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Endocrine
Emergencies. Part I.
FOCAL POINT Endocrine Pancreatic
★Diabetic ketoacidosis is a
common emergency in small
animal practice.
Disorders
KEY FACTS Colorado State University
Deborah S. Greco, DVM, PhD
■ In diabetic ketoacidosis, serum
potassium is usually elevated but
Administration rate:
Deficit (ml) = Dehydration (%) × body weight (kg) 2 ml/kg/hr × hours required to rehydrate (24 hours)
× 1000 ml
■ Estimate losses (vomiting, diarrhea)
Fluid composition:
Phosphorus
1–2 mg/dl 0.03 mmol/kg/hr Monitor serum phosphorus
every 6 hr
cated by hypomagnesemia. The article by Dr. Macintire Approximately one third of ketoacidotic diabetic cats
on disorders of potassium, phosphorus, and magnesium are presented in recumbency and with a serum osmolal-
in this issue of Compendium provides guidelines for the ity in the range of 388 mOsm/L; this may be a mani-
supplementation of serum potassium and other elec- festation of mixed hyperosmolar syndrome.5
trolytes in patients with diabetic ketoacidosis. Treatment of hyperosmolar coma is difficult. Several
Serum and tissue phosphorus may also be depleted guidelines, which differ from the treatment of diabetic
during a ketoacidotic crisis, and some of the potassium ketoacidosis, should be followed. First, fluid therapy
supplementation (one third of the potassium dose) may should be approached cautiously by estimating the flu-
consist of potassium phosphate—particularly for small id needs (dehydration deficit) and replacing 80% of the
dogs and cats, which are most susceptible to hemolysis deficit over a 12- to 24-hour period.5 Isotonic, rather
caused by hypophosphatemia.5,6 Oversupplementation than hypotonic, solutions should be used. Hyper-
of phosphorus can result in metastatic calcification and glycemia should also be reversed very slowly. A lower
hypocalcemia. Cats with diabetic ketoacidosis may also dosage of insulin (1.1 U/kg over 24 hours) is recom-
have a mild increase in mean cell volume because hy- mended for hyperosmolar animals, and insulin therapy
pophosphatemia causes erythrocytes to swell.6 should be delayed until 2 to 4 hours after fluid therapy
Another cause of hemolysis in cats with diabetic begins.5
ketoacidosis is Heinz-body anemia.7 Although Heinz-
body anemia usually does not result in overt hemolysis HYPOGLYCEMIC SEIZURES
by itself, it probably shortens the erythrocyte life span. Causes of hypoglycemia include iatrogenic insulin
When coupled with low phosphorus levels, it may pre- overdose, insulinoma, sepsis, large tumors, hunting dog
cipitate a hemolytic crisis.6 and puppy hypoglycemia, hypoadrenocorticism, por-
The first three steps in the treatment of diabetic ke- tosystemic shunts, hypothyroidism, growth hormone
toacidosis usually correct serum acid–base status. How- deficiency, and (rarely) starvation.8–14 Insulin overdose,
ever, some patients with blood pH under 7.1 or serum hypoadrenocorticism, and insulinoma are the most
bicarbonate below 12 mEq/L need bicarbonate therapy common endocrine disorders that result in hypo-
(see the protocol).5 Caution is recommended because glycemia.
metabolic alkalosis may be difficult to reverse. Treatment should consist of administration of a
slow intravenous bolus of 50% dextrose (0.5 g/kg di-
HYPEROSMOLAR COMA luted 1:4). If no vein is readily accessible, corn syrup
In humans, nonketotic hyperosmolar diabetes is defined or pancake syrup may be applied to the oral mucous
as extreme hyperglycemia (serum glucose >600 mg/dl), membranes with a large syringe. Thereafter, animals
hyperosmolality (>350 mOsm/L), severe dehydration, with hypoglycemia of any cause should be given a
central nervous system depression, and a paucity of ke- continuous infusion of 5% dextrose until they can be
tones or metabolic acidosis.5 Hyperosmolar nonketotic fed.
syndrome in dogs and cats is an unusual syndrome Veterinarians should avoid the temptation to restore
characterized by neurologic and gastrointestinal abnor- blood glucose concentrations to the normal range in
malities (e.g., progressive weakness, anorexia, vomiting, dogs with insulinoma. Administration of higher and
and lethargy). These signs are usually preceded by the higher doses of 50% dextrose in an attempt to restore
classic signs of uncomplicated diabetes mellitus: poly- euglycemia may result in a cycle of rebound hypo-
dipsia, polyuria, weight loss, and polyphagia. glycemia by provoking insulin secretion. The goal of
Physical examination reveals severe dehydration, hy- intravenous glucose therapy is to stop the seizure rather
pothermia, extreme depression, lethargy, and coma.5 than to normalize blood glucose.
Your comprehensive
Long-term management of hypoglycemia depends on
guide to diagnostic the cause. The veterinarian must therefore use appro-
priate diagnostics to identify the cause of the hypo-
ultrasonography glycemia.
The immediate therapy for hypoglycemia resulting
Nautrup and Tobias from insulin overdose is the same as for other causes of
hypoglycemia. However, endogenous glucose stores
may have been depleted by the insulin overdose; it may
take several days for hyperglycemia to recur.5 In these
cases, insulin therapy should be discontinued until hy-
perglycemia recurs. Insulin overdose in animals may
lead to cerebral edema and temporary blindness or be-
havior changes. These signs are often temporary and re-
solve after several weeks or months.
$
149 REFERENCES
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400 pages, hard cover tin Educ Pract Vet 2(6):456-463, 1980.
3. Schaer M: Insulin treatment for the diabetic dog and cat.
1597 illustrations Compend Contin Educ Pract Vet 5(7):579–590, 1983.
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■ Echocardiography, abdominal and pelvic 6. Nichols R, Crenshaw KL: Complications and concurrent
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forms of diabetes mellitus. Vet Clin North Am Small Anim
Pract 25(3):617–624, 1995.
■ Case illustrations using conventional 7. Christopher MM: Hematologic complications of diabetes
radiography, computed microfocal mellitus. Vet Clin North Am Small Anim Pract 25(3):
625–638, 1995.
tomography, specimen photography, 8. Rogers KS: Hyperinsulinism. Compend Contin Educ Pract
and line drawings Vet 7(10):829–841, 1985.
9. Atkins CE: Disorders of glucose homeostasis in neonatal and
■ Recognition of the disease process and juvenile dogs: Hypoglycemia—Part I. Compend Contin Educ
Pract Vet 6(3):197–208, 1984.
courses of treatment 10. Atkins CE: Disorders of glucose homeostasis in neonatal and
juvenile dogs: Hypoglycemia—Part II. Compend Contin
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11. Breitschwerdt EB, Loar AS, Hribernik TN, McGrath RK:
CALL OR FAX TODAY TO ORDER Hypoglycemia in four dogs with sepsis. JAVMA 178:
1072–1076, 1981.
800-426-9119 • Fax: 800-556-3288 12. Leifer CE, Peterson ME, Matus RE, Patnaik AK: Hypo-
glycemia associated with nonislet cell tumor in 13 dogs.
Price valid only in the US, Canada, Mexico, and
JAVMA 186:53–55, 1985.
the Caribbean. Request international pricing.
Email: books.vls@medimedia.com
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drate metabolism and laboratory evaluation. Compend Con- aspects. Compend Contin Educ Pract Vet 6(2):115–125,
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