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1.
急性单纯及混配有机磷农药中毒104例临床分析   总被引:1,自引:0,他引:1  
Zhang J  Zhao J  Sun S  Ma H  Zhao C  Guo Z  Wang F 《中华内科杂志》2002,41(8):544-546
目的 探讨急性单纯及混配有机磷农药中毒的临床表现的差别。方法 对单剂中毒组(S组 ,5 4例 )与混配中毒组 (C组 ,5 0例 )的症状体征、血液三项胆碱酯酶 (ChE) (分别对全血、红细胞、血浆 )活性受抑制程度、血清AST、ALT、磷酸肌酸激酶 (CK)、乳酸脱氢酶 (LDH)活性变化、血清总胆汁酸 (TBiL)浓度、心电图改变等多项指标进行对照分析。结果 S组与C组患者上述指标比较 :(1)入院时症状体征比较 :C组恶心、呕吐的阳性率明显高于S组 (P <0 0 5 ) ,其他症状体征则差异无显著性。(2 )两组入院时血液 3项ChE活性 <0 30分别为 16、14例 ,18、14例 ,2 8、2 5例 ;>0 30~为 2 4、19例 ,2 2、2 1例 ,10、12例 ;0 5 0~ 0 70为 14、17例 ,14、15例 ,16、13例 ;χ2 依次为 0 85 2、1 4 4 4、0 5 0 9,差异均无显著性 (P >0 0 5 )。 (3)S组与C组入院后 72h内的血清AST、ALT、CK、LDH、TBiL的阳检数依次是 :S组为 2 4、18、4 2、2 2、2 1例 ;C组为 2 0、11、32、18、17例 ,各项差异均无显著性 (P >0 0 5 )。 (4)S组与C组入院后 72h内心电图的ST T改变、Q T延长、房室传导阻滞、早搏等变化的总阳性例数分别为 :S组 2 4例 ,C组 19例 ,差异无显著性 (P >0 0 5 )。 (5 )两组病死率 :S组 7 4 1% (4/ 5 4 ) ,C组 6  相似文献   

2.
急性有机磷中毒193例临床分析   总被引:1,自引:0,他引:1  
目的:探讨急性有机磷中毒(AOPP)所致呼吸衰竭(呼衰)、心力衰竭(心衰)以及重度AOPP合并血清淀粉酶升高的危险因素.方法:193例AOPP患者按毒物种类、中毒程度分组,比较各组间呼衰、心衰发生情况有无差异;分析中毒24h内血清胆碱酯酶(CHE)水平与呼衰、心衰的相关性,重度中毒患者血清淀粉酶升高的危险因素.结果:毒物种类对患者呼衰、心衰影响无统计学差异;重度中毒组呼衰、心衰发生率较轻、中度组明显升高(均P<0.05);呼衰组和心衰组血清CHE水平均明显低于非呼衰组和非心衰组(均P<0.05);敌敌畏中毒和中毒24 h内血清CHE水平与血清淀粉酶水平存在一定相关性.结论:中毒程度和血清CHE水平可作为AOPP呼衰、心衰发生的预测指标;敌敌畏中毒和血清CHE水平明显降低是重度AOPP患者血清淀粉酶升高的2个危险因素.  相似文献   

3.
目的 探讨急性有机磷农药中毒的治疗与护理效果.方法 选取我院2007年6月-2010年6月收治的50例急性有机磷农药中毒的患者随机分为两组,每组25例,两组均在常规治疗和护理的基础上,对照组给予阿托品治疗,观察组给予长托宁治疗,比较两组患者的平均用药次数、症状消失时间、胆碱酯酶恢复时间、平均住院时间及不良反应.结果 观察组患者的平均用药次数、症状消失时间、胆碱酯酶恢复时间、平均住院时间与不良反应率分别与对照组比较,差异均有统计学意义(P<0.05).结论 长托宁治疗急性有机磷农药中毒的效果更好,治疗期间加强安全护理措施,有利提高患者的抢救成功率,改善预后.  相似文献   

4.
目的分析探讨有机磷中毒合并呼吸衰竭的临床特点、发生规律及危险因素。方法根据是否合并呼吸衰竭将有机磷中毒患者分为呼衰组及对照组,分析比较两组临床资料及实验室检查结果。结果经比较两组患者在APACHEⅡ评分、ACHE活力、CK、开始洗胃时间、肌颤持续时间、胆碱酯酶活力恢复时间及死亡率方面有显著性差异(P〈0.05)。结论有机磷中毒患者易并发呼吸衰竭,其中洗胃时间延迟、胆碱酯酶活力低下、胆碱酯酶活力恢复延迟及APACHEⅡ评分、肌酸激酶水平可能是预测是否发生呼吸衰竭的相关危险因素。  相似文献   

5.
有机磷农药中毒的中间综合征,出现与急性胆碱能危象之后,迟发性神经病之前,故称中间综合征,通常出现与急性中毒2~4d,个别在7d之后,突出的临床表现为肌无力,出现呼吸麻痹时,可出现不同程度的呼吸困难,严重者引起死亡。  相似文献   

6.
爱福丁中毒致胆碱酯酶下降5例临床分析   总被引:1,自引:0,他引:1  
爱福丁是一种新型高效非有机磷类杀虫剂,但中毒后胆碱酯酶却明显下降,而临床有机磷中毒症状轻,且无烟碱样症状,胆碱酯酶恢复慢,阿托品用量小,预后较好,治疗上与有机磷中毒有很大的不同,报告如下。  相似文献   

