Blunt cerebrovascular injuries: Outcomes from the American Association for the Surgery of Trauma PROspective Observational Vascular Injury Treatment (PROOVIT) multicenter registry.

BACKGROUND: Administering antithrombotics (AT) to the multiply injured patient with blunt cerebrovascular injury (BCVI) requires a thoughtful assessment of the risk of stroke and death associated with nontreatment. Large, multicenter analysis of outcomes stratified by injury grade and vessel injured is needed to inform future recommendations. METHODS: Nine hundred and seventy-one BCVIs were identified from the PROspective Vascular Injury Treatment registry in this retrospective analysis. Using multivariate analysis, we identified predictors of BCVI-related stroke and death. We then stratified these risks by injury grade and vessel injured. We compared the risk of adverse outcomes in the nontreatment group with those treated with antiplatelet agents and/or anticoagulants. RESULTS: Stroke was identified in 7% of cases. Overall mortality was 12%. Both increased with increasing BCVI grade. Treatment with ATs was associated with lower mortality and was not significantly affected by the choice of agent. Withholding ATs was associated with an increased risk of stroke and/or death across all subgroups (Grade I/II: odds ratio [OR], 4.66; 95% confidence interval [CI], 2.48-8.75; Grade III: OR, 7.0; 95% CI, 2.01-24.5; Grade IV: OR, 4.43; 95% CI, 1.76-11.1) even after controlling for covariates. Predictors of death included more severe trauma, Grade IV injury, and the occurrence of stroke. Arterial occlusion, hypotension, and endovascular intervention were significant predictors of stroke. Patients that experienced a BCVI-related stroke were at a 4.2× increased risk of death. The data set lacked the granularity necessary to evaluate AT timing or dosing regimen, which limited further analysis of stroke prevention strategies. CONCLUSION: Stroke and death remain significant risks for all BCVI grades regardless of the vessel injured. Antithrombotics represent the only management strategy that is consistently associated with a lower incidence of stroke and death in all BCVI categories. In the multi-injured BCVI patient with a high risk of bleeding on anticoagulation, antiplatelet agents are an efficacious alternative. Given the 40% mortality rate in patients who survived their initial trauma and developed a BCVI-related stroke, nontreatment may no longer be a viable option. LEVEL OF EVIDENCE: Epidemiological III; Therapeutic IV.

Breast Conserving Surgery Compared With Mastectomy in Male Breast Cancer: A Brief Systematic Review.

The surgical guidelines for male breast cancer (MBC) have been largely guided by female-predominant clinical trials. Because no clinical trial has been conducted to examine the surgical treatment of MBC, we performed a systematic review comparing the survival of patients with MBC who had undergone breast conserving surgery (BCS) and those who had undergone mastectomy and evaluated the patients' radiotherapy compliance after BCS. We performed a systematic search of electronic databases to find MBC cohort studies that had reported ≥ 1 survival outcome (disease-free survival [DFS], disease-specific survival [DSS], or overall survival [OS]) stratified by surgical treatment (BCS and/or mastectomy) and/or radiotherapy compliance with BCS. A total of 1 prospective and 9 retrospective cohort studies were included, with the number of patients ranging from 7 to 6039. Of the BCS patients, compliance with postoperative radiotherapy was low (range, 27%-46%), with the exception of 1 single-institution prospective study that reported 86% compliance (6 of 7 patients). The pooled estimate for all patients with MBC was 83% (95% confidence interval [CI], 78%-88%) for 5-year DSS and 66% (95% CI, 63%-70%) for 5-year OS. Most studies reported no differences in DFS, DSS, or OS for BCS and mastectomy. BCS is a reasonable treatment approach for MBC because it was associated with oncologic outcomes similar to those with mastectomy. However, the low rates of radiotherapy compliance among male patients who underwent BCS is concerning and highlights the importance of shared decision-making with patients with MBC when selecting a surgical treatment strategy.

Direct site endovascular repair as salvage procedure after anastomotic breakdown of primary repair following trauma.

