• M Austin Johnson, Timothy K Williams, Sarah-Ashley E Ferencz, Anders J Davidson, Rachel M Russo, William T O'Brien, Joseph M Galante, J Kevin Grayson, and Lucas P Neff.
• 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 1; 83 (1): 61-70.

BackgroundDespite 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.MethodsTwenty-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.ResultsThere 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).ConclusionIn 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.

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