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The main caveat of this chapter is that all steroids are systemic. Steroids, that is, corticosteroids, may be the first or second most commonly used class of medication in pain clinics, as well as orthopedic and other musculoskeletal clinics. The primary aim of this chapter is to detail the potential adverse events associated with corticosteroids themselves and to briefly review corticosteroid pharmacology and technical aspects. Clinical efficacy evidence is not reviewed here because it has been done extensively elsewhere; instead, a review of steroid-specific risks is presented to aid decision making on whether a steroid should even be used in the first place. If all steroids are systemic, then any adverse event related to steroids could potentially result from steroids administered in the pain clinic, whether or not such has been reported in the literature. Let not steroids be understood the least by those who use them the most.

Spinal injections containing steroids are generally safe. Recent events have focused attention on these procedures, such as the fungal meningitis outbreak caused by contaminated steroids and the recent Food and Drug Administration (FDA) Safety Alert, both of which are explained in detail in this chapter. However, a 7-year retrospective of 4265 epidural steroid injections (ESIs) in 1857 patients found no major complications and a minor complication rate of 2.4%, consisting mostly of increased pain or pain at the injection site or persistent numbness.1 The ASA Closed Claims study reports 114 major complications, including nerve injury, infection, headache, worse pain, brain damage, and death.2 However, in truth, we do not know the complication rate because there is no mandated reporting.3


Cortisone was first isolated from the adrenal gland in 1935.4 As initiates, we may cringe at the word “cortisone” when that is the limit of one's self-report of medical history. “Steroid” for purposes here refers to corticosteroid medications, which are now usually synthetic derivatives of the endogenous corticosteroids produced by the adrenal cortex in response to stimulation by adrenocorticotropic hormone (ACTH). All corticosteroids have mineralocorticoid and glucocorticoid potency in varying proportions and may have metabolic effects on every organ system. As part of the glucocorticoid effect, corticosteroids have powerful anti-inflammatory action.

ACTH is a 39–amino acid peptide cleaved from a larger precursor protein, pro-opiomelanocortin (POMC), and it exerts actions via the melanocortin receptor subtypes (MC2R in the adrenal cortex). ACTH from the pituitary stimulates adrenal cortex production and release of glucocorticoids, mineralocorticoids, and dehydroepiandrosterone. In clinical practice, a synthetic ACTH analog, cosyntropin, is given in a high dose to test the ability of the hypothalamic–pituitary–adrenal (HPA) axis response of increased cortisol production.

The HPA is a cooperation of these three organs in maintaining glucocorticoid levels. Three HPA mechanisms are: (1) diurnal rhythm or fluctuation in steroidogenesis, (2) negative feedback loop wherein excess glucocorticoid decreases ACTH, and (3) positive stress ...

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