A 16-year-old boy presented to a level I trauma center after multiple gun shot wounds and a motorcycle crash. He was in profound hemorrhagic shock and had multiple traumatic injuries, including a right common iliac arterial injury. The vessel was shunted for damage control and subsequently repaired primarily. On hospital day 18, he experienced dehiscence of the anastomosis requiring urgent surgery. The artery was ultimately repaired with an expandable polytetrafluoroethylene stent graft deployed in an open fashion through the site of injury. We discuss the use of stent grafts as an interesting alternative to suture repair after anastomotic disruption.

Renal effects of three endoaortic occlusion strategies in a swine model of hemorrhagic shock.

INTRODUCTION: Trauma patients are predisposed to kidney injury. We hypothesized that in shock, zone 3 REBOA would increase renal blood flow (RBF) compared to control and that a period of zone 3 occlusion following zone 1 occlusion would improve renal function compared to zone 1 occlusion alone. MATERIALS AND METHODS: Twenty-four anesthetized swine underwent hemorrhagic shock, 45 min of zone 1 REBOA (Z1, supraceliac), zone 3 REBOA (Z3, infrarenal), or no intervention (control) followed by resuscitation with shed blood and 5 h of critical care. In a fourth group (Z1Z3), animals underwent 55 min of zone 3 REBOA following zone 1 occlusion. Physiologic parameters were recorded, blood and urine were collected at specified intervals. RESULTS: During critical care, there were no differences in RBF between the Z1 and Z3 groups. The average RBF during critical care in Z1Z3 was significantly lower than in Z3 alone (98.2 ±â€¯23.9 and 191.9 ±â€¯23.7 mL/min; p = 0.046) and not different than Z1. There was no difference in urinary neutrophil gelatinase-associated lipocalin-to-urinary creatinine ratio between Z1 and Z1Z3. Animals in the Z1Z3 group had a significant increase in the ratio at the end of the experiment compared to baseline [median (IQR)] [9.2 (8.2-13.2) versus 264.5 (73.6-1174.6)]. Following Z1 balloon deflation, RBF required 45 min to return to baseline. CONCLUSION: Neither zone 3 REBOA alone nor zone 3 REBOA following zone 1 REBOA improved renal blood flow or function. Following zone 1 occlusion, RBF is restored to baseline levels after approximately 45 min.

Resuscitative endovascular balloon occlusion of the aorta induced myocardial injury is mitigated by endovascular variable aortic control.

BACKGROUND: The cardiac effects of resuscitative endovascular balloon occlusion of the aorta (REBOA) are largely unknown. We hypothesized that increased afterload from REBOA would lead to cardiac injury, and that partial flow using endovascular variable aortic control (EVAC) would mitigate this injury. METHODS: Eighteen anesthetized swine underwent controlled 25% blood volume hemorrhage. Animals were randomized to either Zone 1 REBOA, Zone 1 EVAC, or no intervention (control) for 45 minutes. Animals were then resuscitated with shed blood, observed during critical care, and euthanized after a 6-hour total experimental time. Left ventricular function was measured with a pressure-volume catheter, and blood samples were drawn at routine intervals. RESULTS: The average cardiac output during the intervention period was higher in the REBOA group (9.3 [8.6-15.4] L/min) compared with the EVAC group (7.2 [5.8-8.0] L/min, p = 0.01) and the control group (6.8 [5.8-7.7] L/min, p < 0.01). At the end of the intervention, the preload recruitable stroke work was significantly higher in both the REBOA and EVAC groups compared with the control group (111.2 [102.5-148.6] and 116.7 [116.6-141.4] vs. 67.1 [62.7-87.9], p = 0.02 and p < 0.01, respectively). The higher preload recruitable stroke work was maintained throughout the experiment in the EVAC group, but not in the REBOA group. Serum troponin concentrations after 6 hours were higher in the REBOA group compared with both the EVAC and control groups (6.26 ± 5.35 ng/mL vs 0.92 ± 0.61 ng/mL and 0.65 ± 0.38 ng/mL, p = 0.05 and p = 0.03, respectively). Cardiac intramural hemorrhage was higher in the REBOA group compared with the control group (1.67 ± 0.46 vs. 0.17 ± 0.18, p = 0.03), but not between the EVAC and control groups. CONCLUSION: In a swine model of hemorrhagic shock, complete aortic occlusion resulted in cardiac injury, although there was no direct decrease in cardiac function. EVAC mitigated the cardiac injury and improved cardiac performance during resuscitation and critical care.

