Paper - Diabetes Canina

Vol 10 No 3
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Vol 10 No 3
Published Quarterly
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Diagnosis and
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Focus
The worldwide journal for the companion animal veterinarian
Focus
Long term
management of the
diabetic dog
Prolonging the life
of the feline renal
failure patient
WALTHAM
INSIDE
The worldwide journal for the companion animal veterinarian
A low phosphate, low protein
diet can DOUBLE the life
span of cats with chronic
renal failure see page 10
A low phosphate, low protein
diet can DOUBLE the life
span of cats with chronic
renal failure see page 10
WALTHAM Focus is published quarterly.
Editions are produced in English, Dutch,
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How I treat . . . an anorexic rabbit 2
Frances Harcourt-Brown BVSc, MRCVS
Harrogate, North Yorkshire, UK
Diagnosis and treatment of spinal neoplasia in dogs and cats 4
Bernard Seguin DVM, MS, DipACVS
Colorado State University, USA
Rodney S. Bagley DVM, DipACVIM (Neurology and Internal Medicine)
Gena M. Silver DVM, MS
Washington State University, USA
Prolonging the life of the feline renal failure patient 10
Jonathan Elliott MA Vet MB, PhD, Cert SAC, DipECVPT, MRCVS
Royal Veterinary College, London, UK
WSAVA News 15
Long-term management of the diabetic dog 17
Linda M. Fleeman BVSc, MACVSc
Jacquie Rand BVSc, DVSc, DipACVIM
University of Queensland, Australia
Diagnosis of otitis media in dogs 24
Louis N. Gotthelf DVM
WALTHAM Research News 31
WALTHAM Viewpoint 32
Dietary manipulation of canine odiferous atulence
International Contacts 33
Cover picture:
Cross-section of
canine kidney
ISSN 1354-0157
Contents
Executive Editor
Karyl Hurley BSc, DVM, DACVIM,
DECVIM-CA
Veterinary Communications,
WALTHAM
Managing Editor
Sarah Rusholme BSc ARCS,
PhD, MSc Comm. Sci.
Communications Executive,
WALTHAM
Editor
Richard Harvey PhD, BVSc,
DVD, DipECVD, MIBiol, MRCVS
UK and European Diplomat in
Veterinary Dermatology.
Partner in a small animal
practice seeing rst and
second opinion cases
Editorial Advisors
Prof. J. E. Bauer DVM, PhD,
DipACVN
Dept. of Small Animal Clinical
Studies
College of Veterinary Medicine
Texas A&M University
College Station, Texas, USA
Prof. C .F. Burrows BVetMed,
PhD, MRCVS
Department of Small Animal
Clinical Sciences, University of
Florida, USA
Prof. Dr. J. Leibetseder DVM
Institut fr Ernhrung
Veterinrmedizinische
Universitt
Wien, Austria
Prof. Roger M. Batt BVSc, MSc,
PhD, MRCVS, DipECVIM-CA
Head of Veterinary Research,
WALTHAM
Prof. Dr. R. Moraillon DVM
Ecole Nationale Vtrinaire
dAlfort
Maisons-Alfort, France
Dr. Ralf S. Mueller MAVSc,
DipACVD, FACVSc
School of Veterinary Medicine,
Colorado State University, USA
Waltham Centre for Pet Nutrition 2000 Waltham-on-the-Wolds, Melton Mowbray, Leicestershire, England, LE14 4RT Tel: 44-1664-415400 Fax: 44-1664-415440
WALTHAM
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WALTHAM FOCUS
VOL 10 NO 3
2000
The licensing arrangements for therapeutic agents intended for use in
small animal species vary greatly worldwide. In the absence of a specic
licence, consideration should be given to issuing an appropriate
cautionary warning prior to administration of any such drug.
THE WORLDS LEADING AUTHORITY ON PET CARE AND NUTRITION
Introduction
Feline chronic renal failure (CRF) is a common clinical problem,
particularly affecting the ageing cat population. The rst goal in the
management of clinical CRF is to identify and treat any underlying cause of
renal disease. Where this is not possible, as is often the case, other
treatment goals are to manage the complications of renal failure to improve
the quality of life of the animal (1). In addition, by correcting some of these
complications, it has been suggested that the progression of CRF to its end
stage may be slowed.
Progression of CRF to end stage is thought to be an inevitable process in
some species (2). Experimental evidence seems to suggest that, following
surgical reduction in renal mass in the cat, progressive deterioration of
renal function is difcult to demonstrate over a 12-month period (3, 4). In
clinical patients, however, progressive loss of remaining functioning
nephrons does seem to occur (5, 6) albeit in stepwise decrements at highly
variable intervals rather than as a gradual linear progression. Figures 1a to
c show sequential data from three cats showing the patterns of progressive
deterioration of renal function observed in a recent study (6). Of the
39 cases that died or were euthanised during this study, 21 were
documented to have suffered from deteriorating renal function as the cause
of their death. Most cases that died of renal failure demonstrated stepwise
decrements in renal function as seen in Figures 1a and b. There were very
few examples of cases that showed clear evidence of linear increases in
plasma creatinine concentration accompanied by progressive loss of weight
such as that shown in Figure 1c.
Why do cases of CRF tend to show progressive renal
dysfunction?
There are two main reasons why renal function tends to deteriorate once
CRF has been diagnosed in a clinical patient (7). First, there may be
repeated insults that damage the remaining functioning nephrons and lead
to the stepwise falls in glomerular ltration rate. Secondly, the adaptive
responses the body makes to loss of functional renal tissue, once this has
been reduced to a critical level, lead to the death of further nephrons and a
vicious cycle ensues culminating in end stage renal failure. These responses
can, therefore, be described as maladaptation.
Maladaptation may be contributed to by many of the bodys responses to
azotaemia that lead to the uraemic syndrome (8). Examples include the
following.
Hypersecretion of parathyroid hormone
Hyperparathyroidism results from accumulation of phosphate in the body
(9). In a normal animal, parathyroid hormone (PTH) would cause
increased excretion of phosphate ions in the urine and a restoration of
phosphate balance. With severe loss of functioning nephrons, however, PTH
Prolonging the life of the feline
renal failure patient
Jonathan Elliott MA, Vet MB, PhD, Cert SAC, DipECVPT, MRCVS
Royal Veterinary College, London, UK
KEY POINTS
G Many cases of feline chronic renal failure (CRF) progress to end stage and die of their renal disease.
G Progression can be due to repeated renal insults and/or to maladaptive responses to the uraemic syndrome leading to
loss of functioning nephrons.
G Secondary renal hyperparathyroidism resulting from phosphate retention is one such maladaptive response.
G Control of this syndrome by dietary phosphate restriction leads to increased survival in naturally occurring feline CRF.
10
WALTHAMFocus G Vol 10 No 3 G 2000
Dr. Elliott is a 1985 graduate of
Cambridge University Veterinary
School. After graduating, he
completed an Internship at VHUP
in Philadelphia, a PhD in vascular
biology at the University of
Cambridge and gained his
Certicate in Small Animal
Cardiology. In 1990 he took up a
lectureship at the Royal Veterinary
College in London where he is
currently Senior Lecturer in
Veterinary Pharmacology. In 1998
he was awarded the Pzer
Academic Award for his research
contributions to companion
animal medicine in the areas of
feline chronic renal failure and
equine laminitis. In 1999 he
became a Diplomate of the
European College of Veterinary
Pharmacology and Toxicology.
Jonathan Elliott
MA, Vet MB, PhD, Cert SAC, DipECVPT,
MRCVS
THE WORLD S LEADI NG AUTHORI TY ON PET CARE AND NUTRI TI ON
is unable to rid the body of excess phosphate and the response is
maladaptive because it adds to the problem of hyperphosphataemia by
releasing more phosphate from stores within bone. Calcium is released
with phosphate, soft tissue mineralisation occurs and, some hypothesise,
mineralisation of renal tissues will lead to progressive loss of functioning
nephrons (10).
Glomerular capillary hypertension and hyperltration
Another maladaptation occurs at the level of the glomerulus itself and leads
to glomerular hypertension and hyperltration. This has been documented
to occur in cats with experimentally induced renal failure by surgical
reduction of renal mass (11). The change in glomerular haemodynamics
that accompanies reduction in renal mass is postulated, in species such as
the rat, ultimately to damage the hyperltrating nephrons and lead to their
demise.
Renal adaptation to metabolic acidosis
A nal example of a maladaptation in CRF is the response to metabolic
acidosis, a common disturbance that accompanies CRF (12) but one that
has been poorly studied in the cat. Ammonia generation in the distal tubule
aids hydrogen ion secretion by the remaining functioning nephrons but
excess ammonia may itself be detrimental and lead to activation of
complement and damage to the failing kidney (13). In addition, metabolic
acidosis can cause excessive potassium losses (14), which in turn can lead
to hypokalaemic nephropathy (15).
Prognosis for cats presenting with CRF
It would be helpful for practising veterinary surgeons to be able to predict at
initial diagnosis, which cats with CRF will progress rapidly to end stage renal
failure regardless of the treatment they receive and which, given the right
treatment, will remain stable for a long period of time. One might expect
the plasma creatinine after rehydration at initial presentation to be a
reasonable guide. Many cases where the plasma creatinine concentration
remains above 500 mol/l when the cat has been adequately rehydrated
tend to represent very quickly for further uid treatment and are often very
difcult to manage for the complications of their renal failure. For those
cats that present in stable CRF where the plasma creatinine concentration
is less than 500 mol/l, this biochemical assessment at initial presentation
does not predict which cats will progress and which will remain stable. In a
retrospective study, the correlation between plasma creatinine and survival
in cats that presented with signs of stable CRF was very poor, with only 5%
of the variation in survival time being predicted by the initial plasma
creatinine concentration (5). This nding perhaps merely conrms what a
crude index of renal function plasma creatinine really is and highlights the
need for more sensitive indices to be developed that can be used in routine
11
200
300
400
500
600
2
3
4
5
6
0 50 100 150 200 250 300 350 400
Figure 1 Graphs showing the changes in plasma creatinine and body weight
with time in three clinical cases of naturally occurring chronic renal failure.
