急性避蚊胺中毒致多脏器功能衰竭并死亡1例

急性避蚊胺中毒临床罕见。通过回顾性分析收治的1例急性避蚊胺中毒导致多脏器功能衰竭并死亡患者的临床资料,结合文献,探讨急性避蚊胺中毒的救治措施。患者口服大量避蚊胺后,迅速出现昏迷,循环、呼吸等多器官功能衰竭,予以洗胃、血液灌流、血浆置换清除体内毒物,持续静脉-静脉血液滤过稳定内环境及容量管理,抗休克、保护重要脏器等治疗后,患者循环仍难以维持,最终救治效果不佳而死亡。在避蚊胺中毒救治过程中建议多种血液净化方式联合应用,如循环仍难维持,条件允许可尝试体外膜肺氧合治疗,帮助患者度过急性期,避免因循环衰竭加重脏器功能损伤。     

氟乙酰胺中毒致多脏器功能衰竭45例报告

氟乙酰胺是一种高效、剧毒、内吸收性强的有机氟杀虫剂，农村常用来浸渍食物以诱杀灭鼠，如果被人误食，或者自杀时服用，可引起中毒。从1996年至2001年作者共抢救本院收治的氟乙酰胺中毒并多脏器功能衰竭(MOF)病人45例。现报道如下。     

腹透治疗重症鱼胆中毒致多脏器功能衰竭

我院自1990年1月2002年1月收治重症鱼胆中毒致急性肾功能衰竭伴严重肝损或/和心脏损害符合多脏器功能衰竭病人10例,均以腹膜透析(腹透)方法抢救治疗,取得良好疗效,现报道如下。 1 临床资料 1.1 一般资料本文10例,男6例,女4例,年龄28岁～63岁,平均42岁。10例均以生食鱼胆后出现消化道症状。次日     

误服氯化汞致多脏器功能衰竭一例报告

该文报道一例患者因误服氯化汞(3.0g),超过致死剂量约2.5倍,由于当时处理措施不当,到上级医院虽经各种急救措施救治,终因汞中毒过重,多脏器功能衰竭而死亡。     

鱼胆中毒致多脏器功能失常综合征12例

我科 1990年～ 2 0 0 0年收治鱼胆中毒致多脏器功能失常综合征 (MODS) 12例 ,报告如下 :1　资料与方法1.1　一般资料　男 8例 ,女 4例 ;～ 3岁 1例 ,～ 7岁 5例 ,～ 14岁 6例。服生鱼胆前均无肝、肾疾病史。服生鱼胆 1～2个 ,鱼种为草鱼、鲤鱼、青鱼等。发病急 ,9例在食鱼胆后1～ 4小时发病。1.2　临床表现　患儿均以恶心、呕吐、腹痛、腹泻等胃肠道表现为首发症状 ,症状轻重不一。 12例均有肾损害 ,10例发生急性肾功能衰竭 (ARF) ,均有少尿或无尿 ,多在病后 6小时～ 5天 ,持续 3～ 12天。浮肿 7例 ,腹水 3例 ,胸水 1例。蛋白尿 4例 ,肉…     

百草枯中毒多脏器功能失常综合征1例

本例病人服百草枯后,短时间内出现呼吸衰竭、肾功衰竭、中毒性肝损害、便血等多脏器功能失常表现,治疗效果不佳。     

急性化学物中毒性多脏器功能失常综合征临床分析

目的：探讨急性化学物中毒性多脏器功能失常综合征（MODS）的临床特点。方法：对173例急性重度化学物中毒致多个脏器损害的病例进行分析。 结果：凡能对机体造成重大打击的化学物均可引发MODS,其发病机制主要有两个特点,可为化学物的直接作用或间接作用（继发性损害）,发病类型以原发性多见（占80．76％）,病死率与脏器衰竭的数目,受害程度及急性中毒病因治疗是否及时得当有关。结论：急性化学物中毒性MODS与其它病因所致MODS不尽相同,具有其独特的临床特点。将各脏器功能失常指标分为功能损害和功能衰竭二期可以体现诊断标准的连续动态,功能损害期是早期救治降低MODS病死率的关键时期,在诊断标准中列入相当必要。     