Is Breast-Conserving Therapy Appropriate for Male Breast Cancer Patients? A National Cancer Database Analysis.

BACKGROUND: Current treatment guidelines for male breast cancer are predominantly guided by female-only clinical trials. With scarce research, it is unclear whether breast-conserving therapy (BCT) is equivalent to mastectomy in men. We sought to compare overall survival (OS) among male breast cancer patients who underwent BCT versus mastectomy. METHODS: We performed a retrospective analysis of 8445 stage I-II (T1-2 N0-1 M0) male breast cancer patients from the National Cancer Database (2004-2014). Patients were grouped according to surgical and radiation therapy (RT). BCT was defined as partial mastectomy followed by RT. Multivariable and inverse probability of treatment-weighted (IPTW) Cox proportional hazards models were used to compare OS between treatment groups, controlling for demographic and clinicopathologic characteristics. RESULTS: Most patients underwent total mastectomy (61.2%), whereas 18.2% underwent BCT, 12.4% underwent total mastectomy with RT, and 8.2% underwent partial mastectomy alone. In multivariable and IPTW models, partial mastectomy alone, total mastectomy alone, and total mastectomy with RT were associated with worse OS compared with BCT (p < 0.001 all). Ten-year OS was 73.8% for BCT and 56.3, 58.0 and 56.3% for other treatment approaches. Older age, higher T/N stage, histological grade, and triple-negative receptor status were associated with poorer OS (p < 0.05). Subgroup analysis by stage demonstrated similar results. CONCLUSIONS: In this national sample of male breast cancer patients, BCT was associated with greater survival. The underlying mechanisms of this association warrant further study, because more routine adoption of BCT in male breast cancer appears to translate into clinically meaningful improvements in survival.

Endovascular Perfusion Augmentation for Critical Care: Partial Aortic Occlusion for Treatment of Severe Ischemia-Reperfusion Shock.

BACKGROUND: The resuscitation of patients in shock is materially intensive and many patients are refractory to maximal therapy. We hypothesized that partial inflation of an intra-aortic balloon, termed Endovascular Perfusion Augmentation for Critical Care (EPACC), would minimize material requirements while improving physiologic metrics. METHODS: Swine underwent a 25% controlled bleed and 45 min of complete aortic occlusion to create a severe ischemia-reperfusion shock state. Animals received either standardized critical care (SCC) composed of IV fluids and norepinephrine delivered through an algorithmically controlled platform or EPACC in addition to SCC. Physiologic parameters were collected, and blood was sampled for analysis. Primary outcomes were total IV fluids and average MAP during the critical care phase. Differences (P < 0.05) were measured with t test (continuous data) and Wilcoxon rank-sum test (ordinal data). RESULTS: There were no differences in baseline characteristics. There were no differences in the maximum lactate; however, animals in the EPACC group had a higher average MAP (EPACC 65 mmHg, 95% confidence interval [CI], 65-66; SCC 60 mmHg, 95% CI, 57-63; P < 0.01) and remained within goal MAP for a greater period of time (EPACC 95.3%, 95% CI, 93.2-97.4; SCC 51.0%, 95% CI, 29.5-72.6; P < 0.01). EPACC animals required less IV fluids when compared with the SCC group (EPACC 21 mL/kg, 95% CI, 0-42; SCC 96 mL/kg, 95% CI, 76-117; P < 0.01). There were no differences in final lactate. Animals in the EPACC group had a higher final creatinine (EPACC 2.3 mg/dL, 95% CI, 2.1-2.5; SCC 1.7 mg/dL, 95% CI, 1.4-2.0; P < 0.01), but there were no differences in renal cellular damage on histology (P = 0.16). CONCLUSION: Using a swine model of severe shock, the addition of EPACC to SCC significantly reduced fluid resuscitation requirements and improved blood pressure. This is the first description of a new therapy for patients in refractory shock or in resource-limited settings.

