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The novel total left anterior descending devascularization (TLD) approach in a canine ischemic heart failure model limits collateral flow in the ischemic zone and provides excellent early survival and repeatable development of chronic ischemic heart failure in the canine heart. This work provides a consistent large animal model for investigating heart failure mechanisms and testing novel therapeutics.

Background: Extrinsic control of cardiomyocyte metabolism is poorly understood in heart failure (HF). FGF21 (Fibroblast growth factor 21), a hormonal regulator of metabolism produced mainly in the liver and adipose tissue, is a prime candidate for such signaling. Methods: To investigate this further, we examined blood and tissue obtained from human subjects with end-stage HF with reduced ejection fraction at the time of left ventricular assist device implantation and correlated serum FGF21 levels with cardiac gene expression, immunohistochemistry, and clinical parameters. Results: Circulating FGF21 levels were substantially elevated in HF with reduced ejection fraction, compared with healthy subjects (HF with reduced ejection fraction: 834.4 [95% CI, 628.4–1040.3] pg/mL, n=40; controls: 146.0 [86.3–205.7] pg/mL, n=20, P =1.9×10 −5 ). There was clear FGF21 staining in diseased cardiomyocytes, and circulating FGF21 levels negatively correlated with the expression of cardiac genes involved in ketone metabolism, consistent with cardiac FGF21 signaling. FGF21 gene expression was very low in failing and nonfailing hearts, suggesting extracardiac production of the circulating hormone. Circulating FGF21 levels were correlated with BNP (B-type natriuretic peptide) and total bilirubin, markers of chronic cardiac and hepatic congestion. Conclusions: Circulating FGF21 levels are elevated in HF with reduced ejection fraction and appear to bind to the heart. The liver is likely the main extracardiac source. This supports a model of hepatic FGF21 communication to diseased cardiomyocytes, defining a potential cardiohepatic signaling circuit in human HF.

Background: Ischemia-reperfusion injury (IRI) after hemorrhage is potentiated by aortic occlusion or resuscitative endovascular balloon occlusion of the aorta (REBOA). Given the central role of mitochondrial injury in shock, we hypothesized that Elamipretide, a peptide that protects mitochondria, would mitigate IRI after hemorrhagic shock and REBOA. Methods: Twelve pigs were subjected to hemorrhagic shock and 45 minutes of REBOA. After 25 minutes of REBOA, animals received either saline or Elamipretide. Animals were transfused with autologous blood during balloon deflation and pigs were resuscitated with isotonic crystalloids and norepinephrine for 4.25 hours. Results: Elamipretide-treated animals required less crystalloids than the controls (62.5 [50-90] and 25 [5-30] mL/kg, respectively), but similar amounts of norepinephrine (24.7 [8.6-39.3] and 9.7 [2.1-12.5] mcg/kg, respectively). Treatment animals had a significant reduction in serum creatinine (control: 2.7 [2.6-2.8]; Elamipretide: 2.4 [2.4-2.5] mg/dL; p=0.04), troponin (control: 3.20 [2.14-5.47] ng/mL, Elamipretide: 0.22 [0.1-1.91] ng/mL; p=0.03), and interleukin-6 concentrations at the end of the study. There were no differences in final plasma lactate concentration. Conclusions: Elamipretide reduced fluid requirements and protected the kidney and heart after profound IRI. Further understanding the subcellular consequences of REBOA and mitochondrial rescue will open new therapeutic avenues for patients suffering from IRI after hemorrhage.

