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4 CONGRESSO
FECAVA SCIVAC
EUROPEO
BOLOGNA
18-21
GIUGNO
PROGRAMMA DEFINITIVO
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Tra ing er quio 19
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Ter 15
1998
Con il patrocinio di
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SCIVAC
PALAZZO
TRECCHI
26100
CREMONA
THE
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
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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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
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
SEMINARI PRE-C
S
8,30
A
R
L
E
A
G
D
S
I
T R
ESFM
MEDICINA FELINA
SIDEV
DERMATOLOGIA
ESCG
GASTROENTEROLOGIA
Approccio diagnostico
alle malattie cutanee su
base autoimmune nel
cane e nel gatto (30)
Dominique Heripret (F)
Tecniche per il
trattamento dei tumori colorettali nel cane:
valutazione critica (30)
R.A.S. White (UK)
10,00
Pemfigo e pemfigoide
nel cane e nel gatto
(1a parte)
(30)
Pemfigo e pemfigoide
nel cane e nel gatto
(2a parte)
(30)
Lupus discoideo e
lupus sistemico (60)
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)
TERAPIA
Penetrazione corneale, congiuntivale e
intraoculare dell'acido fusidico per uso
topico nel cane - G. J. McLellan (UK)
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
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)
Tecniche di allenamento
(2a parte) (20)
Dominique Grandjean (F)
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)
10,30
11,00
11,30
Tecniche diagnostiche
impiegabili in medicina
aviare (50)
Peter Scott (UK)
11,50
12,00
9,30
10,00
*
Hills
Gruppo di Studio
ANIMALI ESOTICI
Il prontuario
farmaceutico
cardiologico Tilley
per il veterinario
pratico (60)
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
SEMINARI PRE-C
SALA EUROPA 900
ESFM
MEDICINA FELINA
SIDEV
DERMATOLOGIA
ESCG
GASTROENTEROLOGIA
14,00 Biochimica
clinica felina:
i gatti non sono cani
piccoli da un punto di
vista biochimico !!! (60)
LENTE
Controllo del diabete del cane e cataratta
diabetica
D. Salgado ( CH)
UVEA
Uveite pigmentaria nel Golden Retriever:
43 casi
J.S. Sapienza (USA)
14,30
Diagnosi clinica
differenziale delle
patologie cutanee
autoimmuni (45)
Il linfoma
gastrointestinale del
cane e del gatto (30)
G.Couto (USA)
15,00
Alterazioni vestibolari
nel gatto (60)
15,15
Diagnosi istologica
differenziale delle
patologie cutanee
autoimmuni (45)
RETINA
La retina normale nella Phoca vitulina,
riscontri elettroretinografici e morfologici
E. Bjerkas (N)
Protocolli terapeutici
(e nuove terapie) delle
malattie cutanee
autoimmuni (60)
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)
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)
20
CONGRESSUALI
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)
Gruppo di Studio
ANIMALI ESOTICI
14,00
14,30
Aggiornamenti in tema
di cardiomiopatia
dilatativa nel cane (40)
M. Borgarelli (I)
15,15
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)
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)
Alterazioni
muscolo-tendinee nel cane
atleta (15)
A. Piras (I) e B. Jones (IRL)
Annual General
Meeting of the IEWG
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)
PROGRAMMASCI
S
8,30
A
R
L
E
A
G
D
S
I
T R
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.
EMATOLOGIA
Chairman: Marco Caldin
ORTOPEDIA
Chairman: Antonio Ferretti
OFTALMOLOGIA
Chairman: Stefano Pizzirani
12,00
Livello di Aggiornamento
Livello Avanzato
22
ellArte
S
Sessione Specialistica
O
23
Sessione Interattiva
M
13,00
12,00
RIPRODUZIONE
Chairmen: Matteo Spallarossa (I)
e Patrizia Ponzio (I)
11,00
10,30
4 C O N G R E S S O F E C AVA S C I VA C
DERMATOLOGIA
Sessione specialistica
Chairman: Chiara Tieghi (I)
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?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@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
e@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
?H@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N
?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
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@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7?
L@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J?
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7
?L@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J
e@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
e@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
e1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7?
eL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J?
e?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
e?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7
e?L1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J
f@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7?
fL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
f?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7J?
f?L@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J
g1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7?
gL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@J?
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@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
gh?X?K)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&O2WW?
@@@@
X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W?
?XX6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2W?
)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
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?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O
9,30
N G R
A Z I
E S S O
O N E
8,30
IENTIFICO
PROGRAMMASCI
SALA EUROPA 900
EMATOLOGIA
Chairman:
George Lubas
ORTOPEDIA
Chairman:
Carlo Maria Mortellaro
OFTALMOLOGIA
Chairman:
Claudio Peruccio
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.
