How common is adrenal atrophy in patients taking Glucocorticoids?
Exogenous administration of GCs is the most common cause of adrenal insufficiency, resulting from suppression of adrenocorticotropic hormone (ACTH). Any patient who is Cushingoid in appearance, has received >20 mg of daily prednisone for >3 weeks, has been on ≥5 mg/day for >1 year, or has a fasting morning plasma cortisol <5 to 10 μg/dL should be considered to have a potentially suppressed HPA axis. In some patients, 10 to 15 mg/day of prednisone for as little as 4 to 6 weeks can cause adrenal suppression that cannot respond to physiologic stress. When patients with adrenocortical functional impairment are stressed by infection, trauma, or surgery, they may not be able to respond optimally (the body’s normal cortisol output when under stress is up to 200–300 mg/day) resulting in fluid unresponsive hypotension. Proper management during periods of physiologic stress aims to mimic the normal cortisol response. Full recovery of the HPA axis may take 6 to 9 months after stopping GC therapy. The responsiveness of the adrenal gland to stress can be tested with a short ACTH (Cortrosyn) stimulation test (250 μg [40 IU] intramuscularly [IM], measure baseline and 60-minute plasma cortisol levels). A normal response is doubling of baseline cortisol and a 60-minute level >18 μg/dL. In patients at risk for adrenal insufficiency who are undergoing surgery or experiencing a severe infection, “stress dose steroids” may be needed to prevent hemodynamic instability.
Patients who become hypotensive during a period of “stress” and do not respond to intravenous fluids should immediately receive 100 mg of Solu-Cortef intravenously.