ObjectivesTo expand the number of conditions and interventions explored for their associations with thrombosis in the veterinary literature and to provide the basis for prescribing recommendations.DesignA population exposure comparison outcome format was used to represent patient, exposure, comparison, and outcome. Population Exposure Comparison Outcome questions were distributed to worksheet authors who performed comprehensive searches, summarized the evidence, and created guideline recommendations that were reviewed by domain chairs. The revised guidelines then underwent the Delphi survey process to reach consensus on the final guidelines. Diseases evaluated in this iteration included heartworm disease (dogs and cats), immune-mediated hemolytic anemia (cats), protein-losing nephropathy (cats), protein-losing enteropathy (dogs and cats), sepsis (cats), hyperadrenocorticism (cats), liver disease (dogs), congenital portosystemic shunts (dogs and cats) and the following interventions: IV catheters (dogs and cats), arterial catheters (dogs and cats), vascular access ports (dogs and cats), extracorporeal circuits (dogs and cats) and transvenous pacemakers (dogs and cats).ResultsOf the diseases evaluated in this iteration, a high risk for thrombosis was defined as heartworm disease or protein-losing enteropathy. Low risk for thrombosis was defined as dogs with liver disease, cats with immune-mediated hemolytic anemia, protein-losing nephropathy, sepsis, or hyperadrenocorticism.ConclusionsAssociations with thrombosis are outlined for various conditions and interventions and provide the basis for management recommendations. Numerous knowledge gaps were identified that represent opportunities for future studies.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes a severe ischemia-reperfusion injury. Endovascular Perfusion Augmentation for Critical Care (EPACC) has emerged as a hemodynamic/mechanical adjunct to vasopressors and crystalloid for the treatment of post-REBOA ischemia-reperfusion injury. The objective of the study is to examine the impact of EPACC as a tool for a wean from complete REBOA compared to standard resuscitation techniques.Nine swine underwent anesthesia and then a controlled 30% blood volume hemorrhage with 30 min of supraceliac total aortic occlusion to create an ischemia-reperfusion injury. Animals were randomized to standardized critical care (SCC) or 90 min of EPACC followed by SCC. The critical care phase lasted 270 min after injury. Hemodynamic markers and laboratory values of ischemia were recorded.During the first 90 min the intervention phase SCC spent 60% (54%-73%) and EPACC spent 91% (88%-92%) of the time avoiding proximal hypotension (60 mm Hg), P = 0.03. There was also a statistically significant decrease in cumulative norepinephrine dose at the end of the experiment between SCC (80.89 mcg/kg) versus EPACC (22.03 mcg/kg), P = 0.03. Renal artery flow during EPACC was similar compared to SCC during EPACC, P = 0.19. But during the last hour of the experiment (after removal of aortic balloon) the renal artery flow in EPACC (2.9 mL/kg/min) was statistically significantly increased compared to SCC (1.57 mL/min/kg), P = 0.03. There was a statistically significant decrease in terminal creatinine in the EPACC (1.7 mg/dL) compared to SCC (2.1 mg/dL), P = 0.03.The 90 min of EPACC as a weaning adjunct in the setting of a severe ischemia-reperfusion injury after complete supraceliac REBOA provides improved renal flow with improvement in terminal creatinine compared to SCC with stabilized proximal hemodynamics and decreased vasopressor dose.

Introduction Endovascular variable aortic control (EVAC) is an automated partial resuscitative endovascular balloon occlusion of the aorta (REBOA) platform designed to mitigate the deleterious effects of complete REBOA. Long-term experiments are needed to assess potential benefits. The feasibility of a 24-hour experiment in a complex large animal trauma model remains unknown. Materials and methods Anesthetized swine were subjected to controlled hemorrhage, blunt thoracic trauma, and tibial fractures. Animals were then randomized (N = 3/group) to control (No balloon support), 90 minutes of complete supraceliac REBOA, or 10 minutes of supraceliac REBOA followed by 80 minutes of EVAC. One hundred ten minutes after injury, animals were resuscitated with shed blood, the REBOA catheter was removed. Automated critical care under general anesthesia was maintained for 24 hours. Results Animals in the control and EVAC groups survived to the end of the experiment. Animals in the REBOA group survived for 120, 130, and 660 minutes, respectively. Animals in the EVAC group displayed similar mean arterial pressure and plasma lactate concentration as the control group by the end of the experiment. Histologic analysis suggested myocardial injury in the REBOA group when compared with controls. Conclusions This study demonstrates the feasibility of intermediate-term experiments in a complex swine model of polytrauma with 90 minutes of REBOA. EVAC may be associated with improved survival at 24 hours when compared with complete REBOA. EVAC resulted in normalized physiology after 24 hours, suggesting that prolonged partial occlusion is possible. Longer studies evaluating partial REBOA strategies are needed.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) causes myocardial injury from increased aortic afterload and supraphysiologic cardiac output. However, pharmacologic methods to attenuate high cardiac output and reduce myocardial injury have not been explored. We hypothesized that the use of esmolol during REBOA would reduce myocardial injury.Ten pigs were anesthetized and instrumented. Following 25% total blood volume hemorrhage, animals underwent 45 min of supraceliac (zone 1) REBOA with or without titration of esmolol to maintain heart rate between 80 and 100 beats per minute. Following the REBOA interventions, animals underwent 275 min of standardized critical care.During REBOA, heart rate was significantly lower in the esmolol group compared to control animals (100 [88 - 112] vs 193 [172 - 203] beats/minute, respectively, p0.001) and the average mean arterial pressure (MAP) was lower in the esmolol group (88.0 [80.3-94.9] vs 135.1 [131.7-140.4] mmHg, respectively, p = 0.01). During the critical care phase, there were no differences in heart rate or MAP between groups. Animals in the intervention group received 237.9 [218.7-266.5] µg/kg of esmolol. There was a significant increase from baseline in serum troponins for the control group (p = 0.006) and significantly more subendocardial hemorrhage compared to animals treated with esmolol (3 [3 - 3] and 0 [0 - 0], p = 0.009, respectively).In our porcine model of hemorrhagic shock, zone 1 REBOA was associated with myocardial injury. Pharmacologic heart rate titration with esmolol during occlusion may mitigate the deleterious effects of REBOA on the heart.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) has been proposed as a novel approach to managing non‐traumatic cardiac arrest (NTCA). During cardiac arrest, cardiac output ceases and perfusion of vital organs is compromised. Traditional advanced cardiac life support (ACLS) measures and cardiopulmonary resuscitation are often unable to achieve return of spontaneous circulation (ROSC). During insertion of REBOA a balloon‐tipped catheter is placed into the femoral artery and advanced in a retrograde manner into the aorta while the patient is undergoing cardiopulmonary resuscitation (CPR). The balloon is then inflated to fully occlude the aorta. The literature surrounding the use of aortic occlusion in non‐traumatic cardiac arrest is limited to animal studies, case reports and one recent non‐controlled feasibility trial. In both human and animal studies, preliminary data show that REBOA may improve coronary and cerebral perfusion pressures and key physiologic parameters during cardiac arrest resuscitation, and animal data have demonstrated improved rates of ROSC. Multiple questions remain before REBOA can be considered as an adjunct to ACLS. If demonstrated to be effective clinically, REBOA represents a potentially cost‐effective and generalizable intervention that may improve quality of life for patients with non‐traumatic cardiac arrest.

