Page 856 - Small Animal Internal Medicine, 6th Edition

828 PART VI Endocrine Disorders

concentrations are typically greater than 500 µmol/L in dogs BOX 49.9
with insulin resistance and can exceed 700 µmol/L if resis-
VetBooks.ir tance is severe. Unfortunately, an increased serum fructos- Diagnostic Tests to Consider for Evaluation of Insulin
amine concentration is merely indicative of poor glycemic
Resistance in Diabetic Dogs and Cats
control not insulin resistance, per se.
The severity of insulin resistance is dependent, in part, Complete blood count, serum biochemistry panel,
on the underlying etiology. Insulin resistance may be mild urinalysis
and easily overcome by increasing the dosage of insulin or Bacterial culture of the urine
may be severe, causing marked hyperglycemia regardless of Serum canine/feline pancreatic-specific lipase (Spec cP/
fPL) (pancreatitis)
the type and dosage of insulin administered. Some causes of Serum trypsin-like immunoreactivity (TLI) (exocrine
insulin resistance are readily apparent at the time diabetes is pancreatic insufficiency)
diagnosed, such as obesity and the administration of insulin- Adrenocortical function tests
antagonistic drugs (e.g., glucocorticoids). Other causes of Urine cortisol/creatinine ratio (spontaneous
insulin resistance are not readily apparent and require an hyperadrenocorticism)
extensive diagnostic evaluation to be identified. In general, Low-dose dexamethasone suppression test
any concurrent inflammatory, infectious, hormonal, neo- (spontaneous hyperadrenocorticism)
plastic, or organ system disorder can cause insulin resis- Adrenocorticotropic hormone (ACTH)–stimulation test
tance and interfere with the effectiveness of insulin therapy. (iatrogenic hyperadrenocorticism)
In our experience, the most common concurrent disorders Thyroid function tests
interfering with insulin effectiveness in diabetic dogs include Baseline serum total and free thyroxine
(hypothyroidism and hyperthyroidism)
diabetogenic drugs (glucocorticoids), severe obesity, hyper- Serum thyroid-stimulating hormone (TSH;
adrenocorticism, diestrus, chronic pancreatitis, chronic hypothyroidism)
kidney disease, inflammatory bowel disease, oral cavity Serum progesterone concentration (diestrus in intact
disease, infections of the urinary tract, hyperlipidemia, and female dog)
insulin-binding antibodies in dogs receiving beef insulin. Fasting serum triglyceride concentration (hyperlipidemia)
Obtaining a complete history and performing a thorough Plasma growth hormone or serum insulin-like growth
physical examination is the most important initial step in factor 1 concentration (acromegaly)
identifying these concurrent disorders. If the history and Serum insulin concentration 24 hours after discontinuation
physical examination are unremarkable, a CBC, serum bio- of insulin therapy (insulin antibodies)
chemical analysis, serum canine pancreatic-specific lipase Abdominal ultrasonography (adrenomegaly, adrenal
mass, pancreatitis, pancreatic mass)
(cPL), serum progesterone concentration (intact female Thoracic radiography (cardiomegaly, neoplasia)
dog), abdominal ultrasound, and urinalysis with bacterial Computed tomography or magnetic resonance imaging
culture should be obtained to further screen for concurrent (pituitary mass)
illness. Additional tests will be dependent on results of the
initial screening tests (Box 49.9).
Treatment and reversibility of insulin resistance is depen-
dent on the etiology. Insulin resistance is reversible with awaits their pet. However, clients should be assured that the
treatable disorders, for example, sodium levothyroxine treat- devastating effects of human diabetes (e.g., nephropathy,
ment in a diabetic dog with concurrent hypothyroidism or vasculopathy, coronary artery disease) require 10 to 20 years
ovariohysterectomy in an intact female diabetic dog in dies- or longer to occur and therefore are uncommon in diabetic
trus. In contrast, insulin resistance often persists with disor- dogs.
ders that are difficult to treat such as chronic recurring
pancreatitis. In some situations, measures can be taken to Cataracts
prevent insulin resistance, such as avoidance of glucocorti- Cataract formation is the most common and one of the most
coids in diabetic dogs and an ovariohysterectomy at the time important long-term complications of diabetes mellitus in
diabetes mellitus is diagnosed in an intact female dog. the dog. A retrospective cohort study on the development of
cataracts in 132 diabetic dogs referred to a university referral
CHRONIC COMPLICATIONS OF hospital that found cataract formation in 14% of dogs at the
DIABETES MELLITUS time diabetes was diagnosed, and a time interval for 25%,
Complications resulting from diabetes or its treatment are 50%, 75%, and 80% of the study population to develop cata-
common in diabetic dogs and include blindness and anterior racts at 60, 170, 370, and 470 days, respectively (Beam et al.,
uveitis resulting from cataract formation, hypoglycemia, 1999). The pathogenesis of diabetic cataract formation is
chronic pancreatitis, recurring infection, poor glycemic thought to be related to altered osmotic relationships in the
control, and ketoacidosis (see Box 49.5). Many clients are lens induced by the accumulation of sorbitol and galactitol—
hesitant to treat their newly diagnosed diabetic dog because sugar alcohols produced following reduction of glucose and
of knowledge regarding chronic complications experienced galactose by the enzyme aldose reductase in the lens are
in humans with diabetes and concern that a similar fate potent hydrophilic agents, which cause an influx of water