Updates on hypoadrenocorticism - Veterinary Medicine
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Updates on hypoadrenocorticism
The lack of a stress leukogram in dogs with gastrointestinal signs may signal this potentially life-threatening disease. This review will help ensure that you aren't overlooking other clinical signs and that you know the latest about diagnosing and treating canine hypoadrenocorticism.


Treat hyperkalemia

Any patient with hyperkalemia-induced clinical signs or electrocardiographic signs of cardiotoxicity should receive immediate therapy with intravenous 10% calcium gluconate (Table 4). Calcium gluconate affects the transmembrane potential of myocardial cells, protecting the heart from potassium's toxic effects.2,9 The protective effect will last 30 to 60 minutes, which should allow enough time for other potassium-lowering therapies to start working.9 All patients with hyperkalemia should be given intravenous fluid therapy. Fluid diuresis lowers serum potassium concentrations through dilution and by promoting renal potassium excretion. For patients with mild hyperkalemia and no signs of cardiotoxicity, intravenous fluid therapy alone may correct hyperkalemia.3

For patients with moderate to severe hyperkalemia or signs of cardiotoxicity, additional treatments such as dextrose with or without insulin or sodium bicarbonate are indicated. Insulin drives potassium into the cells, lowering serum potassium concentrations. Insulin should always be administered with dextrose (Table 4). In nondiabetic patients, dextrose may be given to stimulate endogenous insulin release with less risk of iatrogenic hypoglycemia.2 Similarly, sodium bicarbonate drives potassium into the cells, lowering serum potassium concentrations.9 Monitor patients with moderate to severe hyperkalemia with an electrocardiogram (ECG) and serial serum potassium concentration measurements.

Additional treatment considerations

Metabolic acidosis is almost always corrected with intravenous fluid therapy alone.3 However, for patients with a severe acidemia (pH < 7.1) that is unresponsive to volume resuscitation, sodium bicarbonate can be administered.4 For patients with clinically important hypoglycemia, dextrose can be administered.3,4 Make sure to monitor patients for acute renal failure and treat appropriately.9

Myelinolysis of the central thalamus may develop after rapid correction of chronic hyponatremia in dogs.28 Clinical signs of this neurologic condition develop five days after rapid correction and include obtundation, ataxia, tetraparesis, decreased sensory perception, and hypermetria.28 To avoid myelinolysis, correction of chronic hyponatremia should not exceed a 10 to 12 mEq/L increase in serum sodium concentration in a 24-hour period.28


Hypoadrenocorticism is a dynamic condition, and a patient's status may rapidly change, resulting in a life-threatening situation. Careful serial monitoring of physical examination parameters, blood pressure, central venous pressure, an ECG, urine production, serum electrolytes, and renal parameters is prudent. Once appropriate treatment is initiated, many worrisome clinicopathologic abnormalities such as azotemia, hyponatremia, and hyperkalemia will resolve.


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