Objective:Dialysis patients may not have access to conventional renal replacement therapy (RRT) following disasters. We hypothesized that improvised renal replacement therapy (ImpRRT) would be comparable to continuous renal replacement therapy (CRRT) in a porcine acute kidney injury model.Methods:Following bilateral nephrectomies and 2 hours of caudal aortic occlusion, 12 pigs were randomized to 4 hours of ImpRRT or CRRT. In the ImpRRT group, blood was circulated through a dialysis filter using a rapid infuser to collect the ultrafiltrate. Improvised replacement fluid, made with stock solutions, was infused pre-pump. In the CRRT group, commercial replacement fluid was used. During RRT, animals received isotonic crystalloids and norepinephrine.Results:There were no differences in serum creatinine, calcium, magnesium, or phosphorus concentrations. While there was a difference between groups in serum potassium concentration over time (P < 0.001), significance was lost in pairwise comparison at specific time points. Replacement fluids or ultrafiltrate flows did not differ between groups. There were no differences in lactate concentration, isotonic crystalloid requirement, or norepinephrine doses. No difference was found in electrolyte concentrations between the commercial and improvised replacement solutions.Conclusion:The ImpRRT system achieved similar performance to CRRT and may represent a potential option for temporary RRT following disasters.

Diversity, equity, and inclusion (DEI) are crucial elements of successful veterinary emergency and critical care practices across the world. Embracing the elements of DEI creates a work environment that is safe and welcoming for all the members of the team. The American College of Veterinary Emergency and Critical Care DEI committee was formed to enhance and support efforts to increase racial diversity in veterinary emergency and critical care, as well as provide resources that will generate DEI practices across the country. This article provides an overview of the vision of the committee and some of the steps that have been taken to create a welcoming space for all represented in veterinary emergency and critical care.

Background Non-invasive measurement of somatosensory-evoked potentials (SEP) in a large animal model is important to translational cognitive research. We sought to develop a methodology for neurophysiological recording via a transcranial electroencephalography (EEG) cap under an effective sedative regimen with dexmedetomidine, midazolam, and butorphanol that will produce sedation instead of anesthesia while not compromising data quality. Results Pigs received intramuscular dexmedetomidine, midazolam, and butorphanol for SEP assessment with peroneal nerve stimulation. Semi-quantitative sedation assessment was performed after the animal was sufficiently sedated and 30 min later, during the transcranial SEP recording. SEP data were analyzed with commercial software. Binary qualitative analysis of the recording was categorized by an experienced neurophysiologist. All four animals had adequate surface SEP recordings. Animals received 43 [21–47] mcg/kg of dexmedetomidine, 0.3 [0.2–0.3] mg/kg of midazolam, and 0.3 [0.3–0.3] mg/kg of butorphanol IM. All treatments resulted in moderate to deep sedation (Baseline median sedation score 11.5 [11–12]; median score at 30 min: 11.5 [10.5–12]). Heart rate (median [range]) (55 [49–71] beats per minute), respiratory rate (24 [21–30] breaths per minute), and hemoglobin oxygen saturation (99 [98–100]%) and body temperature (37.7 [37.4–37.9] °C) remained within clinically acceptable ranges. There were no undesirable recovery incidents. Conclusions In this pilot study, we demonstrate the feasibility of SEP recording via a transcranial EEG cap under an effective sedative regimen in pigs. Our approach will expand the use of a large animal model in neurotranslational research.