ENDOCRINOLOGIA
Chairman:
Alessandra Fondati
ORTOPEDIA
Chairman:
Aldo Vezzoni
OFTALMOLOGIA
Chairman:
Antonella Vercelli
Masse oculari pigmentate e
non pigmentate (60)
*
Hills
18,00
RELAZIONE
SULLO STATO DELLARTE
Approccio diagnostico
e terapeutico
alliperadrenocorticismo (60)
A.D. Rijnberk (NL)
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
IENTIFICO
SALA BIANCA 200
MEDICINA PER
ANIMALI ESOTICI
Chairman:
Peter Scott
NEUROLOGIA
Sessione interattiva
Chairmen: Massimo Baroni e
Tommaso Furlanello
MALATTIE INFETTIVE
Chairman:
Alessandra Fondati (I)
Il grande dibattito:
vantaggi e svantaggi nelluso
dei corticosteroidi nelle
patologie spinali del cane (60)
15,30
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)
17,00
ellArte
18,00
19,00
E U R O P A
A
E
C O N C E R T O
P O
B E
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
14,30
A new drug for the teatment of canine leishmaniosis: Amphotericin B lipid complex
(Abelcet) - Jacques Lamothe (F)
PROGRAMMASCI
SALA EUROPA 900
ONCOLOGIA
Chairman:
Claudio Capurro
EPATOLOGIA
Chairman:
Marco Caldin
OFTALMOLOGIA
Chairman:
Alberto Crotti
Recenti applicazioni e
interpretazioni degli esami
epatici (60)
9,30
DERMATOLOGIA
Chairman:
Antonella Vercelli
Complicazioni della
chemioterapia ed emergenze
oncologiche (60)
EPATOLOGIA
Chairman:
Ugo Lotti
OFTALMOLOGIA
Chairman:
Adolfo Guandalini
Modificazioni oculari
nellanimale anziano
(60)
12,00
Patologie cutanee da
micobatteri (60)
Novit nellapproccio
terapeutico alle patologie
del fegato (60)
Livello di Aggiornamento
Livello Avanzato
26
IENTIFICO
SALA BIANCA 200
DERMATOLOGIA
Chairman:
Alessandra Fondati
ORTOPEDIA
Sessione specialistica
Chairman: Piermario Piga
NEUROLOGIA
Chairman: Stefano Pizzirani (I)
Discussione clinico-patologica
di casi dermatologici (120)
CITOLOGIA
Chairman:
Davide De Lorenzi
9,30
GM 1 - Gangliosidosis in Alaskan
Huskies
Andreas Moritz (CH)
A case of canine central diabetes insipida caused by a chromophobe cell adenoma of the hypophysis
J.H. Duarte Correia (P)
10,30
CARDIOLOGIA
Chairmen: Claudio Bussadori (I)
e Chris Lombard (CH)
Electrocardiographic features of
Deerhounds - A.R. Bodey (UK)
11,00
12,00
ellArte
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
*
Hills
Fissazione con chiodo
bloccato: un nuovo metodo di
fissazione ossea nei piccoli
animali (60)
8,30
PROGRAMMASC
SALA EUROPA 900
DERMATOLOGIA
Chairman:
Chiara Noli
EMATOLOGIA
Chairman:
Marco Caldin
NEUROLOGIA
Chairman:
Marco Bernardini
Prima parte:
Lesioni cerebrali (40)
15,30
*
Hills
Approccio diagnostico
allalopecia nel cane e nel gatto
(60)
Seconda parte:
Lesioni del midollo spinale (40)
Terza parte:
Lesioni a livello
neuromuscolare (40)
Rick LeCouteur (USA)
e Simon Wheeler (UK)
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)
Trattamento clinico
e chirurgico del paziente
con trauma spinale (60)
Infezioni recidivanti nel cane
(60)
19,00
Livello di Aggiornamento
Livello Avanzato
28
IENTIFICO
SALA BIANCA 200
UROLOGIA E
NEFROLOGIA
Chairman:
Claudio Brovida
ONCOLOGIA
Chairmen: Giorgio Romanelli (I)
e Claudio Capurro (I)
14,30
UROLOGIA E
NEFROLOGIA
Chairman:
Fabio Vigan
ellArte
17,00
18,00
16,30
CHIRURGIA E ORTOPEDIA
Chairmen: Carlo Scotti (I) e
Aldo Vezzoni (I)
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
Tecniche diagnostiche
impiegabili per il
riconoscimento precoce delle
patologie renali (60)
Integrazione dei parametri clinici ed istologici nella prognosi dei tumori mammari
maligni della cagna e della gatta
Ombretta Capitani (I)
PROGRAMMASCI
SALA EUROPA 900
CARDIOLOGIA
Chairman:
Gino DAgnolo
NEUROLOGIA
Chairman:
Marco Bernardini
Tachicardia sopraventricolare
nel cane (60)
9,30
RELAZIONE SULLO STATO
DELLARTE
Trattamento chirurgico delle
lesioni retto-anali, anali,
perianali e perineali (60)
Patologie discali
toraco-lombari: diagnosi e
trattamento (60)
12,00
CARDIOLOGIA
Chairman:
Claudio Bussadori
NEUROLOGIA
Chairman:
Massimo Baroni
Considerazioni terapeutiche
sulla cardiomiopatia dilatativa
del cane (60)
13,00
La Sindrome di Wobbler:
considerazioni sul
trattamento (60)
Livello di Aggiornamento
Livello Avanzato
30
IENTIFICO
SALA BIANCA 200
ODONTOSTOMATOLOGIA
Chairman:
Dea Bonello
CITOLOGIA
Sessione specialistica
Chairman: Mario Caniatti
MEDICINA INTERNA
Chairmen: Tommaso Furlanello (I)
e A.R. Michell (UK)
Citologia linfonodale:
quadri normali, infiammatori e
neoplastici (120)
ODONTOSTOMATOLOGIA
Chairman:
Simon Kleinjan
La radiologia come strumento
diagnostico delle patologie del
cavo orale (60)
ellArte
10,30
Sessione Specialistica
12,00
11,00
Le leucemie (60)
DERMATOLOGIA
Chairmen:
Alessandra Fondati (I) e
Luca Mechelli (I)
ONCOLOGIA
Sessione specialistica
Chairman:
Claudio Capurro
*
Hills
9,30
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
*
Hills
8,30
PROGRAMMASC
SALA ITALIA 350
CARDIOLOGIA
Chairman:
Michele Borgarelli
NEUROLOGIA
Chairman:
Stefano Pizzirani
Meccanismi patogenetici e
trattamento delle patologie
pericardiche (60)
15,30
Polipi auricolari, otite media e
sinusite nel gatto (60)
Esperienze e metodi personali di
trattamento di queste frequenti
patologie chirurgiche del gatto
A. R. Michell (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
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?
Dalla farmacocinetica
allapplicazione clinica (40)
David Aucoin (USA)
15,30
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
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)
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
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
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
MAIN SPONSORS
MAJOR SPONSORS
*
Hills
Animal Health
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
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
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
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
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.
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
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.
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.
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
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.
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
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.
13
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.
Introduction
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.
14
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.
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
DOSAGE
COMMENTS
CHELONIANS
Ketamine HCl
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.
Etorphine
0.3-2.75mg/kg i/m
Ketamine HCl
Alphaxalone/ alphadolone
Propofol
10-15mg/kg i/v
LIZARDS
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
Ketamine HCl
Rapid induction, prolonged recovery. May need to IPPV at higher doses, lower
dose for pre-anaesthetic sedation.
Alphaxalone/ alphadolone
Methohexital sodium
Induction and recovery times rapid, concentration should not exceed 0.5%.