肝硬化并发多脏器功能衰竭67例治疗体会

目的：探讨肝硬化并发多脏器功能衰竭（MOF）的原因及预防措施。方法：对近10年来收治的67例肝硬化合并多脏器功能衰竭的临床资料进行分析。结果：老年组MOF的发生率、衰竭器官数目及死亡率高于非老年组，病死率与衰竭组器官数目呈正相关。结论：早期诊断，严密监护，积极有效地改善肝细胞功能，加强首衰器官的治疗，是除低MOF病死率、提高治愈率的关键。     

急性重度一氧化碳中毒合并多脏器功能衰竭1例报告

1　病例摘要患者谭×× ,男 ,63岁。于 1998年 8月 2 4日晚约 10时入睡 ,因家中煤气管道泄漏 ,大量煤气外溢 ,次日晚 5时许被家人发现昏迷在床上 ,伴抽搐及二便失禁 ,身旁有呕吐物。同室内另一人亦发病 ,症状相同 ,既往身体健康。入院查体　Ｔ 3 7.5℃ ,Ｐ 90次 /分 ,Ｒ 18次 /分 ,ＢＰ 15 0 /10 0ｍｍＨｇ。深昏迷 ,压眶无反应 ,球结膜充血、水肿 ,双瞳孔等大、等圆 ,直径 2毫米。对光反射消失。口唇紫绀 ,左下肺少许干鸣音 ,未闻及湿罗音 ,心率 90次 /分 ,律齐。肝、脾肋下未触及。双下肢无浮肿。双膝反射迟钝 ,双侧巴彬氏征阳性。辅助检…     

酒精中毒并发多脏器功能衰竭20例报告

酗酒是当今世界范围的一个重要的公共卫生问题。它不仅危害社会治安环境等 ,严重影响了人体健康 ,嗜酒者的死亡率比一般人群要高 1～ 3倍。内科急症病情严重者可出现多个器官功能衰竭 ,其中神经系统疾患、肝脏、心血管病的患病率比一般人群高 2 0 %。本文对 2 0例酒精中毒合并多器官功能衰竭的患者加以报告分析。1　临床资料我们于 1999年 12月至 2 0 0 1年 12月共收治酒精中毒患者160例 ,其中并发多脏器功能衰竭 2 0例 ,男 14例 ,女 6例 ,年龄 2 5～ 60岁 ,饮酒史 6～ 32年不等 ,平均每日饮酒量 80～45 0ml (纯酒精含量 )不等 ,且统计表明…     

一例毒蕈中毒致多脏器功能衰竭患者获救

一例毒蕈中毒致多脏器功能衰竭患者获救李凤辉（湖南省衡东县中医院４１２４００）我院于１９９４年５月收治一例毒蕈中毒致多脏器功能衰竭患者［１］，经精心治疗和护理而获救。１临床资料患者，男，４２岁，湖南省衡东县人。因误食大量毒蕈而出现头晕、呕吐、腹痛、昏迷...     

毒蕈中毒致多脏器功能损害10例分析

毒蕈又称毒蘑菇 ,作为一种野生植物在我国内生长的有８０多种 ,不同类型的毒蕈含有不同的有毒成份 ,但一种毒蕈也可含多种毒素。由于不少毒蘑菇与食用蘑菇外形不易区别而误食致群体中毒 ,其毒素可致全身多脏器功能受损 ,病死率高 ,近几年我院收治毒蕈中毒１０例 ,临床分析如下     

儿童苍耳子中毒致多脏器功能障碍1例报告

报道1例儿童因急性苍耳子中毒致多脏器功能障碍的病例资料及救治经过,探讨苍耳子中毒的临床表现和治疗方法,以提高苍耳子中毒的救治成功率.     