Endocrine Effects of Simulated Complete and Partial Aortic Occlusion in a Swine Model of Hemorrhagic Shock.

INTRODUCTION: Low distal aortic flow via partial aortic occlusion (AO) may mitigate ischemia induced by resuscitative endovascular balloon occlusion of the aorta (REBOA). We compared endocrine effects of a novel simulated partial AO strategy, endovascular variable aortic control (EVAC), with simulated REBOA in a swine model. MATERIALS AND METHODS: Aortic flow in 20 swine was routed from the supraceliac aorta through an automated extracorporeal circuit. Following liver injury-induced hemorrhagic shock, animals were randomized to control (unregulated distal flow), simulated REBOA (no flow, complete AO), or simulated EVAC (distal flow of 100-300 mL/min after 20 minutes of complete AO). After 90 minutes, damage control surgery, resuscitation, and full flow restoration ensued. Critical care was continued for 4.5 hours or until death. RESULTS: Serum angiotensin II concentration was higher in the simulated EVAC (4,769 ± 624 pg/mL) than the simulated REBOA group (2649 ± 429) (p = 0.01) at 180 minutes. There was no detectable difference in serum renin [simulated REBOA: 231.3 (227.9-261.4) pg/mL; simulated EVAC: 294.1 (231.2-390.7) pg/mL; p = 0.27], aldosterone [simulated EVAC: 629 (454-1098), simulated REBOA: 777 (575-1079) pg/mL, p = 0.53], or cortisol (simulated EVAC: 141 ± 12, simulated REBOA: 127 ± 9 ng/mL, p = 0.34) concentrations between groups. CONCLUSIONS: Simulated EVAC was associated with higher serum angiotensin II, which may have contributed to previously reported cardiovascular benefits. Future studies should evaluate the renal effects of EVAC and the concomitant therapeutic use of angiotensin II.

Pharmacokinetics of Tranexamic Acid via Intravenous, Intraosseous, and Intramuscular Routes in a Porcine (Sus scrofa) Hemorrhagic Shock Model.

BACKGROUND: Intravenous (IV) tranexamic acid (TXA) is an adjunct for resuscitation in hemorrhagic shock; however, IV access in these patients may be difficult or impossible. Intraosseous (IO) or intramuscular (IM) administration could be quickly performed with minimal training. We investigated the pharmacokinetics of TXA via IV, IO, and IM routes in a swine model of controlled hemorrhagic shock. METHODS: Fifteen swine were anesthetized and bled of 35% of their blood volume before randomization to a single 1g/10mL dose of IV, IO, or IM TXA. Serial serum samples were obtained after TXA administration. These were analyzed with high-pressure liquid chromatography-mass spectrometry to determine drug concentration at each time point and define the pharmacokinetics of each route. RESULTS: There were no significant differences in baseline hemodynamics or blood loss between the groups. Peak concentration (Cmax) was significantly higher in IV and IO routes compared with IM (p = .005); however, the half-life of TXA was similar across all routes (p = .275). CONCLUSION: TXA administration via IO and IM routes during hemorrhagic shock achieves serum concentrations necessary for inhibition of fibrinolysis and may be practical alternatives when IV access is not available.

Endovascular variable aortic control (EVAC) versus resuscitative endovascular balloon occlusion of the aorta (REBOA) in a swine model of hemorrhage and ischemia reperfusion injury.

