Secondary Logo

Journal Logo

Pediatric Anesthesiology: Research Reports

Malignant Hyperthermia and Muscular Dystrophies

Gurnaney, Harshad MBBS, MPH*†; Brown, Amanda MD*†; Litman, Ronald S. DO*†

Editor(s): Davis, Peter J.

Author Information
doi: 10.1213/ane.0b013e3181aa5cf6
  • Free


Malignant hyperthermia (MH) is an uncommon pharmacogenetic condition that results in a hypermetabolic cascade initiated at the skeletal muscle cell on exposure to volatile anesthetics and depolarizing muscle relaxants.1 A life-threatening clinical picture can rapidly evolve, characterized by rhabdomyolysis, lactic acidosis, hyperthermia, disseminated intravascular coagulopathy, and lethal cardiac arrhythmias.2,3 MH susceptibility (MHS) is conferred by specific inherited mutations, most commonly related to the ryanodine receptor involved in the excitation-contraction process of the muscle cell.3–5 When a MHS patient is exposed to a triggering agent, there is destabilization of intracellular calcium regulation resulting in acute MH syndrome.1

The muscular dystrophies encompass a diverse group of disorders with varying modes of inheritance and pathophysiological characteristics. The most prevalent are the X-linked recessive types, Duchenne muscular dystrophy (DMD) and Becker dystrophy (BD). Numerous publications in the anesthesia literature have suggested an association between DMD and BD and an increased risk of a MH episode.6–11

DMD, which occurs in approximately 30 per 100,000 liveborn males, is caused by a recessive mutation on the X-chromosome that prevents normal formation of dystrophin, a muscle-stabilizing protein. Dystrophin is an important part of the dystrophin-glycoprotein complex. The dystrophin-glycoprotein complex is part of a larger complex of proteins associated with dystrophin, which plays a role in sarcolemmal integrity (Figure 1). Loss of dystrophin (partial in BD or complete in DMD) disrupts sarcolemmal integrity and leads to muscular dystrophy.12,13

Figure 1.:
Schematic representation of the organization of the dystrophin-glycoprotein complex (DGC). Various muscular dystrophies (MD) result from defects in the muscle DGC. DMD results from a complete deficiency of dystrophin, whereas a partial deficiency leads to BD. Deficiency in laminin leads to congenital muscular dystrophy and defective glycosylation of the α-dystroglycan leads to limb-girdle muscular dystrophy. BMD = Becker muscular dystrophy; CMD = congenital muscular dystrophy; CYS = cysteine; DG = dystroglycan; DMD = Duchenne muscular dystrophy; LGMD = limb-girdle muscular dystrophy; NOS = nitric oxide synthase. (Adapted with permission from Khurana TS, Davies KE, Nat Rev Drug Discov, 2003, 2, 379-90.)12

DMD usually presents in early childhood as weakness and motor delay. Delayed walking beyond 15-mo-old is a common initial sign. During development, clinical manifestations include progressive lower extremity weakness, pseudohypertrophy of the calves, and markedly elevated creatine kinase levels. Almost all patients with DMD are symptomatic by the age of 5 yr, with difficulty running, jumping, climbing steps, and a waddling gait. Proximal weakness causes patients to use their arms in rising from the floor (Gower’s sign). Progressive and severe muscle atrophy and weakness cause loss of the ability to ambulate by the age of 14 yr. Cardiac disease in both DMD and BD manifests as a dilated cardiomyopathy and/or cardiac arrhythmias. Approximately, one third of the patients with DMD develop cardiomyopathy by the age of 14 yr and almost all patients have cardiomyopathy by the age of 18 yr. Patients with DMD ultimately die in early to midadulthood secondary to a progressive cardiomyopathy and/or ventilatory pump insufficiency.

BD, which occurs in approximately 3-6 per 100,000 male births, is an X-linked recessive inherited disorder that is similar to DMD (progressive muscle weakness of the legs and pelvis), but progresses at a slower rate because of a partial loss of dystrophin. Symptoms usually appear in early adolescence, but may begin later. BD patients can present with cardiomyopathy, which is not consistent with their skeletal muscle weakness. Most patients will have cardiomyopathy by 30 yr of age. Mortality in BD patients typically occurs between 30 and 60 yr from respiratory failure or cardiomyopathy. DMD and BD carrier females may either be asymptomatic or have mild musculoskeletal symptoms, but are at risk of dilated cardiomyopathy. The accuracy of genetic testing in diagnosing DMD and BD is rapidly improving.