CROCODILIANS
Propofol
10-15mg/kg i/v
Succinylcholine*
0.4-1mg/kg i/m
Gallamine triethiodide*
0.6-4mg/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.
16
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
All species. May be used with volatile anaesthetics to reduce induction time and improve
muscle relaxation and analgesia.
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
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.
18
3.
4.
5.
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
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.
20
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-
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
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
22
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.
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
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
24
Calcium mmol/l
Phosphorus mmol/l
2.2-3.5
1.5-3.0
Haematological parameter
Normal range
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
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
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.
Microbiology11
10
Endoscopy
Key words
Reptile, diagnostics, history, clinical examination,
26
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.
27
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.
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
28
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).
29
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.
31
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.
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
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
32
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
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.
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
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
34
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.
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-
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.
Interval
Hemoglobin
Hematocrit
Red blood cells
MCV
MCHC
MCH
Reticulocytes
White blood cells
Neutrophils
Band neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Platelets
Total protein
Fibrinogen
*Modified from deBruijne JJ, Feldman BF: Referentiewaarden van laboratoriumonderzoek bij hond en kat. Analyse 38:11, 248 - 252, 1983.
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.
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
37
.
.I
.
.
.D.
38
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.
39
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.
.
.D.
Systemic and Discoid Lupus Erythematosus are dermatosis associated with circulating auto-antibodies, non specific of cutaneous antigens.
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
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.
40
* 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
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
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
43
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.
.D.
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)
44
- Drug eruption
- Contact irritant dermatitis
- Sub corneal pustular dermatosis
- Sterile eosinophilic pustular dermatitis
- AISD
45
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.
.D.
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
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-
46
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.
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).
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
47
quires long term therapy. Ocular examination is recommended every 4 months even though the cutaneous component is controlled.
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.
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.
49
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.
51
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.
ANATOMICAL CONSIDERATIONS
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
52
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.
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.
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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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.
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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.
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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.
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
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.
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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
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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.
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.
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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.
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
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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.
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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.
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-
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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.
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
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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-
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
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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
73
74
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.
76
77
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-
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-
78
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
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.
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.
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
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.
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.
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.
80
ACQUIRED MYOPATHIES
Potassium-depletion polymyopathy
Infectious polymyositis
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.
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
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.
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
82
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.
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
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.
84
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).
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.
