Suxamethonium Anticholinesterases

Suxamethonium produces a typical depolarising block that is characterised by the appearance of fasciculations before the onset of block, absence of fade in response to tetanic and TOP stimulations, and potentiation of block by anticholinesterase drugs. 

Anticholinesterase drugs if administered in large doses or in the absence of muscle relaxants may produce fasciculations and even a depolarising type of block, similar to that with suxamethonium. Neostigmine prolongs the effect of suxamethonium. 

Gesztes T. Prolonged apnoea after suxamethonium injection associated with eye drops containing an anticholinesterase agent. Br J Anaesth 1966 38(5) 408-9. 

Anticholinesterases oppose the actions of competitive neuromuscular blockers (e.g. tubocurarine) and can therefore be used as an antidote to restore muscular activity following their use. Conversely, anticholinesterases increase and prolong the actions of the depolarising neuromuscular blockers (e.g. suxamethonium (succinylcholine)). Anticholinesterases used to treat Alzheimer s disease may also interact with neuromuscular blockers. 

The depolarising blockers (such as suxamethonium (succinylcholine)) act like acetylcholine to depolarise the motor endplate, but unlike acetylcholine, they are not immediately removed by cholinesterase. The anticholinesterase drugs increase the concentration of acetylcholine at the neuromuscular junction, which enhances and prolongs this type of blockade, and therefore anticholinesterases cannot be used as an antidote for this kind of blocker. Care should be taken if an anticholinesterase has been given to antagonise a competitive neuromuscular block prior to the use of suxamethonium, as the duration of the suxamethonium block may be prolonged. ... 

The manufacturer warns that irinotecan could possibly prolong the neuromuscular blocking effects of suxamethonium (succinylcholine) and antagonise the neuromuscular blockade of competitive (non-depolarising) drugs. This is based on the fact that irinotecan has anticholinesterase activity (see also Neuromuscular blockers + Anticholinesterases , p. 114, for an explanation of this mechanism). 

Distigmine A patient taking the anticholinesterase distigmine bromide for urinary retention underwent ECT facUitated by suxamethonium 1 mg/kg [10 ]. Paralysis after administration of suxamethonium lasted 30 minutes and plasma cholinesterase activity was below the reference range. Reduced plasma cholinesterase activity leads to reduced clearance of suxamethonium and prolonged action, a predictable interaction. 

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