Endocrine emergencies are clinical presentations in which immediate recognition and treatment of the endocrine disorder is
required to decrease patient morbidity and prevent mortality. Endocrine disorders that require this immediate recognition
and treatment are adrenal insufficiency, pheochromocytoma, diabetic ketoacidosis, hyperosmolar diabetes mellitus, insulinoma,
hypoparathyroidism, and myxedema coma in severe hypothyroidism.
Hypoadrenocorticism occurs as a result of a deficiency in glucocorticoids and, in most cases, mineralocorticoids as a result
of progressive destruction of the cortex. Mineralocorticoids and glucocorticoids are important in maintaining vascular tone
and water balance. A deficiency in these hormones could result in circulatory failure and hypovolemic shock.
This is a disease of young to middle aged dogs with a predisposition for females and certain breeds. The classic history
is of waxing and waning lethargy, inappetence, vomiting, and diarrhea that often responds to symptomatic treatment. Weakness,
polyuria, polydipsia, muscle wasting, and regurgitation can occur. More critical patients present with a history of anorexia,
vomiting, diarrhea, melena, and collapse. These dogs may be in hypovolemic shock, laterally recumbent, with pale tacky mucous
membranes, increased capillary refill time, poor pulse quality, bradycardia, and hypothermia. A key identifier of this condition
is a dog presenting in hypovolemic shock with bradycardia as opposed to tachycardia.
Routine laboratory evaluation might reveal a mild non-regenerative anemia, the absence of a stress leukogram, prerenal azotemia,
increased ALT, hypoalbuminemia, hypocholesterolemia, hypoglycemia, increased potassium, decreased sodium, and decreased chloride.
Diagnosis is made with clinical signs and the ACTH stimulation test.
In hypovolemic shock it is important to address hypotension and hypovolemia. Typically this is done with shock rates (80
– 90 ml/kg/hr) of crystalloids until signs of shock resolve. After correcting hypovolemia, fluid rates are adjusted to correct
deficits, maintain hydration and replace losses. Sodium chloride (0.9%) is used initially in dogs with evidence of mineralocorticoid
deficiency because of its higher sodium content. If bradycardia and moderate to severe hyperkalemia (> 8.0 mEq/L) are present
then 10% calcium gluconate can be administered to help maintain a normal membrane potential. Dextrose (± regular insulin)
or sodium bicarbonate should also be given to move potassium into cells. Fluid diuresis will aid in elimination of potassium
through the kidneys and, in animals with mild to moderate hyperkalemia, may be all that is required.
Parenteral glucocorticoids should be given as soon as possible. Glucocorticoids most commonly used are dexamethasone, dexamethasone
sodium phosphate, prednisolone sodium succinate, and hydrocortisone hemisuccinate. If considering glucocorticoids prior to
or during the ACTH stimulation test, dexamethasone-containing formulations and hydrocortisone hemisuccinate are recommended
because they reportedly will not interfere with measuring cortisol during the ACTH stimulation test. Parenteral glucocorticoids
are given until the dog is no longer vomiting, eating and drinking regularly. At this time dogs can be switched to oral prednisone
then tapered to lowest dose necessary once at home and feeling well.
Mineralocorticoids are not necessary in an acute crisis but should be given as soon as a mineralocorticoid deficiency is diagnosed.
Desoxycorticosterone pivalate (DOCP) is a more suitable mineralocorticoid for critical cases because it is an injectable formulation.
Glucocorticoids need to be supplemented with DOCP because of its lack of glucocorticoid activity. Fludrocortisone is an alternative
in a dog that can take oral medications. Fludrocortisone can occasionally be administered without glucocorticoids but in
both instances glucocorticoids should be given initially and then tapered to the lowest dose necessary to maintain appetite
and normal activity levels while minimizing signs of glucocorticoid excess. Treatment is life long and the goals of therapy
are to normalize potassium and control clinical signs. Mild hyponatremia is well tolerated.
With prompt recognition and treatment these dogs should do well short and long term.