Abstract
BackgroundResuscitative endovascular balloon occlusion of the aorta (REBOA) causes physiological, metabolic, end-organ and inflammatory changes that need to be addressed for better management of severely injured patients. The aim of this study was to investigate occlusion time-dependent metabolic, end-organ and inflammatory effects of total REBOA in Zone I in a normovolemic animal model.MethodsTwenty-four pigs (25-35 kg) were randomized to total occlusion REBOA in Zone I for either 15, 30, 60 min (REBOA15, REBOA30, and REBOA60, respectively) or to a control group, followed by 3-h reperfusion. Hemodynamic variables, metabolic and inflammatory response, intraperitoneal and intrahepatic microdialysis, and plasma markers of end-organ injuries were measured during intervention and reperfusion. Intestinal histopathology was performed.ResultsMean arterial pressure and cardiac output increased significantly in all REBOA groups during occlusion and blood flow in the superior mesenteric artery and urinary production subsided during intervention. Metabolic acidosis with increased intraperitoneal and intrahepatic concentrations of lactate and glycerol was most pronounced in REBOA30 and REBOA60 during reperfusion and did not normalize at the end of reperfusion in REBOA60. Inflammatory response showed a significant and persistent increase of pro- and anti-inflammatory cytokines during reperfusion in REBOA30 and was most pronounced in REBOA60. Plasma concentrations of liver, kidney, pancreatic and skeletal muscle enzymes were significantly increased at the end of reperfusion in REBOA30 and REBOA60. Significant intestinal mucosal damage was present in REBOA30 and REBOA60.ConclusionTotal REBOA caused severe systemic and intra-abdominal metabolic disturbances, organ damage and inflammatory activation already at 30 min of occlusion.
Highlights
Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes physiological, metabolic, end-organ and inflammatory changes that need to be addressed for better management of severely injured patients
Multi-trauma patients are exposed to varying degrees of hypoperfusion and reperfusion, complicating the evaluation of the inflammatory response that might be expected from aortic occlusion per se [11, 15, 16]
Hemodynamic and respiratory variables Aortic occlusion in all REBOA groups induced immediate systemic hypertension, tachycardia and increased cardiac output (CO) (Table 1, Fig. 1). These effects gradually subsided throughout the occlusion period in all REBOA groups, with these changes being correspondingly more pronounced in REBOA60 than in REBOA15 at the end of the occlusion period (Table 1, Fig. 1)
Summary
Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes physiological, metabolic, end-organ and inflammatory changes that need to be addressed for better management of severely injured patients. The aim of this study was to investigate occlusion time-dependent metabolic, end-organ and inflammatory effects of total REBOA in Zone I in a normovolemic animal model. Multi-trauma patients are exposed to varying degrees of hypoperfusion and reperfusion, complicating the evaluation of the inflammatory response that might be expected from aortic occlusion per se [11, 15, 16]. The aim of this study was to investigate potential gradual changes in response to occlusion time on systemic and intraabdominal metabolic, inflammatory and organ damage variables with Zone I total REBOA in a non-shock porcine model
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