Perioperative corticosteroid administration

Where are steroids naturally produced, and what type of steroids are they?

The adrenal cortex produces three different classes of steroids derived from the same basic cholesterol molecule: glucocorticosteroids (cortisol), mineralocorticoids (aldosterone), and androgens (testosterone). The adrenal medulla produces catecholamines via a different metabolic pathway, under different neurohumoral control, and derived from the amino acid tyrosine.

What are the physiologic effects of glucocorticosteroids?

Glucocorticosteroids are produced by the adrenal glands in response to stimulation by adrenocorticotropic hormone (ACTH). ACTH is secreted by the pituitary in response to corticotropin-releasing hormone, which is produced in the hypothalamus. Glucocorticosteroids primarily affect intermediary metabolism. They diffuse through cell membranes and bind to specific glucocorticosteroid receptors, creating a complex that migrates to the nucleus and alters gene transcription. Resulting physiologic effects include an increase in blood glucose, mobilization of fatty acids, catabolism, and antiinflammation.

What steroids are available for administration, and what are their equivalent doses?

Dexamethasone (e.g., Decadron), methylprednisolone (e.g., Solu-Medrol), prednisone, and hydrocortisone (e.g., Solu-Cortef [intravenous form], Cortef [oral form]) are the four main steroids available for enteral or parenteral administration (not inhaled or topically applied). Their relative dose equivalents are:

  • Dexamethasone

  • Methylprednisolone

  • Prednisone

  • Hydrocortisone


For example, a patient taking oral prednisone, 5 mg per day, who needs to be changed to an intravenous steroid of identical potency would receive 20 mg of hydrocortisone intravenously.

How much cortisol is normally produced, and what is addison disease?

Under normal conditions, approximately 30 mg of cortisol is produced daily. During periods of extreme stress (e.g., thoracic aortic surgery or septic shock), 300 mg may be produced over the course of 24 hours.

Addison disease results from chronic lack of endogenous cortisol (and usually aldosterone) production. Clinical manifestations include fatigue, weakness, anorexia, increased skin pigmentation, hypotension, hypoglycemia, hyponatremia, and hyperkalemia ( Table 29-1 ). Most cases are idiopathic.

TABLE 29-1

Cushing Syndrome and Addison Disease

Cushing Syndrome Addison Disease
Etiology Excessive cortisol Lack of endogenous cortisol
Cause BAH
Excessive pituitary ACTH
Ectopic ACTH secretion
Exogenous cortisol
Features Hypertension Hypotension
Hyperglycemia Hypoglycemia
Truncal obesity Fatigue
Hirsutism Weakness
Weakness Anorexia
Abdominal striae
Increased skin pigmentation

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Jul 14, 2019 | Posted by in ANESTHESIA | Comments Off on Perioperative corticosteroid administration
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