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T O day' S Ve T erinary Prac T ice | September/October 2016 | tvpjournal.com cO n S ider Thi S c a S e Peer r eviewed 98 o verview of Hypoadrenocorticism Pathophysiology The adrenal gland is composed of an outer cortex and the inner medulla: The adrenal medulla, which is not affected in hypoadrenocorticism, secretes catecholamines, such as epinephrine and norepinephrine. Hypoadrenocorticism results from atrophy or destruction of the adrenal cortex, which is subdivided into 3 layers: • The outer layer— zona glomerulosa—is involved with synthesis and secretion of the mineralocorticoid hormone, aldosterone. • The middle layer—zona fasciculata—synthesizes glucocorticoids. • The inner layer—zona reticularis—produces adrenal sex steroids. Primary versus s econdary d isease Hypoadrenocorticism may be classified as primary or secondary 8 : Primary hypoadrenocorticism results from bilateral destruction of the adrenal cortices, presumed in most cases to result from immune-mediated destruction of the adrenal gland. Less common causes of primary hypoadrenocorticism include trauma (eg, surgical versus other), infections (eg, fungal or bacterial), neoplasia, or medical therapy (eg, mitotane, trilostane, ketoconazole, megestrol acetate). s econdary hypoadrenocorticism results from lack of adrenal gland stimulation due to hypothalamic–pituitary–adrenal axis dysfunction, which most commonly results from inflammation, tumors, or trauma. Exogenous steroid administration may also suppress ACTH release, resulting in adrenal atrophy. s ignalment With hypoadrenocorticism, certain breeds of dogs are over-represented, including standard poodles, Great Danes, Rottweilers, West Highland white terriers, Wheaten terriers, Leonbergers, Portuguese water dogs, Labrador retrievers, bearded collies, Old English sheepdogs, and standard schnauzers. Hypoadrenocorticism is also seen more often in young to middle-aged female dogs. 11-18 c linical s igns Pathophysiologic changes seen with hypoadrenocorticism are directly a result of glucocorticoid and mineralocorticoid deficiencies. Common clinical signs typically include lethargy, inappetence, vomiting, diarrhea, bradycardia, hypotension, weight loss, and, rarely, death. 11 c linical Findings Clinicopathologic findings seen with hypoadrenocorticism include the failure to mount a stress leukogram (resulting in eosinophilia, lymphocytosis, and normal overall white blood cell and neutrophil count) and electrolyte abnormalities secondary to direct aldosterone effects (eg, hyperkalemia, hyponatremia, hypochloremia, metabolic acidosis). Other common laboratory abnormalities include azotemia, isosthenuria (from osmotic diuresis secondary to sodium losses), hypoglycemia (due to impaired gluconeogenesis), hypercalcemia (due to altered renal excretion, reduced gastrointestinal absorption, and decreased resorption of calcium from bone), hypoalbuminemia, and hypocholesterolemia. 11,12 t herapeutic a pproach Without treatment, hypoadrenocorticism can be life-threatening due to dehydration, hypovolemia, severe electrolyte derangements, and ongoing fluid losses. To ensure the best outcome, the hypoadrenocorticism state should be rapidly identified. Treatment for the critically ill patient with hypoadrenocorticism should include symptomatic supportive care, aggressive fluid therapy, correction of electrolyte abnormalities and hypoglycemia, antiarrhythmic therapy (if needed), steroid administration, and mineralocorticoid supplementation, if needed. Appropriate use of steroids needs to be weighed so as not to impair diagnostic testing for baseline cortisol levels or for future ACTH stimulation tests.