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采用三相肿胀生物力学模拟创伤性脑损伤后的脑水肿和迟发性死亡。

Simulating cerebral edema and delayed fatality after traumatic brain injury using triphasic swelling biomechanics.

机构信息

Biomedical Engineering, Columbia University, New York, New York.

Honda R&D, Tochigi, Japan.

出版信息

Traffic Inj Prev. 2019;20(8):820-825. doi: 10.1080/15389588.2019.1663347. Epub 2019 Oct 24.

Abstract

: Contemporary finite element (FE) models, like that from the Global Human Body Models Consortium (GHBMC), have been useful for developing safety systems to reduce the severity of injuries in motor vehicle crashes (MVCs), including traumatic brain injury (TBI). However, not all injury occurs during the MVC. Cerebral edema after TBI contributes to mortality by increasing intracranial pressure (ICP) and preventing adequate cerebral blood supply. The focus of this study was to model post-traumatic cerebral edema and subsequent mortality due to increased ICP.: Brain tissue swells in a manner consistent with triphasic biomechanics, which models biological tissues as a charged deformable porous solid matrix (fixed charge density [FCD]), a solvent, and monovalent counter-ions (cerebrospinal fluid). Fluid uptake into the brain is driven by the Gibbs-Donnan osmotic pressure as the FCD is exposed when cells die. Post-TBI edema was simulated in FEBio (febio.org), which includes triphasic material formulations.The GHBMC mesh was imported into FEBio, and each element was assigned a FCD to represent impact-related cell death based on its maximum principal strain (MPS) experienced during the crash-simulation using the stock GHBMC model and LS-DYNA. The ensuing pathophysiology was simulated in FEBio in two steps. First, the brain swelled in response to exposure of FCD, causing some adjacent elements to compress as fluid was redistributed. Biologically, the compression was assumed to reduce blood flow and cause ischemic cell death, represented by additional exposure of FCD, swelling, and increased ICP. Using published prognostic models of clinical outcome, mortality was predicted based on ICP.: Post-traumatic volume ratio of elements ranged from less than 30% (compaction) to greater than 200% (swelling). Predicted ICP values for a fatal impact were as high as 8.55 kPa (64.1 mmHg), which is associated with a 99% probability of death. To the best of our knowledge, this is the first study to simulate post-traumatic brain swelling to predict outcome. By incorporating swelling, ischemia, and cell death, our novel approach may improve fidelity of predicting outcome after MVCs. A strength of our approach is relying on the validated GHBMC model to predict brain deformation in the crash-scenario. The main goal of the current study was to demonstrate feasibility of simulating post-injury swelling using triphasic biomechanics. We successfully predicted clinically relevant increases in ICP that suggest a high likelihood of death when simulating a fatal impact scenario, however, more validation of our methodology is needed.

摘要

: 当代有限元(FE)模型,如全球人体模型联合会(GHBMC)的模型,已被用于开发安全系统,以降低机动车碰撞(MVC)中伤害的严重程度,包括创伤性脑损伤(TBI)。然而,并非所有损伤都发生在 MVC 期间。TBI 后的脑水肿通过增加颅内压(ICP)和阻止足够的脑血流供应来导致死亡率。本研究的重点是模拟创伤后脑水肿和由于 ICP 升高导致的随后死亡率。: 脑组织以三相生物力学的方式肿胀,该模型将生物组织视为带电荷的可变形多孔固体基质(固定电荷密度[FCD])、溶剂和单价抗衡离子(脑脊液)。当细胞死亡时,FCD 暴露,流体通过 Gibbs-Donnan 渗透压被吸入大脑。FEBio(febio.org)中模拟了 TBI 后水肿,该模型包括三相材料配方。将 GHBMC 网格导入 FEBio,并根据其在使用原始 GHBMC 模型和 LS-DYNA 进行碰撞模拟时经历的最大主应变(MPS),为每个元素分配一个 FCD,以代表与冲击相关的细胞死亡。随后的病理生理学在 FEBio 中通过两步进行模拟。首先,暴露 FCD 会导致脑组织肿胀,导致一些相邻元素压缩,因为流体重新分布。从生物学角度来看,假设压缩会降低血流并导致缺血性细胞死亡,这表现为更多的 FCD 暴露、肿胀和 ICP 增加。使用临床预后模型预测死亡率。: 受影响元素的创伤后体积比范围从小于 30%(压实)到大于 200%(肿胀)。致命冲击的预测 ICP 值高达 8.55 kPa(64.1 mmHg),这与 99%的死亡概率相关。据我们所知,这是第一项模拟创伤后脑肿胀以预测结果的研究。通过纳入肿胀、缺血和细胞死亡,我们的新方法可能会提高预测 MVC 后结果的准确性。我们方法的一个优势是依赖经过验证的 GHBMC 模型来预测碰撞场景中的脑变形。当前研究的主要目标是展示使用三相生物力学模拟损伤后肿胀的可行性。我们成功预测了临床上相关的 ICP 升高,表明在模拟致命冲击场景时死亡的可能性很高,但是需要更多的方法验证。

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