1例多系统脏器功能衰竭抢救成功的护理体会

多系统器官衰竭 (ＭＳＯＦ) ,又称多器官衰竭 ,是指病人因严重感染、创伤、失血、大手术等应激状态下机体出现的两个以上的脏器同时或先后发生的功能衰竭 ,涉及心、肝、脑、肺、肾以及胃肠、代谢、凝血、免疫等各系统功能。据文献报道 ,2个器官受累死亡率为 4 4%～ 6 0 % ,4个以上器官受累死亡率为10 0 % [1] 。我院 2 0 0 0年 12月成功抢救了 1例ＭＳＯＦ ,即 4个脏器受累的病人 ,就此例ＭＳＯＦ病人抢救成功的护理体会作以下介绍。患者女性 ,4 5岁。入院诊断为慢性肾功能不全 ,尿毒症。于 2 0 0 0年 11月 11日行肾移植手术 ,术后第 6天出…     

妊娠合并多脏器功能衰竭15例临床分析

目的：探讨妊娠合并脏器功能衰竭MSOF的致病因素,对母婴的影响及防治方法。方法：分析15例妊娠合并MSOF的临床资料。诊断标准,治疗方法。结果：妊娠合并MSOF是一种后果恶劣的妊娠综合征,本文15例中死亡5例,病死率为33．3％,围产儿死率7例（7／16）,死亡率为437．5‰;结论：妊娠合并MSOF是孕产妇和围产儿死亡的主要原因,应加强围产期的系统管理。高危孕产妇应及时转诊,对MSOF的治疗应针对病因,及时去除或减少引起MSOF的诱因,如出血,感染,子病等,阻止过强的应激反应,使MSOF不发生或程度减轻,对妊娠合并征,并发症在产前出现主要脏器功能损害,应果断终止妊娠,减少继续妊娠对母体的损害,对患者应加强监护,注意支持和对症治疗及人工器官如人工呼吸机,血液秀析等的应用。     

婴幼儿重症肺炎并多脏器功能衰竭52例临床分析

目的分析治疗婴幼儿重症肺炎并多脏器功能衰竭的效果。针对婴幼儿重症肺炎并多脏器功能衰竭,应做到早期诊断,早期治疗,并采取综合措施,有预见性地进行干预治疗。方法 2年来收住婴幼儿重症肺炎314例,并发多脏器功能衰竭52例,经过早期诊断,早期治疗纠正缺氧,保持呼吸道通畅,保护心、脑、肺、胃肠功能、肾功能,尽量不让多个器官受损。结果治愈35例,死亡12例,自动出院5例。其中合并2个系统器官衰竭30例,3个以上系统器官22例,从病史中可以看出多个脏器(3个以上受损,病情越重,病死率越高,达40%;而2个器官以下受损,病死率低,为7.4%。结论对婴幼儿重症肺炎并多脏器功能衰竭,尽量做到超前性干预治疗,可缩短病程,提高治愈率。     