BACKGROUND: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is effective at limiting hemorrhage from noncompressible sources and restoring but causes progressive distal ischemia, supraphysiologic pressures, and increased cardiac afterload. Endovascular variable aortic control (EVAC) addresses these limitations, while still controlling hemorrhage. Previous work demonstrated improved outcomes following a 90-minute intervention period in an uncontrolled hemorrhage model. The present study compares automated EVAC to REBOA over an occlusion period reflective of contemporary REBOA usage. METHODS: Following instrumentation, 12 Yorkshire-cross swine underwent controlled 25% hemorrhage, a 45-minute intervention period of EVAC or REBOA, and subsequent resuscitation with whole blood and critical care for the remainder of a 6-hour experiment. Hemodynamics were acquired continuously, and laboratory parameters were assessed at routine intervals. Tissue was collected for histopathologic analysis. RESULTS: No differences were seen in baseline parameters. During intervention, EVAC resulted in more physiologic proximal pressure augmentation compared with REBOA (101 vs. 129 mm Hg; 95% confidence interval [CI], 105-151 mm Hg; p = 0.04). During critical care, EVAC animals required less than half the amount of crystalloid (3,450 mL; 95% CI, 1,215-5,684 mL] vs. 7,400 mL [95% CI, 6,148-8,642 mL]; p < 0.01) and vasopressors (21.5 ng/kg [95% CI, 7.5-35.5 ng/kg] vs. 50.5 ng/kg [95% CI, 40.5-60.5 ng/kg]; p = 0.05) when compared with REBOA animals. Endovascular variable aortic control resulted in lower peak and final lactate levels. Endovascular variable aortic control animals had less aortic hyperemia from reperfusion with aortic flow rates closer to baseline (36 mL/kg per minute [95% CI, 30-44 mL/kg per minute] vs. 51 mL/kg per minute [95% CI, 41-61 mL/kg per minute]; p = 0.01). CONCLUSIONS: For short durations of therapy, EVAC produces superior hemodynamics and less ischemic insult than REBOA in this porcine-controlled hemorrhage model, with improved outcomes during critical care. This study suggests EVAC is a viable strategy for in-hospital management of patients with hemorrhagic shock from noncompressible sources. Survival studies are needed to determine if these early differences persist over time.

Location is everything: The hemodynamic effects of REBOA in Zone 1 versus Zone 3 of the aorta.

OBJECTIVES: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an emerging technology to augment proximal blood pressure during the resuscitation of patients with noncompressible torso hemorrhage. Currently, placement choice, supraceliac (Zone 1) versus infrarenal (Zone 3) aorta, depends on injury patterns, but remains a highly debated topic. We sought to compare the proximal hemodynamic support provided by Zone 1 versus Zone 3 REBOA placement and the degree of hemodynamic instability upon reperfusion following intervention. METHODS: Eighteen anesthetized swine underwent controlled hemorrhage of 25% total blood volume, followed by 45 minutes of Zone 1 REBOA, Zone 3 REBOA, or no intervention (control). They were then resuscitated with shed blood, aortic balloons were deflated, and 5 hours of critical care ensued prior to euthanasia. Physiologic parameters were recorded continuously, and blood was drawn for analysis at specified intervals. Significance was defined as p < 0.05. RESULTS: There were no significant differences between groups at baseline or during the initial 30 minutes of hemorrhage. During the intervention period, average proximal MAP was significantly greater in Zone 1 animals when compared with Zone 3 animals (127.9 ± 1.3 vs. 53.4 ± 1.1 mm Hg) and greater in Zone 3 animals when compared with control animals (42.9 ± 0.9 mm Hg). Lactate concentrations were significantly higher in Zone 1 animals (9.6 ± 0.4 mmol/L) when compared with Zone 3 animals (5.1 ± 0.3 mmol/L) and control animals (4.2 ± 0.8 mmol/L). CONCLUSIONS: In our swine model of hemorrhagic shock, Zone 3 REBOA provided minimal proximal hemodynamic support when compared with Zone 1 REBOA, albeit with less ischemic burden and instability upon reperfusion. In cases of impending hemodynamic collapse, Zone 1 REBOA placement may be more efficacious regardless of injury pattern, whereas Zone 3 should be reserved only for relatively stable patients with ongoing distal hemorrhage.

Lower extremity cooling reduces ischemia-reperfusion injury following Zone 3 REBOA in a porcine hemorrhage model.