The risks related to anesthesia and sedation for patients with DMD include potentially fatal reactions to certain anesthetics, upper airway obstruction, hypoventilation, atelectasis, congestive heart failure, cardiac dysrhythmias, respiratory failure, and difficulty weaning from mechanical ventilation. Preoperative evaluation in patients with DMD and BD should include a detailed work-up of their pulmonary function, which includes measurement of forced vital capacity, maximum inspiratory pressure, maximum expiratory pressure, and peak cough flow.13 Preoperative training with assist devices should be considered based on their pulmonary function.13 Complete cardiac evaluation should be undertaken before any surgical procedure and a dobutamine stress test should be considered if any abnormalities of cardiac function are present. Medical therapy of any cardiac dysfunction should be optimized before any surgery.14

Myotonic dystrophy, an autosomal dominant disorder, characterized by myotonia, weakness of facial and anterior neck muscles, a progressive distal to proximal weakness of the limbs, and involvement of other systems, will be discussed in a separate article in this series of reviews.

We undertook this systematic analysis of the pertinent literature with the purpose of defining the association between DMD and BD, and MHS, and to describe additional anesthesia-related complications.


We performed a literature search using PubMed, Medline, OVID, and ISI using the search terms “malignant hyperthermia,” “muscular dystrophy,” “Duchenne,” “Becker,” “myopathy,” “rhabdomyolysis,” and “cardiac arrest,” and crossreferenced all with the term “anesthesia.” All languages were included but only reviews of abstracts of non-English language studies were possible. References of identified literature were explored, and identified authors were used as additional search terms.


One hundred seventy-three references were identified and reviewed by the authors. Nearly all involved DMD or BD, and thus, the subsequent discussion will be focused on these specific disease entities.

After an initial review of these published cases and studies, and by consensus of the authors, we broadly identified four categories of anesthetic complications in patients with DMD and BD: disease-related (DMD) intraoperative heart failure, rhabdomyolysis and hyperkalemic cardiac arrest in the absence of succinylcholine administration, acute hyperkalemia after administration of succinylcholine, and MH. Postoperative respiratory failure is also a known contributor to perioperative morbidity and mortality in patients with DMD, but has been recently addressed elsewhere.13

Intraoperative Heart Failure

Most retrospective reports on the anesthetic management of patients with DMD attest to the safe use of inhaled volatile anesthetics without succinylcholine.15–18 Nevertheless, there are several reports of intraoperative heart failure attributable to ventricular insufficiency in patients with known DMD during correction of spinal scoliosis.16,19–22 Characteristic of each was the sudden onset of a nonviable tachyarrhythmia and/or hypotension. The eventual contribution of the general anesthetic agents to the cause of the event cannot be ascertained because events occurred during IV and inhaled anesthetic exposures, without succinylcholine. Gross perturbations of serum electrolytes were not found; however, continuing intravascular volume resuscitation was an aspect of each procedure. In most cases, markers of adequate volume status just before the onset of the event were identified, but the case reports fail to identify whether the volume administered was transiently insufficient considering continuing losses or if the volume loss overstressed an already compromised left ventricle.

Hemodynamic alterations are imposed by prone positioning, positive pressure ventilation, anesthetic exposure, and blood loss.13,23 Preoperative echocardiographic assessment of cardiac function and use of invasive monitoring would appear critical to the successful management of these patients.7

Rhabdomyolysis in the Absence of Succinylcholine

Intraoperative and postoperative cardiac arrests as a result of rhabdomyolysis and hyperkalemia have occurred in patients with DMD and BD in the absence of succinylcholine administration.7,24–27

We identified seven cases of rhabdomyolysis and intraoperative cardiac arrest secondary to hyperkalemia during the use of inhaled anesthetics in patients with DMD.8,28–32 Halothane was the anesthetic in all cases. The muscular dystrophy status of the patients was not known in three of these cases.8,29,31 Bradycardia and tachycardia were both observed to precede complete cardiovascular collapse. The time of onset of the clinically significant cardiac arrhythmia after anesthetic induction was variable. Cardiac arrest occurred in some cases with minimal anesthetic exposure, either shortly after induction or during the early portion of the procedure. Initial serum potassium levels exceeded 8 mEq/dL in four patients with no documentation in the other three. Resuscitations persisted in excess of 60 min, with full recoveries obtained in six patients. Dantrolene was often used empirically after documented concomitant metabolic and respiratory acidosis, with or without modest temperature increases. These cases would suggest a predisposition to rhabdomyolysis on exposure to volatile anesthetics regardless of surgical stress. The components of an effective resuscitation are difficult to discern but reduction of the serum potassium is crucial.

