Suxamethonium muscle fasciculation

Isoflurane in nitrous oxide inhibited suxamethonium-induced muscle fasciculation in children (26). 

Suxamethonium-induced fasciculation or increased muscle tone can be dangerous in patients with fractures or dislocations (especially vertebral, when the drug is relatively contraindicated), in patients with open-eye injuries or after the eyeball is opened surgically, when an increase in abdominal pressure must be avoided (pheochromocytoma, aortic aneurysm, full stomach, ileus), and in patients in whom a rise in arterial pressure may be catastrophic (cerebral aneurysm, raised intracranial pressure). Prolonged paralysis, occasionally lasting hours, is a risk if the patient is, or has been, taking certain 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. 

In 113 patients undergoing general anesthesia, intravenous midazolam 15 mg slowed recovery of the twitch height after vecuronium and atracurium compared with diazepam. The recovery index was not altered (162). However, in another study in 20 patients, midazolam 0.3 mg/kg did not affect the duration of blockade, recovery time, intensity of fasciculations, or adequacy of relaxation for tracheal intubation produced by suxamethonium 1 mg/kg, nor the duration of blockade and adequacy of relaxation for tracheal intubation produced by pancuronium 0.025 mg/kg in incremental doses until 99% depression of muscle-twitch tension was obtained (161). Furthermore, in 60 patients undergoing maintenance anesthesia randomly assigned to one of six regimens (etomidate, fentanyl, midazolam, propofol, thiopental plus nitrous oxide, or isoflurane plus nitrous oxide), midazolam did not alter rocuronium dosage requirements (165). 

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 (t / 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. 

The depolarization of the motor end-plate receptors produced by suxamethonium (either directly or via repetitive discharge generation by the motor nerve terminals) (40) results in generalized and desynchronized contraction of skeletal muscle fibers. These fasciculations result in aching muscle pain (in up to 90% of patients), most commonly in the neck, pectoral region, shoulders, and back. The pain is most often experienced the day after operation and is worse in ambulatory patients. It is more common in women than in men. Children, elderly patients, athletes, and pregnant women (41) complain less often. Africans also seem to be less susceptible (42). 

Myoglobinuria (79) and raised serum creatine kinase activity (44) have been reported after suxamethonium and appear to be evidence of muscle damage, probably resulting from fasciculation. Repeated bolus doses of suxamethonium result in higher plasma myoglobin concentrations (80) and creatine kinase activities (44). Myoglobinemia seems to be much more common in children than in adults (SEDA-10,107) (SEDA-11,121) (81) and is more marked when halothane is used (82). On occasion, myoglobinuria results in renal insufficiency (83-88). 

It exerts a weak and feeble neuromuscular blocking activity which fails to produce signifieant muscle relaxation except imder deep ether anaesthesia. It has been found to potentiate the neuromuscular blockade caused by tubocurarine and to antagonize the action of decamethonium. Paradoxically, it has been used successfully to prolong and potentiate the relaxant effects of suxamethonium chloride. Besides, it has also been reported to decrease suxamethonium-induced muscular fasciculations. 

Thiopental can reduce muscle fascicula-tion associated with suxamethonium [3 ]. In 300 ASA I and n patients, who were randomized to suxamethonium immediately after thiopental or 30 seconds later, the onset of fasciculation was earher in the former and the duration of fasciculation was shorter in addition, there was moderate to severe fasciculation in the latter. The relation between fasciculations and postoperative myalgia has not been well defined. The authors did not comment on the incidence and severity of myalgia after surgery. 

---