河豚毒素中毒48例分析

本院1997年2月～2002年12月收治河豚毒素中毒48例，现将抢救体会介绍如下。     

急性河豚毒素中毒致呼吸衰竭6例抢救成功的体会

我市位于长江中下游 ,因食用河豚而引起中毒者甚多 ,自1998年 1月至 2 0 0 1年 11月 ,我科共收治 74例急性河豚毒素中毒患者 ,其中 6例合并呼吸衰竭 ,均抢救成功。1　临床资料1.1　一般资料　 6例患者中男 5例 ,女 1例 ;年龄 30～ 6 2岁 ,平均年龄 4 5 .3岁 ;发病季节 2～ 4月份 4例 ,9～ 10月份 2例 ;中毒症状出现的时间为食用河豚后 0 .5～ 3.5小时 ,首发症状均为口唇、舌尖、肢端麻木。其中 5例表现为进行性四肢麻木无力、呼吸困难、发绀 ,直至呼吸肌麻痹 ;1例在昏迷 2小时后突然呼吸停止。从出现症状至呼吸衰竭的时间 :10分钟 1例 ,1.5…     

黏液水肿性昏迷1例分析

对我院表现较为典型的黏液水肿性昏迷1例分析如下。 1 病历摘要 男，87岁，因呼之不应4d于2007—12—18T16：00入院。患者入院前4d开始出现进食差、神志淡漠、意识逐渐不清。既往有高血压（3级）、冠心病史。查体：T〈35C，P62次／min，R16次／min，BP120／60mm Hg，昏迷状态，全身皮肤角化而僵硬，双肺可闻及痰鸣音，无哮鸣音，HR62次／min，律齐，未闻杂音，     

河豚鱼中毒患者救治流程的临床应用

目的探讨河豚鱼中毒患者规范的救治流程,以提高抢救成功率。方法在综合治疗的基础上,结合各个救治环节,采取相应的急救流程,包括院前急救流程、院中抢救室急救流程I、CU救治流程、普通病房护理流程,保证及时清除未被吸收的毒素及药物早期应用,适时选择机械通气的最佳时机,确保有效通气,缩短患者在院前急救、院中抢救室停滞的时间,使血液灌流得以早期开展。结果 36例河豚鱼中毒患者平均住院9 d,均抢救成功,康复出院,无并发症。结论河豚鱼中毒及时正确的抢救是治疗的关键,采用院前急救、院中抢救室急救、ICU救治、普通病房护理四位一体的救治流程组合,保证了抢救措施在最快时间内序贯实施,减少了工作的盲目性,提高了工作效率,可以极大地提高抢救成功率。     

河豚毒素中毒致心跳呼吸骤停1例

河豚毒素是河豚鱼含有的一种毒性剧烈的类神经毒素,性质比较稳定,其主要存在于卵、卵巢、皮肤、肝脏和血液中,肌肉一般无毒。河豚毒素有箭毒样作用,中毒后患者先后出现感觉、运动神经麻痹症状,严重者可因呼吸肌麻痹而死亡,目前尚无特效解毒药。我院近日成功抢救1例河豚毒素中毒致心跳呼吸骤停的患者,     

食用过期变质食用油严重中毒致死一例

患者女性 ,5 2岁。于 2 0 0 2年 10月15日食用久置残余变质的粗制葵花子油 (已混浊 ,有异味 )烧菜 ,5人共食。患者进食量较多 ,约于 1ｈ后出现恶心、呕吐 ,并逐渐口唇肢端发绀、头昏、乏力、胸闷、呼吸困难 ,于进食 2ｈ后由家属送入医院。体检 :体温Ｔ36 8℃、脉搏 96次 /ｍｉｎ ,呼吸 2 4次 /ｍｉｎ ,血压 14 / 8ｋＰａ ,(10 5 / 6 0ｍｍＨｇ) ,轻度烦躁不安 ,合作欠佳 ,呼吸急促。口唇、肢端明显紫绀 ,瞳孔对称等园 ,心肺未闻及异常。即往无心、脑、肺、肾疾病史。入院给予吸氧 ,输注葡萄糖液、ＶｉｔＣ、ＶｉｔＢ6 等 ,病情稍有好转 ,即…     