BackgroundExtrinsic control of cardiac contractility and ultrastructure via neurohormonal signaling is well established, but how other organs regulate cardiomyocyte metabolism is less well understood. Fibroblast growth factor-21 (FGF21) a hormonal regulator of metabolism mainly produced in the liver and adipose tissue, is a prime candidate for such signaling.MethodsTo investigate this further, we examined blood and tissue obtained from human subjects with heart failure with reduced ejection fraction (HFrEF) at the time of left ventricular assist device (LVAD) implantation, and correlated serum FGF21 levels with cardiac gene expression, immunohistochemistry, and clinical parameters.ResultsCirculating FGF21 levels were substantially elevated in HFrEF, compared to healthy subjects (HFrEF: 834.4 ± 101.8 pg/mL, n = 40; controls: 145.9 ± 28.6 pg/mL, n = 20, p = 5.5 × 10−8). There was clear FGF21 staining in diseased cardiomyocytes, and circulating FGF21 levels negatively correlated with the expression of cardiac genes involved in ketone metabolism, consistent with cardiac FGF21 signaling. FGF21 gene expression was low in failing and non-failing hearts, suggesting at least partial extracardiac production of the circulating hormone. Circulating FGF21 levels were correlated with BNP and total bilirubin, markers of chronic cardiac and hepatic congestion.ConclusionsCirculating FGF21 levels are elevated in HFrEF. The liver is likely the main extracardiac source, and congestive hepatopathy, common in HFrEF, was likely the proximate signal leading to FGF21 elevations. This supports a model of venous congestion from cardiomyopathy driving hepatic FGF21 communication to diseased cardiomyocytes, defining a potential cardio-hepatic signaling circuit in human heart failure.

While resuscitative endovascular balloon occlusion of the aorta (REBOA) is contraindicated in patients with aortic injuries, this technique may benefit poly-trauma patients with less extreme thoracic injuries. The purpose of this study was to characterize the effects of thoracic injury on hemodynamics during REBOA and the changes in pulmonary contusion over time in a swine model. Twelve swine were anesthetized, instrumented, and randomized to receive either a thoracic injury with 5 impacts to the chest or no injury. All animals underwent controlled hemorrhage of 25% blood volume followed by 45 min of Zone 1 REBOA. Animals were then resuscitated with shed blood, observed during a critical care period, and euthanized after 6 h of total experimental time. There were no differences between the groups at baseline. The only difference after 6 h was a lower hemoglobin in the thoracic trauma group (8.4 ± 0.8 versus 9.4 ± 0.6 g/dL, P = 0.04). The average proximal mean arterial pressures were significantly lower in the thoracic trauma group during aortic occlusion [103 (98–108) versus 117 (115–124) mmHg, P = 0.04]. There were no differences between the pulmonary contusion before REBOA and at the end of the experiment in size (402 ± 263 versus 356 ± 291 mL, P = 0.782) or density (− 406 ± 127 versus − 299 ± 175 HFU, P = 0.256). Thoracic trauma blunted the proximal arterial pressure augmentation during REBOA but had minimal impacts on resuscitative outcomes. This initial study indicates that REBOA does not seem to exacerbate pulmonary contusion in swine, but blunt thoracic injuries may attenuate the expected rises in proximal blood pressure during REBOA.

Introduction Tranexamic acid (TXA) improves survival in traumatic hemorrhage, but difficulty obtaining intravenous (IV) access may limit its use in austere environments, given its incompatibility with blood products. The bioavailability of intramuscular (IM) TXA in a shock state is unknown. We hypothesized that IM and IV administration have similar pharmacokinetics and ability to reverse in vitro hyperfibrinolysis in a swine-controlled hemorrhage model. Methods Twelve Yorkshire cross swine were anesthetized, instrumented, and subjected to a 35% controlled hemorrhage, followed by resuscitation. During hemorrhage, they were randomized to receive a 1 g IV TXA infusion over 10 min, 1 g IM TXA in two 5 mL injections, or 10 mL normal saline IM injection as a placebo group to assess model adequacy. Serum TXA concentrations were determined using liquid chromatography-mass spectrometry, and plasma samples supplemented with tissue plasminogen activator (tPA) were analyzed by rotational thromboelastometry. Results All animals achieved class III shock. There was no difference in the concentration-time areas under the curve between TXA given by either route. The absolute bioavailability of IM TXA was 97%. IV TXA resulted in a higher peak serum concentration during the infusion, with no subsequent differences. Both IV and IM TXA administration caused complete reversal of in vitro tPA-induced hyperfibrinolysis. Conclusion The pharmacokinetics of IM TXA were similar to IV TXA during hemorrhagic shock in our swine model. IV administration resulted in a higher serum concentration only during the infusion, but all levels were able to successfully correct in vitro hyperfibrinolysis. There was no difference in total body exposure to equal doses of TXA between the two routes of administration. IM TXA may prove beneficial in scenarios where difficulty establishing dedicated IV access could otherwise limit or delay its use.