Pre-anaesthetic
Fasting
Volatile anaesthetics
BLOOD GAS
PARTITION
COEFF AT 37OC
PHYSIOLOGICAL
ASPECTS
Halothane
2.3
15-20% metabolised
Isoflurane
1.4
low solubility makes
induction & recovery
very rapid
0.3% metabolised
MAC (1.5-2%)
0.68
quick induction etc
MAC (2-3%)
12.0
50% metabolised,
hang-over
Sevoflurane
Methoxyflurane
GENERAL COMMENTS
85
Injectable anaesthetics
DOSE RATE
COMMENTS
Alphaxalone/alphadalone
Ketamine
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.
1.5-2mg/kg ketamine +
60-85 mg/kg medetomidine
(reversed with atipamazole Antisedan,
250-380 g/kg i/m)
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)
Propofol
1.33mg/kg i/v
Xylazine
86
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.
Monitoring
Injectable anaesthetics
DOSE RATE
COMMENTS
buprenorphine
0.02mg/kg i/m
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).
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.
87
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.
89
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.
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
Eosinophils
Basophils
Lymphocytes
Monocytes
Serology
At present there are not many useful serological tests for
birds in Europe. In the USA there are now tests for poly-
90
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
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.
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.
95
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.
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.
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
96
Antimicrobial selection
Antimicrobial dosing
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-
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
MAIN PROGRAMME
97
99
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.
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.
MAIN PROGRAMME
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.
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
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.
MAIN PROGRAMME
101
102
10.
References
13.
8.
9.
11.
12.
14.
1.
2.
3.
4.
5.
6.
7.
15.
16.
17.
18.
19.
20.
21.
22.
103
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
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
104
Canine herpesvirus1
Rabies2
Bacteria
Leptospira spp.3
Episcleral injection, yellowing of the sclera due to icterus, conjunctival petechia, uveitis.
Brucella canis3
Clostridium tetani4
Borrelia burgdorferi5
Uveitis, endophthalmitis. Examples of bacterial diseases: Pyometra, prostatitis, severe otitis externa.
Protozoa
Toxoplasma gondii2
Leishmania donovani5,6
Babesia spp.2
Chorioretinitis. Rare.
Neospora caninum7
Uveitis, chorioretinitis.
Rickettsia
Rickettsia rickettsii8
(Rocky Mountain spotted fever)
Ehrlichia canis9
(tropical canine pancytopenia)
Conjunctivitis, conjunctival hemorrhage, hyphema, uveitis, keratic precipitates, retinal detachment. Widespread in Europe.
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.
Demodex canis3
Immune-mediated diseases
Uveodermatologic syndrome14
Pemphigus complex15
105
Immune-mediated thrombocytopenia15
Atopy15
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
Hypothyroidism18
Hyperlipoproteinemia19
Central blindness.
Ehler-Danlos syndrome23
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.
Hyperviscosity syndrome26
Neoplasias (metastases)
Malignant lymphoma /
malignant fibrous histiocytoma27,28
Other tumors29
Nutritional deficiencies
Vitamin A deficiency2
MAIN PROGRAMME
Diabetes mellitus16
106
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.
107
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-
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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
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?
Any ocular change, serious eye changes probably due to secondary problems caused by immunosuppression.
Panleukopenia virus12
Central blindness.
Pox virus2
Blepharitis, conjunctivitis.
Bacteria
Bacteria
Mycobacterium tuberculosis14
Chlostridium tetani
Chlamydia psittaci2
Mycoplasma spp.7
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Rickettsia
Hemobartonella felis15 (feline infectious anemia)
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
Blastomyces dermatitidis4
Coccidioides immitis4
America. Uveitis.
Microsporum spp.2
Blepharitis.
Parasites2
Notoedres cati
Blepharitis, pruritic.
Demodex spp.
Toxocara cati
Dirofilaria immitis
Thelazia californiensis
Immune-mediated diseases2
Pemphigus complex
Blepharitis.
Metabolic diseases
Diabetes mellitus19
Central blindness.
Renal failure
See hypertension.
Hyperthyroidism
See hypertension.
Hyperparathyroidism21
Cataract.
Chdiak-Higashi syndrome2
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Cryptoccus neoformans4,17
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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)
Coagulation disorders2
Hyperviscosity syndrome2
Periarteritis nodosa2
Haws syndrome
Nutritional deficiencies
Taurine deficiency28
Thiamin deficiency29
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.
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15.
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
27.
28.
29.
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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.
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Private Practitioner, Moncalieri - Italy
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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.
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
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-
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-
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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.
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the limbs.
The X-ray examination may also reveal the presence of
foreign materials.
Figure 1
Figure 2
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Private Practitioner, Pistoia - Italy
116
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.
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
Figure 4
CORNEAL
SCUTE DERMAL
BONE
NEURAL
ARCH
LATERAL
PROCESS
CENTRUM
SPINAL
CORD
Figure 3
Figure 5
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Celiotomy
118
119
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.
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.
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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.
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-
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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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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
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-
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
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.
127
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
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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.
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.
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%.
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.
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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
131
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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132
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
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-
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.
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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133
134
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.
135
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.
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
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
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136
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.
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.
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
MAIN PROGRAMME
Summary
138
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.
