WARD 6: WHAT YOU MUST KNOW ABOUT HYPOADRENOCORTICISM (ADDISONS DISEASE) Overview Uncommon (perhaps 1 dog in 2,000) 95% of cases are primary and thought to be caused by immune-mediated destruction of the
adrenal glands; uncommonly primary hypoadrenocorticism can be due to or destruction of the
adrenals by op-DDD. Almost all dogs with primary hypoadrenocorticism require supplementation
with both glucocorticoids and mineralocorticoids. 5% of cases are secondary and due to pituitary disease or iatrogenic administration of
corticosteroids (may need to wait 2 weeks to 2 months to assess adrenal function after
discontinuing steroids). Dogs with secondary hypoadrenocorticism usually do not require
mineralocorticoid supplementation. Key to diagnosing this disease is maintaining a high index of suspicion for it Signalment Young to middle aged dogs (usually 4 to 5 years of age) 70% are female Any breed including mixed breeds Some breeds (Standard poodle, Portuguese water dog, Bearded collie, Labrador retriever) may
have a genetic predisposition Rare in cats History and Physical Common signs o Lethargy o Poor appetite or anorexia o Vomiting o Weakness o Weight loss o Dehydration o Waxing and waning course of illness o Diarrhea o Previous history of response to fluids or corticosteroids o Cardiovascular collapse (shock) Less common signs o PU/PD o GI ulceration and melena Routine lab work and radiology CBC o Mild nonregenerative anemia (may be masked by dehydration) o Absolute eosinophilia (20%) and lymphocytosis (10%) are not common but absence of
eosinopenia and lymphopenia in a severely stressed animal should raise suspicion Profile o Hyperkalemia o Low Na:K ratio (< 27) o Hyponatremia o Azotemia o Hyperphosphatemia o Hypochloremia o Hypercalcemia o Metabolic acidosis o Less common: increased liver enzymes, hypoglycemia Urinalysis o USG commonly is low (isosthenuric range or slightly above) despite no intrinsic renal
disease (due to medullary washout of solute). May result in mis-diagnosis of acute renal
failure Hypoadrenocorticism with normal electrolytes (< 5% of cases) o Requires high index of suspicion to recognize o May be due to secondary hypoadrenocorticism (pituitary disease) o May have primary glucocorticoid-dependent hypoadrenocorticism (many of these animals
develop electrolyte abnormalities over the next several weeks or months) o In dogs with glucocorticoid-dependent hypoadrenocorticism, a blunted response of plasma
aldosterone to ACTH stimulation may predict future need for mineralocorticoid
supplementation Thoracic radiographs o Microcardia (due to volume depletion) o Megaesophagus (rare) Electrocardiographic findings o Caused by hyperkalemia: Absent P waves, slow heart rate, prolonged QRS, decreased
amplitude R wave, increased amplitude T wave o Eventually, sinoventricular rhythm and ultimately asystole or ventricular fibrillation Abdominal ultrasound o Not necessary for evaluation o Adrenals are smaller than normal (but some overlap with normal) ACTH stimulation test is the gold standard for diagnosis: DO NOT NEGLECT THIS TEST! o Dogs with hypoadrenocorticism (primary and secondary) have pre- and post-ACTH
cortisol concentrations < 2.0 ug/dl o Dogs with primary hypoadrenocorticism typically have pre- and post-ACTH cortisol
concentrations < 1.0 _g/dL Plasma ACTH concentrations: Primarily of academic interest o Very high in dogs with primary hypoadrenocorticism o Low in dogs with secondary hypoadrenocorticism or iatrogenic corticosteroid exposure Treatment Correct hypovolemia (place IV catheter and start 0.9% NaCl at 40-80 ml/kg/hr) Start ACTH stimulation test! Treat hyperkalemia as necessary (NaHCO 3 recommended as initial treatment) Give corticosteroids (prednisolone sodium succinate if ACTH stimulation test completed;
dexamethasone if ACTH stimulation test in progress) Longterm management (Fludrocortisone OR DOCP) o Fludrocortisone (10-30 _g/kg/day)