We identified eight patients with DMD who developed cardiac arrest secondary to rhabdomyolysis and hyperkalemia in the immediate postoperative period after an uneventful intraoperative course.10,33–38 The diagnosis of DMD was not known in three patients.34,36,38 One patient was a female DMD carrier.37 Nondepolarizing muscle relaxants were used in three patients and reversal drugs administered in two. Inhaled anesthetics included isoflurane, halothane, and sevoflurane. In each case, the patients arrived to the recovery unit awake and hemodynamically stable, only to abruptly develop cardiac arrest shortly thereafter. Four patients survived; two achieved return to baseline function. Four events were fatal. Marked hyperkalemia and metabolic acidosis was consistently identified during the resuscitation, with serum potassium levels in excess of 8 mmol/L in six patients with no documentation in the other two. One patient rapidly responded to defibrillation, but most resuscitation exceeded 45 min to a maximum of 3 h. In these patients, a clear precipitant rhythm or event was difficult to discern.

We identified three patients with BD from 2.5 to 18 yr, who developed anesthesia-related cardiac arrest.28,34,35 One cardiac arrest occurred intraoperatively and two occurred in the recovery room. One arrest was fatal and the other two resulted in prolonged morbidity. All patients received dantrolene sodium to treat hyperkalemia from presumed MH. However, a diagnosis of MH is unlikely because of the absence of a hypermetabolic state preceding the rhabdomyolysis and hyperkalemic event.

In the two patients who survived, the diagnosis of BD had been established before exposure to the inhaled anesthetic. The patient who had a fatal outcome had a family history of BD that was elicited after the crisis occurred and was confirmed in a postmortem muscle biopsy. Because of the delayed appearance of signs and symptoms of patients with BD, it is possible that undiagnosed patients have undergone anesthesia without untoward complications.

Rhabdomyolysis and Life-Threatening Hyperkalemia After Succinylcholine Administration

We identified 37 patients with previously unrecognized DMD who developed succinylcholine-induced hyperkalemic cardiac arrest.17,39–61 The majority of these patients did not manifest clinical signs or symptoms of a myopathy at the time of the succinylcholine administration, and therefore, the adverse event led to the eventual diagnosis of a myopathy. The mortality rate in this group of patients was 30%.

Do Muscular Dystrophy Patients have an Increased Risk of MHS?

Clinical suspicion of MH has been reported in patients with DMD and BD.6,35,45,62 Nine patients with DMD developed unexplained hyperthermia and tachycardia related to the use of halothane,15,56 and six patients had significant rhabdomyolysis without hyperkalemia.24,26,27,49,50,63 A majority of these patients had a diagnosis of muscular dystrophy at the time of the anesthetic. In two patients, the symptoms abated after the volatile anesthetic was withdrawn. Dantrolene was used in some patients because of suspicion of MH.26,31,34,35,42,49 However, the rhabdomyolysis and other clinical characteristics that result from administration of succinylcholine and volatile anesthetics to patients with DMD share signs similar to those arising from a true MH episode; thus, the two entities are difficult to distinguish. The clinical presentation of an episode of MH can be variable and some patients may not demonstrate significant rhabdomyolysis or even lactic acidosis. It seems unlikely that there is a true genetic association between DMD and MH because the genetic mutation associated with DMD is located on the X chromosome, and the mutations associated with MHS are usually found on chromosome 19. Nevertheless, some patients with DMD have demonstrated a positive caffeine-halothane contracture test indicating MHS.6,35,55,62,64 The validity of a caffeine-halothane contracture test in patients who have muscular dystrophy has been debatable as the muscles in these patients may be prone to a positive test on exposure to triggering agents.65–67 However, in all these “clinical MH” cases, the patients suffered acute rhabdomyolysis with hyperkalemia without other classic signs and symptoms of MH, and did not have any evidence of hypermetabolism, which is a hallmark of MH.1,2

Although muscular dystrophy patients are unlikely to have an increased risk of MHS, exposure to volatile anesthetics may be associated with life-threatening rhabdomyolysis and therefore should be used cautiously and when the benefits of their use outweigh the possible risks. Undiagnosed motor delay or loss of motor milestones should prompt neurological evaluation before administration of general anesthetics.