多脏器功能衰竭的代谢与营养支持

The problems of inflammation and infection leading to organ dysfunction and failure continue to be the major concerns after injury and operations and with the intensive care for many diseases and problems.When systemic inflammatory response syndrome (SIRS) goes to multiple organ dysfunction syndrome (MODS) and multiple organ failure (MOF),the mortality ecomes high,ranging from 30-80% depending on the number of failed organs.In MOF or MODS respiratory failure develops with the need for ventilaroty support,accompanied by circulatory instability with depression of cardiac output and a decrease in peripheral resistance,depression of the immune system,coagulation defects,gastrointestinal problems,a rising bilirubin denoting hepatic dysfunction and central nervous depression.The elevation in whole body protein turnover after sepsis and trauma usually is accompanied by an increase in metabolic rate Hepatic output of acute phase proteins rises,lean tissue is catabolized to provide energy substrates for wound and inflammatory tissue.Plasma proteins drop due to inhibition of hepathic synthesis,an increase in capillary permeability,and the dilutional effect of extracellular fluid expansion can be observed.Muscle protein synthesis seems to be decreased.These changes are driven by a combination of the counterregulatory hormones (catecholamines,glucagon,cortisol,growth hormone) and the direct and indirect actions fo the various inflammatory mediators (IL-1,IL-6,and TNF),prostaglandins and kallikreins.The changes in whole body protein turnover seen in MOF are similar to those described in overt sepsis and severe trauma:both synthesis and degradation are elevated,with a higher rate of degradation.This situation result in a loss of body mass, predominantly lean tissue.Although it is not oftern possible to identify the orgin of the “sepsis”,it must be reasonable to regard patients with MOF metabolically as “severely septic”.In recent years,the gastrointestinal tract was thought to be the ongoing inflammatory stimulus and the cause of MOF.In the presence of sepsis and shock and lack of nutrient intake,endotoxin and bacteria translocate from the lumen of the gut into the portal and systemic circulations and set up a systemic inflammatory reaction with release of inflammatory mediators.The evidence for the gastrointestinal tract as the “motor”for MOF,however,is derived largely from animal work,and the direct evidence duppotyinh gut permeability as a cause of MOF in man is less convincing,although early and aggressive enteral feeding afger major abdominal injury has been shown to diminish the incidence of major septic complications.On the other hand,there are problems associated with enteral feeding in MOF.This is due sometimes to local damage from peritoneal sepsis but often from deleterious effects of high levels of sympathetic activation on the gastrointestinal tract,combined with some fo the sedative and cardiovascular drugs used to facilitate artificial ventilation or to support the cardiovascular system that also adversely affect gastrointestinal motility.The use of parnteral nutrition in combination with the so-called minimal enteral nutritional support in critically ill patients is mandatory in order to preserve organ function and to avoid deleterious side effects.This strategy of combining the two ways of artificial nutrition is based on the idea to use the gut,if it works,and to complete the full range of essential nutrient supply by the parenteral route.As energy donors,lipid emulsions are an integral element of parenteral nutrition regiments for critically ill patients.Moreover lipids are not only structural building blocks of cells and tissues but at the same time suppliers of C atoms for a number of biosynthetic pathways as well as carriers of essential fatty acids and fat-soluble vitamins.In addition,faty acids are precursors of prostaglandins other eicosanoids and therefore have important metabolic functions.Over the years,for the supply of lipids in the filed of parenteral nutrition,different concepts have been developed.Lipid emulsions derived from soybean or safflower oil contain excessive quantities of PUFA and insufficient amounts of α-tocopherol.Their parenteral use can rapidly lead to an unbalanced pattern of eicosanoids and is associated with an increased production of peroxidative catabolites.In order to avoid negative effects from these metabolic procucts,it is recommended to use preparations with a reduced content of PUFA in combination with an enrichment in α-tocopherol.Indeed the physical mixture of MCT and LCT is a well-proven concept in the parenteral nutrition of critically ill patients.Having a demonstrably higher utilization rate,MCT-containing lipid emulsions do not impair liver function,produce less immune and no RES function compromise,and do not interfere with pulmonary hemodynmics or gas exchange.Newer preparations based on structured triglycenrides or lilve oil appear to achieve the same goal,I.e.reducing the n- PUFA intake.These new lipid emulsions are safe and wel tolerated.Further studies are necessary to investigate potential benefits compared to the physical mixture of MCT/LCT in a clinical environment.A promising substrato in the evolution of parenteral lipid emulsions can be seen in fish oils (n-3 fatty acids).Their fixed combination in a physical mixture of MCT/LCT displays a great number of fascinating aspects.With regard to current literature,n-3 fatty acids have a beneficial influence on the pathophysiological response to dndotoxins and exert important modulations on eicosanoid and cytokine biology.Furthermore their intravenous use may improve organ perfusion in different critical situations.     

急性甲醇中毒致多脏器损害1例

急性甲醇中毒致多脏器损害１例王玲安蒋淑珍武淑荣王振馥王纪云尚玉惠患者男，３４岁，某材料厂反修腐工。工作程序为将甲苯、丁苯胶投入反应罐内加热至９０℃１小时后成成品。于１９９４年３月２０日原料厂家错把甲醇当成甲苯投出（原料筒无标记），于７时３０分患者将丁...