Both FSLTx and TVLTx offer the same prognosis in terms of patient and graft survival rates for children after a primary and elective liver transplantation. However, TVLTx has a higher morbidity.
SummaryAn acute episode of a maiignant hyperthermia-like syndrome is described which occurred after suxamethonium and isofurane anaesthesia in a 41-year-old healthy male patient undergoing a minor elective hand operation. Dantrolene therapy rapidly reversed the lfe-threatening signs. Laboratory results appeared to confrm the suspicion of malignant hyperthermia. However, the in vitro contracture test, which was carried out according to the standards of the European Malignant Hyperthermia Group. was equivocal. Key wordsAnaesthetics, volatile; isoflurane. Hyper thermia; malignant. Neuromuscular relaxants; suxamethonium.Malignant hyperthennia (MH) is a dangerous complication of anaesthesia. The combination of suxamethonium and a potent volatile anaesthetic agent can act as a trigger, but MH is not frequently associated with isoffurane anaesthesia. In 1982 the first case of MH after isoflurane anaesthesia was described; however, it was not confirmed by a positive in vilro contracture test.' Since then six more cases have been reported, three of whom were confirmed by a positive test.2 Case historyA 41-year-old male patient, weighing 85 kg presented for a local excision of a tumour on the radial side of his left wrist. He had undergone two previous anaesthetic procedures without any complication and was assessed as ASA I . No premedication was given. After insertion of an intravenous line, an interscalene brachial plexus block was performed with 40 ml bupivacaine 0.375% and adrenaline 1:400 000. Anaesthesia, as assessed by pinprick 20 minutes after the injection, appeared to be adequate. However, at skin incision, this proved not to be so, therefore the patient was anaesthetised with thiopentone 425 mg and given suxamethonium 100 mg to facilitate intubation of the trachea. The anaesthetist noticed that the muscles of the neck were rigid, but tracheal intubation was uneventful. Controlled ventilation of the lungs was instituted (Drager: Ventilog 2) and carbon dioxide (CO,) output monitored by capnography (Datex). Anaesthesia was maintained with 30% oxygen in nitrous oxide and isoflurane 1% and a bolus dose of fentanyl 0.15 mg was given. Five minutes after intubation a rapid rise in the end-tidal CO, was noticed (7.8%) despite apparently adequate ventilation. Auscultation of the lungs and ventilatory pressures were normal, expansion of the chest wall was symmetrical and there were no signs of any leak of gas from the breathing system. The ventilator and the capnograph were checked and no defects were found. In 15 minutes the end-tidal C 0 2 increased from 4.1% to greater than 10% (Fig. 1). The heart rate increased to 129 beats/minute, but the blood pressure remained stable. There was no cyanosis and pulse oximetry showed an oxygen saturation of 97%. Blood gas analysis 30 minutes after the induction of anaesthesia revealed a respiratory acidosis (pH 7.11; Paco, 10.4 kPa).Although the temperature of the skin felt normal, MH was suspected. Isoflurane was discontinued and the patient's lungs were hyperventilated with 100%...
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