Hypoadrenocorticism

26 Hypoadrenocorticism



David L. Panciera



1. What are the causes of hypoadrenocorticism?

The most common cause of hypoadrenocorticism is idiopathic destruction of the adrenal cortex. The resulting primary hypoadrenocorticism causes glucocorticoid and mineralocorticoid deficiencies. Primary hypoadrenocorticism can also develop secondary to excessive mitotane administration. Secondary hypoadrenocorticism, which causes a deficiency of glucocorticoid hormone production only, results from decreased secretion of adrenocorticotropic hormone (ACTH) and is most common following withdrawal of long-term glucocorticoid or progestin treatment. Atypical hypoadrenocorticism, an uncommon variant of idiopathic primary hypoadrenocorticism, occurs when only glucocorticoid secretion is impaired.


2. What are the common clinical signs of hypoadrenocorticism?

Hypoadrenocorticism is typically seen in young to middle-aged dogs, with a predisposition for females. In the acute form of hypoadrenocorticism (Addisonian or hypoadrenocortical crisis), weakness, dehydration, weak pulses, collapse, diarrhea, and shaking are often present. Weakness, dehydration, hypothermia, bradycardia, and melena are common physical examination findings.


Clinical signs of more chronic hypoadrenocorticism are weakness, dehydration, hypothermia, bradycardia, and melena, but in milder form than is seen with acute disease. Other findings in dogs with chronic hypoadrenocorticism include weight loss, polyuria, and polydipsia. Typically, the clinical signs follow a waxing and waning course. The dog may have a history of previous nondescript illness that responded to supportive treatment. The finding of bradycardia or a lower than expected heart rate in a dog with dehydration and weak pulses should lead to a suspicion of hyperkalemia.


3. What routine laboratory test abnormalities would be expected in a dog with hypoadrenocorticism?

Hyperkalemia and hyponatremia are present in almost all cases of primary hypoadrenocorticism. Hypochloremia is also usually present. Metabolic acidosis is common and may be severe. Elevated blood urea nitrogen (BUN), creatinine, and phosphorus concentrations are common and may be marked in cases of prerenal azotemia. Mild to moderate hypercalcemia is common. Hypoglycemia is fairly common and the blood glucose level may be low enough to cause clinical signs. Hypoproteinemia and hypoalbuminemia are frequent findings, particularly after rehydration. Mild nonregenerative anemia is the most common abnormality identified from the results of a complete blood count (CBC). Lymphocytosis and eosinophilia may be present in some cases, but often cell counts are normal. The absence of a stress leukogram in an ill dog is another laboratory finding suggestive of hypoadrenocorticism. Another important laboratory finding is a urine specific gravity that is lower (<1.030) than expected in a dog with dehydration and azotemia.


4. Is it possible for a dog without electrolyte abnormalities to have hypoadrenocorticism?

Dogs with atypical hypoadrenocorticism have glucocorticoid deficiency but not electrolyte abnormalities. Clinical signs in these cases include lethargy, weight loss, vomiting, diarrhea, melena, polyuria, polydipsia, regurgitation (due to megaesophagus), weakness, and collapse or seizures related to hypoglycemia; bradycardia is not present. Often these dogs have normal stress leukograms and no evidence of nonregenerative anemia, hypocholesterolemia, hypoalbuminemia, or hypoglycemia. A diagnosis of atypical hypoadrenocorticism requires a high index of suspicion and often is arrived at only after extensive testing fails to identify a primary gastrointestinal or systemic disorder.


5. What electrocardiographic abnormalities occur in dogs in acute hypoadrenocortical crisis?

Electrocardiographic (ECG) abnormalities in dogs with hyperkalemia include bradycardia, prolonged PR interval, evidence of atrial standstill (lack of visible P waves), prolonged QRS duration, high T-wave amplitude, low R-wave amplitude, and evidence of heart block. Atrial standstill and marked prolongation of QRS duration indicate severe hyperkalemia.

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Jul 31, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Hypoadrenocorticism

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