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Hypoadrenocorticism in dogs | VETgirl Veterinary Continuing Education Videos

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In this VETgirl online veterinary continuing education video, we discuss how to recognize and treat hypoadrenocorticism, commonly called Addison’s disease. This is a 4-year-old, male neutered Labrador/Pit bull mixed breed dog, who presented for lethargy and vomiting. The dog had ingested some foam from a bed a week earlier, and subsequently became lethargic, nauseous and anorexic. Several days after ingestion, he presented to the emergency clinic for inability to walk. On presentation, the dog was mild bradycardiac (e.g., 70 bpm) with red injected mucous membranes. The dog was clinically 7-9% dehydrated, and had a non-painful abdomen on palpation. Inital diagnostics included abdominal radiographs and blood work. Radiographs did not show any obstruction; foreign material was seen within the colon. A CBC, biochemistry panel and baseline cortisol were performed next. Although one may treat symptomatically for gastroenteritis and hyperdynamic shock at this point, this case demonstrates the importance of checking blood work. In this patient, a mild azotemia was seen, along with hemoconcentration, hyperkalemia and hyponatremia (with a Na:K ratio of < 27:1). A baseline cortisol level was < 0.5 mcg/dL, consistent with hypoadrenocorticism. Due to concern regarding the low baseline cortisol, a complete adrenocorticotropin hormone (ACTH) stimulation test was submitted. Both pre-ACTH (< 0.5 mcg/dL) and post-ACTH (< 2 mcg/dL) stimulation test results were consistent with hypoadrenocorticism.

Hypoadrenocorticism results from the insufficient secretion of glucocorticoids and/or mineralocorticoids from the adrenal glands. Atypical Addison’s results from only insufficient secretion of glucocorticoids. Common clinical signs typically include lethargy, inappetence, vomiting, diarrhea, bradycardia, hypotension, weight loss, and, rarely, death. Treatment for the hypoadrenocorticism patient should include aggressive fluid therapy, correction of electrolyte abnormalities (with calcium gluconate, insulin/glucose, or sodium bicarbonate), correction of hypoglycemia (e.g., dextrose), symptomatic supportive care, steroid administration, antiarrhythmic therapy (if needed), 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. With adequate management and treatment, the prognosis for dogs with hypoadrenocorticism is good to excellent. This dog was treated with several liters of IV crystalloids, dexamethasone, maropitant, and pantoprazole, and gradually improved within 12 hours. Intramuscular desoxycorticosterone pivalate (DOCP) was also started once the patient was stable. The patient was discharged the following day on a daily physiologic dose of oral prednisone, and and instructed to continue electrolyte monitoring and follow up (including DOCP approximately every 25 days) at the referring veterinarian. 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.

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