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

Objectives To evaluate the association of intraoperative urinary biomarker excretion during cardiac surgery and the subsequent development of acute kidney injury (AKI). Design Prospective, nonrandomized, observational study. Setting Single tertiary-level, university-affiliated hospital. Participants Ninety patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Interventions None. Measurements and Main Results Urinary samples were collected every 30 minutes intraoperatively and then at four, 12, and 24 hours after CPB. Samples were measured for interleukin 18 (IL-18), kidney injury molecule-1 (KIM1), and creatinine concentrations. Urinary biomarker excretion (raw and indexed to creatinine) for four intraoperative and three postoperative points were compared between patients with and those without subsequent AKI defined by increased serum creatinine concentration ≥0.3 mg/dL within the first 48 hours or ≥1.5 times baseline within seven days. Raw and indexed median IL-18 values were similar between AKI groups at all intraoperative points, but became significantly different at 12 hours after CPB. Raw and indexed median KIM1 values were significantly different between AKI groups at multiple intraoperative points and at four and 12 hours after CPB. During intraoperative and postoperative points, patients in the fourth quartile of KIM1 excretion had greater AKI incidence and longer intensive care and hospital lengths of stay than those in the first quartile. Only postoperatively did the differences in these outcomes between the fourth and first quartile of IL-18 excretion occur. Conclusions Intraoperative KIM1 but not IL-18 excretion was associated with postoperative development of AKI.

The use of extracorporeal cardiopulmonary resuscitation (ECPR) to resuscitate patients with refractory out-of-hospital cardiac arrest is increasing in the United States and the developed world. This approach to treatment is appealing, because it can restore prearrest levels of perfusion to the brain and vital organs while the cause of the arrest is addressed. In this article, the authors highlight current ECPR program development and discuss controversies.

Background Resuscitative endovascular balloon occlusion of the aorta (REBOA) may be a novel intervention to improve cardiopulmonary resuscitation (CPR) quality during cardiac arrest. Zone 1 supraceliac aortic occlusion improves coronary and cerebral blood flow. It is unknown if Zone 3 occlusion distal to the renal arteries offers a similar physiologic benefit while maintaining blood flow to organs above the point of occlusion. Methods Fifteen swine were anesthetized, instrumented, and placed into ventricular fibrillation. Mechanical CPR was immediately initiated. After 5 min of CPR, Zone 1 REBOA, Zone 3 REBOA, or no intervention (control) was initiated. Hemodynamic variables were continuously recorded for 30 min. Results There were no significant differences between groups before REBOA deployment. Once REBOA was deployed, Zone 1 animals had statistically greater diastolic blood pressure compared to control (median [IQR]: 19.9 mmHg [9.5–20.5] vs 3.9 mmHg [2.4–4.8], p = .006). There were no differences in diastolic blood pressure between Zone 1 and Zone 3 (8.6 mmHg [5.1–13.1], p = .10) or between Zone 3 and control (p = .10). There were no significant differences in systolic blood pressure, cerebral blood flow, or time to return of spontaneous circulation (ROSC) between groups. Conclusion In our swine model of cardiac arrest, Zone 1 REBOA improved diastolic blood pressure when compared to control. Zone 3 does not offer a hemodynamic benefit when compared to no occlusion. Unlike prior studies, immediate use of REBOA after arrest did not result in an increase in ROSC rate, suggesting REBOA may be more beneficial in patients with prolonged no-flow time. Institutional protocol number FDG20180024A

Accurate assessment of coagulation in porcine studies is essential. We sought to establish normal values for porcine rotational thromboelastometry (ROTEM) according to the American Society for Veterinary Clinical Pathology guidelines and to assess the effects of various preanalytical parameters on those measurements. Healthy Yorkshire-cross pigs (n = 81; 46 males and 35 females) were anesthetized. By using a 18-gauge needle attached to a vacuum phlebotomy tube, blood was acquired from the cranial vena cava. Tubes were filled in the following order: evacuation clot tube, EDTA tube, heparin tube, and 2 citrate tubes. The citrate tubes were randomly assigned to 30 min with or without constant agitation on a rocker. The following parameters were reported according to the manufacturer's recommendations: clotting time, clot formation time, α, (tangent to the clot formation curve when the clot firmness is 20 mm), clot firmness after 10 and 20 min, maximal clot firmness, maximum lysis, and lysis indexes at 30 and 45 min. Reference intervals were reported as mean ± 2 SD (parametric distribution) or 2.5th and 97.5th percentile of the population's results (nonparametric distribution). The effects of sex, sampling order, and agitation on ROTEM results were analyzed through linear regression. Neither sex nor sample agitation influenced any of the ROTEM parameters. Combined reference intervals were established for each ROTEM parameter by pooling data from the nonagitated tubes for both male and female pigs. This study is the first to establish ROTEM reference intervals from a large number of male and female adult Yorkshire-cross pigs and to provide a detailed description of preanalytical sample processing.

