Rachel M. Russo

Extending the golden hour: Partial resuscitative endovascular balloon occlusion of the aorta in a highly lethal swine liver injury model.

BACKGROUND Combat-injured patients may require rapid and sustained support during transport; however, the prolonged aortic occlusion produced by conventional resuscitative endovascular balloon occlusion of the aorta (REBOA) may lead to substantial morbidity. Partial REBOA (P-REBOA) may permit longer periods of occlusion by allowing some degree of distal perfusion. However, the ability of this procedure to limit exsanguination is unclear. We evaluated the impact of P-REBOA on immediate survival and ongoing hemorrhage in a highly lethal swine liver injury model. METHODS Fifteen Yorkshire-cross swine were anesthetized, instrumented, splenectomized, and subjected to rapid 10% total blood loss followed by 30% liver amputation. Coagulopathy was created through colloid hemodilution. Randomized swine received no intervention (control), P-REBOA, or complete REBOA (C-REBOA). Central mean arterial pressure (cMAP), carotid blood flow, and blood loss were recorded. Balloons remained inflated in the P-REBOA and C-REBOA groups for 90 minutes followed by graded deflation. The study ended at 180 minutes from onset of hemorrhage or death of the animal. Survival analysis was performed, and data were analyzed using repeated-measures analysis of variance with post hoc pairwise comparisons. RESULTS Mean survival times in the control, P-REBOA, and C-REBOA groups were, 25 ± 21, 86 ± 40, and 163 ± 20 minutes, respectively (p < 0.001). Blood loss was greater in the P-REBOA group than the C-REBOA or control groups, but this difference was not significant (4,722 ± 224, 3,834 ± 319, 3,818 ± 37 mL, respectively, p = 0.10). P-REBOA resulted in maintenance of near-baseline carotid blood flow and cMAP, while C-REBOA generated extreme cMAP and prolonged supraphysiologic carotid blood flow. Both experimental groups experienced profound decreases in cMAP following balloon deflation. CONCLUSION In the setting of severe ongoing hemorrhage, P-REBOA increased survival time beyond the golden hour while maintaining cMAP and carotid flow at physiologic levels.

Emerging Endovascular Therapies for Non-Compressible Torso Hemorrhage

ABSTRACT Management of non-compressible torso hemorrhage (NCTH) remains a challenge despite continued advancements in trauma resuscitation. Resuscitative thoracotomy with aortic cross-clamping and recent advances in endovascular aortic occlusion, including resuscitative endovascular occlusion of the aorta, have finite durations of therapy due to the inherent physiologic stressors that accompany complete occlusion. Here, we attempt to illuminate the current state of aortic occlusion for trauma resuscitation including explanation of the deleterious consequences of complete occlusion, potential methods and limitations of existing technology to overcome these consequences, and a description of innovative methods to improve the resuscitation of NCTH. By explaining the complexity and potential deleterious effects of resuscitation augmented with aortic occlusion, our goal is to provide practitioners with a real-world perspective on current endovascular technology and to encourage the continued innovation required to overcome existing obstacles.

Extending resuscitative endovascular balloon occlusion of the aorta: Endovascular variable aortic control in a lethal model of hemorrhagic shock

BACKGROUND The duration of use and efficacy of resuscitative endovascular balloon occlusion of the aorta (REBOA) is limited by distal ischemia. We developed a hybrid endovascular-extracorporeal circuit variable aortic control (VAC) device to extend REBOA duration in a lethal model of hemorrhagic shock to serve as an experimental surrogate to further the development of endovascular VAC (EVAC) technologies. METHODS Nine Yorkshire-cross swine were anesthetized, instrumented, splenectomized, and subjected to 30% liver amputation. Following a short period of uncontrolled hemorrhage, REBOA was instituted for 20 minutes. Automated variable occlusion in response to changes in proximal mean arterial pressure was applied for the remaining 70 minutes of the intervention phase using the automated extracorporeal circuit. Damage-control surgery and whole blood resuscitation then occurred, and the animals were monitored for a total of 6 hours. RESULTS Seven animals survived the initial surgical preparation. After 20 minutes of complete REBOA, regulated flow was initiated through the extracorporeal circuit to simulate VAC and provide perfusion to distal tissue beds during the 90-minute intervention phase. Two animals required circuit occlusion for salvage, while five animals tolerated sustained, escalating restoration of distal blood flow before surgical hemorrhage control. Animals tolerating distal flow had preserved renal function, maintained proximal blood pressure, and rapidly weaned from complete REBOA. CONCLUSION We combined a novel automated, extracorporeal circuit with complete REBOA to achieve EVAC in a swine model of uncontrolled hemorrhage. Our approach regulated proximal aortic pressure, alleviated supranormal values above the balloon, and provided controlled distal aortic perfusion that reduced ischemia without inducing intolerable bleeding. This experimental model serves as a temporary surrogate to guide future EVAC catheter designs that may provide transformational approaches to hemorrhagic shock.

