Other than the medical emergencies related to diabetes mellitus (i.e., diabetic ketoacidosis, nonketotic hyperosmolar diabetic syndrome), there are seven other endocrine disorders of dogs and cats that may present as an emergency. These include hypoglycemia, adrenocortical insufficiency, hyperthyroidism, hypocalcemia, hypercalcemia, pheochromocytoma and hypothyroidism.
Common causes of hypoglycemia include lab error, liver disease, excessive insulin (iatrogenic or endogenous), hypoglycemia of toy breed puppies, and "hunting dog" hypoglycemia. Other potential causes of hypoglycemia are hypoadrenocorticism, glycogen storage diseases, non-insulin secreting neoplasia, pregnancy, sepsis, uremia, starvation and severe polycythemia. Severe hypoglycemia (BG < 45 mg/dl; < 2.5 mmol/L) is most common with insulin-secreting tumors, portosystemic shunts, and in toy breed puppies. The patient's signalment and history will often help distinguish among the different etiologies for hypoglycemia. Signs of hypoglycemia result from either neuroglycopenia or increased adrenergic tone. Clinical signs include seizures, paresis, weakness, collapse, tremors, lethargy, dullness, behavior changes, ataxia, exercise intolerance, decerebrate posture, and coma. While hypoglycemia results from another disorder that usually requires definitive therapy, emergency treatment to correct hypoglycemia is often required. Hypoglycemia is initially treated with the slow IV bolus administration of 1 ml/kg 50% dextrose, given over 5 – 10 minutes. Following bolus loading, a continuous infusion of 2.5-5% dextrose should be administered until the animal can be fed. Refractory seizures may require additional treatment with corticosteroids or anticonvulsants. If hypoglycemia is due to insulinoma, surgical resection of the primary tumor and any metastatic lesions is the treatment of choice. Long-term medical therapy of insulinoma is usually needed, including dietary management and the use of various drugs, such as diazoxide.
Adrenocortical Insufficiency (Hypoadrenocorticism)
Hypoadrenocorticism is an uncommon endocrinopathy typically occurring in young to middle-aged female dogs characterized by deficient mineralocorticoid and/or glucocorticoid secretion. Adrenal insufficiency is due to atrophy or destruction of both adrenal cortices (primary or Addison's disease) or, less commonly, deficient pituitary ACTH production (secondary hypoadrenocorticism).
Acute adrenocortical insufficiency (addisonian crisis) is a medical emergency requiring immediate therapy. Almost all dogs that present as an emergency have the primary form of the disorder (Addison’s disease). The most common signs in these dogs include depression, lethargy, weakness or collapse, anorexia, vomiting, diarrhea, weight loss, and abdominal pain. Lack of aldosterone causes a lack of renal sodium and water retention, as well as impaired potassium excretion. Although the findings of hyperkalemia and hyponatremia (Na/K < 23:1) strongly suggest hypoadrenocorticism, the absolute diagnosis depends on demonstration of absent or minimal adrenocortical response to an IV injection of corticotropin (ACTH). Rapid administration of large volumes of intravenous fluids, preferably 0.9% saline, is the cornerstone of initial therapy. Fluid therapy is initiated at a rate of 40-80 ml/kg/hr for 1-2 hours and then adjusted as needed. Fluids are tapered to a maintenance rate and eventually discontinued over a few days based on the dog’s clinical status, urinary output, and laboratory parameters. Another important part of treatment of the addisonian crisis is the IV administration of a rapid-acting glucocorticoid. Hydrocortisone sodium succinate or phosphate is probably the best initial glucocorticoid preparation because it also possesses mineralocorticoid activity; hydrocortisone is best administered as an IV infusion (0.5 mg/kg/hr) until the dog can be changed to oral supplementation. Alternatively, dexamethasone sodium phosphate (0.1-0.2 mg/kg, IV) or prednisolone sodium succinate (1-2 mg/kg, IV) can be administered. Glucocorticoid therapy is gradually tapered to a maintenance dosage of glucocorticoid administered parenterally until vomiting has ceased; chronic oral glucocorticoid and mineralocorticoid replacement therapy is then initiated.
In cats, severe hyperthyroidism can present as a medical emergency as a result of the associated hypermetabolic state. Clinical signs in affected cats experiencing “thyrotoxic crisis” or “thyroid storm” include severe tachycardia (>240 bpm), open-mouthed breathing, hypoxia, hyperthermia, ventral neck flexion, and a "panic-attack" mental status. These cats may become aggressive and/or hysterical with handling. Less commonly, cats present in fulminate collapse. On cardiac examination, heart murmurs, gallop rhythm, or arrhythmia are frequent. In some cats, severe hypertension or congestive heart failure may be present. All of the signs associated with thyrotoxic crisis are typically manifested as a result of advanced, long-standing hyperthyroidism and are almost always preceded by a history of weight loss despite a good appetite.
In the acute management of the cat in hyperthyroid (thyrotoxic) crisis, one must attempt to minimize the cat’s stress level. Too much handling or restraint (e.g., related to blood collection, catheter placement, or other procedures) may exacerbate catecholamine release and precipitate a fatal cardiac arrhythmia. If the cat is dyspneic, supplemental oxygen and cage rest should be provided. One should never, however, attempt to place an oxygen facemask on a hypoxic cat in thyroid crisis. A beta-blocking agent (i.e., atenolol or propranolol) should be administered orally, and the cat started on oral antithyroid drug treatment (methimazole or carbimazole) as soon as it is possible.
