Page 259 - Problem-Based Feline Medicine

15 – THE CAT WITH POLYURIA AND POLYDIPSIA 251

Urine specific gravity is usually dilute. tion and doses greater than 1.5 U/kg q 12 h are often
required. Poor glycemic control is often still present
Identification of a mass on palpation or imaging.
despite higher than normal doses of insulin.
Biopsy and histology is required for a definitive diag-
nosis. Thin, fragile skin that bruises easily is a common
sign. Some cats have extremely fragile skin, and nor-
mal grooming, or lifting the skin for injection or
HYPERADRENOCORTICISM
restraint results in severe skin tears.
Classical signs Poor unkempt hair coat, patchy alopecia, or skin
infections including demodicosis may be evident.
● Diabetes mellitus.
● Polyuria and polydipsia. Potbelly, which may be reported by the owner as weight
● Weight loss. gain or abdominal enlargement.
● Fragile skin and poor hair coat.
Muscle wasting.
See main reference on page 324 for details (The Cat Hepatomegaly.
With Weight Loss and a Good Appetite).
Other concomitant infections may occur, e.g. bacterial
cystitis, pyothorax.
Pathogenesis
Hyperadrenocorticism is a rare disease in cats.
Diagnosis
Usually occurs in middle-aged to older cats (average
Diagnosis is based on consistent clinical signs and an
age 10–11 years).
abnormal dexamethasone suppression test, i.e. fail-
Pituitary-dependent form is most common (approxi- ure of cortisol to suppress below 41 nmol/L
mately 75–80% of cases); a functional adrenocortical (1.5 μg/dl) at both 4 and 8 h after IV dexamethasone.
tumor is less frequent (20–25%). ● Because up to 20% of normal cats do not suppress
using 0.01 mg/kg dexamethasone, a higher dose is
Clinical iatrogenic hyperadrenocorticism is less pro-
recommended in cats, i.e. 0.1 mg/kg.
nounced in cats as they are more resistant to the effects
● It is important not to stress the cat when doing this
of excess exogenous glucocorticoids than dogs. PU/PD
test.
may occur with exogenous steroids, but is less dramatic
● Cats with pituitary-dependent hyperadrenocorti-
than in dogs.
cism may fail to suppress, or exhibit suppression at
Chronic insulin resistance from excess endogenous 3–4 hours followed by “escape” of suppression at 8
steroid may result in diabetes mellitus. hours. The latter pattern is diagnostic for pituitary-
dependent disease, and makes further testing
unnecessary.
Clinical signs
A normal urine cortisol:creatinine ratio is useful for
Polyuria, polydipsia is typical, which may be marked
excluding hyperadrenocorticism, but lacks specificity
(>120 ml/kg/24 h) if concurrent diabetes is present.
for diagnosis.
Weight loss occurs as a result of poorly controlled dia-
The corticotropin (ACTH) stimulation test is best
betes.
used to differentiate endogenous from iatrogenic hyper-
Lethargy is common. adrenocorticism, rather than as a diagnostic test for
hyperadrenocorticism, because 15–30% of cats with
Many of the common signs are attributable to poorly
hyperadrenocorticism have a normal response.
controlled diabetes mellitus (although not all cats with
hyperadrenocorticism have diabetes). The diabetes The combined dexamethasone suppression/ACTH
tends to be insulin resistant. Normal doses of insulin stimulation test has been used successfully to diag-
often produce a minimal decrease in glucose concentra- nose hyperadrenocorticism in cats. The combined test