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.
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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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
?
?
?
+/+++
+/-
(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.
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
141
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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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,
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
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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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.
145
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.
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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-
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
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149
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.
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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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.
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.
151
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
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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Private Practitioner, Milano - Italy
152
- 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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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:
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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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
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
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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.
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.
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.
Key words
Reptile, emergency, trauma, shock, haemorrhage,
drowning, gastro-intestinal obstruction, hypothermia, hyperthermia, pneumonia, fluid therapy.
References
1.
2.
3.
4.
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Green
iguana
160
5.
6.
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.
161
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
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Summary
162
163
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,
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Leucocyte cytograms
165
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
HEMOGRAM
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166
167
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.
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169
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
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170
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.
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
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
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171
173
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)
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)
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)
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)
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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
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)
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)
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)
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)
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)
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)
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
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)
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)
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)
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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
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)
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)
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)
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)
177
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-
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-
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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.
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.
179
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181
2) Production of smears
Principles
I) METHODOLOGY
1) Equipment
Sampling: variable methodology, depending on the tissue aspirated
Smears: slides with frosted ends
Centrifuges / cytocentrifuges
Microscopes / objective lenses
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.
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Summary
182
Techniques
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.
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.
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.
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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-
185
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.
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.
MAIN PROGRAMME
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.
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
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187
189
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
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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).
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
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-
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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192
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
193
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-
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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
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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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.
197
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
198
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.
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.
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
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
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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-
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.
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.
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.
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)
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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-
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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-
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.
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.
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.
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2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Key words
16.
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.
207
Dermatological manifestations
of internal diseases
Dominique Heripret
Med Vet, CES DV, Dipl ECVD
Private Practitioner, Arcueil, Paris - France
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209
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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
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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
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
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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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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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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.
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-
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.
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.
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
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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.
may be fatal if appropriate steps to reduce intracranial pressure (hyperventilation and mannitol administration) are not
instituted immediately.
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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.
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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
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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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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-
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-
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F. SPECIFIC NEUROPATHIES
1. Motoneuron Disorders
Inherited and acquired motoneuron disorders have been
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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
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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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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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A. INTRODUCTION
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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.
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-
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
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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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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
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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.
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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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.
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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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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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.
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
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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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.
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
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-
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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247
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
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specific infections:
neoplasias
5. Therapy of ventricular
tachyarrhythmias
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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
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.
253
iv. Bolus
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
1c
(2 and 4)
1 mg/kg
repeat 1-2x
maint. 8 mcg/kg/min
5-10 mcg/kg/min
Propafenone
Sotalol
Amiodarone
Maintenance
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-
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Substance name
255
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.
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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
- hyperthyroidism
- hypertension
- metastat. neoplasia
- pericardial disease
- other
thoracic radiographs
thoracic radiographs
ECG
ECG
BP-measurement
Echocardiogram ECG
Echocardiogram
thoracic radiographs
hematocrit or hemogram,
evt. chemistry profile
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-
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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
257
258
RVH
LVH
RVH
- hypertrophic CMP
- hypertrophic CMP
- 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.
- restrictive CMP
- dilated CMP (rare)
- hyperthyroidism (rare)
PPDH
Pericardial effusion
Dilated cardiomyopathy
pericardium normal
foreign structures
(liver, gas-filled bowel loops etc.)
next to the heart
severe hypokinesis
of both ventricles
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:
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260
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.
restrictive CMP
unknown, idiopathic
(possible previous myocarditis)
hyperthyroidism,
systemic arterial hypertension (CRF)
aortic stenosis, mitral regurgitation
(chron. valvular degeneration)
neoplastic infiltration, acromegaly
LV-cavity: small
normal to high
mostly normal,
moderate to severe turbulence with AS
Thromboembolization: yes
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.
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.
263
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
Weeks of age
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.
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.
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264
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.
8th
Weeks of age
REGENERATIVE ANEMIA
Figure 3 - Reticulocyte count and NRBCs in young Beagle dogs5,6,11.
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
Eosi
1st
2nd
3rd
4th
6th
8th
12th
16th
20th
24th
Baso
Weeks of age
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266
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-
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-
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),
MAIN PROGRAMME
267
268
9.
10.
11.
12.
13.
14.
269
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
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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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
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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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.
273
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-
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
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
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.
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.
MAIN PROGRAMME
277
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.
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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
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.
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
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
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
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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281
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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282
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
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.
MAIN PROGRAMME
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
285
Introduction
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
MAIN PROGRAMME
Summary
286
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.
References
1.
2.
3.
Other indices
4.
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.
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Clearance measurements
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289
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.
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
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.
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292
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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Klahr, S. (1996) Role of dietary protein and blood pressure in the progression of renal disease. Kidney Int. 49: 1783-1786.
Wingen, A.M., Fabian-Back, C., Schaefer, F. and Mehls, O. (1997)
Randomized multicentre study of a low protein diet on the progression of chronic renal failure in children. Lancet 349: 1117-1123.