The pitfalls of resuscitative endovascular balloon occlusion of the aorta: Risk factors and mitigation strategies

ABSTRACT Despite technological advancements, REBOA is associated with significant risks due to complications of vascular access and ischemia-reperfusion. The inherent morbidity and mortality of REBOA is often compounded by coexisting injury and hemorrhagic shock. Additionally, the potential for REBOA-related injuries is exaggerated due to the growing number of interventions being performed by providers who have limited experience in endovascular techniques, inadequate resources, minimal training in the technique, and who are performing this maneuver in emergency situations. In an effort to ultimately improve outcomes with REBOA, we sought to compile a list of complications that may be encountered during REBOA usage. To address the current knowledge gap, we assembled a list of anecdotal complications from high-volume REBOA users internationally. More importantly, through a consensus model, we identify contributory factors that may lead to complications and deliberate on how to recognize, mitigate, and manage such events. An understanding of the pitfalls of REBOA and strategies to mitigate their occurrence is of vital importance to optimize patient outcomes.ABSTRACT Despite technological advancements, REBOA is associated with significant risks due to complications of vascular access and ischemia-reperfusion. The inherent morbidity and mortality of REBOA is often compounded by coexisting injury and hemorrhagic shock. Additionally, the potential for REBOA-related injuries is exaggerated due to the growing number of interventions being performed by providers who have limited experience in endovascular techniques, inadequate resources, minimal training in the technique, and who are performing this maneuver in emergency situations. In an effort to ultimately improve outcomes with REBOA, we sought to compile a list of complications that may be encountered during REBOA usage. To address the current knowledge gap, we assembled a list of anecdotal complications from high-volume REBOA users internationally. More importantly, through a consensus model, we identify contributory factors that may lead to complications and deliberate on how to recognize, mitigate, and manage such events. An understanding of the pitfalls of REBOA and strategies to mitigate their occurrence is of vital importance to optimize patient outcomes.

Potential benefit of early operative utilization of low profile, partial resuscitative endovascular balloon occlusion of the aorta (P-REBOA) in major traumatic hemorrhage

A 28-year-old man with multiple gunshot wounds to the chest and upper extremities was transported by private vehicle to a community hospital with limited trauma capabilities. On arrival he developed pulseless electrical activity and cardiopulmonary resuscitation was initiated. He was intubated, transfused with 4 units of packed red blood cells, and resuscitated with 2 L of crystalloid prior to regaining spontaneous circulation. Left-sided tube thoracostomy immediately drained 1600 mL of bright red blood. He was transiently stable for a short transport to the nearest level 1 trauma center. On arrival the patient was normotensive with tachycardia. Chest X-ray demonstrated persistent left-sided hemothorax despite a well-positioned chest tube. Focused Assessment with Sonography for Trauma (FAST) examination was negative for pericardial fluid, but positive for intra-abdominal fluid. During the secondary examination the patient became hypotensive with systolic blood pressure (SBP) in the 70 s. A massive transfusion protocol was initiated, tranexamic acid was administered, and the patient was promptly transported to the operating room. The patient transiently responded to the massive transfusion. While instruments were being opened in the operating room, he again became hypotensive with SBP in the 50 s. The patient was acidotic (pH of 6.87, base excess −14.6), coagulopathic (international normalized ratio of 1.5) and …

Mass Casualty Disasters: Who Should Run the Show?

