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Aortic branch vessel flow during resuscitative endovascular balloon occlusion of the aorta

Hoehn, Melanie R., MD; Teeter, William A., MD; Morrison, Jonathan J., FRCS; Gamble, William B., MD; Hu, Peter, PhD; Stein, Deborah M., MD; Brenner, Megan L., MD; Scalea, Thomas M., MD

Journal of Trauma and Acute Care Surgery: January 2019 - Volume 86 - Issue 1 - p 79–85
doi: 10.1097/TA.0000000000002075
ORIGINAL ARTICLES
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BACKGROUND Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a torso hemorrhage control adjunct. Aortic branch vessel flow (BVF) during REBOA is poorly characterized and has implications for ischemia-reperfusion injury. The aim of this study is to quantify BVF in hypovolemic shock with and without REBOA.

METHODS Female swine (79–90 kg) underwent anesthesia, 40% controlled hemorrhage and sonographic flow monitoring of the carotid, hepatic, superior mesenteric, renal, and femoral arteries. Animals were randomized to REBOA (n = 5) or no-REBOA (n = 5) for 4 hours, followed by full resuscitation and balloon deflation for 1 hour.

RESULTS All animals were successfully induced into hemorrhagic shock with a mean decrease of flow in all vessels of 50% from baseline (p < 0.001). Deployment of REBOA resulted in a 200% to 400% increase in carotid flow, but near complete abolition of BVF distal to the balloon. The no-REBOA group saw recovery of BVF to 100% of baseline in all measured vessels, except the hepatic at 50% to 75%. two-way analysis of variance confirmed a significant difference between the groups throughout the protocol (p < 0.001). During resuscitation, the REBOA group saw BVF restore to between 25% and 50%, but never achieving baseline values. The lactate at 4 hours was significantly higher in the REBOA versus no-REBOA group (17.2 ± 0.1 vs. 4.9 ± 1.4; p < 0.001).

CONCLUSION REBOA not only abolishing BVF during occlusion, but appears to have a post-REBOA effect, reducing visceral perfusion. This may be a source of REBOA associated ischemia-reperfusion injury and warrants further investigation in order to mitigate this effect.

From the R Adams Cowley Shock Trauma Center, (M.R.H., W.A.T., J.J.M., W.B.G., P.H., D.M.S., M.L.B., T.M.S.); and Shock, Trauma and Anesthesiology Research Center (W.A.T., W.B.G.), University of Maryland, School of Medicine, Baltimore, Maryland.

Submitted: February 18, 2018, Accepted: July 27, 2018, Published online: September 24, 2018.

Address for reprints: Melanie R Hoehn, MD, R Adams Cowley Shock Trauma Center 22 S. Greene Street Baltimore, MD 21201; email: mhoehn@emory.edu.

© 2019 Lippincott Williams & Wilkins, Inc.