Suxamethonium Halothane

Stirt JA, Katz RL, Murray AL, Schehl DL, Lee C. Modification of atracurium blockade by halothane and by suxamethonium. A review of clinical experience. Br J Anaesth 1983 55(Suppl l) S71-5. 

The case is interesting in that although episodes of mass-eter spasm, rigidity, rhabdomyolysis, and malignant hyperpyrexia are well known after the use of halothane and suxamethonium, they have only rarely been reported when suxamethonium was not used. 

A 6-year-old boy sustained pelvic injuries and a femoral fracture. The first anesthetic he received consisted of thiopental, suxamethonium, isoflurane, and nitrous oxide. He also received two units of blood. He subsequently underwent four halothane anesthetics over 6 weeks for dilatation of a urethral stricture. Two days after the last anesthetic he was noted to be jaundiced. He had a negative viral screen but was positive for antitrifluoroacetyl IgG antibodies. He developed fulminant hepatic failure with grade 2 hepatic encephalopathy and underwent an auxiliary Uver transplantation 24 days after his last exposure to halothane. He died of septicemia 18 days later. Both at autopsy and on a previous hepatobiliary scan he was noted to have had extensive native Uver regeneration. 

There have been reports of rhabdomyolysis after anesthesia with halothane, enflurane, and isoflurane in patients with muscular dystrophy, in whom suxamethonium was not used. Rhabdomyolysis has also been reported after sevoflurane anesthesia (46). 

Bradycardia and other dysrhythmias are common (80% in some series) and occur after the first and subsequent injections of suxamethonium in infants and children. In adults, these effects are seen more commonly after second or later injections, particularly when the interval between the doses is 2-5 minutes. However, it has been suggested that bradycardia and asystole may now be more frequently seen than previously in adults after a single injection of suxamethonium, as a result of the increased use of fentanyl or the omission of atropine beforehand (6). Nodal rhythm and wandering pacemaker are frequent. The bradycardia is sometimes extreme (asystoUc periods of 15-30 seconds duration have been reported). Usually these minor dysrhythmias revert to normal after a few minutes. Halothane can prolong their presence. The incidence of bradycardic asystole is not known, as atropine (the effective therapy) is usually quickly given. 

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). 

Inhalational agents potentiate muscle relaxants, which is of more clinical importance with regard to non-depolarizing agents. Tachyphylaxis and phase II block develop earlier and after smaller total doses of suxamethonium when volatile agents such as halothane, enflurane, or isoflurane (306,307) are used instead of balanced anesthesia. Halothane can increase the incidence of cardiac dys-rhjdhmias, especially bradycardia and nodal rhythm, after suxamethonium. Atropine and glycopyrrolate, particularly when given intravenously just before, afford some protection (SEDA-5,136) (308). 

Tammisto T, Airaksinen M. Increase of creatine kinase activity in serum as sign of muscular injury caused by intermittently administred suxamethonium during halothane anaesthesia. Br J Anaesth 1966 38(7) 510-15. 

Reduction of secretions and vagal reflexes Muscarinic antagonists, usually hyoscine, are used to prevent salivation and bronchial secretions and, more importantly, to proteci the heart from arrhythmias, particularly bradycardia caused by halothane, propofol, suxamethonium and neostigmine. Hyoscine is also iiniiemeiic and produces some amnesia. 

In children receiving suxamethonium, those who had anaesthesia induced and maintained with halothane had much higher levels of serum myoglobulin than those undergoing intravenous induction with thiopental followed by halothane. This suggests that prior use of halothane may have potentiated suxamethonium-induced muscle damage. ... 

As pointed out in SED VIII, this is an extremely rare condition which may occur after any form of general anaesthesia. Suxamethonium and halothane most frequently... 

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