7.
目的 探讨急性有机磷中毒与心房颤动(房颤)的关系. 方法 回顾分析322例老年急性有机磷中毒患者的临床资料,选取其中36例发生房颤患者,同时选取年龄和性别均匹配的38例非房颤患者作为对照.对两组患者的胆碱酯酶(ChE)、心肌损伤标志物如肌酸肌酶(CK)及其同工酶(CK-MB)、肌钙蛋白(cTn-Ⅰ)进行对比分析. 结果 两组患者ChE均降低,房颤组ChE 10~3300U/L,平均(1126.42±1047.02)U/L,非房颤组ChE(178~3700)U/L,平均(1604.82±934.06)U/L,房颤组低于非房颤组(t=2.077,P=0.041).CK、CK-MB、cTn-Ⅰ两组患者均有不同程度增高.CK:房颤组(80~2212)U/L,平均(609.97±597.84)U/L;非房颤组50~2200 U/L,平均(462.84±530.71)U/L,两组差异无统计学意义(t=1.121,P=0.266).CK-MB:房颤组8~468 U/L,平均(97.31±104.50)U/L;非房颤组6~300 U/L,平均(55.16±69.62)U/L,房颤组高于非房颤组(t=2.052,P=0.044).cTn-Ⅰ:房颤组1.2~5.0 μg/L,平均(2.39±0.88)μg/L,非房颤组0.1~6.0 μg/L,平均(1.81±1.38)μg/L,房颤组高于非房颤组(t=2.132,P=0.036). 结论 急性有机磷中毒致房颤与ChE活力降低、乙酰胆碱(ACh)蓄积、心肌损伤可能有密切关系.  相似文献   

8.
本文分析73例有机磷农药中毒患者的临床资料并统计处理,发现心电图异常改变的患者中,神志不清的明显增多,且血胆碱酯酶活力明显降低或消失的心电图异常发生率明显增高,与正常者相比, 均有显著差异。提示心电图异常可反映临床病情轻重。  相似文献   

9.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

10.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

11.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

12.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

13.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

14.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

15.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

16.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

17.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

18.
Objective To explore the relationship between acute organophosphate poisoning and atrial fibrillation (AF). Methods Three hundred and twenty-two acute organophosphorus poisoning of elderly patients treated from January 2000 to June 2008 in our hospital were analyzed. Among these patients, 36 cases with AF were selected as case group and 38 age-gender-matched cases without AF were selected as control group. Serum cholinesterase (ChE), myocardial damage markers such as creatine kinase (CK), creatine kinase-MB isoenzyme (CK-MB) and Troponin- Ⅰ (cTn-Ⅰ) were compared between the two groups. Results ChE was decreased in the two groups, and ChE was lower in case group than in control group [(1126. 42±1047.02) vs. (1604.82±934.06)U/L, t= 2.07, P=0. 0414]. CK, CK-MB and cTn-Ⅰ were increased in different degree in the two groups. There was no difference in CK between the two groups [(609.97±597.84) U/L vs. (462.84± 530. 71)U/L, t= 1. 121, P= 0. 266]. CK-MB and cTn-I were higher in case group than in control group [(97.31±104.50) vs. (55. 16±69.62)U/L, t=2. 052,P=0. 0438; (2.39±0. 88) vs. (1.81± 1.38) μg/L, t = 2. 132, P = 0. 036, respectively9 . Conclusions AF caused by acute organophosphate poisoning may be related to the decrease of ChE activity, acetylcholine accumulation and myocardial injury.  相似文献   

19.
对急性有机磷农药中毒(AOPP)后反跳及中间综合征(I MS)等并发症的认识,使得AOPP的病死率显著下降,本文对重症AOPP并发呼吸衰竭与I MS诊治方面进行探讨。临床资料根据国家“急性有机磷农药中毒及分级诊断标准”[1]进行诊断及分级诊断,我院诊治的急性有机磷农药重度中毒并发呼吸衰竭45例(男3,女42),年龄22~71岁,平均年龄(26±8.2)岁,均为口服中毒,服毒量为50~350ml,其中DDV8例,160510例,105927例。中毒后20min内就诊5例,30min内10例,1h内15例,外院转诊15例。出现呼吸衰竭最早45min,最晚9h,平均5.5h。45例中有8例合并有I MS(男1,女…  相似文献   

20.
有机磷农药属有机磷酸酯类化合物,可经消化道、呼吸道、皮肤黏膜侵入人体,在体内与胆碱酯酶(CHE)结合形成较为稳定的磷化胆碱酶,而失去分解乙酰胆碱(Ach)的能力,造成Ach在体内大量蓄积,导致胆碱能神经与部分靶神经过度兴奋,继而转入抑制,出现一系列毒蕈碱样、烟碱样及中枢神经系统中毒等症状和体征[1,2].急性有机磷农药中毒(AOPP)是基层医疗机构急诊常见病症之一,如抢救不及时或治疗不当,患者可迅速死亡[3].本文就在急诊科对AOPP患者快速、彻底清除体内残留毒物,及早、正确、适量地使用阿托品和复能剂,并配合周密详尽的护理措施的临床疗效进行评价.  相似文献   

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