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
non-diabetic renal diseases; a meta-analysis. Ann. Intern. Med. 124:
627-632.
Holm, E.A. and Solling, K. (1996) Dietary protein restriction and the
progression of chronic renal insufficiency: a review of the literature.
J. Intern. Med. 239: 99-104.
Bovee, K.C. (1992) High dietary protein intake does not cause progressive renal failure in dogs after 75% nephrectomy or ageing. Sem.
Vet. Med. Surg. (Small Anim) 7: 227-236.
Brown, S.A. (1992) Dietary protein restriction: some unanswered
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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Canine hypertension:
a difficult but fascinating disease
A.R. Michell
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
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
Hypertension in dogs
Essential (primary) hypertension is rare in dogs, though
an interesting genetic model exists1. The main causes of hy-
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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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
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-
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
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.
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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
References
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
11)
303
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.
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Summary
304
Figure 3 - Neurectomy of the ventral capsule of the hip joint, medial view.
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.
305
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.
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DVM
Veterinar Chirurgische - KI der Universitat Zurich - Switzerland
306
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.
307
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
MAIN PROGRAMME
DVM
Veterinar Chirurgische - KI der Universitat Zurich - Switzerland
308
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.
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.
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Results
311
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.
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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312
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.
313
7. To enhance colouring;
8. To reduce the quantity of undigested residues.
MAIN PROGRAMME
Conclusions
315
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.
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317
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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
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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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
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-
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
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
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
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Treatment
325
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Summary
326
References
1.
2.
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.
10.
11.
12.
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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.
327
329
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.
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.
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332
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).
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.
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.
333
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.
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.
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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
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-
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
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.
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.
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.
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
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.
MAIN PROGRAMME
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.
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.
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.
341
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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342
References
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
1.
2.
23.
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
i
SLIT LAMP EXAMINATION.
NORMAL EYE.
K CORNEAL SLIT
I IRIDAL SLIT
L ANTERIOR CAPSULE SLIT
i
k
SUBLUXATION
i
k
POSTERIOR LUXATION
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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
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.
345
v v
12
Figure 1
3v
MAIN PROGRAMME
346
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.
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.
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.
4.
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
349
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
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-
351
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
MAIN PROGRAMME
352
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.
353
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
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
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-
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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356
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.
3.
4.
5.
6.
7.
8.
9.
10.
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.
11.
12.
13.
14.
15.
16.
17.
18.
357
19.
20.
21.
22.
23.
24.
25.
26.
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359
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.
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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360
(+)
+++
+++
(+)
+++
+++
+++
+++
(+)
(+)
+++
+++
WPW, Wolff-Parkinson-White syndrome; AV, atrioventricular; +++, common mechanism; (+), rare or questionable mechanism
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.
Route
Adenosine
Amiodarone
Ajmaline
Atenolol
Quinidine sulfate
Diltiazem
Endrophonium
chloride
Esmolol
Flecainid
Metildigoxin
IV
PO
IV
PO
IV
PO
IV
PO
IV
IV
IV
IV
PO
Metoprolol
Procainamide
Propafenone
PO
IV
PO
IV
PO
IV
Sotalol
Verapamil
PO
PO
IV
Propranolol
PO
BSA, body surface area
361
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.
MAIN PROGRAMME
362
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.
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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364
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.
References
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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.
MAIN PROGRAMME
367
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.
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
MAIN PROGRAMME
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
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
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
369
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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370
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.
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
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Report of the WHO/ISFC task force on the definition and classification of cardiomyopathies, (1980), Br Heart J, 44: 672-673.
Wynne J, Braunwald E, (1997), The cardiomyopathies and myocarditides, In: Braunwald E (ed), Heart Disease, a Textbook of Cardiovascular Medicine, 5th ed, WB Saunders, Philadelphia, 14041463.
OGrady MR, Horne R, (1995), Occult dilated cardiomyopathy in the
Doberman pinscher, Proc 13th ACVIM Forum, 1072-1074.
Lombard CW, (1984), Echocardiographic and clinical signs of canine
dilated cardiomyopathy, J Small Anim Pract, 25: 59-70.
Calvert CA, Chapmann WL Jr, Toal RL, (1982), Congestive Cardiomyopathy in Doberman pinscher dogs, J Am Vet Med Assoc, 181: 598-602.
Koch J, Jensen AL, Fredholm M et al., (1997), Juvenile dilated cardiomyopathy in Doberman pinscher, Proc WSAVA Congress, 273.
Harpster NK, (1983), Boxer cardiomyopathy, In: Kirk RW (ed), Current Veterinary Therapy VIII, WB Saunders, Philadelphia, 329-337.
Freeman LM, Michel KE, Brown DJ et al., (1996), Idiopathic dilated
cardiomyopathy in Dalmatians: Nine cases, J Am Vet Med Assoc, 9:
1592-1596.
Staaden RV, (1981), Cardiomyopathy in English cocker spaniels, J
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Brownlie SE, (1991), The giant breed research project to the end
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Dec WG, Fuster V, (1994), Idiopathic dilated cardiomyopathy, New
Engl J Med, 331: 1564- 1575.
