In Reply:—
Thank you for the opportunity to comment on the remarks made by Drs. Wappler and Fiege regarding our case report. We agree that the clinical course of malignant hyperthermia (MH) is variable and that postoperative rhabdomyolysis can be the only symptom of MH.
In response to the questions posed by Drs. Wappler and Fiege, our patient had no history of anesthesia induction, and neither he nor his family members had a history of muscle diseases or anesthetic problems. Except for an increase of creatine kinase (CK) up to 13,409 IU/l, he did not show signs of MH perioperatively (e.g., muscle rigidity, metabolic acidosis, hypercapnia, tachycardia, or fever). The results of arterial blood gas analysis did not show abnormal findings during or after the operative procedure. Other pathologic findings included thoracolumbar paravertebral muscle necrosis, which was confirmed by computed tomography, and ischemic dermal damage on the back. Immediately after emerging from the anesthesia, the patient reported severe back pain. At the involved area, pneumatic support was placed in the hyperlordotic supine position for 11 h; therefore, the cause of elevated CK is due to the ischemic damage by the enforced hyperlordotic position.
According to the Clinical Grading Scale, 1our patient had a raw score of 15 (i.e., CK elevation), but this scale should be estimated within 24 h after the administration of an anesthetic. The CK level 24 h later was 3,544 IU/l, and increased to a maximum of 13,409 IU/l at 30 h. These data suggest that our patient did not have MH. Further, review of the literature revealed that CK levels after intraoperative-pressure muscle ischemia are lower (< 75,000 U/l), 2which is compatible with our data. Our patient’s preoperative CK level of 168 IU/l was within the normal range (20–180 IU/l) seen in our hospital. Thirty days later, this patient underwent a second operation for closure of the jejunostomy, which proceeded uneventfully using the same method and agents of anesthesia as in the first operation.
We still conclude that rhabdomyolysis was induced by the pneumatic device, not by MH.
