雷氏综合征的病因、病理生理及治疗

Gudisa Bereda
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摘要

雷氏综合征是一种致命的双相疾病,临床表现为先前的病毒性疾病、脑病发病前1至2天的持续性呕吐和肝功能障碍。雷氏综合征的特征可表现为谵妄、发热、抽搐、呕吐、呼吸系统衰竭、麻木、癫痫发作或昏迷等一系列症状,通常是早期病毒性疾病后的症状。脑病可在24至48小时内由昏睡迅速发展为昏迷。普遍线粒体损伤和甘油三酯积累是雷氏综合征的基础病因学。高浓度氨的积累导致脑病和无黄疸性肝炎,肝酶升高3倍。雷氏综合征常见的病理生理机制是诱导线粒体通透性转变。该综合征与高死亡率相关,治疗是对症的,包括重症监护管理,纠正代谢异常,特别是低血压、低血糖和酸中毒,控制抽搐,监测脑水肿引起的颅内高压。通常也使用降低血清氨浓度的药物,最常用的是硫酸新霉素或乳果糖。应给予昂丹司琼等止吐药以抑制呕吐和潜在的误吸。
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Etiology, pathophysiology and management of reye’s syndrome
Reye’s syndrome is defined as a fatal biphasic disorder that clinically described by preceding viral illness, protracted vomiting from one to two days before the onset of encephalopathy and liver dysfunction. Reye’s syndrome can be characterized as a constellation of delirium, fever, convulsions, vomiting, respiratory collapses, stupor, seizures, or coma typically following an earlier viral illness. Encephalopathy can be frequently progresses rapidly from lethargy to coma within twenty four to forty eight hrs. Both universal mitochondrial injury and triglyceride accumulations are the cornerstone etiology of Reye’s syndrome. Accumulation of high concentration of ammonia leads to encephalopathy and anicteric hepatitis with three times rise in liver enzymes. A frequent pathophysiological mechanism of Reye’s syndrome is induction of the mitochondrial permeability transition. The syndrome is correlated with a high mortality rate and the treatment is symptomatic including intensive care management with correction of metabolic abnormalities especially of hypotension, hypo glycaemia and acidosis, control of convulsions, and monitoring of intracranial hypertension due to cerebral edema. Agents to decrease serum ammonia concentrations are also usually used, the most frequent being are neomycin sulfate or lactulose. Anti-emetic such as ondansetron should be given to inhibit vomiting and potential aspiration.
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