Correspondence  |   April 2000
Malignant Hyperthermia as a Cause for Postoperative Rhabdomyolysis
Author Notes
  • University Hospital Eppendorf
  • Associate Professor
  • Staff Anesthesiologist
  • Department of Anesthesiology
  • University Hospital Eppendorf
  • Martinistr. 52
  • Hamburg, Germany
Article Information
Correspondence   |   April 2000
Malignant Hyperthermia as a Cause for Postoperative Rhabdomyolysis
Anesthesiology 4 2000, Vol.92, 1206. doi:
Anesthesiology 4 2000, Vol.92, 1206. doi:
To the Editor:—
We read with great interest the article by Dr. Uratsuji concerning a case of rhabdomyolysis after abdominal surgery in the hyperlordotic position. 1 The authors concluded that rhabdomyolysis and the increase of creatine kinase (CK), lactate dehydrogenase, and serum myoglobin were sufficiently explained by lumbar muscle damage. However, malignant hyperthermia (MH) as another possible cause was not ruled out.
First, it is important to know whether this patient was anesthetized before this incident and whether the patient’s family members had anesthetic complications or a history of muscle disease. This patient had an elevated CK of 168 U/l at rest, which might be caused by subclinical myopathy. Furthermore, it is well known that MH is characterized by a hypermetabolic response to inhalational anesthetics (e.g.,  sevoflurane) or depolarizing muscle relaxants, leading to muscle rigidity, metabolic acidosis, hypercapnia, tachycardia, and fever. However, relevant clinical parameters necessary for interpretation of this syndrome, such as temperature, end-tidal carbon dioxide concentration, arterial blood gases, heart rate, and muscle tone (i.e.,  rigidity or masseter spasm) were not presented. With these clinical parameters, it would be possible to predict the qualitative likelihood of susceptibility to MH using the Clinical Grading Scale (CGS). 2 In this case, the raw-score rank of the CGS has a minimum of 15 points (CK elevation > 10.000 U/l; MH rank 3, which is defined as somewhat less than likely). However, one might speculate that the use of all clinical indicators of the CGS might produce a higher MH rank. 3 
The clinical course of MH is highly variable (e.g.,  fulminant, moderate, and mild forms) and postoperative rhabdomyolysis may be the only symptom of MH. Although the probability of MH susceptibility in patients with anesthesia-induced rhabdomyolysis is only 0.07, 4 the in vitro  contracture tests with halothane and caffeine are necessary for diagnosis of MH susceptibility. 5,6 This view is also emphasized in several case reports that present clinical courses of postoperative rhabdomyolysis after the use of volatile anesthetics. 7–9 
We recommend that the qualitative likelihood of susceptibility to MH should be assessed using the CGS in all cases with MH-like symptoms. Furthermore, all patients with clinical suspicion of MH should undergo muscle biopsy for in vitro  contracture tests, histologic examination, and genetic screening.
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