[Hypercapnia and mixed acidosis as the only sign of malignant hyperthermia (MH)?].
CASE REPORT: A 34-year-old male (190 cm/100 kg) was scheduled for surgery of the nasal septum. He had had uneventful anaesthesia for appendicectomy 14 years earlier: following 600 mg thiopentone, 180 mg suxamethonium and up to 2 vol.% halothane for 20 min had been used and no symptoms of malignant hyperthermia (MH) were recorded. Following oral premedication with 2 mg flunitrazepam at 7.00 a.m. anaesthesia was induced with a priming dose of atracurium at 8.45 a.m. followed by 0.2 mg fentanyl, 500 mg thiopentone, and 100 mg suxamethonium. Endotracheal intubation was accomplished easily, and the patient was ventilated manually in a semi-closed circle system until spontaneous ventilation resumed. Enflurane (1.5% for 5 min, 1.0% for 10 min, and 0.8% until the diagnosis of MH was suspected) was given in 33% O2/66% N2O. Seventy minutes after induction it was noted that the spontaneous respiratory rate and minute volume had risen continuously from 10/min and 6 l/min, respectively, to 20/min and 12 l/min. Attempts at deepening anaesthesia with repeated doses of fentanyl up to a total dose of 0.95 mg failed to reduce the hyperventilation. In spite of a high fresh gas flow of 6 l/min and assisted manual ventilation, the FIO2 started to fall from 0.34 to 0.28 at 10:20 a.m. The O2/N2O ratio was changed to 1:1, but the FIO2 remained at 0.3. MH was suspected, enflurane was discontinued, and an arterial blood gas analysis was done (Table 2). When marked acidosis and hypercarbia were found, dantrolene 2.5 mg/kg was given, the operation was terminated, and the patient's trachea was extubated and he was monitored closely in the intensive care unit for 24 h. Vital signs were stable (Table 3) and no further complications were observed. The patient did not mention pain or uneasiness postoperatively. About 6 months later, a muscle biopsy was done according to the European MH Protocol and the patient was found to be MHEh. DISCUSSION: In this case five main reasons for the hypercarbia and mixed acidosis must be considered (Table 1). Firstly, hypoventilation does not seem to be reasonable as the patient was ventilated with 8 to 12 l/min, which is within the range of 80-120 ml/kg.min. Secondly, we can exclude shock and hypoperfusion because the patient had a normal blood pressure and heart rate (within 65-90 beats/min), his fingertips and skin were well perfused, his body temperature was 37 degrees C, and there was no sign of muscle rigidity. Thirdly, a defect of the CO2 absorber as well as CO2 admixture to the N2O and O2 ventilation gases can cause hypercarbia. We use two absorbers in sequence of which one is changed every day, and found neither a change in colour of the indicator nor an abnormally raised temperature of the absorbers. A postoperative check of the ventilator showed no defect in the O2/N2O supply and a correctly functioning anaesthesia apparatus. A malfunction of both CO2 absorbers resulting in intraoperative hypercarbia could not explain a postoperative mixed acidosis lasting for more than 6 h. Anaesthesias performed at the same time using soda lime from the same canisters were totally uneventful. CONCLUSION: It is concluded that the hypercarbia and mixed acidosis were caused by hypermetabolism. A thorough postoperative examination by an internist did not reveal any thyroid, pulmonary, endocrine, or circulatory reason for our intra- and postoperative findings. Iatrogenic factors like superficial anaesthesia or systemic side effects of adrenaline admixture to local anaesthetics can cause hypermetabolism without striking clinical signs, but they do not cause mixed acidosis lasting longer than 6 h (Table 2). The most suitable explanation in this case is an abortive form of MH. Even patients who are MHS positive on muscle biopsy do not necessarily go through an MH crisis every time they have stress or undergo anaesthesia. The diagnosis of a fulminant MH crisis is a clinical one. Therefore, we are aware that there is no direct scientific ev