氟乙酰胺中毒50例心电图分析

目的利用心电图描记术了解氟乙酰胺中毒致心肌损害的情况及其对病情的判断。方法对50例氟乙酰胺中毒患者的心电图改变进行分析。结果32例心电图表现为正常图形者均为氟乙酰胺轻、中度中毒;12例重度中毒者心电图均有ST—T相应改变;2例频发室早;3例出现QT延长;2例重度中毒者因并发中毒性心肌炎、心力衰竭而死亡。结论心电图描记的心肌缺血的图形改变与氟乙酰胺中毒的严重程度呈正相关,心电图的改变可作为判断病情的一个指标。     

急性氟乙酰胺中毒患者的心肌酶测定及其意义

氟乙酰胺(ｆｌｕｏｒｏａｃｅｔａｍｉｄｅ)是一种高效、剧毒、高残留的有机氟类杀虫剂,也曾用作杀鼠剂,纯品为无臭、无味、不易挥发的白色针状结晶,易溶于水。我院自1996年1月至1998年12月共收治急性氟乙酰胺中毒患者42例,并检测了急性氟乙酰胺中毒患者的心肌酶,旨在探讨其变化与中毒程度及预后的关系。一、资料与方法1临床资料:本组42例急性氟乙酰胺中毒者均为急救中心住院病人,男30例,女12例,年龄3～56岁,其中误服37例,自杀5例,误服者均服食带有氟乙酰胺的食物,自杀者服食市售氟乙酰胺液2～4ｍｌ,服后至就诊时间长者118ｍｉｎ,最短为26ｍ…     

肝性脑病中氧化应激参与氨中毒的研究进展

肝性脑病是一种严重的肝脏衰竭综合征,临床表现出一系列神经精神病学和神经肌肉上的症状.肝性脑病的病理生理学基础尚不明确,目前普遍认为氨在其中起到关键作用.近年,人们发现氧化应激参与到肝性脑病的病理生理学级联反应中,并与氨中毒学说存在一定的联系.此文将着重就氧化应激与氨中毒学说的研究进展作一综述.     

急性氟乙酰胺中毒的抢救及护理

氟乙酰胺是一种高效、剧毒、残留性强的有机氟杀鼠剂,为神经毒。进入人体主要造成神经系统及心肌的损害。氟乙酰胺中毒如抢救不及时,可使细胞产生难以逆转的病理改变,甚至死亡。如果救治及时,可痊愈出院。我院自1997年12月-1998年6月共收治7例氟乙酰胺中毒患,经积极抢救和采取和效护理措施,除1人严重中毒死亡之外均痊愈出院。现将抢救中的护理体会报告如下。     

8例氟乙酰胺中毒患者的急救护理

氟乙酰胺是一种毒鼠药,纯品为无味无嗅的白色针状结晶,易溶于水,是一种高效剧毒有机氟杀虫农药。误服后经消化道吸收而引起中毒,既往对于有机磷中毒的报道很多,但对于氟乙酰胺中毒的服道甚少,仅在近几年才有报道,氟乙酰胺进入机体主要损害中枢神经系统,消化系统,心血管系统及糖代谢。在短期内损害或     

氟乙酰胺中毒35例救治体会

目的总结氟乙酰胺中毒临床救治经验,提高救治水平。方法对35例氟乙酰胺中毒患者的临床资料进行回顾性分析。结果 35例患者入院时均已处于昏迷、频繁抽搐、呼吸衰竭和休克状态,经紧急救治,治愈出院33例(94.3%),死亡2例(5.7%)。结论早期确诊、及时清除毒物和使用特效解毒剂、控制抽搐及脑水肿、针对性地处理呼吸衰竭是氟乙酰胺中毒救治成功的关键。     

42例急性氟乙酰胺中毒患者的血清心肌酶谱变化及意义

1998年1月～2005年12月，我们共检测了42例急性氟乙酰胺中毒患者和30例健康查体者的血清心肌酶谱。旨在探讨急性氟乙酰胺中毒患者心肌酶谱的变化特点及其与中毒程度、预后的关系。     

急性氟乙酰胺中毒致肾脏损害16例临床分析

氟乙酰胺是一种高效剧毒、残留性强的有机氟杀鼠剂。中毒后常致心、脑、肺、肝、肾等多脏器损害。近年对心血管、肝脏及中枢神经系统损害已屡见报道 ,但对肾脏损害报道较少。现将我院近 6年来收治的 6 3例急性氟乙酰胺中毒患者中有肾脏损害的 16例作一临床分析。临床资料一般资料　 6 3例患者中有肾脏损害表现的 16例 ,占2 5 %。其中男 9例 ,女 7例 ;年龄 4～ 6 8岁 ,平均 2 6 .8岁。 16例均为口服中毒 ,服毒至就诊时间 0 .5～ 16ｈ。临床表现均有呕吐、抽搐、惊厥及心肌酶谱异常等氟乙酰胺中毒的典型症状。对其中 10例的毒饵或洗胃液进行毒…     