(a) A 12-year-old female neutered domestic short-haired cat where there
were two progressive increases in creatinine, two and 15 months following
initial diagnosis. The cat was euthanised 17 months following diagnosis.
(b) A 16-year-old male neutered domestic long-haired cat where stable renal
function was demonstrated for the rst three months and a rapid
deterioration occurred ve months following initial diagnosis. This cat was
euthanised after six months. (c) A four-year-old male neutered domestic
long-haired cat where a gradual increase in plasma creatinine
accompanied by loss of weight was noted at each visit. This cat was
euthanised nine months following initial diagnosis.
200
300
400
500
600
2
3
4
5
6
0
50 100 150 200
200
300
400
500
600
2
3
4
5
6
0
50 100 150 200
Time (days)
Plasma creatinine
(mol/l)
Body weight
(kg)
Plasma creatinine
(mol/l)
Body weight
(kg)
Plasma creatinine
(mol/l)
Body weight
(kg)
Figure 1a
Figure 1b
Time (days)
Time (days)
Figure 1c
clinical practice. Alternatively, it may support the contention that
progressive deterioration of renal function is not a linear uniform process
but occurs in discrete steps separated by highly variable periods of time
during which renal function remains very stable. This would mirror the
situation in experimental nephrectomy models of feline renal failure where
glomerular ltration rate (GFR) remains stable for at least 12 months after
induction of renal failure (3, 4, 16).
One haematological nding that may be of prognostic value is that of
anaemia. In a retrospective study, one-third of the stable CRF cases were
anaemic at initial diagnosis and these fared much worse in terms of their
survival when compared with those whose packed cell volume was above
0.27 l/l on rst presentation (5). Further studies are required involving
large populations of cats with stable CRF to determine what other factors
might be of useful prognostic value in determining their longevity following
initial diagnosis.
Repeated renal insults from exogenous factors
One insult that may repeatedly damage the feline kidney was proposed over
thirty years ago to be bacterial infection (17). A proportion of cases of feline
CRF presenting for the rst time, or those that represent after a period of
stability, will have subclinical bacteriuria. In a prospective survey of 36 cats
with naturally occurring CRF, 268 urine samples were collected by
cystocentesis and submitted for bacteriological culture (18). A positive
culture was found in 22 samples obtained from 11 cats giving the
prevalence of subclinical bacteriuria as 8.2% and the incidence as 30.5%.
A signicantly higher incidence was noted in female cats (53%) when
compared with male cats (14.3%), suggesting these infections were
ascending. Urine collected by cystocentesis and its submission for culture
would, therefore, seem to be a necessary part of any routine procedure in
the monitoring a cat with CRF. Examining the urine sediment for evidence
of bacteriuria (see Figure 2) is a fairly simple procedure that, when
performed carefully, will detect the majority of cases where positive cultures
are obtained. Thus, even if the owner is not prepared to pay for routine
cultures, monitoring can be achieved in all clinical cases.
Early detection of a lower urinary tract infection and appropriate
treatment with antibiotic therapy may prevent an infection from ascending
to the kidney and causing further renal damage. It would be logical to
assume that cats with CRF where bacterial urinary tract infections have
been identied have some renal involvement and so should receive
antibacterial treatment that is appropriate for pyelonephritis (19). The
course of treatment should be of 4 to 6 weeks duration. In addition, the
choice of drug should be based on a sensitivity test that uses the plasma
concentration of the drug achieved by the proposed dose rate. In the
prospective study referred to above (18), all the isolates cultured were
E. coli and all proved sensitive to uoroquinolone antibacterial drugs. The
only other groups of drugs to which more than 90% of the isolates were
sensitive were potentiated sulphonamides and tetracyclines, neither of
which was particularly appropriate for these cases. Empirical treatment
should be avoided and antibacterial drug selection should, where possible,
be based on culture and sensitivity testing. What proportion of feline CRF
cases seen in general practice deteriorate because of an ascending bacterial
infection remains to be determined but this is one cause of further renal
damage that, through careful monitoring and appropriate treatment, can be
prevented.
Effects of phosphate and protein restriction on
survival
Experimental studies in the rat and dog have demonstrated the positive
value of phosphate restriction in slowing the progressive deterioration of
renal function in animals with surgically reduced renal mass (20, 21). As
discussed above, hypersecretion of PTH can be considered maladaptive.
How much PTH itself contributes directly to this process is controversial
and difcult to determine because PTH, phosphate, and calcium are all
intrinsically linked and difcult to study individually. At the very least,
plasma PTH concentrations probably serve to indicate those animals that
are overloaded with phosphate and would therefore benet from phosphate
restriction.
Secondary renal hyperparathyroidism is an extremely common nding in
feline CRF, even in those animals that are normophosphataemic (9). In
many cases where treatment is possible, dietary phosphate restriction
results in a reduction in plasma PTH concentration, which lags behind the
fall in plasma phosphate (22). A study of the effects of phosphate restriction
and control of PTH on the survival times of cats with naturally occurring
CRF has been undertaken in a prospective clinical trial (6). Fifty cats were
entered into this trial, 29 were successfully fed phosphate-restricted (diets
used provided a phosphate intake of no more than 0.25 g/MJ) and 21
received standard maintenance diets (estimated phosphate intake of about
1.14 g/MJ) owing to limited intake of the renal diets by the cats or the
owner being resistant to diet change. The clinical diets fed in this study
(WALTHAM Veterinary Diet: Whiskas
Feline Low Phosphorus Low Protein)

are also moderately restricted in protein, lower in sodium, higher in energy
and supplemented with B vitamins when compared with standard
maintenance cat foods. Plasma phosphate and PTH concentrations were
assessed at the mid-survival time point in each group. A signicant increase
in PTH had occurred with time in the group that were not phosphate
restricted, whereas PTH concentrations were lower than at the time of entry
to the study in 69% of the group receiving phosphate restriction (see
Table 1).
Kaplan Meier survival curves were constructed for the two groups of cats
and are presented in Figure 3. The Kaplan Meier analysis gave median
12
Plasma phosphate and parathyroid hormone values from cats with CRF at initial diagnosis and mid-survival time
Value (reference range)* Maintenance diet group Restricted phosphate group
Initial diagnosis (n) Mid-survival (n) Initial diagnosis (n) Mid-survival (n)
Plasma phosphate 1.85 0.12 (21) 2.18 0.22 (21) 2.04 0.17 (29) 1.50 0.08 (29)
(0.68 to 1.86 mmol/l)
Plasma PTH 119.7 32.2 (21) 215.7 50.4 (21) 162.7 26.2 (29) 86.3 18.2 (29)
(2.5 to 25.5 pg/ml)
* Where appropriate, the laboratory or aged-matched reference range is quoted
(Data are taken from reference 6)
Table 1
survival times of 264 days (interquartile range of 190 to 535 days) and
633 days (interquartile range of 338 to 950 days) for the maintenance diet
and phosphate-restricted groups respectively. When the two curves were
compared by log rank analysis, a highly signicant difference was found
(P = 0.0036) suggesting that the effect of feeding the phosphate- and
protein-restricted diet was to increase survival time.
Although this study was non-randomised and open rather than double
blind and placebo controlled, the cats that accepted the phosphate-
restricted treatment regimen lived considerably longer than those that were
fed standard maintenance diets. It cannot be concluded that phosphate
restriction was the only factor responsible for this nding but it seems likely
to have played a major part given the evidence from other species,
including the dog (21). Based on the results of this study and the evidence
from experimental studies, phosphate restriction should be a standard part
of any treatment regimen for CRF in cats.
Hypertension and progression
Systemic hypertension has been recognised to occur in a proportion of cats
with naturally occurring CRF (23). In human medicine, prospective clinical
studies have shown progressive renal damage can be slowed by lowering
arterial blood pressure. Moreover, the target arterial blood pressure
required should be based on the degree of proteinuria recorded in each
patient (24). One maladaptation to renal failure described above was the
increase in glomerular capillary pressure and hyperltration that can be
detected in experimental models of CRF involving a reduction in renal
mass. Hyperltration and glomerular hypertension will lead to increased
losses of small amounts of albumin across the ltration membrane.
Glomerular capillary pressure has been shown to be raised in cats where
renal mass has been surgically reduced and that hyperltration occurs
leading to increased protein loss (25).
From this information derived from experimental animal studies and
human clinical studies there seem to be a number of questions that need
to be addressed in cats with CRF. Currently, antihypertensive therapy is
prescribed for those cats with systolic arterial blood pressures that are
persistently elevated above 175 mmHg. This is done primarily to protect
these cats from catastrophic events such as brain haemorrhage or retinal
detachments. Lowering blood pressure below 170 mmHg seems to achieve
this goal and the drug that consistently produces this response is the
calcium channel blocker, amlodipine. In a recent study of the prevalence of
systemic hypertension in cats with CRF, approximately 30% of the cases
had systemic blood pressure of between 130 and 175 mmHg (26). How
many of these cats would benet from antihypertensive therapy? What
should the target systemic arterial blood pressure be in order to produce a
protective effect on the nephrons of the failing kidney? What drugs should
be used to lower glomerular capillary pressure and will this therapy prove
benecial in naturally occurring feline CRF?
