叠氮化钠中毒临床及神经电生理特点

Clinical and nerve electrophysiological features of sodium azide poisoning

目的 探讨叠氮化钠中毒的临床及神经电生理特点。方法 回顾性分析11例叠氮化钠中毒患者的临床资料。结果 本组中,以肢体麻木为首发症状4例,以乏力为首发症状3例,行走不稳2例,头晕、恶心2例。主要临床表现为肢体麻木8例,乏力6例,行走不稳4例,头晕、恶心3例,声弱2例,复视2例,四肢肌力减退7例,肌张力减低3例,腱反射减弱3例,皮肤针刺觉减退3例。电生理主要表现为运动神经传导速度（MCV）减慢、远端潜伏期（DML）延长和波幅（AMP）减低、感觉神经传导速度（SCV）减慢和AMP减低;脑干听觉诱发电位（BAEP）、视觉诱发电位（VEP）及躯体感觉诱发电位（SEP）潜伏期（Lat）及波间期延长,AMP减低。与治疗前比较,治疗后正中神经、尺神经、腓深神经的MCV、AMP、DML,正中神经、尺神经、腓浅神经及腓肠神经的SCV、AMP,SEP的AMP的异常率差异无统计学意义（均P〉0.05）。与治疗前比较,治疗后BAEP、VEP、SEP的Lat,BAEPⅢ-Ⅴ波间期及BAEP、VEP的AMP的异常率差异有统计学意义（P〈0.05~0.01）。结论 叠氮化钠中毒主要表现为肢体麻木、乏力、行走不稳、头晕、复视,电生理检查主要表现为MCV减慢、远端DML延长和AMP减低及SCV减慢和AMP减低;诱发电位Lat及波间期延长,AMP减低。

Objective To observe the clinical and nerve electrophysiological features of sodium azide poisonin. Method The clinical data of 11 patients with sodium azide poisonin were analyzed retrospectively. Results In this group, the first symptoms was numbness in 4 cases, weakness in 3 cases, walking instability in 2 cases, dizziness and nausea in 2 cases. The major clinical manifestations were numbness in 8 cases, weakness in 6 cases, walking instability in 4 cases, dizziness and nausea in 3 cases, leptophonia in 2 cases, diplopia in 2 cases, limb muscle strength loss in 7 cases, reducing muscle tension in 3 cases, weakened tendon reflex in 3 cases, skin needle drops in 3 cases. Electrophysiological examination showed motor nerve conduction velocity （MCV） was slower, distal latency （DML） and amplitude （AMP） were reduced; the sensory nerve conduction velocity （SCV） was slower, and AMP was reduced. The latency （Lat） and wave interval of brainstem auditory evoked potential （BAEP） and visual evoked potential （VEP）, somatosensory evoked potentials （SEP） were prolonged, and AMP was reduced. Compared with pre-treatment, the abnormal rates of MCV, AMP, DML of median nerve, ulnar nerve, deep peroneal nerve and SCV, AMP of median nerve, ulnar nerve, superficial peroneal nerve, sural nerve and AMP of SEP after treatment had no statistically significant （ all P 〉 0. 05 ）. Compared with pre-treatment, the abnormal rates of Lat of BAEP, VEP, SEP and Ⅲ-Ⅴ of BAEP and AMP of BAEP, VEP had no statistically significant （P 〈 0. 05 - 0.01 ）. Conclusions The major clinical symptoms of sodium azide poisoning are numbness, weakness, unstable walking, dizziness, diplopia. Electrophysiological examination showed MCV is slower, DML and AMP are reduced; SCV is slower, and AMP is reduced. The Lat and wave interval of evoked potential are prolonged, and AMP is reduced.