Possible Mechanism of Anesthetic-Induced Hyperkalemia in DMD/BD

The pathophysiology underlying the development of inhaled anesthetic-induced rhabdomyolysis in patients with DMD and BD is not precisely known. It is possible that, in dystrophic patients, inhaled anesthetics exacerbate breakdown of already frail and vulnerable muscle membranes that are further disrupted by patient movement or administration of reversal drugs.68 It was speculated that calcium regulation might be deranged in the dystrophic muscle.69–71 There are signs of altered membrane permeability, such as elevated levels of muscle-specific cytoplasmic proteins (e.g., creatine kinase), in the serum of patients with DMD and BD.69

There are two general mechanisms underlying succinylcholine-induced hyperkalemia: excess potassium release as a result of up-regulation of abnormal extrajunctional acetylcholine receptors (e.g., burns, denervation, atrophy, etc.) and development of hyperkalemia as a result of rhabdomyolysis that occurs in patients with clinically evident, as well as subclinical, myopathic disease states, such as DMD.72–74 Muscular dystrophy patients may not demonstrate up-regulation of abnormal extrajunctional acetylcholine receptors.74 All these patients required prolonged resuscitation. One speculation is that the prolonged resuscitation was in response to continuous and prolonged leakage of potassium from the muscle cells secondary to rhabdomyolysis.72

Succinylcholine should not be administered to patients with known DMD or BD unless required as a last resort for a life-threatening airway emergency, when IV access has not been established. All children presenting for administration of general anesthesia or sedation should be screened for motor milestones. Inability to walk past 18-mo-old or other signs of motor loss or delay should prompt suspicion of a subclinical myopathy and should warrant neurological evaluation and genetic testing before elective surgery.75 Most cases of DMD and BD will be detected by genetic testing.


We did not find an increased risk of MHS in patients with DMD or BD. Exposure to volatile anesthetics in patients with muscular dystrophy may be associated with life-threatening rhabdomyolysis and therefore should be used cautiously, and when the benefits of their use outweigh the possible risks. Succinylcholine administration is associated with life-threatening hyperkalemia and should be avoided in patients with DMD and BD.