BACKGROUND: New strategies to mitigate ischemia during REBOA and to prolong its maximal duration are needed. We hypothesized that simple external cooling of the hind limbs would decrease ischemia-reperfusion injury following prolonged Zone 3 REBOA. METHODS: Twelve swine were anesthetized, instrumented, splenectomized, and then underwent 15% total blood volume hemorrhage. Animals were randomized to hypothermia or control followed by 4 hours of Zone 3 REBOA, resuscitation with shed blood, and 3 hours of critical care. Physiologic parameters were continuously recorded, and laboratory specimens were obtained at regular intervals. Baseline and end-of-study muscle biopsies were obtained for histologic analysis. RESULTS: There were no significant differences between groups at baseline or after hemorrhage. Maximum creatine kinase was significantly lower in the hypothermia group compared with the normothermia group (median [interquartile range] = 3,445 U/mL [3,380-4,402 U/mL] vs. 22,544 U/mL [17,030-24,981 U/mL]; p < 0.01). Maximum serum myoglobin was also significantly lower in the hypothermia group (1,792 ng/mL [1,250-3,668 ng/mL] vs. 21,186 ng/mL [14,181-24,779 ng/mL]; p < 0.01). Fascial compartment pressures were significantly lower during critical care in the hypothermia group (p = 0.03). No histologic differences were observed in hind limb skeletal muscle. CONCLUSIONS: External cooling during prolonged Zone 3 REBOA decreased ischemic muscle injury and resulted in lower compartment pressures following reperfusion. Hypothermia may be a viable option to extend the tolerable duration of Zone 3 occlusion, beyond what is currently achievable. Future survival studies are required to assess functional outcomes.

Coagulopathy and Mortality in Combat Casualties: Do the Kidneys Play a Role?

Background: Acute traumatic coagulopathy (ATC) is a common condition after traumatic injury and is known to be associated with an increase in morbidity and mortality in trauma patients. ATC has been implicated as a causative factor in both early hemorrhage and late organ failure in this population, yet the pathophysiology remains largely unknown. Additionally, acute kidney injury (AKI) is a common condition among critically injured trauma patients. AKI has been associated with an elevated International Normalized Ratio (INR) and warfarin use, but its development has not been well studied in the setting of ATC. We hypothesized that the presence of ATC influences the development of AKI and may mediate mortality in combat casualties. Methods: Data were obtained from the Department of Defense Trauma Registry, Medical Data Store and Composite Healthcare System, and the Armed Forces Medical Examiner System. A retrospective review was conducted of US service members injured in Iraq or Afghanistan between February 1, 2002 and February 1, 2011, who required ICU level care and survived evacuation out of theater. Exclusions were made for missing data. Cox proportional hazard regression was performed to determine the effect of ATC (a priori defined as first INR > 1.3) on the development of AKI. Further analysis was conducted to determine the influence of these variables on 30-d mortality, and multiple sensitivity analyses were performed to determine the effect of ATC on both AKI and mortality. Results: A total of 1,288 patients were identified for analysis. ATC was a risk factor for subsequent AKI after adjustment (HR 1.67, 95% CI 1.28-2.18; p < 0.001). However, ATC was not a risk factor for mortality after adjustment in the full model (HR 1.87, 95% CI 0.95-3.65; p = 0.069). On sensitivity analyses exploring alternate definitions of ATC, an INR of 1.2 remained associated with AKI (HR 1.46, 95% CI 1.13-1.88; p = 0.004) and an INR of 1.5 became significant for mortality (HR 1.76, 95% CI 1.32-2.35; p < 0.001). Conclusion: ATC is independently associated with the development of AKI. Although ATC is associated with mortality in the unadjusted model, it is not significant after adjustment for AKI. This implies that the kidneys may play a role in the adverse outcomes observed after ATC. Increased awareness and monitoring for coagulopathy and the subsequent development of AKI in combat casualty patients may lead to earlier diagnosis and treatment of these conditions, possibly decreasing morbidity and mortality.

Presenting hypertension, burn injury, and mortality in combat casualties.

