The inflammatory sequelae of aortic balloon occlusion in hemorrhagic shock

被引:93
作者
Morrison, Jonathan J. [1 ,2 ,3 ]
Ross, James D. [4 ]
Markov, Nickolay P. [2 ]
Scott, Daniel J. [2 ,4 ]
Spencer, Jerry R. [4 ]
Rasmussen, Todd E. [2 ,4 ,5 ]
机构
[1] Royal Ctr Def Med, Acad Dept Mil Surg & Trauma, Birmingham, W Midlands, England
[2] US Army Inst Surg Res, Ft Sam Houston, TX USA
[3] Glasgow Royal Infirm, Acad Surg Unit, Glasgow G4 0SF, Lanark, Scotland
[4] Joint Base San Antonio, Med Wing 59, Lackland AFB, TX USA
[5] Uniformed Serv Univ Hlth Sci, Norman M Rich Dept Surg, Bethesda, MD 20814 USA
关键词
Resuscitative endovascular balloon occlusion of the aorta; REBOA; Noncompressible torso hemorrhage; Hemorrhagic shock; Resuscitation; NONCOMPRESSIBLE TORSO HEMORRHAGE; TUMOR-NECROSIS-FACTOR; PORCINE MODEL; INTERLEUKIN-6; MORTALITY; DEATHS; INJURY; PATHOPHYSIOLOGY; MANAGEMENT; SURVIVAL;
D O I
10.1016/j.jss.2014.04.012
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a hemorrhage control and resuscitative adjunct that has been demonstrated to improve central perfusion during hemorrhagic shock. The aim of this study was to characterize the systemic inflammatory response associated and cardiopulmonary sequelae with 30, 60, and 90 min of balloon occlusion and shock on the release of interleukin 6 (IL-6) and tumor necrosis factor alpha. Materials and methods: Anesthetized female Yorkshire swine (Sus scrofa, weight 70-90 kg) underwent a 35% blood volume-controlled hemorrhage followed by thoracic aortic balloon occlusion of 30 (30-REBOA, n = 6), 60 (60-REBOA, n = 8), and 90 min (90-REBOA, n = 6). This was followed by resuscitation with whole blood and crystalloid over 6 h. Animals then underwent 48 h of critical care with sedation, fluid, and vasopressor support. Results: All animals were successfully induced into hemorrhagic shock without mortality. All groups responded to aortic occlusion with a rise in blood pressure above baseline values. IL-6, as measured (picogram per milliliter) at 8h, was significantly elevated from baseline values in the 60-REBOA and 90-REBOA groups: 289 +/- 258 versus 10 +/- 5; P = 0.018 and 630 +/- 348; P = 0.007, respectively. There was a trend toward greater vasopressor use (P = 0.183) and increased incidence of acute respiratory distress syndrome (P = 0.052) across the groups. Conclusions: REBOA is a useful adjunct in supporting central perfusion during hemorrhagic shock; however, increasing occlusion time and shock results in a greater IL-6 release. Clinicians must anticipate inflammation-mediated organ failure in post-REBOA use patients. Published by Elsevier Inc.
引用
收藏
页码:423 / 431
页数:9
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