Tandem use of gastroesophageal resuscitative occlusion of the aorta followed by resuscitative endovascular balloon occlusion of the aorta in a lethal liver laceration model.

BACKGROUND: Gastroesophageal resuscitative occlusion of the aorta (GROA) has been shown effective in creating zone II aortic occlusion capable of temporarily improving survival in animal models of lethal noncompressible torso hemorrhage. In this study, tandem application of GROA transitioning to resuscitative endovascular balloon occlusion of the aorta (REBOA) is explored to demonstrate feasibility as a potential point-of-injury bridge to more advanced care, using a swine model of lethal abdominal hemorrhage. METHODS: Swine (n = 19) were anesthetized, instrumented, and subjected to a combination of controlled and uncontrolled hemorrhage from a grade-V liver laceration. Animals were designated as intervention (n = 9; GROA to REBOA) or control (n = 10), for 60 minutes. Following intervention, devices were deactivated, and animals received blood and crystalloid resuscitation. Animals were monitored for 4 hours. RESULTS: Injury resulted in onset of class IV shock in all animals with a mean arterial pressure (SD) of 24.5 (4.11) mm Hg at the start of intervention. Nine of 10 controls died during the intervention period with a median (interquartile) survival time of 8.5 (9.25) minutes. All animals receiving the intervention survived both the 60-minute intervention period demonstrating a significant survival improvement ( p = 0.0007). Transition from GROA to REBOA was successful in all animals with a transition time ranging from 30 to 90 seconds. Mean arterial pressure significantly improved in animals receiving GROA to REBOA for the duration of intervention, regardless of the method of aortic occlusion, with a range of 70.9 (16.04) mm Hg to 101.1 (15.3) mm Hg. Additional hemodynamics, metrics of shock, and oxygenation remained stable during intervention. CONCLUSION: Less invasive technologies such as GROA may present an opportunity to control noncompressible torso hemorrhage more rapidly, with a subsequent transition to more advanced care such as REBOA.

Gastroesophageal resuscitative occlusion of the aorta prolongs survival in a lethal liver laceration model.

BACKGROUND: Noncompressible torso hemorrhage management remains a challenge especially in the prehospital setting. We evaluated a device designed to occlude the aorta from the stomach (gastroesophageal resuscitative occlusion of the aorta [GROA]) for its ability to stop hemorrhage and improve survival in a swine model of lethal liver laceration and compared its performance to resuscitative endovascular balloon occlusion of the aorta (REBOA) and controls. METHODS: Swine (n = 24) were surgically instrumented and a 30% controlled arterial hemorrhage over 20 minutes was followed by liver laceration. Animals received either GROA, REBOA, or control (no treatment) for 60 minutes. Following intervention, devices were deactivated, and animals received whole blood and crystalloid resuscitation. Animals were monitored for an additional 4 hours. RESULTS: The liver laceration resulted in the onset of class IV shock. Mean arterial blood pressure (MAP) (standard deviation) decreased from 84.5 mm Hg (11.69 mm Hg) to 27.1 mm Hg (5.65 mm Hg) at the start of the intervention. Seven of eight control animals died from injury prior to the end of the intervention period with a median survival (interquartile) time of 10.5 minutes (12 minutes). All GROA and REBOA animals survived the duration of the intervention period (60 minutes) with median survival times of 86 minutes (232 minutes) and 79 minutes (199 minutes) after resuscitation, respectively. The GROA and REBOA animals experienced a significant improvement in survival compared with controls (p = 0.01). Resuscitative endovascular balloon occlusion of the aorta resulted in higher MAP at the end of intervention 114.6 mm Hg (22.9 mm Hg) compared with GROA 88.2 mm Hg (18.72 mm Hg) (p = 0.024), as well as increased lactate compared with GROA 13.2 meq·L-1 (1.56 meq·L-1) versus 10.5 meq·L-1 (1.89 meq·L-1) (p = 0.028). Histological examination of the gastric mucosa in surviving animals revealed mild ischemic injury from both GROA and REBOA. CONCLUSION: The GROA and REBOA devices were both effective at temporarily stanching lethal noncompressible torso hemorrhage of the abdomen and prolonging survival.

