The neuromuscular blocking action of Suxamethonium is terminated by the enzyme plasma cholinesterase and prolonged apnoea may occur in patients with an atypical enzyme or with low enzyme activity. Apnoea may also occur following development of phase II block after high or repeated doses of suxamethonium chloride, although tachyphylaxis may also occur with repeated doses.
Administration of Suxamethonium results in transient fasciculations during the onset of depolarizing block. Rhabdomyolysis, myoglobinaemia, and myoglobinuria have been reported and may be associated with
muscle damage following fasciculations. Postoperative muscle pain occurs in some patients but is not directly related to the degree of fasciculation. A transient rise in intra-gastric pressure may occur secondary
to fasciculation of abdominal muscles. A transient increase in intra-ocular pressure often occurs.
Depolarization of skeletal muscle procedures an immediate increase in plasma-potassium concentration and this can have serious consequences in some patients.
Stimulation of the vagus nerve and parasympathetic ganglia by suxamethonium chloride may be followed by bradycardia, other arrhythmias, and hypotension, and may be exacerbated by the raised plasma potassium concentration; cardiac arrest has been reported.
Tachycardia and an increase in blood pressure due to stimulation of ganglia have also been reported.
Suxamethonium may cause an increase in salivary, bronchial, and gastric secretion and other muscarinic effects. Salivary gland enlargement has occurred.
Direct release of histamine from mast cells occurs but this is not the main mechanism of hypersensitivity reactions. Flushing, skin rash, bronchospasm, and shock have been reported.
Other reported effects include prolonged respiratory depression and apnoea.
Administration of suxamethonium chloride is implicated in the development of malignant hyperthermia in those patients with a genetic predisposition to the syndrome.
Treatment of Adverse Effects:
Following administration of suxamethonium assisted respiration should be maintained until spontaneous respiration has been fully restored. Transfusion of fresh whole blood, frozen plasma, or other source pf plasma cholinesterase will help the destruction of the suxamethonium when prolonged paralysis is a result of atypical or low serum concentrations of plasma cholinesterase. Anticholinesterases should not normally be used since they potentiate the usual phase I block. If the neuromuscular block ceases to be depolarizing in type and acquires some features of a competitive block (phase II block) the cautions use of an anticholinesterase may be considered. A short-acting anticholinesterase such as edrophonium may be given intravenously and if an obvious improvement is maintained for several minutes, neostigmine may be given with atropine.
Severe hypersensitivity reactions should be treated promptly with supportive and symptomatic measures. If malignant hyperthermia develops, it may be treated.
The muscarinic effects of suxamethonium chloride, such as bradycardia and excessive salivary secretin may be reduced by giving an antimuscarinic such a atropine before suxamethonium. A small dose of a
competitive neuromuscular blocker given before suxamethonium has been to reduce some of the adverse effects of suxamethonium on the muscles.