Abstract

Transforaminal epidural steroid injections (TFESIs) are associated with rare but devastating neurologic complications. Every published case has been associated with a particulate steroid suspension, and the presumed but not proven mechanism is embolization and occlusion of end arterioles. Through an in vivo murine model and in vitro experiments on human red blood cells (RBCs), the study by Laemmel et al (1) in this issue of Radiology elucidates the potential mechanisms for steroid-induced vascular compromise. Unlike dexamethasone (a nonparticulate steroid solution), saline, and the particulate steroid cortivazol, other particulate steroids (prednisolone, methylprednisolone, and triamcinolone) caused often immediate and complete cessation of capillary blood flow, with RBC (not steroid particle) aggregates and alteration of RBC morphologic structure into spiculated RBCs. Thus, the study strengthens evidence in support of the higher safety profile in TFESI for dexamethasone, the nonparticulate and U.S. Food and Drug Administration-recommended steroid of choice, compared with particulate steroids. The results should not be considered proof that cortivazol has not or could not cause neurologic infarction during a TFESI. Rather, experiments such as those by Laemmel et al should foster more research, particularly in the arena of novel therapeutic agents (nonparticulate steroids and nonsteroidal drugs alike).

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