanelli Med Vet
Libero professionista, Ferrara, Italy
A seven month old Pitbull was presented for the apparent absence of the upper left canine tooth. No abnormalities were reported about deciduous dentition. The clinical examination showed the presence of a crown, similar to that of a canine, palatally to
the normally eruption site. Moreover, the absence of the lower right fourth premolar was reported. The x-ray examination confirmed the presence of a morphologically normal canine partially included in the maxillary bone. The apex was located in a
topographically normal position while the root and a portion of the crown crossed the maxilla medio-distally, erupting almost
in the middle of the palate. The absence of the lower right fourth premolar was confirmed. The dog was therefore put under
general inhalant anaesthesia for the extraction of the paratopic canine, because the portion of palatal mucosa surrounding the
palatally erupted crown was already inflamed and packed with food debris. The buccal mucosa was incised with a scalpel
blade, proximal to the projection of the canine on the maxilla, from the root apex to the eruption site in the palate. A similar
incision was made on the gingiva, from the upper left third incisor to the first premolar of the same side and two mucosal
flaps, palatal and buccal, were elevated to expose the underlining maxillary bone. A high-speed handpiece with a surgical dental bur (size1557) was used to incise the bone deeply to the canine surface, following its mesial border, with a result of a deep
fracture of the left maxilla. This solution was adopted, because it wouldnt have been possible to carry out the standard technique for the upper canine extraction, given that the complete removal of all the bone on the buccal side of the canine would
weakened severely the entire maxilla. The canine was entirely extracted with the combined action of an elevator inserted
around the erupted crown to luxate the tooth and of a scalpel inserted into the bony incision to dilate the paratopic alveolus allowing for the canine passage. The buccal and palatal mucosal flaps were reconstructed with a single interrupted pattern with
an absorbable suture (PDS 3-0).
The controls made 7, 15 days and 1 year later didnt reveal any abnormality.

ADENOCARCINOMA OF A LABIAL MINOR SALIVARY GLAND IN A CAT


D. Tontis1 DVM, F. Dakoronia2 DVM
Laboratory of Pathology, Faculty of Veterinary Medicine, University of Thessaly, Karditsa, Greece
2
Small Animal Clinic, Athens, Greece

Neoplasms derived from salivary glands are uncommon in domestic animals. Particularly, minor (labial, bucal, palatine, lingual) salivary gland tumors are very rarely reported in veterinary literature.
In this paper, after a brief review of feline primary and secondary neoplasms of the salivary glands (major and minor), compared to similar tumors in other animals and man, the clinical and histological features of a minor salivary gland adenocarcinoma in a 13-year-old, male, Siamese cat are described.
The cat was referred because of a swollen and painfull lower lip, a decreasing appetite and excessive salivation, noticed by the
owner. During clinical examination, a palpable, hyperaemic and slightly ulcerated, mass of 2.5 cm in diameter, was revealed
between the left internal surface of the lower lip and gingiva. The mass was surgically excised and biopsied. Microscopic examination showed that the tumor was an adenocarcinoma of a labial minor mixed salivary gland, with negative surgical margins. Fine needle aspiration cytology of the regional lymph nodes, indicated that metastasis had not yet occured.
The prognosis for long-term survival was guarded, since the only method of therapy was complete surgical excision of the
cancer with no postoperative radiotherapy or chemotherapy. The recurrence of the tumor at the primary site, with metastasis to
the regional lymph nodes, was noticed 14 months after surgery. This portended a poor prognosis, the animal was euthansized
and no autopsy was performed upon the owners request.

SHORT COMMUNICATIONS

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ULTRASOUND MONITORING OF FETAL DEATH IN THE QUEEN: A CLINICAL CASE


I. Vannozzi DVM, S. Romagnoli DVM MS, F. Camillo DVM
Dept of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University of Pisa, Italy
A feline pregnancy of a 6 year old Persian queen was followed by ultrasound from day 18 after breeding every 3-4 days, using
a Concept 2000 Dinamic Imaging ultrasound unit with a 5.0 MHz probe. On day 18 at least 3 embryonic vesicles were observed. Days of pregnancy and ultrasonographic parameters (embryonic-fetal vesicle diameter, roundness, homogeneity and
presence of heart beat) are presented in the table. On day 33 lack of growth of fetal vesicular diameter, absence of fetal heart
beat and alteration of roundness and homogeneity were observed. On day 43 absence of fetal image in one vesicle was observed. From day 45 on the queen was treated with bromocriptine (10 mcg/kg BID) to cause expulsion of uterine content,
which occurred on day 48 when the queen expelled an empty vesicle and 3 dead fetuses. Microbiological and virological tests
on aborted fetuses proved negative, while on necropsy all fetuses showed incomplete development of maxillary bones and
presence of cleft palate, and one of them showed also lissencephaly. Although all ultrasonographic parameters became altered
on the same day, loss of vesicular roundness and lack of growth of vesicular diameter were the most easily identifiable signs
of fetal death.
Ultrasound parameters
vesicular diam.(mm)
roundness
homogeneity
heart beat