Hypocalcemia can affect multiple organ systems, but the effects on neuromuscular function (e.g., muscle twitching, tetany, seizures) usually predominant. Most conditions associated with hypocalcemia are transient or result in only mild decreases in serum calcium, do not cause obvious clinical signs, and only rarely require any treatment. Of the conditions associated with severe symptomatic hypocalcemia requiring emergency treatment, puerperal tetany (eclampsia) in lactating bitches is the most common. Hypoparathyroidism, the other major cause of symptomatic hypocalcemia, is generally characterized by parathyroid hormone (PTH) deficiency. Unlike puerperal tetany, in which only acute calcium infusion is generally required, both acute and chronic treatment with vitamin D, as well as calcium, is necessary in hypoparathyroidism.
Hypocalcemic tetany is treated with the slow IV administration of calcium at a dose of 5 -15 mg of elemental calcium/kg (0.5-1.5 ml/kg of 10% calcium gluconate) over 15 minutes. Parenteral calcium gluconate is then given at 60-90 mg of elemental calcium/kg/day, adjusted to maintain serum calcium values of 8-9 mg/dl (2-2.25 nmol/L), and oral calcium and vitamin D is initiated as soon as possible.
Oral calcium is administered at the dosage of 25-50 mg/kg/day of elemental calcium. Calcium carbonate is the preferred calcium salt because it contains the highest percent of elemental calcium (40%). Of the vitamin D preparations, calcitiol is generally recommended because it has the most rapid onset of action and shortest biologic half-life. Calcitriol is given at a loading dose of 20-30 ng/kg/day (divided) for 3 to 4 days, then decreased to a maintenance dose of 5 to 15 ng/kg/day until further adjustments are indicated based on monitoring of serum calcium.
Hypercalcemia is an uncommon but important electrolyte disorder, which can deleteriously effect cellular function and result in significant gastrointestinal, cardiovascular, neurological, and renal dysfunction. Clinical signs are most severe when hypercalcemia develops rapidly, whereas animals that develop severe hypercalcemia gradually may have only minimal signs. Therefore, the clinical condition of the animal ultimately dictates how aggressive treatment needs to be, but serum calcium values > 16 mg/dl (> 4 nmol/L) generally deserved emergency treatment. Signs of hypercalcemia include polydispsia, polyuria, anorexia, vomiting, constipation, lethargy, weakness, seizures, stupor, and coma. Causes of hypercalcemia include neoplasia, hypoadrenocorticism, renal failure, primary hyperparathyroidism, and vitamin D toxicosis.
Acute treatment of hypercalcemia involves a combination of therapeutic interventions depending on the severity of the hypercalcemia and the patient's status. Volume expansion with 0.9% saline (100-125 ml/kg/day, IV) should be provided to promote calcium excretion into the urine. In addition, furosemide (2-4 mg/kg, q 8-12 hrs) is indicated to promote renal excretion of calcium. Infusion of sodium bicarbonate (1mEq/kg, IV as a slow bolus; up to 4 mEq/kg total dose) reduces ionized calcium concentrations and may be helpful in crisis management along with other treatments. Corticosteroids can be useful but should not be administered until a diagnosis of lymphoma has been excluded. Other agents available for treatment of hypercalcemia include calcitonin, bisphosphonates, and mithramycin. The underlying cause must also be treated, if possible.
Pheochromocytoma is a rare tumor of the adrenal medulla in dogs and cats, most commonly identified as an incidental finding on ultrasound examination of the abdomen or at necropsy. These tumors may be benign or malignant, but are often invasive. Clinical signs, when present, result from oversecretion of catecholamines (e.g., norepinephrine, epinephrine). Signs often vague and may wax and wane. Hypertension is present in about half of animals tested. Collapse and death from sudden catecholamine release and resultant hypertension can occur. Tumor embolism or hemorrhage from invasion of tumor into a major vessel (e.g., vena cava) may also develop.
The treatment of choice is surgical removal of the adrenal tumor, after a 2-3 week period of medical therapy to reverse the effects of catecholamine excess. Alpha-adrenergic blockade (phenoxybenzamine, 0.2-1.5 mg/kg, BID, to effect) should be utilized to control hypertension prior to surgery. Beta blockade to control arrhythmias or tachycardia (propanolol, 0.15-0.5 mg/kg, TID) is also indicated but should never be attempted without concurrent alpha-blockade.
Myxedema coma is a rare, life-threatening presentation of chronic, advanced hypothyroidism in the dog. In addition to the classical signs of hypothyroidism, severe mental dullness progressing to stupor and coma, hypothermia, bradycardia, hypotension, hypoventilation, and myxedema may be present. If this condition is suspected, treatment should be instituted immediately, even prior to documenting subnormal thyroid hormone concentrations.
Treatment consists of thyroid hormone supplementation and supportive care. Due to unpredictable absorption of agents from the gastrointestinal tract, IV administration of thyroid hormone is recommended (levothyroxine, 22 ug/kg/day) until oral administration can be instituted. In addition, supportive care is extremely important in these dogs and includes fluid therapy for circulatory support, passive, slow rewarming, and correction of hypoglycemia.
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