Paralysis is preceded by muscular fasciculation, and this may be the cause of the muscle pain experienced commonly after its use. The pain may last 1-3 days and can be minimised by preceding the suxamethonium with a small dose of a competitive blocking agent. Suxamethonium is the neuromuscular blocker with the most rapid onset and the shortest duration of action. Tracheal intubation is possible in less than 60 seconds and total paralysis lasts up to 4 min with 50% recovery in about 10 min (t1/, for effect). It is particularly indicated for rapid sequence induction of anaesthesia in patients who are at risk of aspiration — the ability to secure the airway rapidly with a tracheal tube is of the utmost importance. If intubation proves impossible, recovery from suxamethonium and resumption of spontaneous respiration is relatively rapid. Unfortunately, if it is impossible to ventilate the paralysed patient's lungs, recovery may not be rapid enough to prevent the onset of hypoxia.
Suxamethonium is destroyed by plasma pseudo-cholinesterase and so its persistence in the body is increased by neostigmine, which inactivates that enzyme, and in patients with hepatic disease or severe malnutrition whose plasma enzyme concentrations are lower than normal. Approximately 1 in 3000 of the European population have hereditary defects in amount or kind of enzyme, and cannot destroy the drug as rapidly as normal individuals.7 Paralysis can then last for hours and the individual requires ventilatory support and sedation until recovery occurs spontaneously.
Repeated injections of suxamethonium can cause bradycardia, extrasystoles, and even ventricular arrest. These are probably due to activation of cholinoceptors in the heart and are prevented by atropine. It can be used in caesarian section as it does
7 There are wide inter-ethnic differences. When cases are discovered the family should be investigated for low plasma cholinesterase activity and affected individuals warned.
not readily cross the placenta. Suxamethonium depolarisation causes a release of potassium from muscle, which in normal patients will increase the plasma potassium by 0.5 mmol/1. This is a problem only if the patient's plasma potassium was already high, for example in acute renal failure. In patients with spinal cord injuries and those with major burns, suxamethonium may cause a grossly exaggerated release of potassium from muscle, sufficient to cause cardiac arrest.
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