Glomerular pressure cannot be measured in clinical practice. The use of
drugs to lower glomerular capillary pressure seems a logical therapeutic
goal. Angiotensin-converting enzyme inhibitors (ACE-I) would seem to be
the obvious choice of drugs for this purpose since angiotensin-II
preferentially constricts the efferent arteriole in the glomerulus and hence
raises intraglomerular pressure. Avoidance of systemic hypotension would
be an important precaution hence the introduction of an ACE-I such as
benazepril or enalapril should be accompanied by monitoring of systemic
arterial blood pressure and should, ideally, be used only in cats where they
would be benecial. The effect of amlodipine on glomerular
haemodynamics remains to be studied although several properties of this
drug suggest that it too may be benecial in counteracting the adaptation
that occurs within the glomeruli of failing kidneys.
At the present time there are no published data from cats with naturally
occurring CRF to suggest that antihypertensive treatment slows progression
or that address the questions raised above. In one study, hypertensive cats
that responded to antihypertensive treatment fared no better than those
whose blood pressure remained poorly controlled (27). The difculty of
assessing the true arterial blood pressure of individual cats in the clinic is
one problem that will hamper any clinical studies in this area. Nevertheless,
this is certainly an area where further work may well lead to new drug
treatments that could prove to be renoprotective and prolong the survival of
cats with CRF.
13
Figure 3 Kaplan Meier survival curves. Dotted line represents the data from
the normal maintenance diet (NMD) group with the blue symbols
representing those animals still alive at the time of analysis. Solid line
represents the restricted phosphate diet (RPD) group with the red symbols
representing those animals still alive at the time of analysis.
Reprinted with permission from reference 6.
Figure 2 A photomicrograph of urine sediment viewed at 400x
magnication under a phase contrast microscope. The rod-shaped
organisms in focus were found to be E. coli on urine culture. White blood
cells were also present but are out of focus on this eld of view.
0 200 400 600 800 1000 1200
0.2
0.4
0.6
0.8
1.0
RPD Group Dead
RPD Group alive
NMD dead
NMD alive
Survival time (days)
P
r
o
p
o
r
t
i
o
n

o
f

c
a
t
s

s
u
r
v
i
v
i
n
g
Diet group
Conclusion
Improving the quality of life of our renal failure patients is far more
important than increasing their life span. Nevertheless, many do enjoy good
quality of life for extended periods such that some die of diseases other
than their renal failure. It is important to remember that any treatment
needs to be appropriate for the stage of renal failure in each individual
patient. Monitoring these patients for the presence of urinary tract
infections is an important part of any management regimen as prompt and
effective treatment may well prevent further renal damage occurring.
Scientic evidence supports a benecial effect of restricting phosphate
intake in many cases and the positive benet of this measure appears to
include extending the survival of feline CRF patients. Many other areas of
management remain to be explored in detail. Antihypertensive therapy may
well be a promising area for future development but several important
questions remain to be answered.
Surgical renal transplantation may be an option for feline CRF cases in
the future on a more routine basis. We should remember, however, to
compare the quality of life of transplanted patients with that which can
currently be achieved medically with current and future developments
before adopting renal transplantation as the routine method.
.
14
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proteinuria, and the progression of renal disease. The modication of diet in
renal disease study. Annals of Internal Medicine 1995; 123: 754762.
25. Brown, S. A., Brown, C. A. Single-nephron adaptations to partial renal
ablation in cats. American Journal of Physiology 1995; 269: R1002R1008.
26. Elliott, J., Rawlings, J. M., Markwell, P. J, Barber, P. J. Prevalence of
hypertension in cats with naturally occurring chronic renal failure. Journal of
Veterinary Internal Medicine 1999; 13: 251 (abstract 100).
27. Littman, M. P. Spontaneous systemic hypertension in 24 cats. Journal of
Veterinary Internal Medicine 1994; 8: 7986.
GREFERENCES G
Introduction
Diabetes mellitus is a common endocrine disease of middle-aged and older
dogs characterised by an absolute or relative deciency of insulin (1).
Insulin administration is the mainstay of therapy in all affected dogs, with
long-term treatment involving injections given once or twice each day by the
owner. The cause of diabetes in dogs has been poorly characterised and is
undoubtedly multifactorial. Genetic predisposition exists (1) and immune-
mediated destruction of pancreatic beta-cells has been shown to occur in
affected dogs (25).
Clinical presentation
Dogs with uncomplicated diabetes mellitus classically present with polyuria,
polydipsia, weight loss, an increased appetite, and lethargy. Most affected
dogs are over seven years of age and females are at greater risk than males
(6, 7). The onset of these classic clinical signs is typically chronic, ranging
from weeks to months (6), and may initially be unnoticed or considered
insignicant by the dogs owner. If ketosis and metabolic acidosis develop,
more serious systemic signs, such as vomiting and anorexia, are seen and
prompt owners to seek veterinary care more rapidly. Approximately 40% of
Long-term management of
the diabetic dog
Linda M. Fleeman BVSc, MACVSc
Jacquie S. Rand BVSc, DVSc, DipACVIM
University of Queensland, Australia
KEY POINTS
G Insulin is the mainstay of therapy for diabetic dogs.
G The majority of diabetic dogs require twice-daily administration of insulin to control their signs.
G Insulin and dietary recommendations need to be tailored for each diabetic dog.
G A consistent insulin-dosing and feeding routine is optimal, although not critical. For practical reasons, a certain amount
of compromise may be necessary, and is often not associated with signicant clinical consequences.
G The diet fed should primarily be palatable and nutritionally balanced.
G Results of recent studies indicate that improved glycaemic control may be achieved in the majority of diabetic dogs if their
diet contains increased insoluble bre.
G Decreased dietary fat content is recommended if there is concurrent disease of the exocrine pancreas.
G Blindness due to cataract formation occurs in the majority of diabetic dogs.
16
Dr. Fleeman graduated with
honours from the University of
Queensland in 1984. She worked in
rst opinion small animal practice
for eight years and subsequently in
referral practice for ve years. She
completed a three year medicine
internship at Murdoch University
and a Clinical Residency at the
University of Melbourne. Currently
she is completing a PhD research
project investigating canine
diabetes mellitus at the University
of Queensland, working with
Dr Rand.
Linda Fleeman
BVSc, MACVSc
Dr. Rand graduated with honours
from the University of Melbourne
in 1975. She worked in private
practice for eight years before
completing a residency and
doctorate at the University of
Guelph in Canada. After a three-
year position as a Clinical
Registrar at the University of
Zurich in Switzerland she
returned to Australia in 1990.
Currently she is an Associate
Professor in companion animal
sciences at the University of
Queensland. Her primary area of
research is in canine and feline
diabetes and obesity.
Jacquie Rand
BVSc, DVSc, DipACVIM
diabetic dogs were found to have already developed ketosis by the time they
were rst presented to a university teaching hospital (6). This progression
to a more complicated diabetic patient often coincides with the
development of concurrent disease such as pancreatitis or bacterial
infection of the skin, mucosal surfaces, or urinary tract.
Cataract formation is the most common and one of the most important
long-term complications associated with diabetes in the dog (1). It is an
irreversible process once it begins, and can progress quite rapidly. One
survey found that approximately 30% of diabetic dogs already had reduced
vision at presentation, and about half of the remaining dogs became blind
within two years (8). A larger study concluded that cataracts will develop
within ve to six months of diagnosis in the majority of diabetic dogs, and
that within 16 months approximately 80% will have signicant cataract
formation (9).
Insulin deciency results in altered carbohydrate, fat, and protein
metabolism. Abnormal carbohydrate metabolism manifests as
hyperglycaemia and glycosuria and is responsible for the polyuria,
polydipsia, and cataract formation seen in diabetic dogs. The
hyperlipidaemia, ketone production, and hepatic changes seen in these
dogs primarily result from altered fat metabolism. Decreased tissue
utilisation of glucose, amino acids, and fatty acids is the cause of the
lethargy, weight loss, reduced stimulation of the satiety centre, poor coat,
and reduced immunity that is characteristic of untreated diabetic dogs.
Therapy
Aims of therapy
The three primary aims of long-term therapy for diabetic dogs are:
G Resolution of all clinical signs
G Avoidance of insulin-induced hypoglycaemia
G Resumption of usual lifestyle and exercise level
Lethargy tends to resolve rapidly and dogs become more active and
responsive soon after initiation of insulin therapy. Weight loss is usually
arrested before optimal glycaemic control is achieved, but complete
resolution of the polyuria and polydipsia will not occur until the blood
glucose can be kept below the renal threshold. In the majority of diabetic
dogs the process of cataract formation has unfortunately already been
initiated before adequate control of hyperglycaemia can be achieved
(Figure 1).
Insulin
A variety of insulin preparations with both prompt and prolonged actions
are commonly available (Table 1). Regular and semilente insulins are
characterised by rapid action and short duration of effect and are generally
not useful for the long-term management of diabetic dogs. Longer-acting
preparations such as ultralente, protamine zinc insulin (PZI), and
isophane (NPH) are more suited as they provide continued insulin
supplementation for many hours after a single injection. Premixed
combinations of short- and longer-acting insulins are valuable for the
17
Figure 1 Diabetic cataracts: (a) Photograph of a diabetic dog shortly after
diagnosis of diabetes mellitus. (b) The same dog three months later and
after successful stabilisation on insulin therapy. Diabetic cataracts had
developed rapidly and the dogs owners had reported sudden loss of vision.
(c) The same dog following phacoemulsication surgery to remove the
cataract from the right eye.
a
b
c
Commonly available insulin preparations and their effects
following subcutaneous injection in dogs.
Type of Source Onset of Time of Duration
insulin effect maximal effect of effect
Regular* and Recombinant 1030 min 15 h 410 h
semilente human
Bovine
Isophane* (NPH) Recombinant 0.53 h 210 h 424 h
human
Lente** Puried porcine < 1 h 48 h (10) 1424 h (56)
Recombinant 210 h (1) 624 h (1)
human
Bovine
Protamine zinc
insulin 90% bovine, 14 h 414 h (1) 628 h (10)
(PZI) 10% porcine
100% bovine 820 h (10)
Ultralente Recombinant 18 h 416 h 828 h
human
*Premixed combinations of human NPH and regular insulin are available:
20% Regular/80% NPH; 30% Regular/70% NPH; 50% Regular/50% NPH.
