Endocrinology Made Simple : Acute Adrenal Insufficiency

Acute Adrenal Insufficiency:

This is of two main types

Primary adrenal insufficiency

This occurs due to impairment of the adrenal glands.

80% are due to an autoimmune disease called Addison's disease or autoimmune adrenalitis.

One subtype is called idiopathic, or of unknown cause.

Other cases are due to congenital adrenal hyperplasia or an adenoma (tumor) of the adrenal gland.

Secondary adrenal insufficiency

This is caused by impairment of the pituitary gland or hypothalamus.

This also takes place in setting of long term exposure to glucocorticoids medications that can cause chronic suppression of hypothalamic-pituitary adrenal axis resulting in secondary or tertiary adrenal insufficiency due to decrease in plasma ACTH and cortisol levels respectively.

Pathophysiology And Clinical Features:

Signs and symptoms include:

Hypoglycemia

Dehydration

Weight loss

Disorientation.

Weakness

Tiredness

Dizziness

Low blood pressure that falls further when standing (orthostatic hypotension),

Cardiovascular collapse

Muscle aches

Nausea,

Vomiting

Diarrhea.

These problems may develop gradually and insidiously.

ACTH doesnot control release of mineralocorticoids from zona glomerulosa of the adrenal glands and hence patients have normal plasma aldosterone levels and are normotensive.

However such patients can develop vascular collapse under stressful situations such as infection due to decrease in cortisol which is hormone responsible for maintenance of vascular tone.

Cortisol also promotes synthesis of catecholamines in adrenal medulla,cortisol deficient patients are unable to mount a good pressor response during stress.

Hypotension in this patient should respond to fluid repletion and stress dose of corticosteroids.

In secondary and tertiary adrenal failure,there is no significant abnormal mineralocorticoid levels.

Management

Primary goal of treatment in patients with acute adrenal insufficiency is to reverse the hypotension,correct the electrolyte abnormality and replace cortisol.

Prompt administration of intravenous steroids is indicated without watching for confirmation of the diagnosis.

Intravenous dexamethasone is preferred because it is long acting and doe snot interfere with measurement of serum or urinary steroids during subsequent cosyntropin stimulation test ACTH