The Effects of Balloon Occlusion of the Aorta on Cerebral Blood Flow, Intracranial Pressure, and Brain Tissue Oxygen Tension in a Rodent Model of Penetrating Ballistic-Like Brain Injury.

Zachary S Bailey,Deborah Shear,Todd E Rasmussen,Katherine Cardiff,Lai Yee Leung,Xiaofang Yang,Janice Gilsdorf

doi:10.3389/fneur.2019.01309

Abstract

Trauma is among the leading causes of death in the United States. Technological advancements have led to the development of resuscitative endovascular balloon occlusion of the aorta (REBOA) which offers a pre-hospital option to non-compressible hemorrhage control. Due to the prevalence of concomitant traumatic brain injury (TBI), an understanding of the effects of REBOA on cerebral physiology is critical. To further this understanding, we employed a rat model of penetrating ballistic-like brain injury (PBBI). PBBI produced an injury pattern within the right frontal cortex and striatum that replicates the pathology from a penetrating ballistic round. Aortic occlusion was initiated 30 min post-PBBI and maintained continuously (cAO) or intermittently (iAO) for 30 min. Continuous measurements of mean arterial pressure (MAP), intracranial pressure (ICP), cerebral blood flow (CBF), and brain tissue oxygen tension (PbtO2) were recorded during, and for 60 min following occlusion. PBBI increased ICP and decreased CBF and PbtO2. The arterial balloon catheter effectively occluded the descending aorta which augmented MAP in the carotid artery. Despite this, CBF levels were not changed by aortic occlusion. iAO caused sustained adverse effects to ICP and PbtO2 while cAO demonstrated no adverse effects on either. Temporary increases in PbtO2 were observed during occlusion, along with restoration of sham levels of ICP for the remainder of the recordings. These results suggest that iAO may lead to prolonged cerebral hypertension following PBBI. Following cAO, ICP, and PbtO2 levels were temporarily improved. This information warrants further investigation using TBI-polytrauma model and provides foundational knowledge surrounding the non-hemorrhage applications of REBOA including neurogenic shock and stroke.

Highlights

Traumatic hemorrhage is the leading cause of potentially preventable death in both civilian and military populations [1, 2]
It is important to understand the effects of resuscitative endovascular balloon occlusion of the aorta (REBOA) on concomitant traumatic brain injury (TBI) because the significant hemodynamic shift induced by the occlusion likely impacts the cerebral perfusion, intracranial pressure (ICP), and oxygen delivery following injury
The distal mean arterial pressure (MAP) measured at the femoral artery was significantly reduced but maintained at ∼20 mmHg which likely resulted from collateral circulation during full occlusion

Summary

Introduction

Traumatic hemorrhage is the leading cause of potentially preventable death in both civilian and military populations [1, 2]. Medical response to a traumatic event is limited by the lack of technology to control non-compressible hemorrhage which has prompted the development and implementation of resuscitative endovascular balloon occlusion of the aorta (REBOA) [3,4,5,6,7]. The REBOA procedure includes the placement of a balloon catheter into the descending aorta to temporarily occlude distal blood flow and augment cerebral and myocardial perfusion. Traumatic events often involve complex injury patterns and patients are often faced with polytrauma. Neurologic injury, including traumatic brain injury (TBI), is among the most common factor in polytrauma patients and can worsen outcome [8, 9]. It is important to understand the effects of REBOA on concomitant TBI because the significant hemodynamic shift induced by the occlusion likely impacts the cerebral perfusion, intracranial pressure (ICP), and oxygen delivery following injury

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