Cobb MA, (1992), Idiopathic dilated cardiomyopathy: Advances in
aetiology, pathogenesis and management, J Small Anim Pract, 33:
113-118.
Mestroni L, (1997), Dilated cardiomyopathy: a genetic approach,
Heart 77: 185-188.
Hein S, Schaper J, (1996), Pathogenesis of dilated cardiomyopathy
and heart failure: Insights from cell morphology and biology, Curr
Opinion Cardiol, 11: 293-301.
Matsumori A, (1996), Cytokines in myocarditis and cardiomyopathies, Curr Opinion Cardiol, 11: 302-309.
Keene BW, (1993), Evidence for the role of myocarditis in the pathophysiology of dilated cardiomyopathy, Proc 11th ACVIM Forum,
565-566.
Ware WA, (1994), Congestive heart failure: pathophysiology and
therapeutic implications, Proc Waltham/OSU Symposium for the
treatment of small animal diseases, 15-23.
Schober KE, Kirbach B, Oechtering G, (1998), Noninvasive assessment
of myocardial cell injury in suspected canine cardiac contusion and
heart disease: preliminary findings, Proc BSAVA congress, (in press).
Weber KT, Janicki JS, (1989), Pathogenesis of heart failure, Card
Clin 7: 11-24.
Sisson DD, Thomas WP, (1995), Myocardial Diseases, In: Ettinger
SJ, Feldman EC, Textbook of Veterinary Internal Medicine, 4th ed,
WB Saunders, Philadelphia: 995-1032.
Rihal CS, Nishimura RA, Hatle LK et al., (1994), Systolic and diastolic dysfunction in patients with clinical diagnosis of dilated cardiomyopathy, Circulation, 90: 2772-2779.
Koch J, Pedersen HD, Flagstad A, (1993), Dilated cardiomyopathy in
dogs, Dansk Veterinartidsskrift, 76: 785-795.
Calvert CA, Hall G, Jacobs GJ et al., (1997), Clinical and pathologic
findings in Doberman pinschers with occult cardiomyopathy that
died suddenly or developed congestive heart failure: 54 cases (19841991), J Am Vet Med Assoc, 210: 505-511.
Goodwin JK, Cattiny G, (1995), Further characterization of Boxer
cardiomyopathy, Proc 13th ACVIM Forum, 1072-1074.
Tidholm A, Jnsson L, (1996), Dilated cardiomyopathy in the Newfoundland: A study of 37 cases (1983-1994), J Am Anim Hosp Assoc,
32: 465-470.
Calvert CA, Jacobs GJ, Pickus CW, (1996), Bradycardia-associated
episodic weakness, syncope, and aborted sudden death in cardiomyopathic Doberman pinschers, J Vet Int Med, 10: 88-93.
Monnet E, Orton EC, Salman M et al. (1995), Idiopathic dilated cardiomyopathy in dogs: Survival and prognostic indicators, J Vet Int
Med, 9: 12-17.
Lunney J, Ettinger S, (1991), Canine cardiomyopathies, Walth Int Focus, 1: 16-21.
Keene B, (1994), Dilated cardiomyopathy in dogs: Diagnosis and
long-term management, Proc Waltham/OSU Symposium for the
treatment of small animal diseases, 27-32.
Veldhuisen DJ, DeGraff PA, Remme WJ et al. (1996), Value of
Digoxin in heart failure and sinus rhythm: New features of an old
drug, J Am Coll Cardiol, 1996, 28: 813-819.
Packer M, Gheorgiade M, Young JB, et al., (1993), Withdrawal of
digoxin from patients with chronic heart failure treated with angiotensin-converting-enzyme inhibitors (radiance study), N Engl J
Med, 329: 1-7.
Vitarelli A, Fedele F, Dagianti A et al., (1995), A reexamination of the
hemodynamic effects of digitalis relative to ventricular dysfunction,
Cardiol, 86: 94-104.
Smith TW, (1993), Digoxin in heart failure, N Engl J Med, 329: 51-53.
Slatton ML, Irani WN, Hall SA et al., (1997), Does Digoxin provide
additional hemodynamic and autonomic benefit at higher doses in patients with mild to moderate heart failure and normal sinus rhythm?,
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Gheorghiade M, Pitt B, (1997), Digitalis Investigation Group (DIG)
371
36.
37.
38.
39.
40.
41.
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43.
44.
45.
46.
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48.
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50.
51.
52.
53.
54.
55.
56.
57.
MAIN PROGRAMME
373
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.
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
374
Notes on diet
Australian Parakeets
Budgerigar.
Cockatiel.
Kakariki
Lovebirds
Large seeds, small nuts, berries, apple and carrot. Green foods are
popular. Soft fruits.
Moustache parakeets,
Slaty-headed parakeets, Alexandrines,
Indian Ringnecks.
Large seeds, small nuts, berries, apple and carrot. Green foods
are popular. Soft fruits.
Cockatoos
Conures
Macaws
Eclectus
Vosmaeri.