1. Litman RS, Rosenberg H. Malignant hyperthermia: update on susceptibility testing. JAMA 2005;293:2918–24
2. Rosenberg H, Davis M, James D, Pollock N, Stowell K. Malignant hyperthermia. Orphanet J Rare Dis 2007;2:21
3. Stowell KM. Malignant hyperthermia: a pharmacogenetic disorder. Pharmacogenomics 2008;9:1657–72
4. Jurkat-Rott K, McCarthy T, Lehmann-Horn F. Genetics and pathogenesis of malignant hyperthermia. Muscle Nerve 2000;23:4–17
5. Sambuughin N, Holley H, Muldoon S, Brandom BW, de Bantel AM, Tobin JR, Nelson TE, Goldfarb LG. Screening of the entire ryanodine receptor type 1 coding region for sequence variants associated with malignant hyperthermia susceptibility in the North American population. Anesthesiology 2005;102:515–21
6. Takagi A. [Malignant hyperthermia of Duchenne muscular dystrophy: application of clinical grading scale and caffeine contracture of skinned muscle fibers]. Rinsho Shinkeigaku 2000;40:423–7
7. Morris P. Duchenne muscular dystrophy: a challenge for the anaesthetist. Paediatr Anaesth 1997;7:1–4
8. Benton NC, Wolgat RA. Sudden cardiac arrest during adenotonsillectomy in a patient with subclinical Duchenne’s muscular dystrophy. Ear Nose Throat J 1993;72:130–1
9. Peluso A, Bianchini A. Malignant hyperthermia susceptibility in patients with Duchenne’s muscular dystrophy. Can J Anaesth 1992;39:1117–8
10. Kelfer HM, Singer WD, Reynolds RN. Malignant hyperthermia in a child with Duchenne muscular dystrophy. Pediatrics 1983;71:118–9
11. Goresky GV, Cox RG. Inhalation anesthetics and Duchenne’s muscular dystrophy. Can J Anaesth 1999;46:525–8
12. Khurana TS, Davies KE. Pharmacological strategies for muscular dystrophy. Nat Rev Drug Discov 2003;2:379–90
13. Birnkrant DJ, Panitch HB, Benditt JO, Boitano LJ, Carter ER, Cwik VA, Finder JD, Iannaccone ST, Jacobson LE, Kohn GL, Motoyama EK, Moxley RT, Schroth MK, Sharma GD, Sussman MD. American College of Chest Physicians consensus statement on the respiratory and related management of patients with Duchenne muscular dystrophy undergoing anesthesia or sedation. Chest 2007;132:1977–86
14. American Academy of Pediatrics Section on Cardiology and Cardiac Surgery. Cardiovascular health supervision for individuals affected by Duchenne or Becker muscular dystrophy. Pediatrics 2005;116:1569–73
15. Sethna NF, Rockoff MA, Worthen HM, Rosnow JM. Anesthesia-related complications in children with Duchenne muscular dystrophy. Anesthesiology 1988;68:462–5
16. Shapiro F, Sethna N, Colan S, Wohl ME, Specht L. Spinal fusion in Duchenne muscular dystrophy: a multidisciplinary approach. Muscle Nerve 1992;15:604–14
17. Smith CL, Bush GH. Anaesthesia and progressive muscular dystrophy. Br J Anaesth 1985;57:1113–8
18. Lerman J. Inhalational anesthetics. Paediatr Anaesth 2004;14:380–3
19. Reid JM, Appleton PJ. A case of ventricular fibrillation in the prone position during back stabilisation surgery in a boy with Duchenne’s muscular dystrophy. Anaesthesia 1999;54:364–7
20. Irwin MG, Henderson M. Cardiac arrest during major spinal scoliosis surgery in a patient with Duchenne’s muscular dystrophy undergoing intravenous anaesthesia. Anaesth Intensive Care 1995;23:626–9
21. Smelt WL. Cardiac arrest during desflurane anaesthesia in a patient with Duchenne’s muscular dystrophy. Acta Anaesthesiol Scand 2005;49:267–9
22. Schmidt GN, Burmeister MA, Lilje C, Wappler F, Bischoff P. Acute heart failure during spinal surgery in a boy with Duchenne muscular dystrophy. Br J Anaesth 2003;90:800–4
23. Breucking E, Reimnitz P, Schara U, Mortier W. [Anesthetic complications. The incidence of severe anesthetic complications in patients and families with progressive muscular dystrophy of the Duchenne and Becker types]. Anaesthesist 2000;49:187–95
24. Takahashi H, Shimokawa M, Sha K, Sakamoto T, Kawaguchi M, Kitaguchi K, Furuya H. [Sevoflurane can induce rhabdomyolysis in Duchenne’s muscular dystrophy]. Masui 2002;51:190–2
25. Hayes J, Veyckemans F, Bissonnette B. Duchenne muscular dystrophy: an old anesthesia problem revisited. Paediatr Anaesth 2008;18:100–6
