Abstract

Beggs et al.1 presented two interesting case reports postulating an association between rocuronium and malignant hyperthermia (MH). Although the observed fever in these patients declined after discontinuation of rocuronium, several points need further discussion. First, the definition of MH includes hypercapnia, lactic acidosis, and skeletal muscle hypermetabolism due to excessive sarcoplasmic calcium release via mutated ryanodine receptors after exposure to triggering agents.2 As both patients had complex medical conditions (e.g., acute respiratory distress syndrome, history of cardiopulmonary resuscitation, sepsis), disorders such as metabolic acidosis might have occurred for various reasons. Although MH certainly could have been one reason, this seems rather unlikely since the acidosis was not even temporally related to the use of rocuronium. Second, the body temperature in the reported cases remained elevated for several days, which is not typical of MH crisis. Even though there have been several reports of MH with hyperthermia as the only symptom,3 other findings, such as the modest creatine kinase elevation (351 units/L in patient 1), are inconsistent with a diagnosis of MH. Furthermore, unexplained fever among patients in the intensive care unit is very common and associated with a large variety of differential diagnoses.4

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