窒息引起急性心肌损伤和Ⅲ度房室传导阻滞一例

窒息引起急性心肌损伤和Ⅲ度房室传导阻滞(AVB)者临床较为少见,现将我们遇到1例报道如下: 患儿女性,4岁。因洋金花中毒昏迷6天在当地治疗无效,1990年6月20日以洋金花中毒、中毒性脑病被收入我院。21日10时10分患儿突然窒息,面     

8例氟乙酰胺中毒患者的急救护理

氟乙酰胺是一种毒鼠药，纯品为无味无嗅的白色针状结晶，易溶于水，是一种高效剧毒有机氟杀虫农药。误服后经消化遭吸收而引起中毒，既往对于有机磷中毒的报道很多，但对于氟乙酰胺中毒的服道甚少，仅在近几年才有报道，氟乙酰胺进入机体主要损害中枢神经系统，消化系统，心血管系统及糖代谢。在短期内损害或破坏人体某些组织器官的生理功能或组织结构而引起一系列症状和体征，甚至危及生命。     

Reversible leukoencephalopathy caused by 2 rodenticides bromadiolone and fluroacetamide: A case report and literature review

Rationale:With the easy access, rodenticide poisoning has been a public health problem in many countries. Characteristics of central nervous system (CNS) lesions induced by rodenticides are scarcely reported.Patient concerns:We presented a case of a 40-year-old man with seizure and consciousness disorder, coagulation dysfunction, and symmetric lesions in white matter and corpus callosum.Diagnosis:He was diagnosed with rodenticide poisoning due to bromadiolone and fluoroacetamide.Interventions:He was treated with vitamin K, hemoperfusion, acetamide, and calcium gluconate.Outcomes:His leukoencephalopathy was reversed rapidly with the improvement of clinical symptoms.Lessons:This report presented the impact of rodenticide poisoning on CNS and the dynamic changes of brain lesions, and highlighted the importance of timely targeted treatments.     

Clinical manifestations of childhood lead poisoning

Clinical characteristics of 58 patients admitted to Bustamante Hospital for Children with lead poisoning are described. The most common source of lead exposure was backyard battery smelters and most (58%) of the patients were aged below 3 years. Lead toxicity was more severe in younger children as evidenced by higher lead levels and greater incidence of encephalopathy. Patients with lower haemoglobin values had relatively higher lead levels and significantly higher incidence of encephalopathy. Radiological evidence of lead poisoning was present in 96% of our patients demonstrating the usefulness of X-rays in diagnosis, particularly in areas where blood lead levels are not easily available.     

Clinical and radiological studies on 15 cases of acute phosgene poisoning]

A clinical and radiological observation on 15 cases of acute phosgene poisoning were reported. The pulmonary edema after acute phosgene poisoning can be classified into two types: interstitial and alveolar. The X-ray findings were described in detail in correlation with the clinical symptoms. Taking X-ray early can benefit on preventing and treating acute pulmonary edema. Meanwhile, the patients with chronic respiratory or digestive diseases can develop pulmonary encephalopathy or upper gastrointestinal bleeding after acute phosgene poisoning.     

Liver transplantation in mushroom poisoning

Liver transplantation plays an important role in the treatment of patients with fulminant hepatic failure (FHF). Early determination of prognosis in cases of FHF is important to allow prompt decision-making regarding the need for liver transplantation. Mushroom poisoning is a rare cause of FHF, and as a result, prognostic criteria are not well recognized. It appears that the severity of coagulopathy and encephalopathy predicts a poor outcome, whereas the degree of bilirubin elevation may not. We present a case of FHF related to mushroom poisoning that required liver transplantation. The clinical presentation, medical management, and prognostic criteria in mushroom poisoning are discussed.     

Uncommon sources and some unsual manifestations of lead poisoning in a tropical developing country

Lead-containing cooking utensils, sometimes used in South Indian homes, and indigenous medications, widely used in India and increasingly in developed countries, may be responsible for lead intoxication in adults. We report chronic lead poisoning in five adult patients. Not all patients had abdominal colic, while dramatic weight loss, depression and encephalopathy were seen. Once recognized, lead poisoning is treatable and sometimes preventable. Response to chelation therapy with agents such as calcium ethylenediaminetetraacetate (CaEDTA) is impressive, although several courses of therapy may be necessary.     

