Page 836 - Small Animal Internal Medicine, 6th Edition

808 PART VI Endocrine Disorders

puppy or kitten is usually caused by idiopathic hypoglycemia,
starvation, congenital portosystemic shunt, or sepsis. In BOX 49.3
VetBooks.ir young adult dogs or cats hypoglycemia is usually caused by Medical Therapy for Acute Hypoglycemic Seizures
hepatobiliary disease, portosystemic shunt, hypoadrenocor-
ticism, or sepsis. In older dogs or cats, hepatobiliary disease,
β-cell neoplasia, extrapancreatic neoplasia, hypoadrenocor- Seizures at Home
Step 1. Apply sugar solution to pet’s gums.
ticism, and sepsis are the most common causes. Step 2. Once pet is sternal, feed a small meal.
Hypoglycemia tends to be mild (>45 mg/dL) and is often Step 3. Call the veterinarian.
an incidental finding in dogs and cats with hypoadrenocor-
ticism or liver insufficiency. Additional clinical pathologic Seizures in Hospital
alterations are usually present (e.g., hyponatremia and hyper- Step 1. Administer 1 to 5 mL (depending on dog size) of
kalemia in animals with hypoadrenocorticism or increased 50% dextrose (diluted) IV slowly over 1 to 2 minutes
alanine aminotransferase [ALT] activity, hypocholesterol- followed by continuous infusion of 5% dextrose in
water (i.e., D5W).
emia, hypoalbuminemia, low blood urea nitrogen [BUN] Step 2. Once animal is sternal, feed a small meal.
concentration in animals with hepatobiliary disease). A Step 3. Initiate long-term medical therapy if necessary
baseline serum cortisol concentration, adrenocorticotropic (see Box 49.14).
hormone (ACTH) stimulation test or liver function test (i.e.,
preprandial and postprandial bile acids) may be required to Intractable Seizures in Hospital
confirm the diagnosis. Severe hypoglycemia (<40 mg/dL) Step 1. Administer 2.5% to 5% dextrose in water
may develop in neonates and juvenile kittens and puppies intravenously at 1.5 to 2 times maintenance fluid rate.
(especially toy breeds) and in animals with sepsis, β-cell neo- Step 2. Add 0.5 to 1 mg of dexamethasone/kg to IV
plasia, and extrapancreatic neoplasia, most notably hepatic fluids and administer over 6 hours; repeat every 12 to
adenocarcinoma and leiomyosarcoma. Sepsis is readily 24 hours, as necessary.
identified on the basis of physical examination findings and Step 3. If previous step fails, administer IV glucagon USP
(Eli Lilly) by constant-rate infusion at an initial dosage
abnormal CBC findings, such as a neutrophilic leukocytosis of 5 to 10 ng/kg/min.
(typically > 30,000/µL), a shift toward immaturity, and signs Step 4. If preceding steps fail, control seizure activity
of toxicity. Extrapancreatic neoplasia can usually be identi- with diazepam or phenobarbital until medical
fied on the basis of the physical examination, abdominal or treatment becomes effective in controlling
thoracic radiography, and findings on abdominal ultraso- hypoglycemia.
nography. Dogs with β-cell neoplasia typically have normal
physical examination findings with no abnormalities other IV, Intravenous.
than hypoglycemia identified on routine blood and urine
tests. Measurement of baseline serum insulin concentration
when the blood glucose is less than 60 mg/dL (preferably < patients with diabetes may become a viable option for treat-
50 mg/dL) is necessary to confirm the diagnosis of a β-cell ing severe hypoglycemia in diabetic dogs and cats (Zeug-
tumor. swetter et al., 2012). If collapse, seizures, or coma develops
in the hospital, a blood sample should be obtained to measure
Treatment the glucose concentration before reversing the signs with IV
Whenever possible, therapy should be directed at eliminat- administration of 50% dextrose, diluted, followed by con-
ing the underlying cause of the hypoglycemia. If the disorder tinuous IV infusion of 5% dextrose. Dextrose should be
cannot be eliminated and the clinical signs of hypoglycemia administered in small amounts slowly (1-5 mL aliquots)
persist, long-term symptomatic therapy designed to increase rather than in large boluses rapidly. This is especially impor-
the blood glucose concentration may be necessary to mini- tant in dogs with suspected β-cell neoplasia, in which aggres-
mize clinical signs (see p. 850). Such therapy is usually sive glucose administration can result in severe hypoglycemia
required for animals with metastatic β-cell or extrapancre- after excessive insulin secretion by the tumor in response to
atic neoplasia. glucose. Dogs and cats with hypoglycemia usually respond
Symptomatic therapy for animals with severe hypo- to glucose administration within 2 minutes. Recurrence of
glycemia of acute onset relies on the administration of hypoglycemia is dependent on the ability to correct the
glucose (Box 49.3). If the dog or cat is having a hypoglycemic underlying cause.
seizure at home, the client should rub a sugar solution on Occasionally, a dog or cat with severe central nervous
the pet’s buccal mucosa. Most animals respond within 1 to system signs (e.g., blindness, coma) does not respond to
2 minutes. Clients should be instructed never to place fingers initial glucose therapy. Irreversible cerebral lesions may
into, or pour the sugar solution down, the pet’s mouth. Once result from prolonged severe hypoglycemia and the resultant
the dog or cat is sternal and cognizant of its surroundings, it cerebral hypoxia. The prognosis in these animals is guarded
should be fed a small meal and brought to the veterinarian. to poor. Therapy is directed at providing a continuous supply
Although clinical trials are needed, at-home glucagon emer- of glucose by administering a 2.5% to 5% solution intrave-
gency kits used to treat severe hypoglycemia in human nously or by increasing hepatic gluconeogenesis with a