Source: Marketing Authorisation Holder Revision Year: 2022
Suxamethonium is a depolarizing, noncompetitive, skeletal muscle relaxant. As with acetylcholine, it combines with nicotinic cholinoceptors to produce depolarization. This depolarization may be experienced as painful muscle fasciculation. Subsequent inhibition of neuromuscular transmission will occur if adequate concentration of suxamethonium remains at the motor end plate. The result of this is flaccid paralysis. The paralysis is selective, initially involving in order of occurrence, the levator muscles of the face, muscles of the glottis and finally the intercostals and the diaphragm and all other skeletal muscles.
When suxamethonium is given over a prolonged period of time, the characteristic depolarizing neuromuscular block (phase 1 block) may change to a block with characteristics superficially resembling a nondepolarizing block. Suxamethonium causes a slight, transient increase in intraocular pressure.
Suxamethonium has a rapid onset and a short duration of action. It acts in about 30 seconds following intravenous injection and has a duration of action averaging 4 to 6 minutes. Suxamethonium is hydrolysed by pseudocholinesterases in plasma and body tissues; only a small proportion of the dose is excreted in the urine unchanged. Suxamethonium does not readily cross the placenta following administration of normal doses.
RYR1 and CACNA1S are polymorphic genes and multiple pathogenic variants have been associated with malignant hyperthermia susceptibility (MHS) in patients receiving succinylcholine, including suxamethonium. Case reports as well as ex vivo studies have identified multiple variants in RYR1 and CACNA1S associated with MHS. Variant pathogenicity should be assessed based on prior clinical experience, functional studies, prevalence information, or other evidence (see section Contraindications and Warnings).
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