Background Current resuscitative endovascular balloon occlusion of the aorta (REBOA) literature focuses on improving outcomes through careful patient selection, diligent catheter placement, and expeditious definitive hemorrhage control. However, the detection and treatment of post-REBOA ischemia-reperfusion injury (IRI) remains an area for potential improvement. Herein, we provide a review of the metabolic derangements that we have encountered while managing post-REBOA IRI in past swine experiments. We also provide data-driven clinical recommendations to facilitate resuscitation post-REBOA deflation that may be translatable to humans. Methods We retrospectively reviewed the laboratory data from 25 swine across three varying hemorrhagic shock models that were subjected to complete REBOA of either 45 minutes, 60 minutes, or 90 minutes. In each model the balloon was deflated gradually following definitive hemorrhage control. Animals were then subjected to whole blood transfusion and critical care with frequent electrolyte monitoring and treatment of derangements as necessary. Results Plasma lactate peaked and pH nadired long after balloon deflation in all swine in the 45-minute, 60-minute, and 90-minute occlusion models (onset of peak lactate, 32.9 ± 6.35 minutes, 38.8 ± 10.55 minutes, and 49.5 ± 6.5 minutes; pH nadir, 4.3 ± 0.72 minutes, 26.9 ± 12.32 minutes, and 42 ± 7.45 minutes after balloon deflation in the 45-, 60-, and 90-minute occlusion models, respectively). All models displayed persistent hypoglycemia for more than an hour following reperfusion (92.1 ± 105.5 minutes, 125 ± 114.9 minutes, and 96 ± 97.8 minutes after balloon deflation in the 45-, 60-, and 90-minute occlusion groups, respectively). Hypocalcemia and hyperkalemia occurred in all three groups, with some animals requiring treatment more than an hour after reperfusion. Conclusion Metabolic derangements resulting from REBOA use are common and may worsen long after reperfusion despite resuscitation. Vigilance is required to detect and proactively manage REBOA-associated IRI. Maintaining a readily available "deflation kit" of pharmacological agents needed to treat common post-REBOA electrolyte abnormalities may facilitate management. Level of evidence Level V.

Background Partial resuscitative endovascular balloon occlusion of the aorta (pREBOA) and intermittent REBOA (iREBOA) are techniques to extend the therapeutic duration of REBOA by balloon titration for distal flow or cyclical balloon inflation/deflation to allow transient distal flow, respectively. We hypothesized that manually titrated pREBOA would reduce blood losses and ischemic burden when compared with iREBOA. Methods Following 20% blood volume controlled hemorrhage, 10 anesthetized pigs underwent uncontrolled hemorrhage from the right iliac artery and vein. Once in hemorrhagic shock, animals underwent 15 minutes of complete zone 1 REBOA followed by 75 minutes of either pREBOA or iREBOA (n = 5/group). After 90 minutes, definitive hemorrhage control was obtained, animals were resuscitated with the remaining collected blood, and then received 2 hours of critical care. Results There were no differences in mortality. Animals randomized to iREBOA spent a larger portion of the time at full occlusion when compared with pREBOA (median, 70 minutes; interquartile range [IQR], 70-80 vs. median, 20 minutes; IQR, 20-40, respectively; p = 0.008). While the average blood pressure during the intervention period was equivalent between groups, this was offset by large fluctuations in blood pressure and significantly more rescue occlusions for hypotension with iREBOA. Despite lower maximum aortic flow rates, the pREBOA group tolerated a greater total amount of distal aortic flow during the intervention period (median, 20.9 L; IQR, 20.1-23.0 vs. median, 9.8 L; IQR, 6.8-10.3; p = 0.03) with equivalent abdominal blood losses. Final plasma lactate and creatinine concentrations were equivalent, although iREBOA animals had increased duodenal edema on histology. Conclusion Compared with iREBOA, pREBOA reduced the time spent at full occlusion and the number of precipitous drops in proximal mean arterial pressure while delivering more distal aortic flow but not increasing total blood loss in this highly lethal injury model. Neither technique demonstrated a survival benefit. Further refinement of these techniques is necessary before clinical guidelines are issued.

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.

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.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 p0.05.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).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.

Background Early adrenaline administration is associated with return of spontaneous circulation (ROSC) and survival in out-of-hospital cardiac arrest (OHCA). Animal data demonstrate a similar rate of ROSC when early intramuscular (IM) adrenaline is given compared to early intravenous (IV) adrenaline. Aim To evaluate the feasibility of protocolized first-dose IM adrenaline in OHCA and it’s effect on time from Public Safety Access Point (PSAP) call receipt to adrenaline administration when compared to IO and IV administration. Methods This is a before-and-after feasibility study of adult OHCAs in a single EMS service following adoption of a protocol for first-dose IM adrenaline. Time from PSAP call to administration and outcomes were compared to 674 historical controls (from January 1, 2013–February 8, 2021) who received at least one dose of adrenaline by IV or IO routes. Results During the study period, first-dose IM adrenaline was administered to 99 patients (December 1, 2019–February 8, 2021). IM adrenaline was given a median of 12.2 min (95% CI 11.4–13.1 min) after the PSAP call receipt compared to 15.3 min for the IV route (95% CI 14.6–16.0 min) and 15.3 min for the IO route (95% CI 14.9–15.7 min) with a time savings of 3 min (95% CI 2–4 min). Rates of survival to hospital discharge appeared similar between groups: 10% for IM, 8% for IV and 7% for IO. However, results related to survival were underpowered for statistical comparison. Conclusions Within the limitations of a small sample size and before-and-after design, first-dose IM adrenaline was feasible and reduced the time to adrenaline administration.

