Abstract

To the Editor: We read with interest the recent case report by Michalek-Sauberer et al. [1] describing the management of a suspected malignant hyperthermia episode during desflurane anesthesia. Their diagnosis was based on the development of hypercarbia, temperature increase, and increase in heart rate. We are less convinced by the data presented, and we have several questions regarding their management. Clearly, the increase in end-tidal CO2 (from 29 to 85 mm Hg over 90 min) is significant. We are, however, given no information regarding the minute ventilation over this time period. The report does not indicate whether any increase in end-tidal CO2 was noted before the patient's inspiratory efforts. These efforts occurred at roughly the time that resolution of the vecuronium neuromuscular blockade would be expected. Could inadequate minute ventilation in a paralyzed patient have led to hypercarbia that was noticed only when the blockade diminished sufficiently? An increase in core temperature of 0.7[degree sign]C over 90 min in a patient completely draped and with no heat loss through a surgical wound is, in our experience, not unusual. This is particularly true if the initial 36.1[degree sign]C baseline was recorded after the initial redistribution of heat seen with induction of anesthesia. The increase in heart rate (from a relatively slow 55 bpm to >95 bpm) was not particularly dramatic in this setting, certainly no more than might be expected in a young healthy patient with significant hypercarbia. The initial blood gas values of pHa 7.25, PaCO2 62 mm Hg, and PaO (2) of 119 mm Hg seems to be most consistent with a respiratory acidosis. The subsequent correction of the pHa 7.33, with restoration of a normal PaCO2 45 mm Hg supports this conclusion. We see no indication of the metabolic acidosis expected with malignant hyperthermia [2]. Finally, the postoperative creatine phosphokinase level of 34 U/L is in the low normal range. Again, this value is inconsistent with an episode of malignant hyperthermia [3]. Using only the data presented, our evaluation using the clinical grading scale cited in the report [4] resulted in a "somewhat less than likely" chance that this was, in fact, an episode of malignant hyperthermia (Table 1).Table 1: Clinical Grading ScaleThe authors' working diagnosis was, in fact, malignant hyperthermia-why was a relatively small dose of dantrolene (1.3 mg/kg) given? Why was dantrolene treatment delayed until after tracheal extubation and transfer to the intensive care unit? If their suspicion of a malignant hyperthermia episode remained strong, would it be reasonable to perform a muscle biopsy test on the patient, despite his age of 13 yr? The authors' stated policy of not testing patients less than 14 yr of age has serious implications for this patient. If this testing were not possible, should the patient's father have been tested? Finally, even if the increase in end-tidal CO2 truly represented a sudden increase in CO2 production, we believe that the acidosis and increase in heart rate may be the results of hypercarbia. Would the authors advocate canceling or interrupting any surgical procedure based on a rise in end-tidal CO2 in conjunction with clinical signs consistent with the effects of hypercarbia? Robert Lowes, MD James F. Mayhew, MD Department of Anesthesiology; University of Texas Medical Branch; Galveston, TX 77555-0591

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