26. Obata R, Yasumi Y, Suzuki A, Nakajima Y, Sato S. Rhabdomyolysis in association with Duchenne’s muscular dystrophy. Can J Anaesth 1999;46:564–6
27. Rubiano R, Chang JL, Carroll J, Sonbolian N, Larson CE. Acute rhabdomyolysis following halothane anesthesia without succinylcholine. Anesthesiology 1987;67:856–7
28. Bush A, Dubowitz V. Fatal rhabdomyolysis complicating general anaesthesia in a child with Becker muscular dystrophy. Neuromuscul Disord 1991;1:201–4
29. Breucking E, Mortier W. Anesthesia in neuromuscular diseases. Acta Anaesthesiol Belg 1990;41:127–32
30. Sethna NF, Rockoff MA. Cardiac arrest following inhalation induction of anaesthesia in a child with Duchenne’s muscular dystrophy. Can Anaesth Soc J 1986;33:799–802
31. Marchildon MB. Malignant hyperthermia. Current concepts. Arch Surg 1982;117:349–51
32. Miller ED Jr, Sanders DB, Rowlingson JC, Berry FA Jr, Sussman MD, Epstein RM. Anesthesia-induced rhabdomyolysis in a patient with Duchenne’s muscular dystrophy. Anesthesiology 1978;48:146–8
33. Boba A. Fatal postanesthetic complications in two muscular dystrophic patients. J Pediatr Surg 1970;5:71–5
34. Chalkiadis GA, Branch KG. Cardiac arrest after isoflurane anaesthesia in a patient with Duchenne’s muscular dystrophy. Anaesthesia 1990;45:22–5
35. Kleopa KA, Rosenberg H, Heiman-Patterson T. Malignant hyperthermia-like episode in Becker muscular dystrophy. Anesthesiology 2000;93:1535–7
36. Nathan A, Ganesh A, Godinez RI, Nicolson SC, Greeley WJ. Hyperkalemic cardiac arrest after cardiopulmonary bypass in a child with unsuspected duchenne muscular dystrophy. Anesth Analg 2005;100:672-4, table of contents
37. Tokunaga C, Hiramatsu Y, Noma M, Takahashi M, Horigome H, Iwasaki N, Takahashi S, Mizutani T, Sakakibara Y. [Delayed onset malignant hyperthermia after a closure of ventricular septal defect]. Kyobu Geka 2005;58:201–5
38. Girshin M, Mukherjee J, Clowney R, Singer LP, Wasnick J. The postoperative cardiovascular arrest of a 5-year-old male: an initial presentation of Duchenne’s muscular dystrophy. Paediatr Anaesth 2006;16:170–3
39. Linter SP, Thomas PR, Withington PS, Hall MG. Suxamethonium associated hypertonicity and cardiac arrest in unsuspected pseudohypertrophic muscular dystrophy. Br J Anaesth 1982;54:1331–2
40. Lewandowski KB. Rhabdomyolysis, myoglobinuria and hyperpyrexia caused by suxamethonium in a child with increased serum creatine kinase concentrations. Br J Anaesth 1981;53:981–4
41. Seay AR, Ziter FA, Thompson JA. Cardiac arrest during induction of anesthesia in Duchenne muscular dystrophy. J Pediatr 1978;93:88–90
42. Pedrozzi NE, Ramelli GP, Tomasetti R, Nobile-Buetti L, Bianchetti MG. Rhabdomyolysis and anesthesia: a report of two cases and review of the literature. Pediatr Neurol 1996;15:254–7
43. Kerr TP, Duward A, Hodgson SV, Hughes E, Robb SA. Hyperkalaemic cardiac arrest in a manifesting carrier of Duchenne muscular dystrophy following general anaesthesia. Eur J Pediatr 2001;160:579–80
44. Farrell PT. Anaesthesia-induced rhabdomyolysis causing cardiac arrest: case report and review of anaesthesia and the dystrophinopathies. Anaesth Intensive Care 1994;22:597–601
45. Ohkoshi N, Yoshizawa T, Mizusawa H, Shoji S, Toyama M, Iida K, Sugishita Y, Hamano K, Takagi A, Goto K, Arahata K. Malignant hyperthermia in a patient with Becker muscular dystrophy: dystrophin analysis and caffeine contracture study. Neuromuscul Disord 1995;5:53–8
46. Parker SF, Bailey A, Drake AF. Infant hyperkalemic arrest after succinylcholine. Anesth Analg 1995;80:206–7
47. Sullivan M, Thompson WK, Hill GD. Succinylcholine-induced cardiac arrest in children with undiagnosed myopathy. Can J Anaesth 1994;41:497–501
48. Stelzner J, Kretz FJ, Rieger A, Reinhart K. [Anesthetic-induced heart arrest. A case report of 2 infants with previously unrecognized muscular dystrophy]. Anaesthesist 1993;42:44–6
49. Tang TT, Oechler HW, Siker D, Segura AD, Franciosi RA. Anesthesia-induced rhabdomyolysis in infants with unsuspected Duchenne dystrophy. Acta Paediatr 1992;81:716–9