Acute liver injury,acute liver failure and acute on chronic liver failure: A clinical spectrum of poisoning due to Gyromitra esculenta

Gyromitra esculenta, also known as “false morel” is one of the most poisonous mushrooms. This species is found all over the world, growing in coniferous forest in early spring time. Common manifestation of poisoning includes gastrointestinal symptoms which include varied degrees of liver impairment.We describe three cases: acute liver injury, acute liver failure and acute-on-chronic liver failure due to G. esculenta poisoning. At admission patients presented with encephalopathy and features of liver failure. Two of them recovered completely following supportive management while the remaining patient who also had preexisting liver disease developed multiorgan failure and subsequently died.Although a rare occurrence, G. esculenta poisoning should be considered in the differential diagnosis of acute liver failure.     

Neurological Manifestation of Recreational Fatal and Near-Fatal Diethylene Glycol Poisonings: Case Series and Review of Literature

Diethylene glycol is a common industrial solvent which is responsible for accidental and epidemic poisoning as early as the 1930s. Due to the unavailability and unaffordability of ethanol, people in Qatar among the low income group are consuming household chemicals, some of which contain diethylene glycol, for recreational purposes.The history of ingestion is usually not volunteered and the initial clinical presentation is usually nonspecific, making it difficult to diagnose from the clinical presentation. Moreover, the biochemical profile varies with time, making the diagnosis more difficult. The neurological course and toxicity is less well characterized than its renal counterpart. Moreover, reports in the literature of such recreational poisoning is lacking particularly in the region.Three cases of recreational diethylene glycol poisoning seen in Hamad General Hospital, Doha, Qatar from 2009 to 2012 are detailed here.These illustrate the clinical course with emphasis on the neurological sequelae that include encephalopathy and multiple cranial and peripheral neuropathies with fatal and near-fatal outcomes. Neuroimaging in 2 were initially normal, but follow-up imaging showed brain atrophy. The third patient’s neuroimaging showed diffuse brain edema with evidence of transtentorial herniation. Nerve conduction studies were performed in 2 of the 3 cases and showed evidence of mixed sensorimotor neuropathy. The outcomes were death in 1 and severe neurological morbidity and disability in 2 cases.Diethylene glycol is a dangerous substance when ingested and can result in mortality and severe morbidity, particularly from the renal and neurological manifestations. Whereas the mechanism of damage is less well known, the damage is likely dose related. The typical clinical pattern of evolution of the poisoning in the absence of cost-effective ways to detect it in the serum can help clinicians in making the diagnosis.Neurological manifestations may include encephalopathy and multiple cranial and peripheral neuropathies with subsequent brain atrophy. Public awareness of the danger of such recreational use should be raised.     

高压氧联合机械通气治疗重度急性一氧化碳中毒的疗效简

目的 探讨高压氧联合机械通气治疗重度急性一氧化碳中毒的疗效.方法 选取2010年1月～2012年12月于我院MICU进行治疗的28例重度CO中毒患者为研究对象,将其分为对照组（高压氧组）和观察组（高压氧联合机械通气组）各14例,两组患者均同时给予预防感染、防治脑水肿、促进脑细胞代谢等治疗.结果 观察组平均住院时间、昏迷时间短于对照组;迟发性脑病发生率低于对照组;总有效率高于对照组.治疗后6 h,24 h观察组的血氧分压（PaO2） 、碱剩余增加高于对照组,血二氧化碳分压（PaCO2）、CRP、TNF-α、心肌酶谱水平均低于对照组.结论 高压氧联合机械通气治疗重度急性一氧化碳中毒可明显减轻病情,缩短住院时间,改善预后.     

Urea cycle disorders

Deficiency of any of the five enzymes in the urea cycle results in the accumulation of ammonia and leads to encephalopathy. Episodes of encephalopathy and associated symptoms are unpredictable and, if untreated, are lethal or produce devastating neurologic sequelae in long-term survivors. Although these disorders do not produce liver disease, the consequences of hyperammonemia resemble those seen in patients with hepatic failure or in a transient interference with the urea cycle, as seen in some forms of organic acidemias. Therefore, investigation for hyperammonemia in any infant or child with altered mental status (in the absence of obvious causes, such as trauma, infection, or poisoning) is essential for prompt diagnosis of urea cycle disorders and institution of treatment to avoid brain damage and death. This article addresses the function of the urea cycle and the diagnosis and management of urea cycle disorders.     

Acute kidney failure caused by paracetamol poisoning

Paracetamol poisoning is manifested by hepatotoxicity, but acute renal failure is very rare, especially when there is no fulminant hepatic damage with encephalopathy or severe haemodynamic alterations. We present here the case of a 22-year-old woman who presented with acute renal failure after the ingestion of 11.5 g of acetaminophen. The clinical course and laboratory data were consistent with tubular necrosis. The patient required hemodialysis, but finally renal function returned to normal. The acetaminophen pharmacology and the differential diagnosis of acute azotemia in paracetamol overdosage are reviewed.