Hyperadrenocorticism offers obstacles in diagnosis, treatment - DVM
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Hyperadrenocorticism offers obstacles in diagnosis, treatment


DVM Best Practices


Treatment Dogs that have pituitary-dependent hyperadrenocorticism, inoperable adrenocortical tumors or metastatic disease, or have owners who will not allow adrenal tumor removal often respond to medical treatment with mitotane, starting initially at a minimum dosage of 50 mg/kg per day orally for seven to 10 days, perform the ACTH stimulation test, and then start the dog on a maintenance dose of mitotane if the ACTH stimulation test results are decreased (<5 mg/dl). The daily loading dose of mitotane is continued until the ACTH stimulation test results done every seven to 10 days are decreased. Mitotane is usually successful in controlling the clinical signs and, in some cases, may also result in adrenal tumor shrinkage. The effectiveness of mitotane therapy is best monitored using recurrence of previous clinical signs and the ACTH stimulation test. Other therapeutic approaches may be tried for the treatment and control of adrenal-dependent hyperadrenocorticism, but unfortunately they just do not work as well as mitotane therapy.

Successful treatment of adrenocortical tumors involves surgical removal of the adrenal mass (tumor) or use of medical therapy with mitotane. Adrenalectomy should be reserved for those dogs without extensive tumor invasion of local structures or evidence of metastasis. The surgical approach may be done by way of a midline or paracostal approach. The midline approach allows good visualization of both adrenal glands and other abdominal structures; however, the paracostal approach allows better exposure of the affected adrenal gland, less hemorrhage involved, and avoids the risk associated with poor healing of a midline incision. After unilateral adrenalectomy, normal adrenal gland tissue is atrophic and, therefore, supplemental glucocorticoid and sometimes mineralocorticoid therapy is necessary during the perioperative and postoperative period. The glucocorticoid support could include the addition of a rapid acting glucocorticoid in the intravenous fluids that is administered over six hours as soon as the adrenocortical tumor is identified. The mineralocorticoid support may include fludrocortisone or deoxycorticosterone pivalate administered 12 to 24 hours before surgery. Blood pressure, serum electrolyte concentrations, and blood glucose levels should be monitored before, during, and after surgery. After surgery, parenteral glucocorticoids could be continued for 48 to 72 hours or until the dog is bright, alert, and eating. Oral supplementation with prednisone can then replace the parenteral therapy. Supplementation with mineralocorticoids if administered initially should be discontinued after two doses and the dog monitored for the development of hyperkalemia or hyponatremia. The prognosis for those dogs without metastatic disease that survive the initial postoperative period is excellent.

Prognosis The long-term prognosis is always guarded in affected dogs because of the many complications associated with mitotane therapy or adrenal surgery. Frequent complications from hyperadrenocorticism in older dogs are mitotane toxicosis; poor wound healing; pulmonary thromboembolism; infection; hypertension; diabetes mellitus; pancreatitis; progressive heart, liver, and/or kidney failure; and metastatic disease. The ACTH stimulation tests should be done every three to six months to assess adrenal gland function throughout mitotane therapy, as well as the dog should be re-evaluated on how it is doing at home - attitude, appetite, weight loss/gain, and other observations.

Summary Hyperadrenocorticism may be caused by the presence of an adrenocortical tumor or from excessive production of adrenocorticotropic hormone from the pituitary gland that results in bilateral adrenal gland hyperplasia. Exogenous administration of glucocorticoids may also result in clinical signs of hyperadrenocorticism. Dogs that have pituitary-dependent hyperadrenocorticism, adrenocortical tumors or metastatic disease, or have owners who will not allow adrenal tumor removal often respond to medical treatment with mitotane. Successful treatment of adrenocortical tumors involves surgical removal of the adrenal mass (tumor) or use of medical therapy with mitotane. The long-term prognosis is always guarded in affected dogs because of the many complications associated with mitotane therapy or adrenal surgery.

Suggested Reading

  • Behrend EN, Kemppainen RJ, Clark TP, et al: Diagnosis of hyperadrenocorticism in dogs: a survey of internists and dermatologists. JAVMA 220:1643, 2002.
  • Feldman EC, Feldman MS, Nelson RW: Use of low- and high-dose dexamethasone suppression tests for distinguishing pituitary-dependent from adrenal tumor hyperadrenocorticism in dogs. JAVMA 209:772, 1996.
  • Ristic JME, Ramsey IK, Heath FM, et al: The use of 17-hydroxyprogesterone in the diagnosis of canine hyperadrenocorticism. J Vet Intern Med 16:433, 2002.


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Source: DVM Best Practices,
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