Endovascular Variable Aortic Control

Introduction

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is increasingly utilized for patients with exsanguinating truncal hemorrhage. This treatment has proven effective at rapidly restoring perfusion to the heart and brain, while simultaneously minimizing hemorrhage below the level of occlusion. However, this intervention is encumbered by the progressive ischemic burden that begins at the moment of balloon occlusion. To address these issues, partial flow strategies have been developed and tested in applied research models and are increasingly being utilized in the care of patients. To date, these partial flow modalities have been performed manually, which represents a significant limitation to widespread adoption. These limitations include the demand for continuous monitoring of the balloon and the difficulty in maintaining a stable degree of partial aortic flow. To address some of the fundamental limitations surrounding real-world implementation of these partial flow strategies, the concept of endovascular variable aortic control (EVAC) has been developed. EVAC is an automated technology that controls aortic flow by precisely regulating inflation and deflation of a balloon catheter. As it applies to hemorrhage control, EVAC can specifically be used to achieve a low-volume distal aortic flow to strike a delicate balance between ongoing hemorrhage and progressive ischemic injury, a therapeutic modality we have termed regional perfusion optimization (REPO).

The Problems With REBOA

REBOA prolongs survival prior to definitive surgical hemostasis by decreasing distal hemorrhage below the level of occlusion and augmenting proximal perfusion to the heart, lungs, and brain. However, the benefits of REBOA are quickly offset by progressive ischemia below the level of occlusion (limiting its duration of use to 40 to 60 minutes; Fig. 12.1 ). Severe hypertension above the balloon may be detrimental to patients with noncompressible torso hemorrhage (NCTH) and concomitant traumatic brain injuries. It has been reported that the mortality rate in brain-injured patients requiring REBOA as a resuscitative adjunct approaches 50%, with case reports demonstrating increased intracranial hemorrhage volumes after brief periods of REBOA. Physicians within the trauma community have hypothesized that the supraphysiologic blood pressure and carotid blood flow created by REBOA may account for these early clinical findings.

In addition, complete aortic occlusion with REBOA poses challenges at the time of balloon deflation, where abrupt washout of ischemic metabolites during reperfusion can produce life-threatening electrolyte abnormalities and acid-base disturbances. Additionally, balloon deflation may result in profound hemodynamic instability, in part due to the loss of distal vascular tone, which is compounded by the ensuing ischemia reperfusion injury ( Table 12.1 ). However, this currently remains the most expeditious manner of managing NCTH, particularly in austere environments.