Trauma-induced acute kidney injury (AKI) has affected many U.S. warfighters throughout history. We seek to provide a historical review of the epidemiology of combat-acquired AKI and to highlight the importance of adapting current renal replacement therapy (RRT) capabilities to prepare for the next armed conflict. While severe AKI was rare in the recent conflicts in Iraq and Afghanistan, an analysis of prior wars suggests that it will be more common in future combat operations characterized by prolonged evacuation times, limited resuscitation capabilities, and delayed aeromedical evacuation. Therefore, the military community must develop RRT capabilities to satisfy the demands of prolonged field care and austere environments. We propose a series of solutions such as re-enforcing forward deployment of conventional RRT capabilities as well as novel therapies such as improvised dialysis systems or sorbent-based RRT.

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.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.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).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.

While hemorrhagic shock might be the result of various conditions, hemorrhage control and resuscitation are the corner stone of patient management. Hemorrhage control can prove challenging in both the acute care and surgical settings, especially in the abdomen, where no direct pressure can be applied onto the source of bleeding. Resuscitative endovascular balloon occlusion of the aorta (REBOA) has emerged as a promising replacement to resuscitative thoracotomy (RT) for the management of non-compressible torso hemorrhage in human trauma patients. By inflating a balloon at specific levels (or zones) of the aorta to interrupt blood flow, hemorrhage below the level of the balloon can be controlled. While REBOA allows for hemorrhage control and augmentation of blood pressure cranial to the balloon, it also exposes caudal tissue beds to ischemia and the whole body to reperfusion injury. We aim to introduce the advantages of REBOA while reviewing known limitations. This review outlines a step-by-step approach to REBOA implementation, and discusses common challenges observed both in human patients and during translational large animal studies. Currently accepted and debated indications for REBOA in humans are discussed. Finally, we review possible applications for veterinary patients and how REBOA has the potential to be translated into clinical veterinary practice.

Risk prediction is important during combat operations because resources are limited and triage decisions must be rapid and accurate. We evaluated 2 point-of-care urinary biomarker tests for risk prediction in combat casualties.This was an observational cohort study of critically injured military personnel admitted to Craig Joint Theater Hospital in Afghanistan from October 2012 to December 2013. We collected urine within 3 hours of admission and measured urinary biomarkers with NephroCheck and a neutrophil gelatinase-associated lipocalin dipstick (NGALds) to evaluate their ability to predict a combined end point of need for renal replacement therapy or death. Odds ratios (ORs) were calculated and receiver operator characteristic curves were generated for both tests.A total of 89 patients were included for analysis. The median Injury Severity Score was 18 and the combined end point occurred in 12 (13.5%) patients. NephroCheck was not associated with the combined end point (OR 1.56; 95% CI 0.81 to 3.03; p = 0.19) and the area under the curve of the receiver operator characteristic curve was 0.65. The NGALds was highly associated with the combined end point (OR 4.93; 95% CI 2.18 to 11.14; p0.001) and the area under the curve of the receiver operator characteristic curve was 0.84. The NGALds remained significantly associated with the combined end point in a logistic regression model that included Injury Severity Score as a covariate (OR 4.10; 95% CI 1.74 to 9.67; p = 0.001).Measurement of urinary biomarkers with an NGALds, but not NephroCheck, predicts poor outcomes in combat casualties. An NGALds is a simple urine dipstick that could be deployed to combat zones to prioritize aeromedical evacuation, help with triage decisions, and predict resource use.

While resuscitative endovascular balloon occlusion of the aorta (REBOA) is contraindicated in patients with aortic injuries, this technique may benefit poly-trauma patients with less extreme thoracic injuries. The purpose of this study was to characterize the effects of thoracic injury on hemodynamics during REBOA and the changes in pulmonary contusion over time in a swine model.Twelve swine were anesthetized, instrumented, and randomized to receive either a thoracic injury with 5 impacts to the chest or no injury. All animals underwent controlled hemorrhage of 25% blood volume followed by 45 min of Zone 1 REBOA. Animals were then resuscitated with shed blood, observed during a critical care period, and euthanized after 6 h of total experimental time.There were no differences between the groups at baseline. The only difference after 6 h was a lower hemoglobin in the thoracic trauma group (8.4 ± 0.8 versus 9.4 ± 0.6 g/dL, P = 0.04). The average proximal mean arterial pressures were significantly lower in the thoracic trauma group during aortic occlusion [103 (98-108) versus 117 (115-124) mmHg, P = 0.04]. There were no differences between the pulmonary contusion before REBOA and at the end of the experiment in size (402 ± 263 versus 356 ± 291 mL, P = 0.782) or density (- 406 ± 127 versus - 299 ± 175 HFU, P = 0.256).Thoracic trauma blunted the proximal arterial pressure augmentation during REBOA but had minimal impacts on resuscitative outcomes. This initial study indicates that REBOA does not seem to exacerbate pulmonary contusion in swine, but blunt thoracic injuries may attenuate the expected rises in proximal blood pressure during REBOA.

