A 9-year-old boy undergoing anaesthesia including suxamethonium and halothane suffered cardiac arrest on two occasions. Clinical and laboratory examination subsequently showed that the patient had suffered from acute rhabdomyolysis. The eventual recovery was satisfactor

JERUSALEM, S.

MAIER, C.

SCHAER, H.

STEINMANN, B.

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Br.J. Anaesth. (1977), 49, 495RHABDOMYOLYSIS INDUCED BY ANAESTHESIAWITH INTRAOPERATIVE CARDIAC ARRESTH. SCHAER, B. STEINMANN, S. JERUSALEM AND C. MAIERSUMMARYA 9-year-old boy undergoing anaesthesia including suxamethonium and halothane suffered cardiacarrest on two occasions. Clinical and laboratory examination subsequently showed that the patienthad suffered from acute rhabdomyolysis. The eventual recovery was satisfactory.Acute paroxysmal rhabdomyolysis with myoglobin-uria is a rare syndrome which is attributed to a varietyof causes. In many cases the syndrome is precipitatedby a "trigger" event, such as severe physical exercise,infection, fever or the administration of certain drugs.Death may occur at the height of the attack becauseof hyperkalaemia, paralysis of respiratory muscles, orrenal failure (Haase and Engel, 1960; Rowland andPenn, 1972). This report is of acute rhabdomyolysiswithout hyperpyrexia, associated with intraoperativecardiac arrest precipitated by an anaesthetic involvingsuxamethonium and halothane.CASE REPORTA 9-year-old boy, weighing 37 kg and with no historyof muscle weakness at the first consultation, under-went surgery for correction of strabismus. After pre-medication with atropine 0.4 mg and pethidine 40 mgi.m., anaesthesia was induced with nitrous oxide inoxygen and halothane. Suxamethonium 1 mg/kg wasinjected i.v. to facilitate tracheal intubation which,however, was difficult because of incomplete relax-ation of the jaw muscles. At this moment the patientwas suspected of having malignant hyperpyrexia andthe temperature was monitored. Spontaneous respi-ration resumed within 5 min after administration ofthe suxamethonium and anaesthesia was continuedwith 50% nitrous oxide in oxygen with 1% halothanein a rebreathing circuit. Arterial pressure was 80/60 mm Hg and heart rate 100 beat/min. The cardio-vascular measurements remained stable for the next20 min until, suddenly, the pulse became impalpableand the surgeon observed an enlargement of thepupil. The e.c.g. showed cardiac arrest in asystole.After 30 s of external cardiac massage, spontaneousH. SCHAER, M.D., Department of Anaesthesia; C. MAIER,M.D., Department of Medicine; Kreisspital, CH-8708Mannedorf-Zurich, Switzerland. B. STEINMANN, M.D.,Department of Paediatrics; S. JERUSALEM, M.D., Departmentof Neurology; University of Zurich.cardiac activity started again and the e.c.g. showedenlarged ventricular complexes at a rate of about100/min. Arterial pressure was 120/80 mm Hg. Theoperation was terminated quickly. About 15 minlater the heart rate slowed again and a further cardiacarrest in asystole occurred. The second resuscitationwas difficult. Only after more than 15 min of externalcardiac massage, repeated i.v. administrations ofincreasing doses of adrenaline up to 0.5 mg, calciumgluconate 1.0 g, infusion of sodium bicarbonate84 mmol/litre, frusemide 200 mg and 100 ml of 20%human albumin solution did ventricular fibrillationappear which was converted to a sinus rhythm accom-panied by frequent extrasystoles; these could besuppressed by an infusion of lignocaine. The pupilsremained small throughout resuscitation and the tem-perature did not exceed 36.5 °C. At this time thepatient showed signs of regaining consciousness andwas sedated with diazepam 5 mg and paralysed withpancuronium 2 mg. After 1 h of controlled ventilation,. spontaneous respiration recommenced