误食河豚鱼内脏中毒1例抢救分析

2008-01我院成功抢救1例误食河豚鱼内脏呼吸衰竭的患者[1],现将抢救体会报告如下。 1病历摘要 男,37岁。于2008-01-02误食了河豚鱼内脏,10 m in后感觉口唇、舌尖发麻,立即送往医院,途中随即出现四肢麻木无力、语言障碍、呼吸困难,30 m in后到急诊科,患者四肢肌肉麻痹、不能行走、血压测不到、HR 135次/m in、呼吸浅、慢,3次/m in;言语不清、甚至模糊。立即成立抢救小组组织抢救。经洗胃、气管插管、呼吸机辅助呼吸;静脉滴注呼吸兴奋剂可拉明、洛贝林、纳络酮,多巴胺、阿拉明持续静脉泵入9 h后患者神志清醒,自主呼吸恢复,转入监护病房,7 d后出院。     

脑梗死致急性假性球麻痹的临床护理

报告５０ 例脑梗死致急性假性球麻痹的临床护理。２４ 例为完全性假性球麻痹,２６ 例为不全性假性球麻痹。其主要表现为：吞咽困难、饮水呛咳、构音障碍。可致营养不良,吸入性肺炎,甚至窒息死亡。做好心理护理,有重点地针对吞咽困难所采取的鼻饲、喂食的护理和吞咽肌训练,加强呼吸道管理和其它基础护理对疾病的转归起重要作用。     

Metabolic acidosis and coma due to an overdose of nalidixic acid

A case of severe metabolic acidosis and coma after taking 28 g of nalidixic acid is described. After administration of 600 mEq of sodium bicarbonate the patient developed a respiratory alkalosis with secondary tetany. She recovered her state of consciousness nine hours later and the acid-base disturbance resolved after sixty hours.     

Prolonged coma due to cerebral fat embolism: report of two cases

Fat embolism syndrome remains a rare, but potentially life threatening complication of long bone fractures. The true incidence is difficult to assess as many cases remain undiagnosed. Cerebral involvement varies from confusion to encephalopathy with coma and seizures. Clinical symptoms and computed tomography are not always diagnostic, while magnetic resonance imaging is more sensitive in the detection of a suspected brain embolism. Two cases of post-traumatic cerebral fat embolism, manifested by prolonged coma and diffuse cerebral oedema, are presented. The clinical course of the disease as well as the intensive care unit management are discussed.     

Reversible tetraplegia due to polyneuropathy in a diabetic patient with hyperosmolar non-ketotic coma

Critical illness polyneuromypathy has not previously been reported as a complication of diabetic coma. We describe a patient with hyperosmolar non-ketotic coma (HONK) complicating gram-negative sepsis in whom persistent coma and profound tetraplegia caused considerable concern. Although, initially, it was feared that the patient had suffered a central neurological complication such as stroke or cerebral oedema, a diagnosis of critical illness motor syndrome (CIMS) was subsequently confirmed neurophysiologically. Profound limb weakness associated with HONK is not necessarily due to a catastrophic cerebral event, rather it may be a result of CIMS, which has an excellent prognosis for full neurological recovery. Received: 4 June 1999 Accepted: 22 September 1999     

Serum pancreatic enzymes in patients with coma due to head injury or acute stroke

Serum amylase and lipase were measured in 32 patients with cerebral ischemia, 19 with spontaneous cerebral hemorrhage, 15 with head injury and intracranial bleeding, and 22 with head injury without intracranial bleeding; 20 healthy subjects were also studied as controls. Serum pancreatic isoamylase concentrations were assayed in hyperamylasemic sera. The overall incidence of hyperamylasemia was 14% (12 of 88 patients: 4 with cerebral ischemia, 4 with spontaneous cerebral hemorrhage, 1 with head injury and intracranial bleeding, and 3 with head injury without intracranial bleeding). In 4 of the 12 patients the hyperamylasemia was of pancreatic origin: 1 patient with cerebral ischemia, 1 patient with spontaneous cerebral hemorrhage, 1 patient with head injury and intracranial bleeding, and 1 patient with head injury without intracranial bleeding. The incidence of hyperlipasemia was 7% (6 of the 88 patients: 1 patient with cerebral ischemia, 2 with spontaneous cerebral hemorrhage, and 3 with head injury without intracranial bleeding). We conclude that hyperamylasemia is more frequent than hyperlipasemia in patients with an altered state of consciousness due to head injury or stroke and is usually of non-pancreatic origin. This knowledge may save these patients from invasive and costly examinations.