INTRODUCTION: The effect of presenting hypertension is poorly studied in combat casualties. We hypothesized that elevated mean arterial pressure (MAP) on presentation to combat hospitals would be associated with poor outcomes. METHODS: Data was obtained from the Department of Defense Trauma Registry and the Armed Forces Medical Examiner System. Variables analyzed included presenting vital signs to Role II-III military theater hospital, demographic variables, injury severity score (ISS), location and mechanism of injury, presence of traumatic brain injury (TBI), acute kidney injury (AKI), and mortality. Patients were stratified by decile of MAP and logistic regression analysis was employed to adjust for confounders. RESULTS: A total of 4072 subjects injured from February 2002 to February 2011 were identified. Compared to patients in the middle deciles of presenting MAP, patients in the highest and lowest MAP deciles were the only groups that demonstrated a higher mortality on univariate analysis (OR 2.06, 95% CI 1.16-2.31 and OR 2.86, 95% CI 1.76-4.67, respectively), and this relationship persisted after adjustment for ISS, HR, temperature, presence of burn injury, TBI, and AKI. Burn injury was associated with mortality in the full multivariate analysis. However, further analysis limited to patients without burn injury did not demonstrate an association between high MAP and mortality (OR 0.84, 95% CI 0.36-1.99; p=0.70). Conversely, when limited to patients with burn injury, high MAP was associated with mortality (OR 3.78, 95% CI 1.74-8.20; p=0.001). CONCLUSION: The relationship between mortality and presenting MAP appears to be U-shaped, demonstrating increased mortality in the lowest and highest deciles. However, mortality in the highest MAP decile appears to be limited to casualties with associated burn injury, even after adjustment for TBI, AKI, and ISS, which takes into account the severity of the burn injury. Physicians should recognize that burn patients presenting with an elevated MAP are at an increased risk for poor outcomes. LEVEL OF EVIDENCE: III.

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

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.

A novel model of highly lethal uncontrolled torso hemorrhage in swine.

INTRODUCTION: A reproducible, lethal noncompressible torso hemorrhage model is important to civilian and military trauma research. Current large animal models balancing clinical applicability with standardization and internal validity. As such, large animal models of trauma vary widely in the surgical literature, limiting comparisons. Our aim was to create and validate a porcine model of uncontrolled hemorrhage that maximizes reproducibility and standardization. METHODS: Seven Yorkshire-cross swine were anesthetized, instrumented, and splenectomized. A simple liver tourniquet was applied before injury to prevent unregulated hemorrhage while creating a traumatic amputation of 30% of the liver. Release of the tourniquet and rapid abdominal closure following injury provided a standardized reference point for the onset and duration of uncontrolled hemorrhage. At the moment of death, the liver tourniquet was quickly reapplied to provide accurate quantification of intra-abdominal blood loss. Weight and volume of the resected and residual liver segments were measured. Hemodynamic parameters were recorded continuously throughout each experiment. RESULTS: This liver injury was rapidly and universally lethal (11.2 ± 4.9 min). The volume of hemorrhage (35.8% ± 6% of total blood volume) and severity of uncontrolled hemorrhage (100% of animals deteriorated to a sustained mean arterial pressure <35 mmHg for 5 min) were consistent across all animals. Use of the tourniquet effectively halted preprocedure and postprocedure blood loss allowing for accurate quantification of amount of hemorrhage over a defined period. In addition, the tourniquet facilitated the creation of a consistent liver resection weight (0.0043 ± 0.0003 liver resection weight: body weight) and as a percentage of total liver resection weight (27% ± 2.2%). CONCLUSIONS: This novel tourniquet-assisted noncompressible torso hemorrhage model creates a standardized, reproducible, highly lethal, and clinically applicable injury in swine. Use of the tourniquet allowed for consistent liver injury and precise control over hemorrhage. Recorded blood loss was similar across all animals. Improving reproducibility and standardization has the potential to offer improvements in large animal translational models of hemorrhage. LEVEL OF EVIDENCE: Level I.

Comparison of direct site endovascular repair utilizing expandable polytetrafluoroethylene stent grafts versus standard vascular shunts in a porcine (Sus scrofa) model.

