V A Reva1, Y Matsumura2,3, T Hörer4, D A Sveklov5, A V Denisov5, S Y Telickiy5, A B Seleznev5, E R Bozhedomova5, J Matsumoto6,7, I M Samokhvalov5, J J Morrison8,9. 1. Department of War Surgery, Kirov Military Medical Academy, 6, Lebedeva Str., Saint-Petersburg, 194044, Russian Federation. vreva@mail.ru. 2. R. Adams Cowley Shock Trauma Center, University of Maryland, 22 S Green St, Baltimore, MD, 21201, USA. 3. Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8677, Japan. 4. Department of Cardiothoracic and Vascular Surgery, Örebro University Hospital, Fakultetsgatan, 1, 702 81, Örebro, Sweden. 5. Department of War Surgery, Kirov Military Medical Academy, 6, Lebedeva Str., Saint-Petersburg, 194044, Russian Federation. 6. Departments of Emergency and Critical Care Medicine, Saint-Marianna University School of Medicine, 2-1-16, Sugao, Miyamae-ku, Kawasaki, Kanagawa, 216-8511, Japan. 7. Department of Radiology, National Hospital Organization Disaster Medical Center, Tachikawa, Tokyo, 190-0014, Japan. 8. Department of Vascular Surgery, South Glasgow University Hospital, 1345 Govan Rd, Glasgow, G51 4TF, UK. 9. The Academic Department of Military Surgery and Trauma, Royal Centre for Defence Medicine, Mindelsohn Way, Birmingham, B15 2TH, UK.
Abstract
PURPOSE: The aim of this study is to evaluate the early survival and organ damage following 30 and 60 min of thoracic resuscitative endovascular balloon occlusion of the aorta (REBOA) in an ovine model of severe hemorrhagic shock. METHODS: Eighteen sheep were induced into shock by undergoing a 35 % controlled exsanguination over 30 min. Animals were randomized into three groups: 60-min REBOA 30 min after the bleeding (60-REBOA), 30-min REBOA 60 min after the bleeding (30-REBOA) and no-REBOA control (n-REBOA). Resuscitation with crystalloids and whole blood was initiated 20 and 80 min after the induction of shock. Animals were observed for 24 h with serial potassium and lactate measurements. Autopsy was performed to evaluate organ damage. RESULTS: Two animals of the n-REBOA group died within 90 min of shock induction; no hemorrhagic deaths were observed in the REBOA groups. Twenty-four-hour survival for the 60-, 30-, and n-REBOA groups was 0/6, 5/6, and 4/6 (P = 0.002). In 60-REBOA, potassium and lactate were increased at 270-min time point: from 4.3 to 5.1 mEq/l and from 3.7 to 5.1 mmol/L, respectively. Both these values were significantly higher than in the n-REBOA group (P = 0.029 for potassium and P = 0.039 for lactate). Autopsy revealed acute tubular necrosis in all died REBOA group animals. CONCLUSIONS: In this ovine model of severe hemorrhagic shock, REBOA can be used to prevent early death from hemorrhage; however, 60 min of occlusion results in significant metabolic derangement and organ damage that offsets this gain.
PURPOSE: The aim of this study is to evaluate the early survival and organ damage following 30 and 60 min of thoracic resuscitative endovascular balloon occlusion of the aorta (REBOA) in an ovine model of severe hemorrhagic shock. METHODS: Eighteen sheep were induced into shock by undergoing a 35 % controlled exsanguination over 30 min. Animals were randomized into three groups: 60-min REBOA 30 min after the bleeding (60-REBOA), 30-min REBOA 60 min after the bleeding (30-REBOA) and no-REBOA control (n-REBOA). Resuscitation with crystalloids and whole blood was initiated 20 and 80 min after the induction of shock. Animals were observed for 24 h with serial potassium and lactate measurements. Autopsy was performed to evaluate organ damage. RESULTS: Two animals of the n-REBOA group died within 90 min of shock induction; no hemorrhagic deaths were observed in the REBOA groups. Twenty-four-hour survival for the 60-, 30-, and n-REBOA groups was 0/6, 5/6, and 4/6 (P = 0.002). In 60-REBOA, potassium and lactate were increased at 270-min time point: from 4.3 to 5.1 mEq/l and from 3.7 to 5.1 mmol/L, respectively. Both these values were significantly higher than in the n-REBOA group (P = 0.029 for potassium and P = 0.039 for lactate). Autopsy revealed acute tubular necrosis in all died REBOA group animals. CONCLUSIONS: In this ovine model of severe hemorrhagic shock, REBOA can be used to prevent early death from hemorrhage; however, 60 min of occlusion results in significant metabolic derangement and organ damage that offsets this gain.
Entities:
Keywords:
Hemorrhagic shock; Ischemia–reperfusion injury; Ovine model; REBOA; Resuscitative endovascular balloon occlusion of the aorta
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