Siegel John H, Belwadi Aditya, Smith Joyce A, Shah Chirag, Yang King
New Jersey Medical School: UMDNJ, Newark, New Jersey, USA.
J Trauma. 2010 Jun;68(6):1375-95. doi: 10.1097/TA.0b013e3181dcd42d.
Despite advances in the surgical therapy of aortic injury (AI) using endovascular prostheses, more than 60% of motor vehicle crash (MVC) induced AIs die at the scene. In 80 cases of MVC AI, both change in velocity on impact (Delta V) and impact energy (IE) were correlated with autopsy or surgical findings. Of the 34 AIs due to lateral impact MVCs (LMVC), 91% had an aortic isthmus laceration. Computer simulation is used to study the cause of LMVC AI.
To delineate AI mechanism, 10 real life LMVCs (8 left, 2 right) were simulated using a computer-based finite element numerical model. Each began with the initial vehicle impact with another vehicle or fixed object, followed by the vehicle's compartment structures' impact with the patient's chest wall, causing a rise in intra-aortic pressure and the resulting location and pattern of aortic wall stresses and strains. In the real LMVCs, the Delta V ranged from 27.5 to 62 kph with impact energies of from 46,051 to 313,502 joules. In both real-life and the model, the main cause of the chest wall impact was intrusion of the car's B-pillar. Dynamic simulations delineate increased stress and strains at the aortic Isthmus. In some LMVCs, the B-pillar intrusion was also seen to impact the head in the AI cases.
In the simulations, aortic pressure rose from 100 mm Hg precrash to as high as 1,322 mm Hg. Both the maximum aortic longitudinal tensile strain and the von Mises Stress were proportional to the maximum force impacted on the chest wall. Aortic isthmus maximum stresses ranged from 1.1 Mega Pascal (MPa) to 3.2 MPa, with longitudinal tensile strains ranging from 8.2% to 48.5%. The simulation dynamics demonstrated that the proximal pressurized turgid aorta initially moves toward the LMVC impact. As a result, the ascending aorta and aortic arch (proximal ascending aorta) rotate about the fulcrum of the great vessels, so that this aortic unit, acting as the long-arm of an Archimedes lever system, exerts the maximum stress and strain at the aortic isthmus or short-arm, where the real-life aortic rupture occurs.
Simulation supports the lever hypothesis that the force on the short-arm aortic isthmus is proportionally greater than at the long-arm proximal aorta. Simulation also suggests improved vehicle construction techniques, which increase the strength and resistance to deformation of the B-pillar and vehicle side structure plus a B-pillar airbag will limit the intrusion forces causing LMVC AIs and reduce the incidence of associated head injuries.
尽管使用血管内假体治疗主动脉损伤(AI)的外科手术取得了进展,但超过60%的机动车碰撞(MVC)导致的AI患者在现场死亡。在80例MVC导致的AI病例中,撞击时的速度变化(ΔV)和撞击能量(IE)均与尸检或手术结果相关。在34例因侧面碰撞MVC(LMVC)导致的AI病例中,91%存在主动脉峡部撕裂。计算机模拟用于研究LMVC导致AI的原因。
为了阐明AI的机制,使用基于计算机的有限元数值模型模拟了10例真实的LMVC(8例左侧,2例右侧)。每个模拟均从车辆与另一车辆或固定物体的初始碰撞开始,随后车辆的车厢结构撞击患者的胸壁,导致主动脉内压力升高以及主动脉壁应力和应变的产生位置和模式。在真实的LMVC中,ΔV范围为27.5至62公里/小时,撞击能量为46,051至313,502焦耳。在现实生活和模型中,胸壁撞击的主要原因是汽车B柱的侵入。动态模拟显示主动脉峡部的应力和应变增加。在一些LMVC导致的AI病例中,还观察到B柱侵入对头部的影响。
在模拟中,主动脉压力从碰撞前的100毫米汞柱升至高达1,322毫米汞柱。主动脉最大纵向拉伸应变和冯·米塞斯应力均与施加在胸壁上的最大力成正比。主动脉峡部的最大应力范围为1.1兆帕斯卡(MPa)至3.2 MPa,纵向拉伸应变范围为8.2%至48.5%。模拟动力学表明,近端受压膨胀主动脉最初向LMVC撞击方向移动。结果,升主动脉和主动脉弓(近端升主动脉)围绕大血管的支点旋转,因此这个主动脉单元作为阿基米德杠杆系统的长臂在主动脉峡部或短臂处施加最大应力和应变,而现实生活中的主动脉破裂就发生在此处。
模拟支持杠杆假说,即短臂主动脉峡部上的力比长臂近端主动脉上的力成比例地更大。模拟还表明改进车辆制造技术,增加B柱和车辆侧面结构的强度和抗变形能力,再加上B柱安全气囊,将限制导致LMVC导致AI的侵入力,并减少相关头部损伤的发生率。