Malignant hyperthermia suxamethonium

Malignant hyperthermia has been described in a 10-year-old boy who received thiopental and suxamethonium for induction of anesthesia, followed by desflurane for maintenance of anesthesia (15). 

Susceptibility factors and prophylaxis Although malignant hyperthermia is usually associated with the muscle relaxant suxamethonium, all inhalational anesthetics have been implicated and will be unsafe if risk factors for this condition are present, for example a family history or one of the congenital muscle disorders (76). This must be considered in patients at risk, as there are readily acceptable alternatives, such as propofol (77) and midazolam (78). 

Other cases of malignant hyperthermia have been reported in patients who received sevoflurane (50,51). Although it is highly likely that sevoflurane caused malignant hyperpyrexia in these cases, suxamethonium was also given and was also a suspect. 

Anaphylactoid reactions have been documented, and signs suggestive of histamine release are not uncommon. These are mostly mild such as flushing of the skin. Occasionally bronchospasm and/or hypotension can lead to circulatory arrest. Suxamethonium is the relaxant most commonly associated with the syndrome of malignant hyperthermia. 

Tachycardia and a rise in blood pressure are occasionally seen. Other supraventricular and ventricular dysrhythmias are much less common. Ventricular fibrillation associated with suxamethonium is usually the result of hyperkalemia, but has also been reported in hypercalcemia (22) and is often seen in the course of malignant hyperthermia. Atropine, especially when given intravenously just before suxamethonium, is the most effective agent for the prevention of dysrhythmias. Hexafluorenium, D-tubocurarine, pancuronium, and other non-depolarizer blockers have also been reported as being effective in prevention. Severe hypotension can occur in patients with anaphylactoid reactions. 

There is an association between (latent) muscular dystrophy (usually of the Duchenne or Becker type) and the production of rhabdomyolysis by suxamethonium (84,85,89,90). Suxamethonium can cause excessive muscle damage in these patients, as manifested not only by severe myoglobinemia and raised serum creatine kinase activity but also by acute exacerbation of muscle weakness postoperatively (SEDA-11, 121) (7,29,84,91,92). Massive potassium release can result in hyperkalemic cardiac arrest. Such patients may also develop features suggestive of the syndrome of malignant hyperthermia (93,94). Suxamethonium should not be used in patients with Duchenne muscular dystrophy or who have a family history suspect for the condition. 

All of these anaesthetics (and suxamethonium, see page 235) have the potential to cause malignant hyperthermia. This is a rare but potentially lethal complication of anaesthesia. It is characterized by a rapid rise in body temperature, due to excessive muscle contractions, together with increased heart rate and acidosis. It is treated as an emergency with dantrolene, which causes muscle relaxation. 

Side effects of suxamethonium are bradycardia and, rarely, malignant hyperthermia. Individuals with genetically determined less active plasma pseudocholinesterase levels are likely to experience prolonged paralysis with suxamethonium (see Chapter 2, page 23). 

Body temperature Malignant hyperthermia occurred 3 hours after the start of an operation for esophageal resection in an 82-year-old man after anesthesia induced with propofol and suxamethonium and maintained with sevoflurane [6 ]. Masseter spasm was not a feature. End-tidal CO2 rose to 55 mmHg and body temperature exceeded 39.0°C. The patient responded promptly to dantrolene. Reports of malignant hyperthermia in patients over the age of 80 years are unusual. Both suxamethonium and sevofiur-ane are potent triggers. 

---