and the trachealtube was removed. At this time the following bloodmeasurements were obtained: sodium 131 mmol/litre,potassium 5.8 mmol/litre, chloride 92 mmol/litre,calcium 1.37 mmol/litre, phosphate 3.7 mmol/litre,protein 82 g/litre, s.g.o.t. 865 i.u., s.g.p.t. 241 i.u.,c.p.k. 16 860 i.u. The abnormal values of calcium andphosphate had returned to normal by the nextmorning. After urethral catheterization 750 ml ofred-coloured urine was obtained. The presence ofmyoglobin was confirmed by the Blondheim reaction,by gel nitration and by electrophoresis (Adams andRozman, 1970). During the period that followed, urineconcentrations of myoglobin, creatine and amino acidswere measured daily together with c.p.k. in serum(table I). On the 4th day a biopsy of the quadricepsmuscle was obtained for histology, histochemistryand electron microscopy (Jerusalem and Bischhausen,1975) (figs 1 and 2). The e.m.g. (by courtesy ofE. Meyer, Zurich) showed low voltage and brief496 BRITISH JOURNAL OF ANAESTHESIATABLE I. Course ofc.p.k. values in serum and urinary excretion of myoglobin, creatine, camosine,fi-alanine and taurine {expressed as tng/g of creatinine excreted). {Note: parallel normalizationof the urinary metabolites)Timeafter op.Day 01234567Month 2612Bloodc.p.k.(i.v.)16 86077 39049 32021 740850024201170680178272260Myoglobin102065502630330180trace000Creatine2310662015607702050202040UrineCamosine104640(3-Alanine14120Taurine1891848105duration action potentials in the quadriceps, tibialisanterior, triceps bracchii and biceps bracchii muscles.The subsequent clinical course was uneventful andthe patient left the hospital on the 10th day withoutany residual symptoms.After this event inquiry revealed that the patienthad complained about muscle pains up to the age of6 yr and that family walks had had to be stoppedbecause of these complaints. Physical examinationrevealed a normally grown boy without any myo-pathic signs (except strabismus). After ischaemicforearm exercise and exercise on an ergometer for3 min, a normal rate of increase in serum lactic acidconcentration occurred, indicating normal glycolysisand glycogenolysis. A normal carnitine concentrationin serum and muscle and a normal carnitine palmityl-transferase activity in muscle were determined (bycourtesy of A. G. Engel, Mayo Clinic, Rochester,U.S.A.). The e.m.g. at 6 and 12 months after thecardiac arrest was normal.The younger sister of the patient had never com-plained about muscle pain and had not sufferedstrabismus. A series ofc.p.k. estimations was: 140,425, 108 i.u. The e.m.g. and the increase in lacticacid were normal. The parents of the patient hadnormal c.p.k. values.DISCUSSIONThe clinical course and the biochemical and histo-logical findings in this patient confirm the diagnosis ofparoxysmal myoglobinuria as a result of a clinicallyinapparent myopathy. The biochemical examinations,.however, gave no clue to the nature of the muscledisease. In particular, no indication of a disorder oflipid metabolism, glycogenolysis and glycolysis couldbe found (Rowland and Perm, 1972; Engel andAngelini, 1973; Bank et al., 1975).The normal c.p.k. values in the parents, but theincreased values in both children are indicative of anautosomal recessive mode of inheritance. The occur-rence of cardiac arrest could be explained by rapidelectrolyte changes across the cell membrane, especi-ally of calcium during destruction of muscle.Such low calcium and high phosphate valuesare typical of the early phase of acute rhabdo-myolysis (Grossman et al., 1974; Cifuentes et al.,1976).The interest in complications resulting from theaction of suxamethonium and potent anaestheticagents on myopathic muscle has been focused mainlyon the syndrome of malignant hyperpyrexia. It isrecognized less