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目的分析三甲基氯化锡(TMT)中毒的临床特征和诊疗要点。方法收集1998—2006年13起TMT中毒事故76例病例,对其症状、体征、实验室检查结果和治疗方法进行统计学分析。结果有12起中毒事故为塑料加工引起,1起为食用TMT污染猪油所致;TMT中毒的潜伏期为12h～26d,多数为3～6d,平均住院时间22.3d;主要症状为乏力(81.6%)、头晕(47.4%)、食欲不振(39.5%)、胸闷(21.1%)、腹痛(13.2%)、发热(13.2%)、记忆力下降(11.8%)、恶心(11.8%),肢体麻木(10.5%)和昏迷(7.9%)等;低钾血症发生率为81.6%,多数可持续1周以上,血钾下降与尿碱化有相关性,关联系数为0.526(P<0.001);有些病例中5种心肌酶水平升高;肝损伤指标如丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总胆红素(TBIL)约30%升高;心电图主要表现为窦性心动过缓和窦性心律不齐,分别达48.7%和51.3%,部分病例出现U波、ST-T段改变等;尿锡浓度<0.168～927.000mmol/L,中毒程度与尿锡浓度无相关性。2例为代谢性酸中毒;47例中毒者尿钾浓度与血钾下降、中毒程度亦有相关性(P<0.01)。主要治疗方法是早期、足量、持续补钾,除1例中毒昏迷2d后才送院治疗发生死亡外,其余75例均治愈。结论低钾血症是TMT中毒的主要临床表现之一,中毒较重的病例还可出现大脑边缘系统损伤症状;早期持续足量补钾,积极改善脑组织代谢是有效的治疗措施。
Objective To analyze the clinical features and diagnosis and treatment of TMT poisoning. Methods Totally 76 cases of 13 cases of TMT poisoning were collected from 1998 to 2006, and their symptoms, signs, laboratory tests and treatment methods were statistically analyzed. RESULTS: Twelve poisonings were caused by plastic processing and one was caused by TMT-contaminated lard. The latent period of TMT poisoning was 12h-26d, mostly 3-6d, and the average length of stay was 22.3d. The main symptoms were fatigue (81.6% , Dizziness (47.4%), loss of appetite (39.5%), chest tightness (21.1%), abdominal pain (13.2%), fever (13.2%), memory loss (11.8%), nausea %), And coma (7.9%). The incidence of hypokalemia was 81.6%, most of whom were able to continue for more than one week. The correlation between serum potassium and urine alkalization was correlated (0.526, P <0.001) (P <0.05). The levels of 5 kinds of myocardial enzymes increased in patients with acute myocardial infarction. The indicators of liver injury such as ALT, AST and TBIL increased about 30%. The ECG mainly showed sinus beats Over mild sinus arrhythmia, respectively, 48.7% and 51.3%, U wave in some cases, ST-T segment changes; urinary tin concentration <0.168 ~ 927.000mmol / L, the degree of toxicity and urinary tin concentration was not related. 2 cases of metabolic acidosis; 47 cases of poisoning urinary potassium concentration and serum potassium decreased, the degree of poisoning is also related (P <0.01). The main treatment is the early, adequate, continuous potassium, in addition to 1 case of poisoning coma after 2d hospital death occurred, the remaining 75 cases were cured. Conclusions Hypokalemia is one of the main clinical manifestations of TMT poisoning. Serious poisoning may also lead to brain injury in the limbic system. It is an effective therapeutic strategy to continue potassium supplement in early stage and improve cerebral metabolism actively.