BACKGROUND A clear command structure ensures quality patient care despite overwhelmed resources during a mass casualty incident (MCI). The American College of Surgeons has stated that surgeons should strive to occupy these leadership roles. OBJECTIVE We sought to identify whether surgeons, as compared to emergency physicians, are sufficiently prepared to assume command in the event of a mass disaster. METHODS We surveyed hospital-affiliated surgeons and emergency physicians to assess their knowledge of MCI response principles and to gauge opinions regarding who should be in charge during a disaster. RESULTS One hundred and forty-nine (58%) surveys were completed, 78 by surgeons and 71 by emergency physicians. Both groups demonstrated a critical lack of knowledge regarding fundamental principles and key logistical components of preparedness and MCI response. Surgeons as a group were even less prepared than emergency physicians. Of those surgeons who had reviewed their hospitals disaster plan, half (50%) still did not know where to report for an MCI activation. Nonetheless, both groups believed they had sufficient training and both asserted they ought to occupy command positions during a disaster scenario. CONCLUSIONS Errors in disaster triage have been known to increase mortality as well as the monetary cost of disaster response. Funding exists to improve hospital preparedness, but surgeons are lagging behind emergency physicians in taking advantage of these opportunities. Overall, it is imperative that physicians improve their understanding of the MCI response protocols they will be tasked to implement should disaster strike.

Small changes, big effects: The hemodynamics of partial and complete aortic occlusion to inform next generation resuscitation techniques and technologies

BACKGROUND The transition from complete aortic occlusion during resuscitative endovascular balloon occlusion of the aorta can be associated with hemodynamic instability. Technique refinements and new technologies have been proposed to minimize this effect. In order to inform new techniques and technology, we examined the relationship between blood pressure and aortic flow during the restoration of systemic circulation following aortic occlusion at progressive levels of hemorrhage. METHODS An automated supraceliac aortic clamp, capable of continuously variable degrees of occlusion, was applied in seven swine. The swine underwent stepwise removal of 40% of their total blood volume in four equal aliquots. After each aliquot, progressive luminal narrowing to the point of complete aortic occlusion was achieved over 5 minutes, sustained for 5 minutes, and then released over 5 minutes. Proximal and distal blood pressure and distal aortic flow were continuously recorded throughout the study. RESULTS Upon release of the clamp, hyperemic aortic flow was observed following 10% and 20% hemorrhage (1,599 ± 785 mL/min, p < 0.01; and 1,070 ± 396 mL/min, p < 0.01, respectively). Proximal blood pressure exhibited a nonlinear relationship to aortic flow during clamp removal; however, distal blood pressure increased linearly with distal flow upon clamp opening across all hemorrhage volumes. CONCLUSIONS Hyperemic blood flow following return of circulation may contribute to cardiovascular collapse. Reintroduction of systemic blood flow after aortic occlusion should be guided by distal blood pressure rather than proximal pressure. Awareness of hemodynamic physiology during aortic occlusion is of paramount importance to the clinical implementation of next-generation resuscitative endovascular balloon occlusion of the aorta techniques and technologies.

Automated variable aortic control versus complete aortic occlusion in a swine model of hemorrhage

