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Adrenal Crisis (Acute Adrenal Insufficiency, Adrenal Apoplexy) And Primary Hyperaldosteronism (Conn’s Syndrome)

Updated on February 11, 2014

Patient With Adrenal Crisis

Sudden withdrawal of ACTH or steroid therapy, infections, trauma, surgery, drugs like morphine, diarrhea, vomiting, physical or psychological stress and obstetric accidents precipitate acute adrenal failure in patients with chronic adrenal cortical i
Sudden withdrawal of ACTH or steroid therapy, infections, trauma, surgery, drugs like morphine, diarrhea, vomiting, physical or psychological stress and obstetric accidents precipitate acute adrenal failure in patients with chronic adrenal cortical i | Source

Adrenal Apoplexy Or Adrenal Crisis

Sudden development of adrenal cortical failure leads to adrenal crisis. It is a medical emergency which is fatal if undiagnosed. Prompt recognition and replacement of glucocorticoids and mineralocorticoids, with other supportive measures give prompt relief. Adrenal crisis may complicate chornic adrenal insufficiency or it may occur acutely in subjects who develop fulminant infections.

Causes: Sudden withdrawal of ACTH or steroid therapy, infections, trauma, surgery, drugs like morphine, diarrhea, vomiting, physical or psychological stress and obstetric accidents precipitate acute adrenal failure in patients with chronic adrenal cortical insufficiency.

During meningococcal septicemia occurring in otherwise normal subjects, hemorrhagic necorsis of the adrenal may develop (Water-house-Friederichsen Syndrome) leading to shock. Infarction of the adrenal, accidental destruction of the adrenal by trauma or surgery and neonatal adrenogenital syndrome are rare causes.

Clinical Features: Severe vomiting, diarrhea, and profound shock are the prominent symptoms. Blotchy purpura develops in septicemia. If untreated, coma supervenes and death follows within hours.

Diagnosis: It is based on clinical features. Biological parameters and plasma cortisol levels help, if facilities are available.

Management: Glucose saline (10%) should be started immediately. The rate is adjusted to maintain normal blood pressure, serum electrolytes and blood sugar level. Intravenous infusion may have to be continued for days. Drug of choice in an emergency is hydrocortisone hemisuccinate sodium in a dose of 100 mg given intravenously initially and repeated every 4- 6 hours. Parenteral medication is continued till the patient is fit for oral therapy. If the blood pressure does not come up promptly, or is tends to drop, fluodrocortisone 0.1 mg oral or DOCA 2-5 mg is given intramuscularly in addition. After tiding over the crisis, long term management for adrenal failure is instituted. When the condition is secondary to sepsis or other causes, these should receive prompt attention.

Hypertension In Conn's Syndrome

The condition is characterized by hypertension, unprovoked hypokalemia and low plasma rennin activity. Normal aldosterone level is suppressible by intravenous infusion of saline. The triad of low serum potassium, low plasma rennin activity and a high
The condition is characterized by hypertension, unprovoked hypokalemia and low plasma rennin activity. Normal aldosterone level is suppressible by intravenous infusion of saline. The triad of low serum potassium, low plasma rennin activity and a high | Source

Primary Hyperaldosteronism (Conn’s Syndrome)

This is a rare disorder caused by a primary increase in the production of aldosterone. Around 60- 75% of cases are due to aldosterone producing adenoma of the adrenal cortex. The second type called idiopathic hyperaldosteronism is probably due to bilateral adrenal hyperplasia. There is a rare sub-group of idiopathic hyperaldosteronism which is suppressible by glucocorticoids.

The condition is characterized by hypertension, unprovoked hypokalemia and low plasma rennin activity. Normal aldosterone level is suppressible by intravenous infusion of saline. The triad of low serum potassium, low plasma rennin activity and a high non-suppressible plasma aldosterone confirms the diagnosis. Demonstration of raised aldosterone levels in the adrenal venous blood obtained by selective catheterization helps to identify the side of lesion. Large tumours can be detected by CT scanning and isotopic imaging.

The condition has to be differentiated from malignant hypertension, uni- or bilateral renal ischemia and potassium losing nephropathies.

Treatment: Adenomas have to be treated by surgery. Those with idiopathic hyperaldosteronism have to be treated medically with spironolactone. 50- 100 mg thrice daily. In intractable cases, bilateral adrenalectomy can be done. The blood pressure returns to normal after several months.

© 2014 Funom Theophilus Makama

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