EMERGENCY TREATMENT

The clinical presentation for hypoadrenocorticism can vary from mild, vague clinical signs to severe critical illness. For dogs that present with mild clinical signs, maintenance therapy may be initiated immediately. Dogs that present in crisis will require more aggressive initial management.

Table 4: Emergency Treatment of Critically Ill Dogs with Hypoadrenocorticism*

With these objectives in mind, place an intravenous catheter, and administer intravenous fluids, typically 0.9% sodium chloride solution. Many patients will require aggressive fluid resuscitation to correct hypovolemia, and their fluid requirements will fluctuate over the first few days of therapy.² Tailor the amount of intravenous fluid administered to the patient's specific needs based on the evaluation of physiologic end points such as heart rate, blood pressure, central venous pressure, and mental status. For dogs with life-threatening cardiac arrhythmias secondary to hyperkalemia, initiate immediate treatment (see "Treat hyperkalemia").

Replace glucocorticoids

It is essential that glucocorticoids are administered with an intravenous injection of dexamethasone sodium phosphate, prednisolone sodium succinate, or hydrocortisone phosphate when hypoadrenocorticism is suspected in a critically ill dog (Table 4).¹³ Continue injectable glucocorticoids until maintenance therapy is instituted.

ACTH stimulation test timing. Ideally, an ACTH stimulation test should be performed before you administer glucocorticoids. However, glucocorticoids should not be withheld pending the results of the test. If an ACTH stimulation test cannot be performed immediately, administer glucocorticoids until hypoadrenocorticism is confirmed. Dexamethasone is an ideal glucocorticoid in this situation since it is rapid-acting and, unlike other glucocorticoids, will not directly interfere with the cortisol assay.^9,13 A single intravenous injection of dexamethasone at ≤ 1 mg/kg does not significantly decrease post-ACTH stimulation plasma cortisol concentrations 24 hours after dexamethasone administration in dogs.²⁷

Although 5 mg/kg dexamethasone administered intravenously significantly decreases post-ACTH stimulation plasma cortisol concentrations 24 hours after the dexamethasone administration (control dogs' cortisol concentrations 15.1 ± 3.1 μg/100 ml; dexamethasone-treated dogs' cortisol concentrations 10.6 ± 1.7 μg/100 ml), this degree of suppression would be unlikely to result in an inappropriate diagnosis of hypoadrenocorticism.²⁷ However, it is important to consider that long-term glucocorticoid administration will eventually lead to adrenal cortical atrophy and a lack of cortisol production post-ACTH stimulation. For this reason, ACTH stimulation testing should be performed as soon as possible in any dog suspected of having hypoadrenocorticism, and the results should be interpreted in light of previous exogenous glucocorticoid administration.