50. Wang JM, Stanley TH. Duchenne muscular dystrophy and malignant hyperthermia—two case reports. Can Anaesth Soc J 1986;33:492–7
51. Wilhoit RD, Brown RE Jr, Bauman LA. Possible malignant hyperthermia in a 7-week-old infant. Anesth Analg 1989;68:688–91
52. Delphin E, Jackson D, Rothstein P. Use of succinylcholine during elective pediatric anesthesia should be reevaluated. Anesth Analg 1987;66:1190–2
53. Henderson WA. Succinylcholine-induced cardiac arrest in unsuspected Duchenne muscular dystrophy. Can Anaesth Soc J 1984;31:444–6
54. McKishnie JD, Muir JM, Girvan DP. Anaesthesia induced rhabdomyolysis—a case report. Can Anaesth Soc J 1983;30:295–8
55. Brownell AK, Paasuke RT, Elash A, Fowlow SB, Seagram CG, Diewold RJ, Friesen C. Malignant hyperthermia in Duchenne muscular dystrophy. Anesthesiology 1983;58:180–2
56. Larsen UT, Juhl B, Hein-Sorensen O, de Fine Olivarius B. Complications during anaesthesia in patients with Duchenne’s muscular dystrophy (a retrospective study). Can J Anaesth 1989;36:418–22
57. Genever EE. Suxamethonium-induced cardiac arrest in unsuspected pseudohypertrophic muscular dystrophy. Case report. Br J Anaesth 1971;43:984–6
58. Schaer H, Steinmann B, Jerusalem S, Maier C. Rhabdomyolysis induced by anaesthesia with intraoperative cardiac arrest. Br J Anaesth 1977;49:495–9
59. Gibbs JM. A case of rhabdomyolysis associated with suxamethonium. Anaesth Intensive Care 1978;6:141–5
60. Rosenberg H, Gronert GA. Intractable cardiac arrest in children given succinylcholine. Anesthesiology 1992;77:1054
61. Larach MG, Rosenberg H, Gronert GA, Allen GC. Hyperkalemic cardiac arrest during anesthesia in infants and children with occult myopathies. Clin Pediatr (Phila) 1997;36:9–16
62. Oka S, Igarashi Y, Takagi A, Nishida M, Sato K, Nakada K, Ikeda K. Malignant hyperpyrexia and Duchenne muscular dystrophy: a case report. Can Anaesth Soc J 1982;29:627–9
63. Umino M, Kurosa M, Masuda T, Kubota Y. Myoglobinuria and elevated serum enzymes associated with partial glossectomy under enflurane anesthesia in a patient with muscular dystrophy. J Oral Maxillofac Surg 1989;47:71–5
64. Heiman-Patterson TD, Natter HM, Rosenberg HR, Fletcher JE, Tahmoush AJ. Malignant hyperthermia susceptibility in X-linked muscle dystrophies. Pediatr Neurol 1986;2:356–8
65. Adnet PJ, Krivosic-Horber RM, Krivosic I, Haudecoeur G, Reyford HG, Adamantidis MM, Medahoui H. Viability criterion of muscle bundles used in the in vitro contracture test in patients with neuromuscular diseases. Br J Anaesth 1994;72:93–7
66. Gronert GA, Fowler W, Cardinet GH III, Grix A Jr, Ellis WG, Schwartz MZ. Absence of malignant hyperthermia contractures in Becker-Duchenne dystrophy at age 2. Muscle Nerve 1992;15:52–6
67. Heytens L, Martin JJ, Van de Kelft E, Bossaert LL. In vitro contracture tests in patients with various neuromuscular diseases. Br J Anaesth 1992;68:72–5
68. Yemen TA, McClain C. Muscular dystrophy, anesthesia and the safety of inhalational agents revisited; again. Paediatr Anaesth 2006;16:105–8
69. Berchtold MW, Brinkmeier H, Muntener M. Calcium ion in skeletal muscle: its crucial role for muscle function, plasticity, and disease. Physiol Rev 2000;80:1215–65
70. Whitehead NP, Yeung EW, Allen DG. Muscle damage in mdx (dystrophic) mice: role of calcium and reactive oxygen species. Clin Exp Pharmacol Physiol 2006;33:657–62
71. Wallace GQ, McNally EM. Mechanisms of muscle degeneration, regeneration, and repair in the muscular dystrophies. Annu Rev Physiol 2009;71:37–57
72. Gronert GA. Cardiac arrest after succinylcholine: mortality greater with rhabdomyolysis than receptor upregulation. Anesthesiology 2001;94:523–9
73. Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology 2006;104:158–69
74. Theroux MC, Olivant A, Akins RE. C Histomorphology of neuromuscular junction in Duchenne muscular dystrophy. Paediatr Anaesth 2008;18:256–9
75. Wijnhoven TM, de Onis M, Onyango AW, Wang T, Bjoerneboe GE, Bhandari N, Lartey A, al Rashidi B. Assessment of gross motor development in the WHO Multicentre Growth Reference Study. Food Nutr Bull 2004;25:S37–45
© 2009 International Anesthesia Research Society