Adrenal Insufficiency, Acute or Secondary

Risk of adrenal insufficiency: 1/1000 to 1/10,000 (if steroids used in prior y).

With steroids >20 mg/d (cortisol equivalent), >7 to 14 d within 1 y (large variability in pt response to dose, route(s), duration and timing of prior steroid use).

Clinical signs worsen with stress, such as trauma, surgery, or infection.

Increases CV instability, fever, CHF, lyte abnormalities.

High cardiac output failure, or low-output state (hypovolemia) with signs of tissue hypoperfusion.

Often evidence of systemic vasodilation with decreased reactivity to fluid or vasopressors.

GI: N/V, dehydration (adrenal crisis).

Anemia; neutropenia with androgen deficiency: Rare.

CV response; decreased SVR, decreased left ventricular stroke work index and decreased vascular responsiveness to maintain perfusion pressure; steroids necessary for blood vessel. responsiveness to catecholamines.

Hyperkalemia with or without hyponatremia (usually aldosterone deficiency); hypoglycemia, acidosis, hypercalcemia, and anemia; cardiac conduction abnormalities.

Adrenal insufficiency results from inadequate production of glucocorticoids (cortisol), mineralocorticoids (aldosterone), and/or androgens.

Adrenal insufficiency can be acute or chronic, primary or secondary.

Primary adrenal insufficiency: Associated with >90% destruction of the adrenal glands and deficiency in both cortisol and aldosterone.

Secondary adrenal insufficiency develops from the HPA axis dysfunction or failure.

Inadequate mineralocorticoid production can cause hyperkalemia, hyponatremia, and metabolic acidosis, with or without signs of dehydration.

Inadequate glucocorticoid production may cause signs of hemodynamic instability (hypotension) during stress.

Acute adrenal (Addisonian) crisis may develop in periop period when another stress is present (infection, hemorrhage, or major or prolonged surgery), leading to hyponatremia, hyperkalemia, dehydration, abdominal symptoms, and shock. (See also Addison Disease.)

May present without symptoms until stress.

Adrenals secrete around 5 to 20 mg of cortisol daily at baseline, 150 mg in periop period, and up to 300 mg during the maximal stress.

Recovery of the adrenal function may take up to 9 to 12 min after withdrawal of exogenous steroids (>20 mg/d of prednisone × 5 d) and the supplementation of daily cortisol production is advised.

Critical illness may produce a state of relative adrenal dysfunction. Critically ill pts may appear to have sepsis without an obvious source of infection.

Chronic adrenal insufficiency from use of steroids in prior year may manifest as weakness, fatigue, nausea, emesis, weight loss, and a variety of psychiatric disturbances.

Primary adrenal insufficiency: Autoimmunity, infection (TB, HIV, CMV), hemorrhage (meningococcal sepsis, trauma, HIT, anticoagulants), drugs (etomidate, antifungals), infiltration (sarcoidosis, amyloidosis, histoplasmosis), metastatic disease (breast, lung, melanoma).

Secondary adrenal insufficiency: Glucocorticoid therapy (systemic, inhaled, topical), drugs (fluticasone, megestrol, medroxyprogesterone, ketorolac tromethamine), brain injury, pituitary or hypothalamic tumors.

Pts on corticosteroids (even topical) have a reduced basal secretion of cortisol and a reduced response to stress as a result of negative feedback of the HPA axis.

Workup: Screening test) am cortisol: Should be greater than 10 mg/dL; if lower, Cortisol stimulation test (ICU setting; suspected perioperative hypocortisolism should be treated empirically): The baseline cortisol level is measured. Synthetic ACTH at a dose of 250 μg IV is administered, and plasma cortisol levels are measured at 30 and 60 min. Usually the plasma cortisol rises at least 9 mg/dL or to a total of at least 18 g/dL at 60 min.