Factors associated with hemispheric hypodensity after subdural hematoma following abusive head trauma in children

儿童虐待性头部外伤后硬膜下血肿导致半球低密度的相关因素

阅读:1

Abstract

Abusive head trauma (AHT) is a unique form of pediatric TBI with increased mortality and neurologic sequelae. Hemispheric hypodensity (HH) in association with subdural blood after AHT has been described. Though risk factors for HH are not understood, we hypothesized that risk factors could be identified. We retrospectively enrolled children under 5 years with TBI secondary to AHT (child advocacy diagnosis) who had undergone initial and interval brain imaging. Records were interrogated for prearrival and in-hospital physiologic and radiographic findings. HH was determined by a blinded observer. Twenty-four children were enrolled and 13 developed HH. HH was not significantly associated with age, initial Glascow Coma Scale, or mortality. Pediatric Intensity Level of Therapy (PILOT) scores (p=0.01) and daily maximal intracranial pressure (ICPmax; p=0.037) were higher in HH. Hypoxia, hypotension, cardiopulmonary arrest, need for blood transfusion, and daily blood glucoses tended to be greater in HH. Whereas all children with HH had acute subdural hematoma (SBH), many children without HH also had subdural blood; the presence of skull fracture was more likely in the children who did not develop HH (p=0.04), but no other intracranial radiographic pattern of injury was associated with HH. Surgical intervention did not appear to protect against development of HH. A variety of insults associated with ischemia, including intracranial hypertension, ICP-directed therapies, hypoxia, hypotension, and cardiac arrest, occurred in the children who developed HH. Given the morbidity and mortality of this condition, larger studies to identify mechanisms leading to the development of HH and mitigating clinical approaches are warranted.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。