18
10
+
+

22
18
+
+

26
20
+
+
+

Days of Pregnancy
29
28
+
+
+

33
25
-

37
25
-

43
26
-

Diameter of fetal vesicles, roundness, homogeneity (similarity among vesicular diameters) and presence of fetal heart beat in a
feline pregnancy ending with fetal death and expulsion.
Research performed with a grant from the University of Pisa (ex60%)

PROLACTIN AND ANTIPROLACTINIC DRUGS IN DOGS AND CATS:


RELATIVE EFFICACY AND MODE OF ACTION OF THE VETERINARY AVAILABLE DRUGS
J. Verstegen DVM, K. Onclin DVM
Department of Small Animal Reproduction, University of Lige, Belgium
Prolactin nowadays appears to be one of the most important hormone regulating several different aspects of dogs and cats
physiology. Prolactin has been demonstrated to play a major role in six different fields of physiology in all vertebrates: water
and electrolyte balance, growth and development, endocrinology and metabolism, brain and behavior, reproduction, immunoregulation and protection. To study the role and importance of this hormone in dogs and cats, the characterization of the
different drugs able to modify prolactin secretion is certainly really important. These drugs could be separated in drugs inhibiting prolactin secretion and drugs able to stimulate and increase prolactin production and liberation whose interest is particularly important in dogs and cats reproduction. Indeed, these drugs could then be utilized to inhibit pseudopregnancy, induce abortion, induce estrus and control anoestrus. Prolactin stimulating agents on the other being of interest in lactation stimulation in
postpartum animals.
In this study we have compared the relative efficacy on prolactin inhibition and the relative duration of action of the veterinary
available prolactin inhibiting agents: bromocriptine, metergoline and cabergoline. Those effects were assessed by evaluating
prolactin and progesterone secretion after the administration of the different inhibitors. From this study, it results that, at
equipotent dosage, cabergoline and bromocriptine have the most important inhibiting effects of prolactin secretion and that only cabergoline is able after only one administration to inhibit prolactin secretion for more than 2 days. Metergoline only reduce
prolactin levels at 50% of preadministration value and for only 1 to 10 hours, bromocriptine reduced Prl secretion to basal but
for a maximum of 6 to 8 hours whereas cabergoline decreased prolactin secretion to basal after 8 to 12 hours and its effects is
observed for more than 2 days. During the same study, the stimulating effects of several dopamine antagonists (Haloperidol,
Metoclopramide and Tiapride) known to stimulate prolactin in other species were tested. Tiapride was demonstrated to be the
most potent prolactin stimulator followed by metoclopramide and haldol.

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PRELIMINARY RESULTS ON THE USE OF CABERGOLINE, A PROLACTIN INHIBITOR,


FOR THE CONTROL OF MAMMARY TUMORS IN THE BITCH BEFORE SURGERY
J. Verstegen DVM, K. Onclin DVM
Department of Small Animal Reproduction, University of Lige, Belgium
Prolactin involvement in mammary tumors incidence and development in the bitch is still uncertain and questionable. Some
studies have demonstrated that repeated pseudopregnancies are associated with an increased risk of mammary tumors whereas
the effects of pregnancy and lactation was unclear. These two conditions are associated with an increase of plasma prolactin
concentrations for several days or weeks. In clinical practice, it is often observed that bitches presented for mammary surgery
show at the same time mammary enlargement due to pseudopregnancy. In this study, we investigated on more than 100 bitches
with mammary tumors, the possible positive effect of cabergoline on mammary tissues before surgery. The animals were treated orally once daily for 5 days at the dosage of 5 g/kg of cabergoline prior to surgery. The results of the histopathology after
surgical resection were also recorded. From this study, 3 different situations were observed: 1) 57% of all bitches (83% of
bitches with pseudopregnancy) displayed a significant reduction of the mammary enlargement thus allowing an easier surgical
approach than that realised without anti-prolactinic pretreatment. The reduction of mammary swelling consented to have a
clearer clinical picture of the tumour because of a better demarcation of the mass, enabling to detect some small size nodules
that could not be observed before treatment with cabergoline. These nodules can be easily removed. 2) 10% of bitches had
some small nodules prior to treatment that totally disappeared whilst some others (12%) with middle (between 1 to 3 cm) or
larger size were observed to decrease after treatment. 3) The remaining bitches (21%) had some tumors among which all carcinomas and sarcomas and some benign tumors that did not show any changes due to the treatment. These preliminary results
indicate the interests of anti-prolactinic treatments and possible usefulness of the use of cabergoline as an aid in mammary
surgery. The possible beneficial effects of this treatment is clear in all cases when mammary hyperplasia and milk secretion is
present mainly if associated to a reduction in size of some tumors before surgery. Potential interests are present to discreminate
between benign and malign tumors, the malignant tumors clearly being not responsive to the treatment. These results clinically
indicate possible implication of prolactin in mammary growth and tumoral development in bitches.

