Characterization of Acute Pediatric Anoxic Brain Injury in Non-fatal Drowning Using MRI

项目摘要/摘要 这是一项初步研究，旨在确认继发性儿童急性缺氧性脑损伤(ABI)的局部损害。 使用磁共振成像(MRI)进行非致命性溺水。溺水是第三大死因 在全世界范围内，意外伤害的发生率最高，幼儿(1-4岁)发病率最高。虽然 溺水(即浸泡/浸泡在液体中)会导致多器官损伤，这是最具破坏性的残疾 脑部损伤的结果。 目前的诊断神经影像表现(主要是通过定性的视觉检查)是非特异性的，并提供 结论急性脑损伤对儿童急性脑损伤的预后及治疗干预无指导意义。 溺水身亡。我们的初步核磁共振研究显示慢性ABI的病变仅限于豆状纹状核。 分布，这是一个动脉末端分水岭，类似于中风的局灶性缺血。我们发现 局限性损伤表现为灰质萎缩和脑白质微结构异常。 在扩散张量图像(DTI)上，通过使用全自动定量成像分析。有趣的是，损伤 仅限于豆纹分布的负担在非致命性溺水和 可能只在儿童中观察到。 不同缺血性神经病变引起的急性ABI在弥散加权图像上可以更早被发现，因为 根据所提供的证据，与其他结构MRI形式(即T1和T2加权图像)进行比较 在文学作品中。例如，在动物的血管系统闭塞后30分钟检测到损伤 扩散加权图像上的笔划模型。此外，焦点微结构损害可以被检测到16% 在弥散加权图像上显示围产期窒息的时间-这显示了类似的损伤模式 透镜状分布。 该提案的总体目标是识别和验证非致命性溺水中ABI的急性成像标志物。 为此，我们试图使用结构磁共振测试3个AIMS。基于当前的文献和我们的 初步工作，我们预计损伤模式局限于豆状纹状血管分布 同时影响灰质和白质。在损伤的急性期，我们将寻求证明 DTI异常(目标1)和T2加权图像(目标2)。此外，我们还将把异常情况与 DTI和住院时间(目标3)，承诺验证诊断和预后成像 记号笔。未来在急性损伤阶段对神经保护剂的测试将利用以下结论 这项可行性研究。

Project Summary/Abstract This is a pilot study to confirm localized lesions in acute pediatric anoxic brain injury (ABI) secondary to nonfatal drowning using magnetic resonance imaging (MRI). Drowning is the third leading cause of death due to unintentional injury worldwide, with the highest incidence in young children (ages 1-4 years). Although drowning (i.e. submersion/immersion in liquid) results in multi-organ damage, the most devastating disability results from brain injury. Current diagnostic neuroimaging findings (largely via qualitative visual inspection) are nonspecific and offer little value for prognosis or for directing therapeutic interventions in the acute injury phase of pediatric ABI post- drowning. Our preliminary MRI studies show that chronic ABI displays lesions limited to the lenticulostriate distribution, which is an end-arterial watershed zone, similar to focal ischemia seen in stroke. We found that this localized pattern of injury exhibits gray matter atrophy and also white matter microstructural abnormalities on diffusion-tensor images (DTI), by using fully automated quantitative imaging analysis. Interestingly, lesion burden limited to the lenticulostriate distribution has not been reported in adults with nonfatal drowning and may be observed only in children. Acute ABI due to different ischemic neuropathologies can be detected sooner on diffusion-weighted images as compared to other structural MRI modalities (i.e. T1 and T2-weighted images) according to evidence provided in the literature. For example, detection of lesions occurs by 30 minutes after occlusion of vasculature in animal stroke models on diffusion-weighted images. Further, focal microstructural compromise can be detected by 16 hours in perinatal asphyxia on diffusion-weighted images—which demonstrates a similar injury pattern in the lenticulostriate distribution. The overall goal of the proposal is to identify and validate acute-imaging markers for ABI in nonfatal drowning. To this end, we seek to test 3 aims using structural MRI. Based on current literature and results from our preliminary work, we expect an injury pattern that is localized to the lenticulostriate vascular distribution affecting both gray and white matter. In the acute phase of injury, we will seek to demonstrate focal abnormalities on DTI (Aim 1) and T2-weighted images (Aim 2). Additionally, we will correlate abnormalities on DTI with duration of hospital stay (Aim 3), which promises to validate diagnostic and prognostic imaging markers. Future testing of neuroprotective agents in the acute injury phase would leverage conclusions from this feasibility study.