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Adrenal function is critical to stability in the surgical milieu in order to maintain hemodynamic stability and end organ perfusion.1,2 The stress of surgery, trauma, and critical illness, and the vasodilation associated with anesthesia, in conjunction with blood loss and fluid shifts, can lead to hypotension and shock in the setting of inadequate adrenal reserves. There are two distinct populations of relevance in this regard: patients with established and confirmed primary or secondary adrenal insufficiency (from cortisol or ACTH deficiency, respectively), and patients with suspected tertiary adrenal insufficiency related to use of exogenous glucocorticoid therapy that suppresses the hypothalamic-pituitary-adrenal (HPA) axis and ACTH release from the hypothalamus.

Primary adrenal insufficiency most commonly results from autoimmune destruction of the adrenal glands.1 Other causes include adrenalectomy, adrenal infarction or hemorrhage, granulomatous disease, infiltrative diseases, tumors, and HIV. Patients with primary AI taking therapeutic replacement steroids will generally require additional supplementation when undergoing a procedure involving significant blood loss, fluid shifts, and anesthesia time. In contrast to patients taking exogenous steroids, patients with primary/secondary AI do not have the ability to mount an appropriate adrenal response to stress and therefore require additional supplementation.

For patients with tertiary adrenal insufficiency from exogenous corticosteroids, suppression of the HPA axis is quite variable depending on dose, frequency, and patient-related factors including age, weight, hepatic function, concomitant drugs metabolized by the P450 system, and concurrent illnesses. However, a reduced response to ACTH stimulation testing is reported to last for 5 days after a similar duration of 25 mg prednisone therapy.3


Clinicians evaluating patients with known primary AI in the preoperative setting should clarify the etiology of the AI. Some patients may have a clear history of adrenalectomy, tuberculosis, sarcoid, or other etiology, evident by history, examination, imaging, or laboratory assessment including morning cortisol determinations and/or ACTH stimulation testing. Others may not have convincing evidence of AI and may have been told that they are “dependent” on steroids, when in fact they have tertiary AI from exogenous corticosteroid use. Conferring with other treating physicians can help to clarify this issue. Corticosteroid dose, frequency (i.e., daily or alternate day dosing), and duration of therapy are key historical elements to help inform decision-making. Physical examination is often limited in utility, but may demonstrate Cushingoid facies, abdominal and flank striae, and centripetal obesity as manifestations or glucocorticoid excess from exogenous supplementation.

A low morning cortisol level and/or a positive ACTH stimulation test (defined as an increase in serum cortisol by less than 7 mg/dl or an absolute cortisol level less than 18 mg/dl 1 hour after the administration of 1 mcg ACTH) helps to confirm the diagnosis; this does not need to be repeated in the perioperative setting unless the diagnosis is in question or if the patient is already taking exogenous corticosteroids thereby limiting ...

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