Suxamethonium-Induced Hyperkalemia: A Short Review of Causes and Recommendations for Clinical Applications.

Henrik Lynge Hovgaard,Peter Juhl-Olsen,Steven Edelstein

doi:10.1155/2021/6613118

Abstract

After the introduction of suxamethonium in 1953, cases of cardiac arrest during induction of anesthesia were recorded. In the following years, hyperkalemia was identified as the cause, and the connection to acetylcholine receptor modulation as the underlying molecular mechanism was made. Activation of the acetylcholine receptor with suxamethonium, acetylcholine, or choline causes an efflux of potassium to the extracellular space. However, certain pathological conditions cause acetylcholine receptor proliferation and the emergence of immature receptors capable of a larger potassium efflux to the bloodstream. These pathologic conditions include upper and lower neuron injuries, major burns, trauma, immobility, muscle tumors, muscular dystrophy, and prolonged critical illness. The latter is more important and relevant than ever due to the increasing number of COVID-19 patients requiring prolonged respiratory support and consequent immobilization. Suxamethonium can be used safely in the vast majority of patients. Still, reports of lethal hyperkalemic responses to suxamethonium continue to emerge. This review serves as a reminder of the pathophysiology behind extensive potassium release. Proficiency in the use of suxamethonium includes identification of patients at risk, and selection of an alternative neuromuscular blocking agent is imperative.

Highlights

Neuromuscular blocking agents are widely used to facilitate endotracheal intubation [1]
Immature or denervated ACh receptors exhibit a slightly different subunit composition. These receptors stay open 2–10 times longer than the mature ACh receptor, facilitating a larger efflux of potassium down its concentration gradient (Figure 1) [4]. Pathologic conditions such as immobilization [5], denervation [6], and critical illness upregulate the ACh receptors by a factor of 2–100 in the neuromuscular junction but ACh receptors proliferate along the muscle cell membrane [4]. e upregulated ACh receptors comprise more immature ACh receptors relative to the healthy neuromuscular junction. erefore, in the mentioned pathologic conditions, the ACh receptors increase in numbers and in distribution which together increases the transmembrane potassium conduction. e upregulation of ACh receptors produces a detectable rise in serumpotassium with suxamethonium administration, which is seen within six hours of, e.g., denervation. e rise in serumpotassium may reach a critical level as early as 72 hours postdenervation [4]
After the introduction of suxamethonium in 1951, cardiac arrests after induction of anesthesia were observed and first reported in burn patients [7]. e underlying mechanism, hyperkalemia, was not elucidated until 1967 [8], and shortly, thereafter, other pathologic conditions resulting in suxamethonium-induced hyperkalemia were identified [5]

Summary

Introduction

Neuromuscular blocking agents are widely used to facilitate endotracheal intubation [1]. Suxamethonium provides excellent conditions for airway management [2] but may cause adverse events such as malignant hyperthermia, rhabdomyolysis, or hyperkalemia. Ese adverse events are potentially life threatening, and it is crucial to identify patients at risk, and, in these patients, choose an alternative neuromuscular blocking agent [3]. Is short review will explain the causes for suxamethonium-induced hyperkalemia, identify patients at risk, and determine the duration of temporary risk factors

Search Strategy

Pharmacology of Suxamethonium

Clinical Implications

Findings

Conclusion