**Lente insulin contains 30% semilente and 70% ultralente insulin.
(Modied from reference 1)
Table 1
treatment of diabetic dogs. One common example is lente insulin, which
contains a mixture of semilente and ultralente, and results in a relatively
predictable and rapidly obtained peak effect (10). A number of
combinations of regular and NPH insulin are also widely available.
When choosing the type of insulin for long-term use in a diabetic dog,
another consideration is the species of the exogenous insulin. Porcine
insulin has exactly the same amino acid sequence as canine insulin and
induces no anti-insulin antibodies with prolonged use in dogs (1114).
Human insulin differs by one amino acid from canine insulin and anti-
insulin antibodies have been detected in only one dog treated with
recombinant human insulin (15). Bovine insulin differs by two amino
acids from canine insulin. Anti-insulin antibodies have been detected in
dogs treated with both puried bovine (11) and mixed bovine/porcine
insulin (13, 15). These anti-insulin antibodies may affect glycaemic control
in some diabetic dogs treated with bovine/porcine insulin (15) and so it
may be advisable to avoid preparations that contain bovine insulin.
Human recombinant insulins are usually sold at a concentration of
100 IU/ml. In some countries, porcine lente insulin or bovine/porcine PZI
insulin are available at a concentration of 40 IU/ml. These more dilute
preparations are useful for smaller dogs, which may require a total insulin
dose of only one or two international units. Syringes that measure
international unit increments are available for both insulin concentrations.
Insulin-dosing pens are obtainable for NPH insulin and the premixed
combinations of regular and NPH insulin. Most of these dosing pens allow
injection of a minimum dose of 2 IU and increase in 1 IU increments,
making them a practical tool for smaller patients.
In a small proportion of diabetic dogs, good glycaemic control can be
attained with once-daily administration of one of the longer-acting insulins.
The majority of diabetic dogs, however, require twice-daily administration
of insulin to control their clinical signs adequately (1, 12, 16). Although
treatment regimens comprising once-daily insulin injections are considered
by many to be simpler and more convenient, most of these regimens
involve feeding meals twice daily. Owners of diabetic dogs often nd that
having to be at home with their dog at set times twice each day is the main
intrusion into their daily routine. Experienced owners rarely report any
difculty with the administration of insulin injections and therefore if they
are required to be at home to feed the dog it is little more effort to give the
dog an insulin injection at the same time. As a result, many clinicians
favour treatment regimens that involve administration of the same dose of
insulin along with feeding of the same-sized meal every 12 hours. If lente
insulin (12) or a premixed combination of regular and NPH insulin is
chosen, the onset of effect and the period of maximal insulin activity will
then roughly match the expected postprandial absorption of nutrients.
Diet
The food fed to diabetic dogs should provide adequate calories to achieve
and maintain optimal body condition. Dogs with poorly controlled diabetes
have a decreased ability to metabolise the nutrients absorbed from their
gastrointestinal tract and lose glucose in their urine, so require more
calories for maintenance than healthy dogs. The diet fed should be
nutritionally balanced and needs to be palatable so that food intake is
predictable. Meals should ideally be timed so that maximal exogenous
insulin activity occurs during the postprandial period (12). Because the
daily insulin-dosing regimen tends to be xed for diabetic dogs, it is also
important that a predictable glycaemic response is achieved following each
meal. Consequently, every meal should contain roughly the same
ingredients and calorie content, and should be fed at the same times each
day. The owners of diabetic dogs should be aware that a consistent insulin-
dosing and feeding routine is optimal although, for practical reasons, a
certain amount of compromise may be necessary in individual cases.
For several decades, there has been a great deal of interest in research
into the composition of an optimal diet for people diagnosed with the
various forms of diabetes mellitus. As a result, it is now recognised that
dietary management plays a central role in the treatment of diabetic people.
More recently, veterinary researchers have started to follow this trend and
comparison can now be made between the dietary recommendations for
diabetic people and those for dogs (Table 2).
Dietary bre and complex carbohydrates current
recommendations for diabetic people
Before the advent of insulin therapy, fat and protein were the main sources
of energy in the diets prescribed for people with diabetes. Dietary
carbohydrate was avoided in an effort to reduce hyperglycaemia. Diets
currently recommended for diabetics are the result of substitution of the
saturated fat content with complex carbohydrates. The primary reason for
this change was the realisation that the risk of death due to cardiovascular
disease could be greatly reduced by lowering plasma cholesterol. Many
protein sources contain signicant amounts of fat and so are not practical
replacements for dietary fat. Consequently, the only option that remained
was to increase the carbohydrate component. It has been consistently
shown that the cholesterol content of low-density lipoproteins is
signicantly reduced in diabetic people when complex carbohydrates are
substituted for the saturated fat content of their diet (20). It is now highly
recommended that 55 to 60% of a diabetic persons total energy should be
provided from carbohydrate and the majority of the carbohydrates should
be complex, containing high amounts of resistant starch and bre (21).
Classication of foods according to their acute glycaemic effects has been
suggested as a means of identifying which carbohydrate-containing foods
are optimal for people with diabetes (17). Foods such as pulses, oats, and
barley, which have been found to have a low glycaemic index, may be the
most benecial.
In human diabetics, high-carbohydrate intake can be associated with
increased blood glucose uctuations and hypertriglyceridaemia. However,
when the effects of high carbohydrate diets containing soluble bre are
compared with those of high-carbohydrate/low-bre diets, patients
consuming soluble bre tend to have lower glycosylated haemoglobin levels
(22), lower postprandial blood glucose values, and the
hypertriglyceridaemic effect is attenuated or abolished (23). Digestible
carbohydrate needs to comprise more than 40% of caloric intake to ensure
maximal benecial effects of the bre. Only soluble bre has a
hypoglycaemic and hypolipidaemic effect, whereas insoluble bre appears
to have no effect at all (24). The primary mechanism appears to be the
ability of certain soluble bres, such as guar gum, to form a viscous gel and
thus impair transfer of nutrients to the absorptive surface of the intestine
(25).
It should be remembered that exogenous insulin has an overwhelming
effect on carbohydrate metabolism. In diabetic people with absolute insulin
deciency, dietary manipulations are still an adjunct to insulin therapy. The
results of a recent study help to put the role of diet into perspective (26).
18
Current nutritional recommendations for human diabetics
(17) and canine diabetics (1) compared with the nutritional
requirements of non-diabetic populations
Dietary factor Human diabetics Canine diabetics
Carbohydrate content Increased Increased
High proportion of soluble High proportion of insoluble
bre and complex bre and complex
carbohydrates carbohydrates (18, 19)
Fat content Decreased Decreased
Protein content Same Same
Table 2
The effects of foods with different glycaemic indexes and bre content were
examined in a small number of well-controlled diabetic patients treated
with intensive insulin therapy. It was found that, although diets with a low
glycaemic index resulted in lower fasting plasma glucose, and diets with
increased soluble bre reduced the postprandial rise in plasma glucose, the
difference was not sufcient to require adjustment of the patients insulin
doses.
What is dietary bre?
Fibre is a term used to describe the most complex and least denable
component of foods of plant origin, encompassing a diverse group of plant
polysaccharides, mucilages, and phenolic compounds (27). Dietary bre is
in fact a shorthand expression that covers a wide variety of entities and
should be considered a concept, rather than a denable substance. Diverse
methods of bre analysis exist, all measuring something different. The
same analysis performed by different laboratories can produce dissimilar
results. Crude bre is the gure most widely quoted on pet food labels and
is the residue remaining after extraction of a food material with dilute acid
or alkali. It substantially underestimates the total dietary bre of common
ingredients used in commercial pet food and dietary bre supplements and
is largely obsolete in the eld of human nutrition (27).
Analysis techniques that quantify the individual sugars comprising the
polysaccharides also partition the dietary bre into soluble and insoluble
fractions, a reection of their properties in an aqueous media. Soluble bre
has great water-holding capacity, forms a viscous solution in water, and is
readily degraded by colonic microora in dogs to produce short-chain fatty
acids that are absorbed across the intestinal mucosa. It has been proposed
that these fatty acids stimulate secretion of intestinal hormones that
modulate the nutrient transport capacity of the gut and promote insulin
secretion, which together facilitate removal of glucose from the circulation
(28). A recent study indicated that dogs fed diets with increased viscosity
may actually have more rapid postprandial glucose absorption, resulting in
higher total postprandial glucose absorption, and are more likely to develop
secretory diarrhoea than dogs fed diets with lower viscosity (29). This
suggests that only diets with an intermediate viscosity level may be
associated with a delay in gastrointestinal transit time and optimal glucose
homeostasis in dogs. Dogs cannot digest the insoluble bre component of
their diet and it is excreted in the faeces. In contrast to soluble bre,
insoluble bre seems to exert relatively little physiological effect in the
canine gut and can be tolerated in fairly high dietary levels (27). Most foods
contain more insoluble than soluble bre, even those that are commonly
quoted as sources of soluble bre, such as guar gum.
Perhaps the most useful method of dening dietary bre is to consider
the source of the bre. Fruits, legumes, oats, barley, and psyllium husks
tend to contain more soluble bre than cereals and vegetables, although
there are exceptions. Pea bre (puried pea hulls), arbocell (puried
cellulose), oat bran, wheat bran, and guar gum are all sources of bre that
are used as ingredients in commercial pet food or as dietary bre
supplements (Figure 2). One of the main advantages of high-bre diets is
that intestinal glucose absorption is slowed, so the bre should always be
incorporated in the food rather than given separately as a supplement.
