A. Cralley1, 2, E. E. Moore1, 2, C. J. Fox3, M. DeBot1, D. Kissau1, T. Schaid1, S. Mitra1, P. Hom1, M. Fragoso1, A. Ghasabyan1, C. Erickson1, A. D’Alessandro1, K. Hansen1, M. Cohen1, C. Silliman1, A. Sauaia1, 2 1University Of Colorado Denver, Trauma Research Center, Aurora, CO, USA 2Denver Health Medical Center, Surgery, Aurora, CO, USA 3University Of Maryland, Vascular Surgery, Baltimore, MD, USA
Introduction: Zone 1 resuscitative endovascular balloon occlusion (REBOA) has been recommended for refractory shock following a dismounted complex blast injury (DCBI) in the austere combat scenario. While REBOA should enhance coronary perfusion, there is a risk of secondary brain injury due to loss of cerebral autoregulation. We developed a combat casualty relevant DCBI swine model to evaluate the effects of Zone 1 REBOA on intracranial pressure and cerebral edema. We hypothesized that Zone 1 REBOA after DCBI increases mean arterial pressure (MAP) but also increases intracranial pressure (ICP) and promotes secondary brain injury.
Methods: 50kg male Yorkshire swine were subjected to a combination DCBI model consisting of blast TBI (50psi, ARA Mobile Shock Laboratory), tissue injury (bilateral femur fractures), hemorrhagic shock (controlled bleeding to a base deficit of 10mEq/l). During the shock phase, pigs were randomized to observation only (control group, n=8), or to 30 minutes of Zone 1 REBOA (REBOA group, n=4). After shock, pigs in both groups received Tactical Combat Casualty Care-based resuscitation and were monitored for an additional 240 minutes until euthanasia/death for a total 6-hour study. ICP was monitored throughout the model, and brains were harvested for water content at conclusion. Linear mixed models for repeated measures were used to compare MAP and ICP between REBOA and control groups.
Results: Following DCBI, the REBOA group had a significantly higher MAP during hemorrhagic shock compared to control (38.8mmgHg vs 16mmHg, p=.004). During balloon occlusion, ICPs were not significantly elevated in the REBOA group vs control, and ICP was significantly lower in the REBOA group at the end of the observation period. In addition, the REBOA group did not have increased brain water content (3.63g water/dry tissue vs 3.50g water/dry tissue, p=0.5, <5% difference). Troponin levels were not different between the groups.
Conclusions: Zone I REBOA in a large animal DCBI model improved proximal MAPs while not significantly increasing ICP during balloon inflation. Observation up to 4 hours post-resuscitation did not show clinical signs of secondary brain or cardiac injury. These data suggest that in a complex DCBI swine model Zone 1 REBOA provides neuroprotection without cardiac stress.
