K Nitahara1, Y Sugi, K Higa, S Shono, T Hamada. 1. Department of Anesthesiology, Fukuoka University School of Medicine, Fukuoka, Japan. nitahara@fukuoka-u.ac.jp
Abstract
BACKGROUND: Little information is available regarding the neuromuscular effects of sevoflurane in patients with myasthenia gravis (MG). We evaluated the neuromuscular effects of sevoflurane alone in patients with MG and in those with normal neuromuscular transmission. METHODS:Sixteen patients with generalized type MG (MG group) and 12 otherwise healthy patients (control group) entered into this study. Anaesthesia was induced with propofol, fentanyl, and midazolam followed by nitrous oxide in oxygen. Neuromuscular monitoring was recorded from the adductor pollicis muscle using electromyography with train-of-four stimulation of the ulnar nerve. After a stabilization period, and before sevoflurane administration, baseline T4/T1 was obtained and MG patients were classified as non-fade MG group (baseline T4/T1 > or = 0.90) (n = 10) and fade MG group (baseline T4/T1 < 0.90) (n = 6). End-tidal sevoflurane concentration was kept constant at 1.7% for 30 min and doubled thereafter to 3.4% and maintained for a further 30 min. RESULTS:Sevoflurane produced a concentration-dependent decrease in T1 and T4/T1 values. At 3.4% sevoflurane, T1 and T4/T1 decreased significantly from baseline values in all three groups. From baseline until the patient woke up from anaesthesia, the T4/T1 of the fade MG group was significantly lower than the other groups. At the end of anaesthesia, T4/T1 returned to values similar to the baseline in all three groups. CONCLUSIONS: During sevoflurane anaesthesia, concentration-dependent inhibition of neuromuscular transmission was observed in MG and control patients. The inhibitory effects of sevoflurane were more prominent in MG patients with baseline T4/T1 <0.90.
RCT Entities:
BACKGROUND: Little information is available regarding the neuromuscular effects of sevoflurane in patients with myasthenia gravis (MG). We evaluated the neuromuscular effects of sevoflurane alone in patients with MG and in those with normal neuromuscular transmission. METHODS: Sixteen patients with generalized type MG (MG group) and 12 otherwise healthy patients (control group) entered into this study. Anaesthesia was induced with propofol, fentanyl, and midazolam followed by nitrous oxide in oxygen. Neuromuscular monitoring was recorded from the adductor pollicis muscle using electromyography with train-of-four stimulation of the ulnar nerve. After a stabilization period, and before sevoflurane administration, baseline T4/T1 was obtained and MGpatients were classified as non-fade MG group (baseline T4/T1 > or = 0.90) (n = 10) and fade MG group (baseline T4/T1 < 0.90) (n = 6). End-tidal sevoflurane concentration was kept constant at 1.7% for 30 min and doubled thereafter to 3.4% and maintained for a further 30 min. RESULTS:Sevoflurane produced a concentration-dependent decrease in T1 and T4/T1 values. At 3.4% sevoflurane, T1 and T4/T1 decreased significantly from baseline values in all three groups. From baseline until the patient woke up from anaesthesia, the T4/T1 of the fade MG group was significantly lower than the other groups. At the end of anaesthesia, T4/T1 returned to values similar to the baseline in all three groups. CONCLUSIONS: During sevoflurane anaesthesia, concentration-dependent inhibition of neuromuscular transmission was observed in MG and control patients. The inhibitory effects of sevoflurane were more prominent in MGpatients with baseline T4/T1 <0.90.