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The Effect of REBOA, Partial Aortic Occlusion and Aggressive Blood Transfusion on Traumatic Brain Injury in a Swine Polytrauma Model.
Journal of Trauma and Acute Care Surgery 2017 April 28
OBJECTIVES: Despite clinical reports of poor outcomes, the degree to which 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 to partial aortic occlusion (PAO) or no intervention.
METHODS: 21 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.
RESULTS: 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%CI 3.6-57.9; REBOA 28.6%, 95%CI 3.7-71.0; and PAO 28.6%, 95%CI 3.7-71.0).
CONCLUSIONS: In an animal model of TBI and shock, REBOA increased carotid flow 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.
LEVEL OF EVIDENCE: Level IV.
METHODS: 21 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.
RESULTS: 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%CI 3.6-57.9; REBOA 28.6%, 95%CI 3.7-71.0; and PAO 28.6%, 95%CI 3.7-71.0).
CONCLUSIONS: In an animal model of TBI and shock, REBOA increased carotid flow 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.
LEVEL OF EVIDENCE: Level IV.
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