EFFICACY OF TERBINAFINE AGAINST DERMATOPHYTOSIS IN CATS AN OPEN RANDOMIZED BLIND-STUDY (PRELIMINARY RESULTS)

Terbinafine is a proven effective treatment for dermatophytosis, especially onychomycosis, in human medicine. The aim of the
present study is to test the efficacy of terbinafine in treatment of dermatophytosis of cats. It is a randomized blind study with
patients of the Internal Medicine Clinic I of the Veterinary University of Vienna. The control comparison consists of patients
treated with griseofulvin, since for ethical and zoonotic reasons we could not administer placebo to infected animals. To enter
the study, patients required a positive culture on a dermatophyte test medium, which proved a dermatophytosis. Two different
dosages of terbinafine were chosen: 12.5 mg/kg BW and 25 mg/kg BW divided BID. The griseofulvin group was treated with
60 mg/kg BW daily also divided in two parts. We monitored CBC and for chemistry-profile ALT and GLDH and creatinine.
Control examination, control culture and CBC were carried out every two weeks. After clinical recovery and a negative culture, we stopped treatment and 4 to 6 weeks later we set up a follow-up examination and a culture. So far we have completed
treatment and follow-up of 7 cats, 3 persian and 4 european short hair cats. They were between 5 months and 12 years old
(mean 2.7 years). Three cats were treated with 25 mg/kg/day, one with 12.5 mg/kg/day terbinafine and three with griseofulvin
60 mg/kg/day. The cats treated with terbinafine were cured (no clinical signs, negative culture) after 13 to 42 days (mean 24,3
days), the cats with griseofulvin-therapy were cured after 28 to 78 days (mean 61,3 days). The follow-ups showed, that two of
the cats in the griseofulvin-group appeared culture-positive again. All others remained negative. There have been no clinical
signs until weeks later. There were no severe alterations in the blood-values and the organ-screenings in any of the groups. In
order to manage dermatophytosis safely in a short time of therapy, terbinafine seems to be an efficient drug to treat dermatophytosis in cats.

SHORT COMMUNICATIONS

B. Hofbauer Dipl Tzt*, R. Wagner Med Vet#


I. Medizinische Klinik, Veterinrmedizinische Universitt Wien#, Novartis Forschungsinstitut Wien*, Austria

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ESTRUS INDUCTION IN CAT WITH CABERGOLINA: PRELIMINARY STUDIES


D. Zambelli Med Vet, S. Belluzzi Med Vet, G. Mari Med Vet
Veterinary Clinical Department, Obstetric Gynaecology Section, Bologna University, Italy
This paper presents the preliminary results obtained between May and August by administering Cabergolina to 5 cats, to induce estrus in subjects to be inseminated or to be synchronised. Before the start of the trial, a colpocytological examination
and hormone dosing was performed to exclude subjects in a state of proestrus, estrus, pregnancy or pseudopregnancy. A total
of 5 European cats, aged between 2 and 5 years, were orally administered 2,5 g/die of Cabergolina for 8 days, and 3 cats
(control), with similar characteristics, with the same volume of saline solution. All the subjects were kept in an unconditioned
environment with a natural photoperiod. A colpocytological examination was made each day and a blood sample taken to measure progesterone (P4) and 17 estradiol (E2) levels. Colpocytology, initially revealed deep cells and numerous cell debris in
all subjects. At start of proestrus, around 8 days after the start of the trial in the 5 cats treated, this exam revealed an increase in
the intermediate and superficial cells. The mean concentration of E2 and P4 in the treated cats, showed initial values of
7.622.30 pg/ml and < 0.20 ng/ml as compared with 28.303.52 pg/ml and < 0.20 ng/ml on the 8th day. On the 9th-10th day,
these subject showed external sign of estrus, keratinization of the superficial cells and mean E2 and P4 concentration of
37.525.48 pg/ml and < 0.20 ng/ml. The treated cats showed a considerable increase in the E2 concentration as compared with
the controls, that showed no sign of estrus. The 5 treated cats were mated and the embryos recovered were 3,4,3,2 NS 2.

