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.
The initial main objectives of therapy in critically ill dogs are reversing life-threatening arrhythmias, administering intravascular
volume resuscitation, replacing glucocorticoids, and correcting hyperkalemia (Table 4).9
Table 4: Emergency Treatment of Critically Ill Dogs with Hypoadrenocorticism*
Administer fluid therapy
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").
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.