that the same agents can produceacute rhabdomyolysis with myoglobinuria in patientswith certain types of muscle disease. In 1964, Bennikeand Jarnum reported a 20-year-old male whodeveloped idiopathic myoglobinuria with subsequentrenal failure after an anaesthetic involving sux-amethonium and halothane. The main finding was amarked increase in the serum concentrations ofcreatine phosphokinase, the transaminases and lactatedehydrogenase. A further patient was reported byMcLaren (1968) after a similar anaesthetic procedure.Jensen and colleagues (1968) have described a caseof myoglobinuria after an overdose of suxamethnoium.Recently another patient with massive myoglo-binuria precipitated by halothane and suxamethoniumc JDFIG. 1. Fresh frozen cross-sections of muscle tissue stained with (A) haematoxylin and eosin and(B) Oil-red-o and reacted for the demonstration of (c) reduced diphosphopyridine nucleotidedehydrogenase (DPNH) and (D) myofibrillar ATPase at pH 9.3. (A) Three muscle fibres showdegenerative changes with invasion of phagocytes, (B) The presence of neutral fat is demonstratedby the Oil-red-o staining, (c) and (D) The normal distribution of different fibre types is preserved.Horizontal bars represent 20 |xm (A, C, D) and 10 |im (B).498 BRITISH JOURNAL OF ANAESTHESIAFIG. 2. Electron micrograph of a longitudinally oriented muscle fibre. The abnormal spaces (arrows)are positioned between the myofibrils, most of them probably represent lipid droplets. Horizontalbar represents 2 (im.but without cardiovascular and renal complications,was reported (Moore, Watson and Summary, 1976).The normal effect of suxamethonium on therelease of myoglobin is well established. In adultpatients the appearance of myoglobin in serum israre, whereas in a group of children aged 0-10 yr,myoglobin (5-15 (xg/ml serum) could be detected in40% of the patients after a single i.v. dose of suxa-methonium 1 mg/kg (Airaksinen and Tammisto,1965; Jensen et al., 1968; Ryan, Kagen and Hyman,1971). Furthermore, congenital factors predisposingto the development of rhabdomyolysis are found incertain types of patients with strabismus more oftenthan in other children (Tammisto et al., 1970). Inaddition, halothane appears to play a role in theproduction of the muscle injury since myoglobinuriaand increased concentrations of c.p.k. did not occurduring nitrous oxide and oxygen anaesthesia (Tam-misto and Airaksinen, 1966). It appears from all thesestudies that the release of minute amounts of myo-globin and a slight increase of c.p.k. after the injectionof suxamethonium may be a frequent response to thisagent in certain groups of patients.However, these insignificant side-effects of suxa-methonium are very different from the excessivemuscle necrosis observed in our patient, who evenone year after the accident still showed increasedc.p.k. values. Therefore we must consider thisRHABDOMYOLYSIS DURING ANAESTHESIA 499incident as a further case of acute rhabdomyolysis orparoxysmal myoglobinuria, precipitated by anaes-thesia with suxamethonium and halothane. Only afew examples of this complication have been reported.However, it must be considered that, in contrast tothe syndrome of malignant hyperpyrexia, thereappears to be no clinical symptom which points tothis complication at the height of the attack. The onlyclinical sign, an inappropriate muscle relaxation aftersuxamethonium, is considered an indication of malig-nant hyperpyrexia.In cases of an unexplained fatal intraoperativecardiac arrest, preservation of plasma, urine and freshfrozen muscle tissue is imperative for further diag-nosis. This is particularly important for the medico-legal clarification of such cases.Moore, W. E., Watson, R. L., and Summary, J. J. (1976).Massive myoglobinuria precipitated