Dietary bre and complex carbohydrates current
recommendations for diabetic dogs
Studies in diabetic dogs indicate that high-bre diets may also be associated
with improved glycaemic control in this species (18, 19, 3032). When
dogs were fed a single meal containing either increased soluble bre or
increased insoluble bre, a greater reduction of postprandial
hyperglycaemia was seen with the meal containing soluble bre (30).
However, when comparison was made following long-term feeding of high-
soluble-bre diets and high-insoluble-bre diets for one or two months
(18, 19), a tendency for improved glycaemic control and fewer side effects
was seen with the diets containing increased insoluble bre. In particular,
signicantly lower glycosylated haemoglobin (18) or fructosamine (19)
levels were recorded. Regardless of the composition of the high-bre diet,
or the length of time over which the dogs are monitored, no signicant
difference in daily insulin requirement (18, 19, 3032) or fasting
triglyceride (18, 32) between groups of diabetic dogs fed low-bre and high-
bre diets has been found.
Importantly, there seems to be marked variation between the responses
of individual diabetic dogs to dietary bre. In one study (32), signicant
improvement of all indices of glycaemic control, including lowered daily
insulin requirement, was seen in nine of 11 dogs when they were fed a
high-bre diet. The remaining two dogs were found to have improved
glycaemic control on the low-bre diet. A similar situation exists for people
because high-carbohydrate high-bre diets are not uniformly effective in all
diabetic subjects (21). This may be partly due to the side effects that are
sometimes associated with high-bre diets, which include poor palatability,
poor weight gain, poor hair coat, voluminous faeces, atulence, diarrhoea,
and constipation.
In comparison with the bulk of literature addressing the inuence of
dietary bre on human diabetes, the number of studies that have
investigated this aspect of canine diabetes is very small. Although there is
no doubt that a considerable amount of the information that is now known
about dietary recommendations for human patients is also relevant to dogs,
it is clear that the specic requirements of diabetic dogs need further
clarication. The inuence of high-bre and low-bre diets has been
studied in diabetic dogs; however, little comparison has been made with
19
Figure 2 Analysis of ve bre supplements used in commercial dog food.
NB. This illustration rst appeared in Bauer, J.E., Maskell, I.E. Dietary bre: Perspectives in
clinical management. In: Wills, J. M., Simpson, K. W. (eds.) The WALTHAM Book of Clinical Nutrition
of the Dog and Cat. Oxford: Pergamon, 1995: 87104. Analysis of ve bre supplements,
demonstrating the poor correlation between total dietary bre and crude bre. Data are from the
analytical laboratory at Pedigree Petfoods, Melton Mowbray.
0
20
40
60
80
100
DF
CF
CF
CF
CF
CF
DF
DF
DF
DF
Dotted line highlights difference between total dietary
bre and crude bre
Pea
Fibre
Arbocell Oat
Bran
Wheat
Bran
Guar
Insoluble DF Soluble DF Starch
Protein Fat Ash
Moisture Crude Fibre
typical maintenance diets to see if increased bre results in measurable
benets compared with a conventional diet. Future studies will help to
determine more accurately the optimal quantity, type, and source of dietary
bre used. The inuence of the manner of processing the dietary bre and
the effect of the composition of the digestible carbohydrate component of
the diet also require elucidation. Ultimately, clinicians will want to know
how commercially available high-bre diets, compared with the typical
maintenance moderate-bre diets, will inuence the clinical management
of their patients. The owners of diabetic dogs, on the other hand, are likely
to be more interested in the palatability and side effects of any high-bre
diets that are recommended for their pets.
Dietary fat
Altered lipid metabolism occurs in both people and dogs with insulin
deciency. In humans, the lipid disorders that occur in association with
diabetes are arthrogenic and predispose to coronary artery disease,
cerebrovascular disease, and peripheral arterial disease (33). Low-fat diets
have been shown to reduce cardiovascular morbidity and mortality in
diabetic people. Fortunately, atherosclerosis and arterial disease are not
clinical concerns in diabetic dogs. However, it has been known for some
time that a large proportion of diabetic dogs have exocrine pancreatic
disease (6, 3440). High-fat diets and hypertriglyceridaemia have been
proposed as possible inciting causes of canine pancreatitis (41) and low-fat
diets are recommended for dogs with chronic pancreatitis and exocrine
pancreatic insufciency. As it can be difcult to identify those diabetic dogs
with subclinical exocrine pancreatic disease (42), it may be prudent to
consider feeding a reduced fat diet to all diabetic dogs.
Dietary protein
The protein composition of the recommended diet for people with diabetes
is the same as that recommended for the non-diabetic population.
However, if microalbuminuria or persistent proteinuria develop, then
protein restriction may help slow the progression of diabetic nephropathy
in these people (24). The optimal dietary protein for diabetic dogs has not
been determined. It is currently recommended that dietary protein should
meet daily requirements, but not be excessive (1). Microalbuminuria and
proteinuria do occur in diabetic dogs (43) and lower dietary protein intake
may be indicated in these animals.
The dietary recommendations for diabetic dogs are summarised in
Table 3.
Information from research using healthy dogs that may prove
relevant for diabetic dogs
Little is known about the glycaemic responses of dogs to various
carbohydrate-containing foods. It has been found that a semimoist food
containing corn syrup, compared with a canned and a dry food that did not
contain corn syrup, resulted in a signicantly greater postprandial
glycaemic response when fed to healthy dogs (44). A more recent study
examining the postprandial effects of ve diets with equivalent starch
content from different cereal sources found marked differences in the
glucose and insulin responses of healthy dogs (45). The rice-based diet
resulted in signicantly higher postprandial glucose and insulin responses.
Sorghum generally caused the lowest postprandial glucose response while
barley produced the lowest insulin response. These ndings form an
interesting basis for future study on the effects of diets containing barley
and sorghum in diabetic dogs, but more work is required before specic
recommendations can be made. It is worth noting that studies in human
beings have found a marked variability in the glycaemic response to
different types of barley (46) and rice (47).
Chromium tripicolinate is a dietary mineral supplement that has been
shown to increase the clearance rate of glucose from the blood by
approximately 10% in healthy dogs (48). Chromium is an essential
nutrient, not a drug, and therefore supplementation may result in benets
only if the individual is decient or marginally decient in chromium. It is
now clear that dietary chromium levels of most people in industrialised
countries are suboptimal (49). Similar information is not available for dogs
and further studies are warranted to try and establish the minimum
recommended dietary chromium intake for healthy dogs. Chromium is
thought to potentiate insulins ability to store glucose and would
theoretically be a useful adjunct to exogenous insulin therapy. It is also
possible that inadequate dietary intake of chromium by dogs may increase
their risk of developing diabetes. It has been postulated that some insulin-
dependent diabetics may lose their ability to convert inorganic chromium to
the biologically active form and may actually need to consume foods that
contain active forms of chromium (50). At this stage, there is little
information available on the effects of chromium supplementation in
human patients requiring insulin therapy (51, 52). Feeding trials using
diabetic dogs are indicated to determine the effects of dietary chromium
supplementation in these animals.
Establishing a practical routine for the owner
The rst aim of long-term therapy of diabetic dogs is resolution of the
20
Summary of current dietary recommendations for diabetic
dogs
Calorie intake Achieve and maintain optimal body condition
Primary nutritional Palatable
requirements Nutritionally balanced
Consistency is important
The same food containing a standard number of calories
should be fed following each insulin injection
Other nutritional Increased complex carbohydrate content with a high
recommendations proportion of insoluble bre incorporated into the food
Decreased fat content, particularly if there is concurrent
disease of the exocrine pancreas
Timing of meals Postprandial period should ideally coincide with the period of
maximal exogenous insulin activity
Feed multiple small meals or two equal-sized meals per day
Diabetic dogs with The nutritional requirements of any concurrent disease should
concurrent disease take precedence over the dietary therapy for diabetes
Regardless of the diet fed, glycaemic control can still be
maintained with exogenous insulin therapy
Table 3
Lethargy
Altered mentition; hypoglycaemic dogs often appear dull
and unaware of their surroundings. Owners may nd it
difcult to attract their attention
Weakness, trembling, ataxia
Collapse and loss of consciousness
Epileptiform seizures
Figure 3 Progression of clinical signs as hypoglycaemia becomes more
severe in dogs.
clinical signs. In other words, well-controlled diabetic dogs are not
lethargic, maintain optimal body condition, drink less than 60 ml of water
per kg body weight during a 24-hour period, and have no ketonuria.
Many different regimens have been used to achieve this successfully and
it is usually possible to introduce a number of modications to the
treatment strategy of individual dogs without compromising their clinical
response. Ideally, exogenous insulin should remain effective throughout
every 24-hour period and meal feeding should be timed so that the
postprandial periods coincide with maximal insulin activity. Typically, this
entails feeding the dog some time after each insulin injection. However, it is
often more convenient for owners to feed their dog at the time of injection
and many prefer this as they feel their pet is rewarded for submitting to the
injection. It is the authors experience that good control of clinical signs can
readily be achieved in diabetic dogs that are fed meals at the time of insulin
injections. Care should be taken to consider each case individually. It is
usually possible to make practical modications to any treatment regimen
in order to reduce the disruption to the owners lifestyle.
The second goal of therapy is avoidance of insulin-induced
hypoglycaemia. Every person in the diabetic dogs household needs to be
aware of this life-threatening complication, which can rapidly develop into a
frightening emergency. The importance of avoiding an insulin overdose
cannot be overemphasised. If some insulin is spilt during injection it
should never be topped up, even if it appears that the dog has received no
insulin. If the owner is ever uncertain, the safest option is to withhold the
injection as the consequences of missing a single insulin dose are
negligible. The clinical signs seen in dogs with hypoglycaemia are listed in
Figure 3. If mild signs of hypoglycaemia develop, the owner should feed a
meal of the dogs usual food. If the dog is unwilling or unable to eat, syrup
containing a high glucose concentration can be administered orally.