Novel intraperitoneal hemostasis device prolongs survival in a swine model of noncompressible abdominal hemorrhage.

BACKGROUND: Noncompressible torso hemorrhage (NCTH) of the abdomen is a challenge to rapidly control and treat in the prehospital and emergency department settings. In this pilot study, we developed a novel intraperitoneal hemostasis device (IPHD) prototype and evaluated its ability for slowing NCTH and prolonging survival in a porcine model of lethal abdominal multiorgan hemorrhage. METHODS: Yorkshire male swine (N = 8) were instrumented under general anesthesia for monitoring of hemodynamics and blood sampling. Animals were subjected to a 30% controlled arterial hemorrhage followed by lacerating combinations of the liver, spleen, and kidney. The abdomen was closed and after 2 minutes of NCTH, and the IPHD was inserted into the peritoneal cavity via an introducer (n = 5). The balloon was inflated and maintained for 60 minutes. At 60 minutes postdeployment, the balloon was deflated and removed, and blood resuscitation was initiated followed by gauze packing for hemostasis. The remaining animals (n = 3) were used as controls and subjected to the same injury without intervention. RESULTS: All animals managed with IPHD intervention (5 of 5 swine) survived the duration of the intervention period (60 minutes), while all control animals (3 of 3 swine) died at a time range of 15 to 43 minutes following organ injury (p = 0.0042). Animals receiving IPHD remained hemodynamically stable with a mean arterial pressure range of 44.86 to 55.10 mm Hg and experienced increased cardiac output and decreased shock index after treatment. Controls experienced hemodynamic decline in all parameters until endpoints were met. Upon IPHD deflation and removal, all treated animals began to hemorrhage again and expired within 2 to 132 minutes despite packing. CONCLUSION: Our data show that the IPHD concept is capable of prolonging survival by temporarily stanching lethal NCTH of the abdomen. This device may be an effective temporary countermeasure to NCTH of the abdomen that could be deployed in the prehospital environment or as a bridge to more advanced therapy.

Gastroesophageal resuscitative occlusion of the aorta: Physiologic tolerance in a swine model of hemorrhagic shock.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) has been shown to be effective for management of noncompressible torso hemorrhage. However, this technique requires arterial cannulation, which can be time-consuming and not amendable to placement in austere environments. We present a novel, less invasive aortic occlusion device and technique designated gastroesophageal resuscitative occlusion of the aorta (GROA). In this study, we aimed to characterize the physiological tolerance and hemodynamic effects of a prototype GROA device in a model of severe hemorrhagic shock and resuscitation and compare with REBOA. METHODS: Swine (N = 47) were surgically instrumented for data collection. A 35% controlled arterial hemorrhage was followed by randomizing animals to 30-minute, 60-minute, or 90-minute interventions of GROA, REBOA, or control. Following intervention, devices were deactivated, and animals received whole blood and crystalloid resuscitation. Animals were monitored for an additional 4 hours. RESULTS: All animals except one GROA 90-minute application survived the duration of their intervention periods. Survival through resuscitation phase in GROA, REBOA, and control groups was similar in the 30-minute and 60-minute groups. The 90-minute occlusion groups exhibited deleterious effects upon device deactivation and reperfusion with two GROA animals surviving and no REBOA animals surviving. Mean (SD) arterial pressure in GROA and REBOA animals increased across all groups to 98 (31.50) mm Hg and 122 (24.79) mm Hg, respectively, following intervention. Lactate was elevated across all GROA and REBOA groups relative to controls during intervention but cleared by 4 hours in the 30-minute and 60-minute groups. Postmortem histological examination of the gastric mucosa revealed mild to moderate inflammation across all GROA groups. CONCLUSION: In this study, the hemodynamic effects and physiological tolerance of GROA was similar to REBOA. The GROA device was capable of achieving high zone II full aortic occlusion and may be able to serve as an effective method of aortic impingement.