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 25-28 September, 2018 | Singapore
WSV18-0101
TIPS FROM THE EXPERTS FOR THE APPROACH OF...
POLYURIA / POLYDIPSIA
G. Segev1
1Koret School of Veterinary Medicine, Israel
Introduction
Polyuria and polydipsia (PUPD) is a common disorder in dogs and cats. As polyuria cannot be easily quantified, the diagnosis mostly relies on daily water consumption. Normal water consumption is ~50 ml/kg, however there is great variability among and within species. The definition of polydipsia is met when the daily water consumption is >100 ml/kg. In most of the cases, polyuria is the primary disorder and polydipsia is a compensatory mechanism
to maintain normal hydration status. Less frequently, polydipsia is deriving the polyuria (e.g., primary polydipsia, neurological disorders, fever and pain). The most common mechanisms for polyuria include osmotic (including solute) diuresis, antidiuretic hormone (ADH) deficiency and conditions that alter the kidney response to ADH. In some disorders the pathophysiology of PUPD is multifactorial, involving both primary polyuria and primary polydipsia.
Establishing presence of PUPD
In some cases the owners do not recognize PUPD
as a problem and in other cases PUPD may be the
chief complaint. Incontinence, nocturia, pollakiuria
or inappropriate urination should not be confused
with PUPD, therefore accurate history is informative. Polydipsia can be confirmed easily by measuring
daily water consumption. If the latter is not possible, urine specific gravity (USG) can be measured. PUPD is suspected when the morning USG is persistently low. The clinician needs to bear in mind that almost any USG can be normal, depending on the concurrent hydration status of the patient.
Diagnostic approach
For a rational diagnostic approach, the clinician needs
to be familiar with the most common differential diagnoses in which PUPD is the presenting compliant. These include diabetes mellitus, chronic kidney disease (including pyelonephritis), hyperadrenocorticism, liver diseases, central diabetes insipidus (CDI), pyometra, and hypercalcemia. Other differential diagnoses that should be considered, however PUPD is less likely to be the main presenting compliant, include drug administration (e.g., phenobarbitone, glucocorticoids, diuretics), hypokalaemia, medullary washout, hypoadrenocorticism, congenital nephrogenic DI, post-obstructive diuresis, high salt or low protein diet. Rare differentials should be considered only when the diagnostic work up suggest that these are likely, or when other causes of PUPD have been excluded. These include primary renal glucosuria, Fanconi’s syndrome and hyperviscosity.
History is an extremely valuable tool to further narrow down the differential diagnosis list, even prior to performing any laboratory test. For example, in a non-spayed female dog that was in estrusin the preceding weeks and also presents systemic clinical signs (e.g., lethargy/anorexia/voting), pyometra should be considered high in the differentials. If concurrent history also include polyphagia, diabetes mellitus, hyperthyroidism (in a cat), and hyperadrenocorticism should be considered. If the latter are also accompanied with weight loss, diabetes mellitus and hyperthyroidism (cat) should be considered. If the PUPD is accompanied with weight loss, CKD is more likely. Dogs and cats
with some diseases are less likely to be bright alert
and responsive (e.g., liver failure, hypoadrenocorticism, pyometra, hypercalcemia, advances CKD), whereas in others (e.g., CDI, primary polydipsia) animals are often bright alert and responsive, and PUPD is the only clinical sign present.
Physical examination findings may also aid in narrowing down the differential diagnosis list and occasionally
be almost indicative of the diagnosis. Presence of anal sac mass in an old dog with PUPD, is highly suggestive of anal sac adenocarcinoma (promoting PUPD due
to hypercalcemia). In most cats with hyperthyroidism,
a cervical nodule can be palpated. Animals with hyperadrenocorticism, may present with concurrent dermatological disorders (alopecia, thinning of the
skin, pot-belly), and animals with diabetes mellitus may present with varying degrees of cataract while small and irregular kidneys are suggestive of CKD.
To reach a final diagnosis, usually ancillary tests are required. Complete blood count, serum chemistry and urinalysis are indicated in animals presenting with PUPD. Urinalysis is an initial diagnostic test in such cases. The USG is usually iso- to hypo-stenuric, but may also be hyperstenuric in animals with diabetes mellitus. Unless USG is very now (<1.006), often times USG by itself does not narrow down substantially the differential diagnoses list. When the urine is extremely diluted, differentials
like CDI, hyperadrenocorticism and primary polydipsia become more likely. Naturally, presence of glucose in the urine is highly suggestive of diabetes mellitus, however, glucosuria may also be present in face of normoglycemia in animals with primary glucosuria, Fanconi’s
syndrome, AKI or in animals with stress/drugs induced hyperglycemia. In the latter the glucosuria is expected to be transient. When bacteriuria and pyuria are present in urinalysis, pyolenephritis should be suspected, even in the absence of systemic clinical signs or changes
in complete blood count (CBC) or chemistry, and urine should be submitted for culture and sensitivity.
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43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS


































































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