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灾难性颅脑损伤致脑膨出的脑肿胀机制——尸检研究。

Mechanism of brain swelling in cases of brain evisceration due to catastrophic craniocerebral injury - an autopsy study.

机构信息

Institute of Forensic Medicine, University of Belgrade - School of Medicine, 31a Deligradska str., Belgrade, 11000, Serbia.

Institute of Pathology, University of Belgrade - School of Medicine, Belgrade, Serbia.

出版信息

Forensic Sci Med Pathol. 2020 Mar;16(1):107-112. doi: 10.1007/s12024-019-00207-1. Epub 2020 Jan 28.

Abstract

Some previously reported cases of brain evisceration in catastrophic craniocerebral injuries showed the presence of brain swelling. The aim of this study was to observe the occurrence of focal or diffuse brain swelling in such cases in order to explain the underlying mechanism. An observational autopsy study included 23 adults, 18 males and 5 females, whose average age was 48 ± 22 years (range: 19-89 years) and who died as the result of catastrophic craniocerebral injury with brain evisceration. In all the examined cases, either focal (12 cases) or diffuse (11 cases) brain swelling was present. Grossly visible brain contusions (either cortical or deep) were rarely present - only in 6 out of 23 cases, while microscopic brain contusions were observed in 22 out of 23 cases, with 1 remaining case of microscopic subarachnoid bleeding. Blood aspiration in the lungs, as a vital reaction, was noted in 20 out of 23 cases. Microscopic examination showed absence of edema in 20 cases and mild edema in only 3 cases, while microscopic signs of moderate or severe edema were absent. Brain swelling in cases of brain evisceration likely represents a biomechanical reaction (i.e. decompression) due to a sudden decrease in intracranial pressure. The rapidity of death, together with marked absence of microscopic signs of edema, suggests that this is not a form of biological response to injury, but rather a pure physical phenomenon, strictly in a living person. In such cases, the occurrence of brain swelling and parenchymal microbleeding should be considered vital reactions.

摘要

一些先前报道的灾难性颅脑损伤导致的脑膨出病例显示存在脑肿胀。本研究旨在观察此类病例中是否存在局灶性或弥漫性脑肿胀,以解释其潜在机制。一项观察性尸检研究纳入了 23 名成年人,其中男性 18 名,女性 5 名,平均年龄为 48±22 岁(范围:19-89 岁),均因灾难性颅脑损伤伴脑膨出而死亡。在所有检查的病例中,均存在局灶性(12 例)或弥漫性(11 例)脑肿胀。肉眼可见的脑挫伤(皮质或深部)很少见——仅在 23 例中的 6 例中存在,而 23 例中有 22 例观察到显微镜下脑挫伤,1 例遗留显微镜下蛛网膜下腔出血。23 例中有 20 例肺部有血液抽吸的生命反应。显微镜检查显示 20 例无水肿,仅 3 例轻度水肿,而无中度或重度水肿的显微镜下表现。脑膨出病例中的脑肿胀可能代表一种生物力学反应(即减压),由于颅内压突然降低所致。死亡的迅速性,加上明显缺乏水肿的显微镜下表现,提示这不是对损伤的生物反应,而是一种纯粹的物理现象,严格来说是在活体中发生的。在这种情况下,脑肿胀和实质微出血应被视为生命反应。

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