Difficult diagnosis of malignant hyperthermia during laparoscopic surgery

Abstract

Editor, Malignant hyperthermia is a hypermetabolic state of skeletal muscle, triggered by volatile anaesthetics and succinylcholine. It is a rare condition, and its clinical manifestations vary widely. A high level of vigilance on the part of the anaesthesiologist is needed to recognise a potential episode of malignant hyperthermia, followed by a timely response and a specific management plan if a lethal outcome is to be avoided. However, some physicians consider malignant hyperthermia to be a thing of the past, in part because modern volatile agents such as desflurane have a low potential for triggering malignant hyperthermia. For this reason, with consent of the patient, we describe this case of a confirmed episode of malignant hyperthermia triggered by desflurane. A 66-year-old male patient (85 kg, 175 cm, BMI 28 kg m−2) with known asymptomatic posterior mitral valve prolapse underwent elective robot-assisted laparoscopic prostatectomy under general anaesthesia. He had no known allergies and took no medication prior to surgery and had had uncomplicated spinal anaesthesia years before. Three milligrams of midazolam were administered intravenously 15 min prior to induction of anaesthesia. General anaesthesia was induced with thiopental, fentanyl and atracurium and was maintained with desflurane, remifentanil and fentanyl. Initial end-tidal CO2 was 4.3 kPa and oesophageal temperature was 36.5°C. Thirty minutes after induction, SBP and heart rate dropped to 80 mmHg and 40 beats min−1, respectively. Ephedrine 10 mg and atropine 0.75 mg were administered intravenously. The patient was positioned in a steep Trendelenburg position for surgery. After insufflation of CO2 into the peritoneal cavity, SBP increased to 180 mmHg. A total of 150 μg clonidine was administered intravenously, divided into four doses. Subsequently, haemodynamic variables remained stable. A forced warm air device (Bair Hugger, 3M, Rueschlikon, Switzerland) was installed to maintain the core temperature, which measured 36.5°C at that time. Over the next 210 min, vital signs remained stable. Minute ventilation was increased shortly after capnoperitoneum from 4.5 to 9.5 l min−1, whereas a constant end-tidal pCO2 was measured to be 4.1 to 4.5 kPa. About 240 min after induction, there was a continuous increase of end-tidal CO2 from 4.5 to 5.3 kPa, as well as a rise in core temperature from 37.1 to 37.7°C. The forced warm air was stopped and minute ventilation was increased from 9.5 to more than 11.5 l min−1. During the next 90 min, the patient's core temperature rapidly increased from 37.7 to 39.4°C, and end-tidal CO2 rose to 8.8 kPa; heart rate increased from 80 to 130 beats min−1, whereas blood pressure remained stable at 110/50 mmHg. A blood gas analysis 390 min after induction showed respiratory acidosis (pH 7.25, paO2 28.9 kPa, paCO2 9.6 kPa, lactate 2.6 mmol l−1, base excess +2.9 mmol l−1, glucose 6.0 mmol l−1, potassium 4.9 mmol l−1). Oxygen saturation remained stable at 99% with an inspiratory oxygen concentration of 50%. At this moment, malignant hyperthermia was suspected. Desflurane was stopped; anaesthesia was maintained by propofol; the ventilator was changed, and dantrolene 200 mg (2.3 mg kg−1) was given as an intravenous bolus. The patient was uncovered and cool wet blankets were applied. Within 30 min, core temperature and end-tidal CO2 returned to 37.2°C and 5.0 kPa, respectively. At that time, surgery had terminated. The patient was transferred to the ICU under controlled ventilation. Serum levels of creatine kinase rose from 284 U l−1 before surgery to 1480 U l−1 4 h thereafter and peaked at 7133 IU l−1 on the next day. The patient's trachea was extubated on the day of surgery and he made a full recovery. Three months after discharge, the patient was tested for malignant hyperthermia susceptibility according to the European Malignant Hyperthermia Group (EMHG) protocol with an open muscle biopsy and an in-vitro contracture test. The two halothane a