Succinylcholine-induced Hyperkalemia in Acquired Pathologic States

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) alpha7 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 up-regulated AChRs.

Different magnitude of resistance to non-depolarizing muscle relaxants in dexamethasone-treated rat diaphragm associated with altered acetylcholine receptor expression

“…The expression of γ-AChR has clinical significance, because the two subtypes have different electrophysiological and drug-binding properties (Martyn et al, 1992). Upregulation and spreading of nAChRs, especially the immature form, can induce resistance to NDMRs, as documented in burns, denervation and immobilization (Martyn et al, 1992;Martyn and Richtsfeld, 2006;Jeevendra et al, 2006). Thus, Dex-induced upregulation of functional nAChRs can lead to resistance to NMBRs (Maestrone et al, 1995).…”

Anesthetic Management of a Patient With Carnitine-Acylcarnitine Translocase Deficiency

“…Residual neuromuscular blockade should be reversed at the completion of the procedure and full recovery documented prior to tracheal extubation. In our patient, we chose to reverse neuromuscular blockade with sugammadex given its limited adverse effect profile and superior efficacy when compared to cholinesterase inhibitors [14].…”

Perioperative Management of an Adolescent With Friedreich’s Ataxia and Hypertrophic Cardiomyopathy

“…Previous reports caution against the use of succinylcholine in patients with FA given there is progressive limb and gait ataxia with skeletal muscle weakness and the theoretical risk of a hyperkalemic response following succinylcholine [14]. The involvement of the central and peripheral nervous system would also theoretically make these patients sensitive to the effects of non-depolarizing NMBAs.…”