INTRODUCTION: The small diameter of temporary vascular shunts for vascular trauma management may restrict flow and result in ischemia or early thrombosis. We have previously reported a clinical experience with direct, open surgical reconstruction using expandable polytetrafluoroethylene stent grafts to create a "sutureless" anastomosis as an alternative to standard temporary vascular shunts. We sought to characterize patency and flow characteristics of these grafts compared with standard shunts in a survival model of porcine vascular injury. METHODS: Twelve Yorkshire-cross swine received a 2-cm-long near-circumferential defect in the bilateral iliac arteries. A 14 Fr Argyle shunt was inserted into one randomly assigned artery, with a self-expanding expandable polytetrafluoroethylene stent deployed in the other. At 72 hours, conduit patency was evaluated by angiography. Arterial flow measurements were obtained at baseline, immediately after intervention, and after 72 hours via direct measurement with perivascular flow meters. Blood pressure proximal and distal to the conduits and arterial samples for histopathology were obtained during the terminal procedure. RESULTS: Angiography revealed no difference in patency at 72 hours (p = 1.0). While there was no difference in baseline arterial flow between arteries (p = 0.63), the stent grafts demonstrated significantly improved blood flow compared with shunts both immediately after intervention (390 ± 36 mL/min vs. 265 ± 25 mL/min, p = 0.002) and at 72 hours (261 ± 29 mL/min vs. 170 ± 36 mL/min, p = 0.005). The pressure gradient across the shunts was greater than that of the stent grafts (11.5 mm Hg [interquartile range, 3-19 mm Hg] vs. 3 mm Hg [interquartile range, 3-5 mm Hg], p = 0.013). The speed of deployment was similar between the two devices. CONCLUSIONS: Open "sutureless" direct site repair using commercially available stent grafts to treat vascular injury is a technically feasible strategy for damage control management of peripheral vascular injury and offers increased blood flow when compared with temporary shunts. Furthermore, stent grafts may offer improved durability to extend the window until definitive vascular repair. The combination of these traits may improve outcomes after vascular injury. LEVEL OF EVIDENCE: Epidemiologic/Prognostic, level III.

Incremental balloon deflation following complete resuscitative endovascular balloon occlusion of the aorta results in steep inflection of flow and rapid reperfusion in a large animal model of hemorrhagic shock.

INTRODUCTION: To avoid potential cardiovascular collapse after resuscitative endovascular balloon occlusion of the aorta (REBOA), current guidelines recommend methodically deflating the balloon for 5 minutes to gradually reperfuse distal tissue beds. However, anecdotal evidence suggests that this approach may still result in unpredictable aortic flow rates and hemodynamic instability. We sought to characterize aortic flow dynamics following REBOA as the balloon is deflated in accordance with current practice guidelines. METHODS: Eight Yorkshire-cross swine were splenectomized, instrumented, and subjected to rapid 25% total blood volume hemorrhage. After 30 minutes of shock, animals received 60 minutes of Zone 1 REBOA with a low-profile REBOA catheter. During subsequent resuscitation with shed blood, the aortic occlusion balloon was gradually deflated in stepwise fashion at the rate of 0.5 mL every 30 seconds until completely deflated. Aortic flow rate and proximal mean arterial pressure (MAP) were measured continuously over the period of balloon deflation. RESULTS: Graded balloon deflation resulted in variable initial return of aortic flow (median, 78 seconds; interquartile range [IQR], 68-105 seconds). A rapid increase in aortic flow during a single-balloon deflation step was observed in all animals (median, 819 mL/min; IQR, 664-1241 mL/min) and corresponded with an immediate decrease in proximal MAP (median, 30 mm Hg; IQR, 14.5-37 mm Hg). Total balloon volume and time to return of flow demonstrated no correlation (r = 0.016). CONCLUSION: This study is the first to characterize aortic flow during balloon deflation following REBOA. A steep inflection point occurs during balloon deflation that results in an abrupt increase in aortic flow and a concomitant decrease in MAP. Furthermore, the onset of distal aortic flow was inconsistent across study animals and did not correlate with initial balloon volume or relative deflation volume. Future studies to define the factors that affect aortic flow during balloon deflation are needed to facilitate controlled reperfusion following REBOA.