Suitable syrups are marketed for use by human diabetics. When the dog
recovers, food should be fed as soon as possible. No more insulin should be
given to the dog until the case is discussed with a veterinarian, at which
point a 50% reduction in insulin dose is usually recommended. Care must
be taken when dispensing insulin syringes to owners to ensure that there is
no confusion regarding dosing. For example, the gradations on many 1 ml
insulin syringes are equal to 2 IU, while gradations of 1 IU are present on
most 0.5 ml insulin syringes. Gradations on syringes designed for use with
100 IU/ml insulin represent a different volume from gradations on syringes
designed for use with 40 IU/ml insulin, and this may lead to dosing errors.
The nal goal of long-term therapy of diabetic dogs is resumption of the
pets usual lifestyle and exercise level. Most owners of diabetic dogs will take
one to two weeks to establish a daily treatment routine and to become
accustomed to administration of subcutaneous injections. A period of
adjustment and stabilisation of therapy follows. Good glycaemic control is
usually attained after at least two months of reappraisal and insulin dosage
adjustment. Once this stage is reached, further clinical improvement may
still be seen for several weeks before the dog achieves an optimal health
and tness level. Many diabetic dogs are elderly and are accustomed to
moderate daily exercise. Younger dogs may resume a very high activity level
and require further adjustment to their daily calorie intake and insulin
dose as a result.
Concurrent disease
Most diabetic dogs are middle aged and older and so are prone to diseases
that commonly affect this age group. Consequently, many suffer concurrent
problems that cause insulin resistance and need to be managed in
combination with the diabetes. Treated diabetic dogs have a similar chance
of survival to that of non-diabetic dogs of the same age and gender,
although the hazard of death occurring is greatest during the rst six
months of therapy (53). Insulin resistance associated with
hyperadrenocorticism is a relatively common problem in diabetic dogs (40)
and can present a diagnostic and therapeutic challenge. Chronic
pancreatitis also complicates the management of some dogs with diabetes.
Reduced immunity often remains a feature of treated diabetic dogs and
many are at increased risk for developing bacterial infections, particularly
of the skin and the urinary tract. Regular urine culture may be advisable,
even if urinary tract signs are not present (54). Ovariohysterectomy is
recommended for entire bitches, as insulin resistance occurs during the
long progesterone phase of their cycle (1).
Blindness and lens-induced uveitis develop sooner or later in the
majority of diabetic dogs and are the single most important sequelae for
this condition (1). Mild or subclinical uveitis is present in most dogs with
diabetic cataracts and can often be satisfactorily managed with oral non-
steroidal anti-inammatory drugs such as aspirin (55). Permanent ocular
damage can result if lens-induced uveitis is not treated (Figure 4). Surgical
removal of diabetic cataracts usually results in restoration of good vision
and marked improvement of the dogs quality of life.
Conclusion
Successful long-term management of a diabetic dog sometimes requires
permanent changes to the lifestyles of both owner and dog and so
21
Figure 4 (a) A hypermature cataract in a diabetic dog. Some scleral
hyperaemia is present, indicating that there is also mild, lens-induced
uveitis. (b) Severe, lens-induced uveitis in a diabetic dog. The eye is red and
painful. There is signicant ocular discharge and posterior synechiae are
present.
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.
individualisation of the advice given is imperative. A relationship based on
trust and co-operation between veterinarian and client invariably leads to
the most satisfactory outcome. The ongoing treatment of a diabetic dog can
be one of the more rewarding experiences of small animal practice and
many diabetic dogs and their owners come to occupy a special place within
the clinic environment.
22
1. Feldman, E. C., Nelson, R. W. Diabetes mellitus. In: Feldman, E. C., Nelson,
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2. Sai, P., Debray-Sachs, M., Jondet, A., Gepts, W., Assan, R. Anti-beta-cell
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3. Alejandro, R., Feldman, E., Shienvold, F. L., Mintz, D. H. Advances in canine
diabetes mellitus research: Etiopathology and results of islet transplantation.
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4. Hoenig, M., Dawe, D. L. A qualitative assay for beta cell antibodies.
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5. Elie, M., Hoenig, M. Canine immune mediated diabetes mellitus: a case
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6. Ling, G. V., Lowenstine, L. J., Pulley, T., Kaneko, J. J. Diabetes mellitus in
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7. Marmor, M., Willeberg, P., Glickman, L. T., Priester, W. A., Cypress, R. H.,
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8. Graham, P. A., Nash, A. S. Rates of blindness and other complications in
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9. Beam, S., Correa, M. T., Davidson, M. G. A retrospective-cohort study on the
development of cataracts in dogs with diabetes mellitus: 200 cases. Veterinary
and Comparative Ophthalmology 1999; 2: 169172.
10. Church, D. B. The blood glucose response to three prolonged duration
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11. Neubauer, H. P., Schone, H. H. The immunogenicity of different insulins in
several animal species. Diabetes 1978; 27: 815.
12. Church, D. B. Canine diabetes mellitus: some therapeutic considerations.
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13. Feldman, E. C., Nelson, R. W., Karam, J. H. Reduced immunogenicity of
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14. Freiherr von Bolcshazy, G. Examination of immune reaction due to use of
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15. Harb-Hauser, M., Nelson, R., Gershwin, L., Neal, L. Prevalence of insulin
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16. Hess, R. S., Ward, C.R. Effect of insulin treatment on glycemic response in
dogs with diabetes mellitus: 221 cases (19931998). Journal of the American
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17. Diabetes and Nutrition Study Group of the EASD. Nutritional
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18. Nelson, R. W., Ihle, S. L., Lewis, L. D. et al. Effects of dietary ber
supplementation on glycemic control in dogs with alloxan-induced diabetes
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19. Kimmel, S., Michel, K., Hess, R., Ward, C. Effect of dietary ber on glycemic
control in diabetic dogs (abstract). In: Proceedings of the 17th Forum of the
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20. Howard, B. V., Abbott, W. G., Swinburn, B. A. Evaluation of metabolic effects
of substitution of complex carbohydrates for saturated fat in individuals with
obesity and NIDDM. Diabetes Care 1991; 14: 786795.
21. Anderson, J. W., Akanji, A. O. Dietary ber an overview. Diabetes Care
1991; 14: 11261131.
22. Buyken, A. E., Toeller, M., Heitkamp, G. et al. Relation of bre intake to
HbA1c and the prevalence of severe ketoacidosis and severe hypoglycaemia.
EURODIAB IDDM Complications Study Group. Diabetologia 1998; 41:
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23. Riccardi, G., Rivellese, A., Pacioni, D., Genovese, S., Mastranzo, P., Mancini,
M. Separate inuence of dietary carbohydrate and bre on the metabolic control
in diabetes. Diabetologia 1984; 26: 116121.
24. Karamanos, B. The dietary management of diabetes. Dialogue Diabetes
Literature Review Service 1998; 3: 1115.
25. Nuttall, F. Q. Dietary ber in the management of diabetes. Diabetes 1993;
42: 503508.
26. Lafrance, L., Rabases-Lhoret, R., Poisson, D., Ducros, F., Chaisson, J.-L.
Effects of different glycaemic index foods and dietary bre intake on glycaemic
control in type 1 diabetic patients on intensive insulin therapy. Diabetic
Medicine 1998; 15: 972978.
27. Bauer, J. E., Maskell, I. E. Dietary bre: Perspectives in clinical
management. In: Wills, JM, Simpson, K. W. (eds.) The Waltham Book of
Clinical Nutrition of the Dog and Cat. Oxford, Pergamon, 1995: 87104.
28. McBurney, M. I., Massimino, S. P., Field, C. J., Sunvold, G. D., Hayek, M. G.
Modulation of intestinal function and glucose homeostasis in dogs by the
ingestion of fermentable dietary bers. In: Reinhart, G. A., Carey, D. P. (eds.)
Recent Advances in Canine and Feline Nutrition. Vol II. Wilmington: Orange
Frazer Press, 1998: 113122.
29. Nelson, R. W., Sunvold, G. D. Effect of carboxymethylcellulose on
postprandial glycaemic response in healthy dogs. In: Reinhart, G. A., Carey, D.
P. (eds.) Recent Advances in Canine and Feline Nutrition. Vol II. Wilmington:
Orange Frazer Press, 1998: 97102.
30. Blaxter, A. C., Cripps, P. J., Gruffydd-Jones, T. J. Dietary bre and post
prandial hyperglycaemia in normal and diabetic dogs. Journal of Small Animal
Practice 1990; 31: 229233.
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31. Graham, P. A., Maskell, I. E., Nash, A. S. Canned high ber diet and
postprandial glycemia in dogs with naturally occurring diabetes mellitus.
Journal of Nutrition 1994; 124: 2712S2715S.
32. Nelson, R. W., Scott-Montcrieff, C., DeVries, S., Davenport, D., Neal, L. Effect
of dietary insoluble ber on control of glycaemia in dogs with naturally acquired
diabetes mellitus. Journal of the American Veterinary Medical Association
1998; 212: 380386.
33. Stamler, J., Vaccaro, O., Neaton, J. D., Wentworth, D. Diabetes, other risk
factors, and 12-yr cardiovascular mortality for men screened in the Multiple
Risk Factor Intervention trial. Diabetes Care 1993; 16: 434444.
34. Schlotthauer, C. F., Millar, J. A. S. Diabetes mellitus in dogs and cats.
Journal of the American Veterinary Medical Association 1951; 118: 3135.
35. Dixon, J. B., Sanford, J. Pathological features of spontaneous canine
diabetes mellitus. Journal of Comparative Pathology 1962; 72: 153167.
36. Cotton, R. B., Cornelius, L. M., Theran, P. Diabetes mellitus in the dog: A
clinicopathologic study. Journal of the American Veterinary Medical
Association 1971; 159: 863870.
