Johnson M Austin, Williams Timothy K, Ferencz Sarah-Ashley E, Davidson Anders J, Russo Rachel M, O'Brien William T, Galante Joseph M, Grayson J Kevin, Neff Lucas P
From the Department of Emergency Medicine, UC Davis Medical Center, Sacramento, California (M.A.J.); Clinical Investigation Facility, David Grant Medical Center, Travis Air Force Base, California (M.A.J., T.K.W., S.-A.E.F., A.J.D., R.M.R., J.K.G., L.P.N.), Heart, Lung and Vascular Center, David Grant Medical Center, Travis Air Force Base, California (T.K.W.); Department of Surgery, UC Davis Medical Center, Sacramento, California (S.-A.E.F., A.J.D., R.M.R., J.M.G.); Department of Surgery, Wright State University Boonshoft School of Medicine, Miami Valley Hospital, Dayton, Ohio (S.-A.E.F.); Department of Radiology, David Grant Medical Center, Travis Air Force Base, California (W.T.O.S.); and Division of Pediatric Surgery, Department of Surgery, Emory University School of Medicine, Atlanta, Georgia (L.P.N.).
J Trauma Acute Care Surg. 2017 Jul;83(1):61-70. doi: 10.1097/TA.0000000000001518.
Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Qcarotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention.
Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals.
There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Qcarotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3%; 95% confidence interval [CI], 3.6-57.9; REBOA, 28.6%; 95% CI, 3.7-71.0; and PAO, 28.6%; 95% CI, 3.7-71.0).
In an animal model of TBI and shock, REBOA increased Qcarotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.
尽管有临床报告显示预后不佳，但主动脉内复苏球囊阻断术（REBOA）加重创伤性脑损伤（TBI）的程度尚不清楚。我们假设，与部分主动脉阻断术（PAO）或不干预相比，REBOA导致的近端平均动脉压（pMAP）、颈动脉血流量（Qcarotid）和颅内压（ICP）升高的综合作用会导致TBI进展。
21头猪通过计算机控制的皮质撞击进行标准化TBI，随后进行25%总血容量的快速出血。低血压30分钟后，将动物随机分为持续低血压60分钟（对照组）、REBOA或PAO。然后对REBOA和PAO动物进行阻断撤机。所有动物通过快速输血器用自体血进行复苏。连续记录生理参数，并在指定间隔进行脑部计算机断层扫描。
基线生理状态或低血压最初30分钟期间无差异。在60分钟的干预期内，REBOA导致更高的最大pMAP（REBOA，105.3±8.8；PAO，92.7±9.2；对照组，48.9±7.7；p = 0.02）和更高的Qcarotid（REBOA，673.1±57.9；PAO，464.2±53.0；对照组，170.3±29.4；p < 0.01）。在血液复苏期间ICP升高最大，对照组动物的ICP峰值最大（对照组，12.8±1.2；REBOA，5.1±0.6；PAO，9.4±1.1；p < 0.01）。CT显示出血进展的动物百分比无差异（对照组，14.3%；95%置信区间[CI]，3.6 - 57.9；REBOA，28.6%；95%CI，3.7 - 71.0；PAO，28.6%；95%CI，3.7 - 71.0）。
在TBI和休克动物模型中，REBOA增加了Qcarotid和pMAP，但未加重TBI进展。PAO导致的生理状态更接近基线，ICP和pMAP升高幅度较小。快速血液复苏而非REBOA导致干预后ICP升高幅度最大，这发生在对照组动物中。需要继续研究主动脉阻断和输血的脑血流动力学，以确定多发伤患者的最佳复苏策略。
