Reperfusion repercussions: A review of the metabolic derangements following resuscitative endovascular balloon occlusion of the aorta

Abstract

BACKGROUND Current resuscitative endovascular balloon occlusion of the aorta (REBOA) literature focuses on improving outcomes through careful patient selection, diligent catheter placement, and expeditious definitive hemorrhage control. However, the detection and treatment of post-REBOA ischemia-reperfusion injury (IRI) remains an area for potential improvement. Herein, we provide a review of the metabolic derangements that we have encountered while managing post-REBOA IRI in past swine experiments. We also provide data-driven clinical recommendations to facilitate resuscitation post-REBOA deflation that may be translatable to humans. METHODS We retrospectively reviewed the laboratory data from 25 swine across three varying hemorrhagic shock models that were subjected to complete REBOA of either 45 minutes, 60 minutes, or 90 minutes. In each model the balloon was deflated gradually following definitive hemorrhage control. Animals were then subjected to whole blood transfusion and critical care with frequent electrolyte monitoring and treatment of derangements as necessary. RESULTS Plasma lactate peaked and pH nadired long after balloon deflation in all swine in the 45-minute, 60-minute, and 90-minute occlusion models (onset of peak lactate, 32.9 ± 6.35 minutes, 38.8 ± 10.55 minutes, and 49.5 ± 6.5 minutes; pH nadir, 4.3 ± 0.72 minutes, 26.9 ± 12.32 minutes, and 42 ± 7.45 minutes after balloon deflation in the 45-, 60-, and 90-minute occlusion models, respectively). All models displayed persistent hypoglycemia for more than an hour following reperfusion (92.1 ± 105.5 minutes, 125 ± 114.9 minutes, and 96 ± 97.8 minutes after balloon deflation in the 45-, 60-, and 90-minute occlusion groups, respectively). Hypocalcemia and hyperkalemia occurred in all three groups, with some animals requiring treatment more than an hour after reperfusion. CONCLUSION Metabolic derangements resulting from REBOA use are common and may worsen long after reperfusion despite resuscitation. Vigilance is required to detect and proactively manage REBOA-associated IRI. Maintaining a readily available “deflation kit” of pharmacological agents needed to treat common post-REBOA electrolyte abnormalities may facilitate management. LEVEL OF EVIDENCE Level V.

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“…4 However, REBOA in its current state is limited in duration by the distal ischemia it induces 5 and the reperfusion injury that results following balloon deflation. 5 This time limitation hinders its utility in a prolonged field care environment. Both civilian and Department of Defense funded researchers are actively investigating ways to overcome these challenges and enhance the practicality of REBOA in the austere setting.…”

Biochemical disturbance in damage control resuscitation: mechanisms, management and prognostic utility

“…With enhanced distal ischaemia and cessation of renal blood flow, potassium will both accumulate more and be excreted less in the presence of aortic occlusion. In animal models of REBOA, severe prolonged hyperkalaemia has been reported [19,20]. Selective aortic arch perfusion (SAAP) reduces sub-diaphragmatic blood flow via balloon aortic occlusion while a retrograde infusion of oxygenated media perfuses proximal organs.…”

Computed tomography imaging of resuscitative endovascular balloon occlusion of the aorta (REBOA): pearls and pitfalls

“…5). Ischemia and reperfusion injury are common [10]; thus, inflation time should be minimized to prevent irreversible ischemic organ injury. Ideally, total aortic occlusion time < 30 min avoids ischemic complications [11].…”