by halothane andsuccinylcholine in a member of a family with elevation ofserum creatine phosphokinase. Anesth. Analg. (Cleve.),55 680Rowland, L. P., and Penn, A. S. (1972). Myoglobinuria.Med. Clin. N. Am., 56, 1233.Ryan, J. F., Kagen, L. J., and Hyman, A. I. (1971).Myoglobinemia after a single dose of succinylcholine.N. Engl.J. Med., 285, 824.Tammisto, T., and Airaksinen, M. (1966). Increase ofcreatine kinase activity in serum as sign of muscularinjury caused by intermittently administered suxa-methonium during halothane anaesthesia. Br.J. Anaesth.,38, 510.Brander, P., Airaksinen, M. M., Tommila, V., andListola, J. (1970). Strabismus as possible sign of latentmuscular disease predisposing to suxamethonium-induced muscular injury. Ann. Clin. Res.. 2; 126.REFERENCESAdams, E. C , and Rozman, M. J. (1970). Differentiation ofhemoglobinuria and myoglobinuria in renal diseases; inLaboratory Diagnosis of Kidney Disease (eds F. W.Sunderman and F. W. Sunderman jr). St Louis, U.S.A.:Green and Warren.Airaksinen, M. M., and Tammisto, T. (1965). Myoglobinuriaafter intermittent administration of succinylcholine duringhalothane anesthesia. Clin. Pharmacol. Ther., 7, 583.Bank, W. J., DiMauro, S., Bonilla, E., Capuzzi, D. M., andRowland, L. P. (1975). A disorder of muscle lipidmetabolism and myoglobinuria. Absence of carnitinepalmityl transferase. N. Engl. J. Med., 252, 443.Bennike. K.-A., and Jarnum S. (1964). Myoglobinuria withacute renal failure possibly induced by suxamethonium.Br.J. Anaesth., 36,730.Cifuentes, E., Norman, M. E., Schwartz, M. W., Maley, B.,and Bason, W. (1976). Myoglobinuria with acute renalfailure in children. The importance of intensive care andperitoneal dialysis. Clin. Pediatr., 15, 63.Engel, A. G., and Angelini, C. (1973). Carnitine deficiency ofhuman skeletal muscle with associated lipid storagemyopathy: A new syndrome. Science, 179, 899.Grossman, R. A., Hamilton, R. W., Morse, B. M.,Penn, A. S., and Goldberg, M. (1974). Non-traumaticrhabdomyolysis and acute renal failure. N. Engl. J Med.,291, 807.Haase, G. R., and Engel, A. G. (1960). Paroxysmal recurrentrhabdomyolysis. Arch. Neurol., 2, 410.Jensen, K., Bennike, K.-A., Hanel, H. K., and Olesen, H.(1968). Myoglobinuria following anaesthesia includingsuxamethonium. Br. J. Anaesth., 40, 329.Jerusalem, F., and Bischhausen, R. (1975). Zur Technik derMuskelbiopsie. Nervenarzt, 46,42.McLaren, C. A. B. (1968). Myoglobinuria following theuse of suxamethonium chloride. A case report. Br. J.Anaesth., 40, 901.RHABDOMYOLYSE PROVOQUEE PARL'ANESTHESIE AVEC ARRET CARDIAQUEINTRAOPERATOIRERESUMEUn garcon de 9 ans subissant une anesthesie a base desuxamethonium et d'halothane a souffert d'un arretcardiaque a deux reprises. Les examens cliniques et ceuxeffectu£s par la suite en laboratoire ont montre que lemalade avait souffert d'une rhabdomyolyse aigue\ Laguerison ulterieure a 6te satisfaisante.DURCH ANASTHESIE EINGELEITETERHABDOMYOLYSE MIT HERZSTILLSTANDWAHREND DER OPERATIONZUSAMMENFASSUNGEin 9-jahriger Junge in einer Suxamethonium- undHalothannarkose erlitt bei zwei Gelegenheit Herzstillstand.Klinische und laboratoriumsmassige Untersuchungen imAnschluss daran zeigten, dass der Patient an akuterRhabdomyolyse gelitten hatte. Die schliessliche Erholungwar zufriedenstellend.RABDOMIOLISIS INDUCIDA MEDIANTEANESTESIA CON PARO CARDIACOINTRAOPERATIVOSUMARIOUn muchacho de 9 afios sometido a anestesia incluyendosuxametonio y halotano padecio de paro cardiaco en dosocasiones. El examen clinico y de laboratorio efectuadosubsiguientemente revelo que el paciente habia sufrido unarabdomiolisis aguda. La recuperation eventual fue satis-factoria.

RHABDOMYOLYSIS INDUCED BY ANAESTHESIA WITH INTRAOPERATIVE CARDIAC ARREST

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