Hypoadrenocorticism in dogs

Hypoadrenocorticism is a condition where there is decreased secretion of adrenocorticotropic hormone. In dogs, it's typically suffered by middle-aged female dogs. In some cases, this is a chronic deficiency for which there is no treatment, in others mineralocorticoid and glucocorticoid therapy is initiated. The causes for hypoadrenocorticism are usually idiopathic, but to some extent it is regarded as an autoimmune disease.

Etiology

Primary

Primary adrenocortical insufficiency is the more common form of hypoadrenocorticism. It involves a deficiency of both mineralocorticoid and glucocorticoid secretion. Most cases are classified as idiopathic, although immune-mediated adrenocortical destruction is a likely cause. Bilateral destruction of the adrenal cortex by neoplasia (e.g. lymphosarcoma), granulomatous disease, or arterial thrombosis can also cause primary adrenocortical insufficiency. The destruction is progressive, although variable in rate, ultimately leading to complete loss of adrenocorotical function. A partial deficiency syndrome may occur initially, with signs manifested only during times of stress (e.g., boarding, travel, surgery).

Secondary

Secondary adrenocortical insufficiency involves only a deficiency of glucocorticoid secretion. Destructive lesions (e.g. neoplasia, inflammation) in the pituitary gland or hypothalamus and chronic administration of exogenous glucocorticoids or megestrol acetate (cats) are the most common causes.^[1]

Clinical Features

Hypoadrenocorticism is typically a disease of young to middle-aged (mean, 4 years; range, 2 months to 12 years) female dogs. No significant breed predilection exists, although genetics probably play a role in Standard Poodles and Portuguese Water Spaniels. The disease is rare in cats. There exists no apparent gender predisposition in cats, but young to middle-aged cats (average, 6 years) are most often affected.

Clinical Signs and Physical Findings

The most common clinical manifestations are related to mental status and gastrointestinal function; they include lethargy, anorexia, vomiting, weight loss, and weakness. Additional findings may include dehydration, bradycardia, weak femoral pulses, and abdominal pain. Polyuria and polydipsia, diarrhea, and shivering are occasionally reported.

Addisonian crisis

If hyponatremia (low sodium) and hyperkalemia (high potassium) are severe, the resulting hypovolemia, prerenal azotemia, and cardiac arrhythmias may result in an Addisonian crisis. In severe cases, the patient may be presented in shock and moribund. Addisonian crisis must be differentiated from other life-threatening disorders such as diabetic ketoacidosis, necrotizing pancreatitis, and septic peritonitis.^[2]

Diagnosis

Hypoadrenocorticism is often tentatively diagnosed on the basis of history, physical findings, clinical pathology, and, for primary adrenal insufficiency, characteristic electrolyte abnormalities.

• Clinical Pathology - Abnormalities that may be identified on CBC, MBA, UA. Hyperkalemia, hyponatremia, and hypochloremia are the classic electrolyte alterations. The sodium/potassium ratio often is <27 (normal is between 27:1 and 40:1)and maybe <20 in animals with primary adrenal insufficiency.
• ECG - The severity of the ECG abnormalities correlates with the severity of the hyperkalemia. Therefore the ECG can be used to identify and estimate the severity of hyperkalemia and to monitor changes in serum potassium during therapy.
• Diagnostic imaging - Abdominal ultrasound may reveal small adrenal glands, suggesting adrenocortical atrophy. However, finding normal-sized adrenal glands does not rule out hypoadrenocorticism. Rarely, megaesophagus is evident on radiographs.
• ACTH Stimulation Test - Confirmation requires evaluation of an ACTH stimulation test. Basline plasma cortisol and urine cortisol/Cr ratios are unreliable for confirming the diagnosis. One major diagnostic criterion is abnormally decreased post-ACTH plasma cortisol. Normal plasma cortisol after ACTH stimulation rules out adrenal insufficiency.

The ACTH stimulation test does not distinguish between primary adrenal insufficiency and secondary insufficiency or adrenocortical destruction caused by mitotane overdose. Differentiation between primary and secondary adrenal insufficiency can be made by periodically measuring serum electrolytes, baseline endogenous ACTH, or possibly serum or plasma aldosterone during the ACTH stimulation test.

Treatment

Aggressiveness of therapy depends on the clinical status of the patient and the nature of the insufficiency (glucocorticoid, mineralocorticoid, or both). Many dogs and cats with primary adrenal insufficiency are presented in Addisonian crisis and require immediate, aggressive therapy. In contrast, secondary insufficiency often has a chronic course.

Addisonian crisis

Treatment is directed towards (1) correcting hypotension, hypovolemia, electrolyte imbalances, and metabolic acidosis; (2) improving vascular integrity, and (3) providing an immediate source of glucocorticoids. Rapid correction of hypovolemia is the first priority.

Most patients show dramatic improvement within 24 to 48 hours of appropriate fluid and glucocorticoid therapy. Over the ensuing 2 to 4 days, a gradual transition from IV fluids to oral water and food is undertaken, and maintenance mineralocorticoid and glucocorticoid therapy is initiated. Failure to make this transition smoothly should raise suspicion of insufficient glucocorticoid supplementation, concurrent endocrinopathy (e.g. hypothyroidism), or cocurrent illness (especially renal damage).

References