Succinylcholine-induced hyperkalemia in acquired pathologic states: Etiologic factors and molecular mechanisms

J. A Jeevendra Martyn, Martina Richtsfeld

Research output: Contribution to journalReview articlepeer-review

247 Scopus citations

Abstract

Lethal hyperkalemic response to succinylcholine continues to be reported, but the molecular mechanisms for the hyperkalemia have not been completely elucidated. In the normal innervated mature muscle, the acetylcholine receptors (AChRs) are located only in the junctional area. In certain pathologic states, including upper or lower motor denervation, chemical denervation by muscle relaxants, drugs, or toxins, immobilization, infection, direct muscle trauma, muscle tumor, or muscle inflammation, and/or burn injury, there is up-regulation (increase) of AChRs spreading throughout the muscle membrane, with the additional expression of two new isoforms of AChRs. The depolarization of these AChRs that are spread throughout the muscle membrane by succinylcholine and its metabolites leads to potassium efflux from the muscle, leading to hyperkalemia. The nicotinic (neuronal) α7 acetylcholine receptors, recently described to be expressed in muscle also, can be depolarized not only by acetylcholine and succinylcholine but also by choline, persistently, and possibly play a critical role in the hyperkalemic response to succinylcholine in patients with upregulated AChRs.

Original languageEnglish (US)
Pages (from-to)158-169
Number of pages12
JournalAnesthesiology
Volume104
Issue number1
DOIs
StatePublished - Jan 2006

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