37. Anderson, N. V., Strafuss, A. C. Pancreatic disease in dogs and cats. Journal
of the American Veterinary Medical Association 1971; 159: 885891.
38. Haines, D. M., Penhale, W. J. Autoantibodies to pancreatic islet cells in
canine diabetes mellitus. Veterinary Immunology and Immunopathology
1985; 8: 149156.
39. Haines, D. M. A re-examination of islet cell cytoplasmic antibodies in
diabetic dogs. Veterinary Immunology and Immunopathology 1986; 11:
225233.
40. Hess, R. S., Saunders, H. M., Van Winkle, T. J., Ward, C. R. Evaluation of
concurrent disorders in dogs with diabetes mellitus (abstract). In: Proceedings
of the 17th Forum of the American College of Veterinary Internal Medicine.
Chicago, USA, 1999: 710.
41. Williams, D. A. Diagnosis and management of pancreatitis. Journal of
Small Animal Practice 1994; 35: 445454.
42. Wiberg, M. E., Nurmi, A.-K., Westermarck, E. Serum trypsin like
immunoreactivity measurement for the diagnosis of subclinical exocrine
pancreatic insufciency. Journal of Veterinary Internal Medicine 1999; 13:
426432.
43. Struble, A. L., Feldman, E. C., Nelson, R. W., Kass, P. H. Systemic
hypertension and proteinuria in dogs with diabetes mellitus. Journal of the
American Veterinary Medical Association 1998; 213: 822825.
44. Holste, L. C., Nelson, R. W., Feldman, E. C., Bottoms, G. D. Effect of dry, soft
moist, and canned dog foods on postprandial blood glucose and insulin
concentrations in healthy dogs. American Journal of Veterinary Research
1989; 50: 984989.
45. Sunvold, G. D., Bouchard, G. F. The glycaemic response to dietary starch.
In: Reinhart, G. A., Carey, D. P. (eds.) Recent Advances in Canine and Feline
Nutrition. Vol II. Wilmington: Orange Frazer Press, 1998: 123131.
46. Liljeberg, H. G., Granfeldt, Y. E., Bjorck, I. M. Products based on a high ber
barley genotype, but not on common barley and oats, lower postprandial
glucose and insulin responses in healthy humans. Journal of Nutrition 1996;
126: 458466.
47. Jarvi, A.E., Karlstrom, B. E., Granfeldt, Y.E., Bjorck, I. M., Vessby, B. O., Asp,
N. G. The inuence of food structure on postprandial metabolism in patients
with non-insulin-dependent diabetes mellitus. American Journal of Clinical
Nutrition 1995; 61: 837842.
48. Spears, J. W., Brown, T. T., Sunvold, G. D., Hayek, M. G. Inuence of
chromium on glucose metabolism and insulin sensitivity. In: Reinhart, G. A.,
Carey, D.P. (eds.) Recent Advances in Canine and Feline Nutrition, Vol II.
1998 Iams nutrition symposium proceedings. Wilmington: Orange Frazer
Press, 1998: 103113.
49. Anderson, R. A. Chromium, glucose intolerance and diabetes. Journal of
the American College of Nutrition 1998; 17: 548555.
50. Anderson, R. A. Chromium, glucose tolerance, and diabetes. Biological
Trace Element Research 1992; 32: 1924.
51. Ravina, A., Slezak, L., Rubal, A., Mirsky, N. Clinical use of the trace element
chromium (III) in the treatment of diabetes mellitus. Journal of Trace
Elements in Experimental Medicine 1995; 8: 183190.
52. Fox, G. N., Sabovic, Z. Chromium picolinate supplementation for diabetes
mellitus. Journal of Family Practice 1998; 46: 8386.
53. Graham, P. A., Nash A. S. Survival data analysis applied to canine diabetes
mellitus (abstract). In: 15th Annual Forum of the American College of
Veterinary Internal Medicine. Lake Buena Vista, USA. 1997: 689.
54. Forrester, S. D., Troy, G. C., Dalton, N., Huffman, J. W., Holtzman, G.
Retrospective evaluation of urinary tract infection in 42 dogs with
hyperadrenocorticism or diabetes mellitus or both. Journal of Veterinary
Internal Medicine 1999; 13: 557560.
55. Bagley, L. H. II, Lavach, J. D. Comparison of postoperative
phacoemulsication results in dogs with and without diabetes mellitus: 153
cases (19911992). Journal of the American Veterinary Medical Association
1994; 205: 11651169.
56. Graham, P. A., Nash, A. S., McKellar, Q. A. Pharmacokinetics of a porcine
insulin zinc suspension in diabetic dogs. Journal of Small Animal Practice
1997; 38: 434438.
31
F
rom 1417 February 2000, the 9th International Symposium on
Urolithiasis took place in the city of Cape Town, South Africa, organised
by Professor Allen Rodgers and his team from The University of Cape
Town. Within this forum, the worlds leading experts in human urology and
nephrology meet every four years to discuss recent innovations and research
in this eld. This year, for the rst time, a new addition was featured on the
programme of scientic events: the WALTHAM Session on Stone Disease in
Animals. Urological diseases are a signicant problem in companion animals
accounting for approximately 3% of dogs and over 7% of cats seen at
veterinary hospitals (1, 2). There are many aspects of stone pathogenesis and
management that are shared between humans and animals. For this reason
WALTHAM collaborated with the congress organisers to include a session
exclusively for presentation of recent research abstracts and discussion on
companion animal urolithiasis, with particular reference to the cat and dog.
Approximately 400 people attended the conference, which contained a mix
of around 300 oral and poster presentations. In addition to the sessions on
urolithiasis in animals, topics included supersaturation and physical
chemistry, crystallisation modulators and macromolecules, nutrition, dietary
risk factors and water intake, epidemiology, genetics, metabolic evaluation,
and medical therapy and endourology.
The WALTHAM session on Stone Disease in Animals was very well
supported with an attendance of around 80 delegates. Some of these were
local veterinarians invited by Masterfoods South Africa, but the majority were
from the main conference, with particular interest shown by the
physiologists. A very stimulating scientic programme was presented with 17
abstracts received from a number of authors and institutions. Peter Markwell,
from the WALTHAM Centre for Pet Nutrition, opened the session by
presenting the overview lecture, entitled Urolithiasis: a comparison of
humans, cats, and dogs. This paper discussed a number of topics including
anatomical distribution, mineral composition, mineral intake, and urine
composition provided an insight into some of the similarities and differences
that exist amongst these three species. Several abstracts addressed the shift in
stone formation away from struvite towards calcium oxalate formation in
both cats and dogs. Data were presented from both Europe (Stevenson et al.,
Waltham Centre for Pet Nutrition; Hesse et al., University of Bonn) and North
America (Bartges et al., University of Tennessee). Professor A. Hesse also
presented a paper on the occurrence of ammonium urate urolithiasis in
Eurasian otters.
A number of papers were presented by Bartges et al. around the
management of urate urolithiasis both in Dalmatian and non-Dalmatian
dogs. Of particular interest was a paper presented on the pharmacokinetics of
allopurinol (a xanthine oxidase inhibitor used in the dissolution and
prevention of urate urolithiasis). WALTHAM presented two other papers
containing recent research. The effect of urine pH on relative
supersaturations of feline urine outlined a study in which the urine pH of cats
was manipulated by addition of either an acidier or an alkaliniser to the diet.
This study concluded that, when compared with a moderately acidic urine pH
of between 6 and 6.5, further acidication (urine pH <6.0) increased
urinary calcium concentration and calcium oxalate saturation, indicating
overacidication may be a risk factor for calcium oxalate formation.
Furthermore addition of an alkaliniser increased urine pH to around 6.8, but
did not reduce calcium oxalate saturation and resulted in urine oversaturated
with struvite. A second paper was presented showing that sodium levels of up
to 1.6 g/400 kcal did not cause an increase in urinary calcium concentration,
as claimed by some researchers. This may be because most human studies
looked at sodium levels far higher than those commonly contained within pet
foods. Dr V. Biorge also presented a paper examining struvite and calcium
oxalate activity product ratios in cats fed a number of acidifying diets. This
generated a particularly interesting discussion comparing the use of activity
product ratios (APR) and relative supersaturation (RSS) in assessing the risk
of stone formation in cats and dogs. Dr W. G. Robertson challenged the use of
APR rather than RSS, pointing out the pitfalls of the former technique and the
fact that very few people in the human eld used it.
At the Gala Banquet on the nal evening of the conference several awards
were presented. Dr. W. G. Robertson received a Lifetime Achievement Award
for 30 years of high-quality research within the eld of stone disease in
humans. For the last four years Dr Robertson has been working as a
consultant for WALTHAM and in his speech he acknowledged the WALTHAM
Centre for Pet Nutrition and the enjoyment he now gets from expanding his
portfolio into cats and dogs. Other awards included the Junior Researcher
Award and awards for the best poster and oral presentation within the
WALTHAM Session on Stone Disease in Animals. The oral presentation was
won by the paper entitled Urine pH and urinary relative supersaturation
in healthy adult cats presented by Abigail Stevenson, WALTHAM Project
Scientist, while the award for the best poster was given to Joseph Barges for
his poster entitled Pharmacokinetics of allopurinol in healthy adult dogs.
See you at the 10th International Symposium on Urolithiasis to be held in
Hong Kong in 2004!!
