Department of Biomedical Engineering, Columbia University, 351 Engineering Terrace MC 8904, 1210 Amsterdam Avenue, New York, NY, 10027, USA.
Department of Mechanical Engineering, Columbia University, 220 S. W. Mudd Building, 500 West 120th Street, New York, NY, 10027, USA.
Ann Biomed Eng. 2024 Oct;52(10):2818-2830. doi: 10.1007/s10439-024-03496-y. Epub 2024 Mar 26.
Poor outcome following traumatic acute subdural hematoma (ASDH) is associated with the severity of the primary injury and secondary injury including cerebral edema and ischemia. However, the underlying secondary injury mechanism contributing to elevated intracranial pressure (ICP) and high mortality rate remains unclear. Cerebral edema occurs in response to the exposure of the intracellular fixed charge density (FCD) after cell death, causing ICP to increase. The increased ICP from swollen tissue compresses blood vessels in adjacent tissue, restricting blood flow and leading to ischemic damage. We hypothesize that the mass occupying effect of ASDH exacerbates the ischemic injury, leading to ICP elevation, which is an indicator of high mortality rate in the clinic. Using FEBio (febio.org) and triphasic swelling biomechanics, this study modeled clinically relevant ASDHs and simulated post-traumatic brain swelling and ischemia to predict ICP. Results showed that common convexity ASDH significantly increased ICP by exacerbating ischemic injury, and surgical removal of the convexity ASDH may control ICP by preventing ischemia progression. However, in cases where the primary injury is very severe, surgical intervention alone may not effectively decrease ICP, as the contribution of the hematoma to the elevated ICP is insignificant. In addition, interhemispheric ASDH, located between the cerebral hemispheres, does not significantly exacerbate ischemia, supporting the conservative surgical management generally recommended for interhemispheric ASDH. The joint effect of the mass occupying effect of the blood clot and resulting ischemia contributes to elevated ICP which may increase mortality. Our novel approach may improve the fidelity of predicting patient outcome after motor vehicle crashes and traumatic brain injuries due to other causes.
外伤性急性硬脑膜下血肿（ASDH）后预后不良与原发性损伤和继发性损伤的严重程度有关，包括脑水肿和缺血。然而，导致颅内压（ICP）升高和高死亡率的潜在继发性损伤机制仍不清楚。脑水肿是由于细胞死亡后细胞内固定电荷密度（FCD）的暴露而发生的，导致 ICP 升高。肿胀组织的增加 ICP 压迫相邻组织中的血管，限制血流，导致缺血性损伤。我们假设 ASDH 的占位效应加剧了缺血性损伤，导致 ICP 升高，这是临床高死亡率的一个指标。本研究使用 FEBio（febio.org）和三相肿胀生物力学，对临床相关的 ASDH 进行建模，并模拟创伤后脑肿胀和缺血，以预测 ICP。结果表明，常见的凸面 ASDH 通过加剧缺血性损伤显著增加 ICP，而去除凸面 ASDH 的手术可能通过防止缺血性进展来控制 ICP。然而，在原发性损伤非常严重的情况下，单独的手术干预可能无法有效降低 ICP，因为血肿对升高的 ICP 的贡献并不显著。此外，位于大脑半球之间的大脑半球间 ASDH 不会显著加重缺血，这支持了一般推荐的大脑半球间 ASDH 的保守手术治疗。血栓的占位效应和由此产生的缺血的联合作用导致 ICP 升高，这可能会增加死亡率。我们的新方法可能会提高对机动车碰撞和其他原因导致的外伤性脑损伤后患者预后的预测准确性。
