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术后谵妄。第 1 部分:发病机制和危险因素。

Postoperative delirium. Part 1: pathophysiology and risk factors.

机构信息

Service d'Anesthésiologie, Centre Hospitalier Universitaire Vaudois et Université de Lausanne, Lausanne, Switzerland.

出版信息

Eur J Anaesthesiol. 2011 Sep;28(9):628-36. doi: 10.1097/EJA.0b013e328349b7f5.

Abstract

Delirium presents clinically with differing subtypes ranging from hyperactive to hypoactive. The clinical presentation is not clearly linked to specific pathophysiological mechanisms. Nevertheless, there seem to be different mechanisms that lead to delirium; for example the mechanisms leading to alcohol-withdrawal delirium are different from those responsible for postoperative delirium. In many forms of delirium, the brain's reaction to a peripheral inflammatory process is considered to be a pathophysiological key element and the aged brain seems to react more markedly to a peripheral inflammatory stimulus than a younger brain. The effects of inflammatory mediators on the brain include changes in neurotransmission and apoptosis. On a neurotransmitter level, impaired cholinergic transmission and disturbances of the intricate interactions between dopamine, serotonin and acetylcholine seem to play an important role in the development of delirium. The risk factors for delirium are categorised as predisposing or precipitating factors. In the presence of many predisposing factors, even trivial precipitating factors may trigger delirium, whereas in patients without or with only a few predisposing factors, a major precipitating insult is necessary to trigger delirium. Well documented predisposing factors are age, medical comorbidities, cognitive, functional, visual and hearing impairment and institutional residence. Important precipitating factors apart from surgery are admission to an ICU, anticholinergic drugs, alcohol or drug withdrawal, infections, iatrogenic complications, metabolic derangements and pain. Scores to predict the risk of delirium based on four or five risk factors have been validated in surgical patients.

摘要

谵妄在临床上表现为不同的亚型,从高警觉到低警觉不等。临床表现与特定的病理生理机制没有明确的联系。然而,似乎有不同的机制导致谵妄;例如,导致酒精戒断性谵妄的机制与导致术后谵妄的机制不同。在许多形式的谵妄中,大脑对周围炎症过程的反应被认为是病理生理的关键因素,衰老的大脑对周围炎症刺激的反应似乎比年轻的大脑更为明显。炎症介质对大脑的影响包括神经递质传递的改变和细胞凋亡。在神经递质水平上,胆碱能传递受损和多巴胺、血清素和乙酰胆碱之间复杂相互作用的紊乱似乎在谵妄的发展中起着重要作用。谵妄的危险因素可分为易患因素和诱发因素。在存在许多易患因素的情况下,即使是轻微的诱发因素也可能引发谵妄,而在没有或只有少数易患因素的患者中,需要重大的诱发因素才能引发谵妄。年龄、合并症、认知、功能、视力和听力障碍以及机构居住等已被充分证明的易患因素。除手术外,重要的诱发因素还包括入住 ICU、抗胆碱能药物、酒精或药物戒断、感染、医源性并发症、代谢紊乱和疼痛。基于四个或五个危险因素预测谵妄风险的评分已在手术患者中得到验证。

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