Abstracts from WALTHAM scientists
Stevenson AE, Wrigglesworth, DJ, Markwell PJ: Urine pH and urinary relative
supersaturation in healthy adult cats. Proceedings of 9th International
symposium on Urolithiasis 2000, 818-820
Stevenson AE, Wrigglesworth, DJ, Markwell PJ: Dietary sodium chloride, urinary
calcium and urinary oxalate in healthy adult dogs. Proceedings of 9th
International symposium on Urolithiasis 2000, 794-796
Stevenson AE, Markwell PJ, Kasidas GP: Preliminary data from quantitative
analysis of canine urolithiasis in Great Britain. Proceedings of 9th International
symposium on Urolithiasis 2000, 792-793
Markwell, PJ, Robertson WG, Stevenson AE: Urolithaisis: A comparison of
humans, cats and dogs. Proceedings of 9th International symposium on
Urolithiasis 2000, 785-788
WALTHAM Research News
1. Lulich, J. P., Osborne, C. A., Bartges, J.W., Polzin, D. J. Canine lower urinary
tract disorders. In: Ettinger, S. J., Feldman, E. C. (eds.) Textbook of Veterinary
Internal Medicine, 4th edn. Philadelphia: W. B. Saunders, 1995: 1833-1881.
2. Osborne, C. A., Kruger, J. M., Lulich, J. P., Polzin, D. J. Disorders of the feline
lower urinary tract. In: Osborne, C. A., Finco, D. R. (eds.) Canine and Feline
Nephrology and Urology. Baltimore: Williams & Wilkins, 1995: 625-680.
GREFERENCES G
Urolithiasis 2000 9th International
Symposium on Urolithiasis
32
F
latulence is widely recognised in dogs as a
social nuisance, a source of humour, and an
occasional cause of abdominal discomfort.
There has been little research into the origins and
nature of canine rectal gases, their physiological
and clinical signicance, or the efcacy of various
remedies purported to reduce atulence in dogs.
Flatulence is a frequent everyday occurrence and is
usually associated with no or very mild discomfort.
However, odoriferous gas production is a common
cause for complaint from the dog-owning public.
From human studies it is known that the major
human rectal gases are nitrogen and oxygen, which
are derived from air swallowing and diffusion from
the blood, plus carbon dioxide, hydrogen, and
methane, which are the products of bacterial
metabolism and non-bacterial reactions within the
bowel. Odoriferous gases constitute less than 1%
by volume of atus and much of the unpleasant
odour is due to sulphur-containing gases,
primarily hydrogen sulphide and methanethiol (1,
2). Aside from their odoriferous qualities, sulphur-
containing rectal gases are potentially toxic and
have been implicated in the pathogenesis of
ulcerative colitis in humans (3). There are,
therefore, potential health as well as social benets
to be obtained from reducing the production or
availability (or both) of sulphur gases in the large bowel.
Studies at the WALTHAM Centre for Pet Nutrition have developed an in
vivo method for the assessment of odiferous canine atulence (4). This
technique involves a monitoring pump with a hydrogen sulphide detector
that generates a real-time measure of individual atulence episodes
allowing normal variation in canine rectal gas production to be determined.
In addition, a predictive model has been developed that enables the relative
noxiousness of each emission to be determined from the levels of hydrogen
sulphide measured on-line. This WALTHAM atulence detection system has
been used to determine the potential of dietary ingredients to ameliorate
the frequency and odour characteristics of atulence in dogs.
WALTHAM atulence detection system
Rectal gases are collected via a perforated Teon tube, which is held close to
the anus of the dog and is attached to a sulphur gas-monitoring pump
carried in a jacket over the dogs shoulders (Figure 1). Dogs wear the coats
for ve hours during each measurement period. The sampling pump is
tted with a hydrogen sulphide sensor that measures hydrogen sulphide
levels, in parts per million (p.p.m.), at 20-second intervals (Figure 2).
WALTHAMViewpoint
Dietary manipulation of canine
odiferous atulence
Catriona Giffard BSc, DPhil
Stella Collins BSc
WALTHAM Centre for Pet Nutrition, UK
0 1 2 3 4 5
0
10
20
30
40
50
60
70
80
Figure 1 Schematic representation of rectal gas sampling device and a representative atulence
prole demonstrating atulence episodes and atulence freeintervals. The baseline is set at 1 ppm
hydrogen sulphide and all readings below this are ignored.
Figure 2
Correlation between
human perception rating
of atulence and levels of
hydrogen sulphide in
rectal gas as measured by
the sampling pump. The
data represents the mean
standard deviation and
scores represent 1 no
odour, 2 slightly
noticeable, 3 mildly
unpleasant, 4 bad
odour, 5 unbearable. Odour Score
Hydrogen Sulphide (ppm) r=0.92
Sulphur Gas
Detecting Pump
Connecting Tube Paper pants
O-ring
0
20
40
60
80
100
11.30 12.30 13.30 14.30 15.30 16.30
S
u
l
p
h
u
r

G
a
s

(
p
p
m
)
Time
Baseline @1ppm
Flatuence Free Interval
Flatuence
Episodes
Three measures of atulence can be calculated from the hydrogen
sulphide data: namely number of episodes (NOE), mean interval free time
(MIFT), and human perception of malodour (Figure 1). The NOE is the
number of times during the sampling period that pump readings were
greater than 1 p.p.m., which is the lower limit of sensory detection for
humans in the same room as dogs. The MIFT is a measure of the frequency
of atulence and is calculated as the cumulative sum of atulence-free
intervals (in minutes) divided by the number of atulence-free intervals. A
atulence-free interval was any 20-second period during which the level of
hydrogen sulphide was less than 1 p.p.m. Human perception of odour
rating for each episode of atulence is calculated according to a power
function, where rating (on a scale of 1 to 5) is equal to 1.51[H
2
S]
0.28
.
These odour ratings are categorised as no odour (= 1), slightly noticeable
(= 2), mildly unpleasant (= 3), bad (= 4), and unbearable (=5), as
shown in Figure 3.
Effect of diet on in vivo odoriferous canine atulence
production (5)
The potential for manipulation of the diet by the addition of activated
charcoal, Yucca shidigera extract, and zinc acetate in an attempt to reduce
the number, frequency, and odour characteristics of atulence in dogs was
evaluated. A prospective double-blinded placebo controlled cross-over study
with eight dogs was used to assess the effects on the production of hydrogen
sulphide when fed a supplemented treat 30 minutes after the dogs ate their
daily rations. The number, frequency and odour characteristics of
atulence were then measured for ve hours using the WALTHAM
atulence detection system.
Feeding this supplemented treat was associated with a small reduction in
the number of atulence episodes (2.05 0.74 vs. 2.47 0.82 ln/
5 hours) and there was no difference between treatment groups and
placebo treats in the mean interval free time (7.55 0.75 and 7.20
0.79 ln minutes, respectively). The distribution of odour ratings for
atulence episodes following feeding of test and placebo treats is shown in
Figure 3. The percentage of episodes rated as 3 (mildly unpleasant), 4
(bad), or 5 (unbearable) was reduced when the dogs were fed the
supplemented treat. Consumption of the activated treat reduced the
percentage of bad and unbearable episodes by 86% compared with the
placebo treats, such that episodes rated as 4 or 5 represented only 2.2% of
all episodes versus 16.1% for the placebo treats.
Conclusion
Oral ingestion of a supplemented treat containing the above-listed
ingredients is associated with a decrease in the frequency of malodorous
atulence episodes that will directly affect one of the social nuisances of dog
ownership and, by reducing the production or availability of hydrogen
sulphide, may be benecial in diseases linked to the toxicity of this gas.
Results from this study form the basis of a patent application. This treat
will be available as Easydose Flatulence Control, as one of a range of
treats of this type within the United Kingdom.
Country Name Fax number
Australia Duncan Hall +612 605 553 47
Bahrain Mustafa El Rafey +971 481 5324
Denmark Charlotte Nilsson +454 245 200
Finland Tuomas Mantere +358 9773 94444
Hong Kong Andrew Baker +852 2369 7920
Ireland Niamh Grogan +353 1478 3687
Korea Eusoo Kim +822 545 3291
Malaysia Carmina R. Herrara +603 758 2861
New Zealand Jeff Herkt +649 261 0901
Norway Christian Soerensen +4640 230 957
Phillippines Mark Antony Baguio +632 818 5307
Singapore Irinda Toh +603 758 2861
Sweden Henrik Birkfeldt +464 023 0957
Taiwan Sunghee Han +886 227 476 767
Thailand Rieantfa Puttekulangkura +662 742 6341
Turkey Elcin Eraksoy +9012 12651 2306
United Arab Emirates Susie Amann +971 481 5324
United Kingdom Sarah Harrod +44 1664 415661
For further information or any queries please contact your local ofce
1. Suarez, F., Furne, J., Springeld, X. et al. Insights into human colonic
physiology from the study of atus composition. American Journal of
Physiology 1997; 272: G1028G1033.
2. Suarez, F. L., Springeld, J., Levitt, M. D. Identication of gases responsible
for the odor of human atus and evaluation of a device purported to reduce this
odor. Gut 1998; 43: 100104.
3. Roediger, W. E., Moore, J., Babidge, W. Colonic sulde in pathogenesis and
treatment of ulcerative colitis. Digestive Diseases and Sciences 1997; 42:
15711579.
4. Collins, S. B., Perez, G., Gettingby, G., Batt, R., Butterwick, R., Giffard, C. J.
Flatulence measurement in dogs: development of a technique, description of
normal variability, and relationship to human organoleptic assessments
(submitted for publication).
5. Collins, S. B., Stoodley, N., Batt, R., Butterwick, R., Giffard, C. Ability of an
anti-atulence treat to reduce the hydrogen sulde content of canine atulence.
ACVIM Forum Proceedings 2000.
GREFERENCES G
0
10
20
30
40
50
1 2 3 4 5
*
*
*
Figure 3 Distribution of atulence episodes according to odour rating in
dogs fed active and control treats. Data are shown as mean frequency, with
signicant differences between treatments denoted by * (p<0.05).
Control
Active
Odour Rating
%

F
l
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Paper - Diabetes Canina

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Paper - Diabetes Canina

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Vol 10 No 3

Feline Low Phosphorus Low Protein)

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