BACKGROUND Future endovascular hemorrhage control devices will require features that mitigate the adverse effects of vessel occlusion. Permissive regional hypoperfusion (PRH) with variable aortic control (VAC) is a novel strategy to minimize hemorrhage and reduce the ischemic burden of complete aortic occlusion (AO). The objective of this study was to compare PRH with VAC to AO in a lethal model of hemorrhage. METHODS Twenty-five swine underwent cannulation of the supraceliac aorta, with diversion of aortic flow through an automated extracorporeal circuit. After creation of uncontrolled liver hemorrhage, animals were randomized to 90 minutes of treatment: Control (full, unregulated flow; n = 5), AO (no flow; n = 10), and PRH with VAC (dynamic distal flow initiated after 20 minutes of AO; n = 10). In the PRH group, distal flow rates were regulated between 100 and 300 mL/min based on a desired, preset range of proximal mean arterial pressure (MAP). At 90 minutes, damage control surgery, resuscitation, and restoration of full flow ensued. Critical care continued for 4.5 hours or until death. Hemodynamic parameters and markers of ischemia were recorded. RESULTS Study survival was 0%, 50%, and 90% for control, AO, and VAC, respectively (p < 0.01). During intervention, VAC resulted in more physiologic proximal MAP (84 ± 18 mm Hg vs. 105 ± 9 mm Hg, p < 0.01) and higher renal blood flow than AO animals (p = 0.02). During critical care, VAC resulted in higher proximal MAP (73 ± 8 mm Hg vs. 50 ± 6 mm Hg, p < 0.01), carotid and renal blood flow (p < 0.01), lactate clearance (p < 0.01), and urine output (p < 0.01) than AO despite requiring half the volume of crystalloids to maintain proximal MAP ≥50 mm Hg (p < 0.01). CONCLUSION Permissive regional hypoperfusion with variable aortic control minimizes the adverse effects of distal ischemia, optimizes proximal pressure to the brain and heart, and prevents exsanguination in this model of lethal hemorrhage. These findings provide foundational knowledge for the continued development of this novel paradigm and inform next-generation endovascular designs.

The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model

BACKGROUND Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Qcarotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention. METHODS Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Qcarotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3%; 95% confidence interval [CI], 3.6–57.9; REBOA, 28.6%; 95% CI, 3.7–71.0; and PAO, 28.6%; 95% CI, 3.7–71.0). CONCLUSION In an animal model of TBI and shock, REBOA increased Qcarotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.OBJECTIVES Despite clinical reports of poor outcomes, the degree to which REBOA exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Qcarotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared to partial aortic occlusion (PAO) or no intervention. METHODS 21 swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA 105.3±8.8; PAO 92.7±9.2; Control 48.9±7.7, p=0.02) and higher Qcarotid (REBOA 673.1±57.9; PAO 464.2±53.0; Control 170.3±29.4, p<0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control 12.8±1.2; REBOA 5.1±0.6; PAO 9.4±1.1, p<0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control 14.3%, 95%CI 3.6-57.9; REBOA 28.6%, 95%CI 3.7-71.0; and PAO 28.6%, 95%CI 3.7-71.0). CONCLUSIONS In an animal model of TBI and shock, REBOA increased carotid flow and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients. LEVEL OF EVIDENCE Level IV.

A pilot study of chest tube versus pigtail catheter drainage of acute hemothorax in swine.

BACKGROUND Evacuation of traumatic hemothorax (HTx) is typically accomplished with large-bore (28–40 Fr) chest tubes, often resulting in patient discomfort. Management of HTx with smaller (14 Fr) pigtail catheters has not been widely adopted because of concerns about tube occlusion and blood evacuation rates. We compared pigtail catheters with chest tubes for the drainage of acute HTx in a swine model. METHODS Six Yorkshire cross-bred swine (44–54 kg) were anesthetized, instrumented, and mechanically ventilated. A 32 Fr chest tube was placed in one randomly assigned hemithorax; a 14 Fr pigtail catheter was placed in the other. Each was connected to a chest drainage system at −20 cm H2O suction and clamped. Over 15 minutes, 1,500 mL of arterial blood was withdrawn via femoral artery catheters. Seven hundred fifty milliliters of the withdrawn blood was instilled into each pleural space, and fluid resuscitation with colloid was initiated. The chest drains were then unclamped. Output from each drain was measured every minute for 5 minutes and then every 5 minutes for 40 minutes. The swine were euthanized, and thoracotomies were performed to quantify the volume of blood remaining in each pleural space and to examine the position of each tube. RESULTS Blood drainage was more rapid from the chest tube during the first 3 minutes compared with the pigtail catheter (348 ± 109 mL/min vs. 176 ± 53 mL/min), but this difference was not statistically significant (p = 0.19). Thereafter, the rates of drainage between the two tubes were not substantially different. The chest tube drained a higher total percentage of the blood from the chest (87.3% vs. 70.3%), but this difference did not reach statistical significance (p = 0.21). CONCLUSION We found no statistically significant difference in the volume of blood drained by a 14 Fr pigtail catheter compared with a 32 Fr chest tube.