TREATMENT WITH FINASTERIDE IN DOGS WITH PROSTATIC PATHOLOGIES


D. Zambelli Med Vet, S. Belluzzi Med Vet, G. Mari Med Vet
Veterinary Clinical Department, Obstetric Gynaecology Section, Bologna University, Italy
The aim of this work was to test the use of finasteride, combined with the specific therapy, to preserve the reproductive performances of subjects with benign prostatic hyperplasia (BPH), prostatitis (P) and prostatic absess (PA). Fifteen subjects with BP,
six subjects with P and eight subjects with PA were treated for a period of seven months with finasteride (5 mg/day per os). In
addition, subjects with P and PA received an antibiotic treatment for 30 days, while those with PA were subjected to omentalization. Before, during (after two month from the beginning) and after (one month from the suspension) the treatment with finasteride, the seminal fluid was valued and the following serous hormones were evaluated: testosterone (TST), dihydrotestosterone (DHT) and 17 estradiol (E2). In the three groups it was observed a clear drop in the mean values of DHT (pg/ml) before and during the therapy (BHP= 294.80 75.1 Vs 105.2060.1; P= 285.5016.5 Vs 68.1027.6; PA= 326.5036.4 Vs
102.6044.2). During the treatment, the mean concentrations of TST and E2 were nearly the same; in all the groups it was observed the disappearance of red blood cells, granulocytes, bacteria and degenerate spermatozoons present in the pre-treatment
ejaculate according to the pathology. All the specific spermatic parameters showed no important variations before, during and
after the treatment, in particularly for the group BHP, the percentage of motility was 73.521.5 Vs 72.721.3 Vs 71.523.1,
and the percentage of normal acrosome was 73.815.3 Vs 73.415.4 Vs 75.213.8. Due to the pain present in the subjects of
the groups P and PA it was not possible to obtain constant data on the pre-treatment ejaculated. During and after the therapy,
the percentage of motility and the percentage of normal acrosome was: P= 66.315.5 Vs 66.318.9 and 47.335.6 Vs 44.837.8;
PA= 77.5613.9 Vs 75.612.9 and 80.815.5 Vs 80.414.5. Our findings shows that it is possible to preserve the reproductive
performances of the subjects with these pathologies by replacing the orchiectomy with the therapy with finasteride, in a definitive or temporary way. During and after that therapy the libido was never lost and it was also possible to obtain good ejaculate
and normal litters for what concerns number and morphology.

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Authors list
click on the name for the abstract
Acocella F.
Annarella S.
Ascher F.
Aucoin D.
Belluzzi S.
Benazzi C.
Bergman J.G.H.E.
Bernardini M.
Bjerks E.
Boari A.
Bodey A.R.
Bonello D.
Brovida C.
Brunetti L.
Bruyre D.
Bufalari A.
Bussadori C.
Caldin M.
Caniatti M.
Capitani O.
Cappello R.
Carlotti D.N.
Chandoga P.
Cinone M.
Correia J.H.D.
Cotto D.
Couto C.G.
Crosta L.
De Lorenzi D.
Della Salda L.
Divers S.J.

Fabbrini F.
Feldman B.F.
Ferrer L.
Ferretti A.
Fournel-Fleury C.
Furlanello T.
Galeotti M.
Guandalini A.
Guglielmini C.
Hartmann K.
Hazewinkel H.A.W.
Hendriks S.
Heripret D.
Jesus S.O.T.S.
Kleemann R.
Kozk M.
Kuffer-Frank M.
LeCouteur R.A.
Lombard C.W.
Lubas G.
Lutz H.
Malleczek D.
Mechelli L.
Meyer D.
Michell A.R.
Millefanti M.
Montavon P.M.
Morello E.
Moritz A.
Mosconi G.
Nmeth T.

Niebauer G.
Novales M.
Pec J.
ar
Peruccio C.
Petersen-Jones S.M.
Pizzirani S.
Rijnberk A.D.
Romussi S.
Rovesti G.L.
Salgado D.
Sarli G.
Scarpa P.
Schneider M.
Schober K.
Scott P.W.
Sesic N.
Smeak D.D.
Sozmen M.
Spillmann T.
Squarzoni P.
Stefanelli E.
Tontis D.
Vannozzi I.
Verstegen J.
Verstraete F.
Vezzoni A.
Von Werthern C.
Wagner R.
Wheeler S.J.
White R.A.S.
Zambelli D.

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