Diagnosis of primary hypoadrenocorticism is based on clinical signs, expected electrolyte disturbances, and confirmation with
an ACTH stimulation test. The technique used for performing the ACTH stimulation test includes:
1) baseline cortisol sample should be collected with the initial blood work and synthetic ACTH should be administered intravenously
during the initial fluid therapy, and
2) one hour after ACTH administration, a second cortisol sample is collected and a glucocorticoid is then administered in
the suspected dog with hypoadrenocorticism. Intramuscular injection of synthetic or gel ACTH may not be absorbed in dogs in
circulatory shock; thus, intravenous administration of synthetic ACTH is preferred. If glucocorticoids must be administered
before cortisol is measured, dexamethasone sodium phosphate is used, because dexamethasone will not interfere with the cortisol
assay used in the diagnostic laboratory. Endogenous plasma ACTH may be measured to determine if the hypoadrenocorticism is
primary or secondary. This specimen must be collected in an EDTA tube, spun within one hour of sampling, and stored in a plastic
container before corticosteroids are administered.
Image 6 and 7.
Dogs with primary hypoadrenocorticism will exhibit a subnormal response to ACTH administration. The baseline cortisol concentration
is usually low or undetectable and the post-ACTH cortisol concentration is also low or undetectable. Endogenous plasma ACTH
concentrations are dramatically increased in animals with primary hypoadrenocorticism as a result of loss of negative feedback
to the pituitary gland caused by decreased serum cortisol concentrations. In the case of secondary hypoadrenocorticism, which
is caused by a pituitary deficiency of ACTH, the endogenous ACTH concentrations are usually decreased (<20 pg/ml). The response
to exogenous ACTH is diminished, but not as dramatically as for primary hypoadrenocorticism. Baseline cortisol and post-ACTH
cortisol concentrations may be in the normal range.
Treatment of the Addisonian crisis includes: 1) fluid therapy for electrolyte stabilization, 2) glucocorticoid replacement
therapy, 3) treatment of gastrointestinal disease, and 4) mineralocorticoid replacement therapy.
Normal saline solution without potassium supplementation is the preferred fluid solution for the hypoadrenal crises. Treatment
of hyperkalemia can be achieved using fluid therapy alone. If hyperkalemia is life-threatening, intravenous administration
of calcium chloride or calcium gluconate may be used to counteract the adverse effects of potassium on the heart. Glucocorticoid
and mineralocorticoid therapy must be initiated after diagnostic tests for hypoadrenocorticism have been performed. Glucocorticoid
therapy, using ultra-short acting corticosteroids such as dexamethasone sodium phosphate and prednisolone sodium succinate,
is indicated. Dexamethasone may be preferred in some dogs that require immediate glucocorticoid administration, as it will
not interfere with the cortisol assay; in addition, a single dose of short-acting corticosteroid will not suppress the hypothalamic
pituitary adrenal axis.
Long-term therapy of primary hypoadrenocorticism involves the use of mineralocorticoid supplementation as oral fludrocortisone
(0.1 mg per 10 lb orally every 24 hours) or injectable deoxycorticosterone pivalate (2 mg/kg every 21-30 days). Electrolytes
should be monitored once weekly until the dog is stable on replacement therapy. Most dogs with secondary hypoadrenocorticism
and those supplemented with deoxycorticosterone pivalate require a low dose of glucocorticoids (0.2 mg/kg orally every 24
hours). About 50 percent of Addisonian cases supplemented with fludrocortisone require glucocorticoid supplementation.