African Greys
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
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
375
Comments
Small seeds
Large seeds
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
Fruit
Vegetables
Sprouted
and soaked pulses
Animal protein
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-
MAIN PROGRAMME
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.
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
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.
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.
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
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.
377
379
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
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.
380
distal barbule
hamuli
rachis
barb
proximal barbule
hypopenna
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-
381
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
382
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.
383
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
Artery
Gill lamella
Vein
Water flow
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.
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
384
Levels of anaesthesia
STAGE
PLANE
SIGNS/INDICATORS
Light sedation
Deep sedation
Partial loss
of equilibrium
Total loss
of equilibrium
Loss of reflex
activity
Medullary
collapse
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.
Specific surgery
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
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.
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Ulcer debridement
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387
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.
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.
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
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.
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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-
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
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.
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390
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.
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-
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.
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-
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
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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
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.
393
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.
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-
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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.
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.
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396
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.
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399
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
Diagnosis
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
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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.
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.
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.
401
Patient evaluation
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.
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
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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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.
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.
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.
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Uncomplicated crown-root
fracture
A fracture involving
enamel, dentine and cementum,
but not exposing the pulp
Complicated crown-root
fracture
Root fracture
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.
405
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.
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.
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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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
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.
407
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.
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.
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408
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:
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
Stage 2
Stage 3
Stage 4
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
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
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410
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.
411
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.
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
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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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.
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
415
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Introduction
416
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
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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418
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-
419
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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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.
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-
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Summary
422
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.
423
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 4 - Mini maxillo facial titanium plate with one screw (1.0 Compact).
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Results
424
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.
Introduction
A special titanium plate for wrist arthrodesis in humans
has been developed by the AO, Switzerland. A study has
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.
425
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.
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426
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
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.
427
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.
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Summary
428
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.
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,
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.
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Serology
Microbiology
Electrodiagnostic testing
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.
431
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.
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.
Structural lesion
No lesion - idiopathic
Extracranial
Toxic (Extra-dog)
Metabolic (Intra-dog)
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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.
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.
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.
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.
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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.
435
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.
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.
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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).
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-
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
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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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.
439
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 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
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.
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).
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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443
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.
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445
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.
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
MAIN PROGRAMME
B Vet Med, PhD, DSAS, DVR, FRCVS, Dipl ACVS, Dipl ECVS
University of Cambridge - United Kingdom
446
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.
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
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.
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
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.
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].
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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
452
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.
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
453
Technique
Personal experience
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
455
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.
SPECIALIST/INTERACTIVE PROGRAMME
456
457
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 6 The targeting device derived from the Grosse & Kempf system
by dr. Rovesti.
SPECIALIST/INTERACTIVE PROGRAMME
458
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.
References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
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
461
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.
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-
463
Extranodal lymphomas
C. Guillermo Couto
DVM, Dipl ACVIM, Department of Veterinary Clinical Sciences, College of Veterinary Medicine
The Ohio State University - Columbus - USA
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
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
464
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
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
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.
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465
467
Follicular dysplasias
Luis Ferrer
Med Vet, Dipl ECVS
Private Practitioner, Cremona - Italy
SPECIALIST/INTERACTIVE PROGRAMME
468
References
1.
2.
3.
4.
5.
6.
7.
469
8.
9.
10.
11.
SPECIALIST/INTERACTIVE PROGRAMME
471
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.
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
472
a
Figure 2 - Frame extension to the carpus and tarsus.
b
Figure 3 - Metaphyseal fixation with wires.
473
Figure 4b - Distal metaphyseal fixation of radius and tibia with wires and
half-pins.
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
SPECIALIST/INTERACTIVE PROGRAMME
474
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.
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.
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.
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.
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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
477
Lymphnode cytology:
normal, inflammatory and neoplastic aspects
Corinne Fournel-Fleury
Laboratoire dImmunopathologie-Hmatologie-Cytologie, Ecole Vtrinaire de Lyon - France
SPECIALIST/INTERACTIVE PROGRAMME
Summary
478
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
Adenitis are partial infiltrations of the lymph node by inflammatory cells. They consist of:
- neutrophilic, acute or subacute
- granulomatous (chronic)
adenitis
- eosinophilic
- mixed
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.
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.
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).
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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.
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 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.
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
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.
SPECIALIST/INTERACTIVE PROGRAMME
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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
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.
485
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.
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.
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
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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.
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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.
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
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SPECIALIST/INTERACTIVE PROGRAMME
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-
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.
SPECIALIST/INTERACTIVE PROGRAMME
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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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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.
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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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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.
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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
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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.
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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%
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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.
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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.
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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.
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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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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.
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F. Fabbrini DVM
Clinica Veterinaria Papiniano 50 - 20123, Milano, Italy
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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.
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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.
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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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Department of Internal Diseases of Solipeds, Small Animals and Birds, University of Veterinary Medicine in Kosice, Slovakia
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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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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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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.
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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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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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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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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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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
526
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%)
527
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
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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.