Abstract
Malignant hyperthermia (MH) occurred during anesthesia with volatile inhalation anesthetics in a patient under treatment with multiple oral antipsychotic drugs and with a history of multi-acting receptor-targeted antipsychotic drug (MARTA)-induced elevation of serum creatine kinase (CK). Since the patient was considered to be at high risk for neuroleptic malignant syndrome (NMS) based on this history, differential diagnosis between MH and NMS was difficult at the time of onset. Later, the patient was found to be predisposed to MH based on abnormal high rate of the Ca2+-induced Ca2+ release (CICR). We concluded that MH was induced by the volatile inhalation anesthetics.
Highlights
Patients under treatment with multiple antipsychotic drugs are at risk for multi-acting receptor-targeted antipsychotic drug (MARTA)-induced elevation of serum creatine kinase (CK), which is a risk factor for neuroleptic malignant syndrome (NMS)
We report a case of malignant hyperthermia (MH) which was difficult to be differentiated from NMS during surgery for trauma
We encountered a patient who developed MH that was difficult to be differentiated from NMS due to oral antipsychotic polypharmacy
Summary
Patients under treatment with multiple antipsychotic drugs are at risk for multi-acting receptor-targeted antipsychotic drug (MARTA)-induced elevation of serum creatine kinase (CK), which is a risk factor for neuroleptic malignant syndrome (NMS). Slow elevation of the end-tidal carbon dioxide concentration (ETCO2) occurred at 270 min after initiation of anesthesia (Sevoflurane exposure 90 min + Desflurane exposure 180 min) when wound closure was started. Bladder temperature rose by 0.5 °C within 15 min When this temperature reached 39 °C, the condition was clinically diagnosed as MH or NMS based on the rapid ETCO2 elevation, respiratory acidosis (pH 7.051, PCO2 114.3 mmHg, HCO3− 31mmoL/L, PO2 391.9 mmHg), 190 bpm tachycardia, and 180/50 mmHg high blood pressure. Treatment in the operating room was completed with an ETCO2 of 37 mmHg, improved acidosis (pH 7.429, PCO2 36 mmHg, HCO3− 23.3mmoL/ L, PO2 525 mmHg), 130 bpm heart rate, 120/50 mmHg blood pressure and 39.6 °C bladder temperature at 50 min after treatment initiation. The CICR rate was abnormally high (positive) using the skinned fiber method (Fig. 2), based on which the patient was definitively diagnosed with a predisposition to MH
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