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 ± 23.9 and 191.9 ± 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.

IntroductionExternal cooling of ischemic limbs has been shown to have a significant protective benefit for durations up to 4 hours.Materials and MethodsIt was hypothesized that this benefit could be extended to 8 hours. Six swine were anesthetized and instrumented, then underwent a 25% total blood volume hemorrhage. Animals were randomized to hypothermia or normothermia followed by 8 hours of Zone 3 resuscitative endovascular balloon occlusion of the aorta, then resuscitation with shed blood, warming, and 3 hours of critical care. Physiologic parameters were continuously recorded, and laboratory specimens were obtained at regular intervals.ResultsThere were no significant differences between groups at baseline. There were no significant differences between creatine kinase in the hypothermia group when compared to the normothermia group (median [IQR] = 15,206 U/mL [12,476−19,987] vs 23,027 U/mL [18,745−26,843]); P = 0.13) at the end of the study. Similarly, serum myoglobin was also not significantly different in the hypothermia group after 8 hours (7,345 ng/mL [5,082−10,732] vs 5,126 ng/mL [4,720−5,298]; P = 0.28). No histologic differences were observed in hind limb skeletal muscle.ConclusionWhile external cooling during prolonged Zone 3 resuscitative endovascular balloon occlusion of the aorta appears to decrease ischemic muscle injury, this benefit appears to be time dependent. As the ischemic time approaches 8 hours, the benefit from hypothermia decreases.

BACKGROUND Potassium-binding polymers have shown promising results in an anephric porcine hyperkalemia model. The benefits of the polymer in a clinically relevant injury model remain unknown. We hypothesized that potassium-binding cartridges would control serum potassium concentration in a porcine hemorrhagic shock model with supraceliac aortic occlusion and a limb crush injury. METHODS Ten Yorkshire-cross swine were anesthetized and instrumented. Pigs underwent splenectomy and bilateral nephrectomy. Hemorrhagic shock was induced for 30 minutes while a leg compression device was applied. Pigs underwent supraceliac aortic occlusion for 60 minutes and were resuscitated with shed blood. The leg compression device was removed 20 minutes after balloon deflation. After 20 minutes of reperfusion, animals were randomized to extracorporeal circulation with (treatment) or without (control) the potassium binding cartridges. In both groups, blood was circulated through a hemodialyzer with a peristaltic pump. In the treatment group, the ultrafiltrate was diverted from the hemodialyzer through cartridges containing the polymer and returned to the extracorporeal circuit. Animals were resuscitated with 0.9% saline boluses and a norepinephrine infusion. The change in serum potassium concentration (ΔK) was calculated as serum [K]T390 - serum [K]T0. RESULTS There was a significant difference in serum potassium concentration between groups (p < 0.001). ΔK was significantly higher in the control than the treatment group (3.75 [3.27-4.42] and 1.15 [0.62-1.59] mmol/L, respectively; p = 0.03). There were no differences in mean arterial pressure (p = 0.14), isotonic crystalloids requirement (p = 0.51), or norepinephrine dose (p = 0.83) between groups. Serum lactate concentration was significantly higher in the control group (p < 0.001). At the end of the experiment, the [K] was reduced by 25% (24.9%-27.8%) across the cartridges. CONCLUSION The cartridges controlled serum potassium concentrations without dialysate and retained potassium binding capabilities over 4 hours. There were no deleterious effects on hemodynamic parameters. Those cartridges might be beneficial adjuncts for hyperkalemia management in austere environments. LEVEL OF EVIDENCE Translational science study, level I.

Background Endovascular methods for hemorrhage control, including Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA), are evolving and are increasingly being applied clinically. Partial flow strategies to mitigate the consequences of complete aortic occlusion have been demonstrated in pre-clinical models to enhance REBOA and expand its application to various shock states. Initial studies demonstrated that controlled partial flow requires precision beyond the capabilities of manual balloon volume adjustment, therefore automation is required. Our group previously developed a proof-of-concept computer-controlled extracorporeal flow circuit capable of precision aortic flow regulation, but it was not clinically applicable. To bring this concept closer to clinical applicability, we have developed the first endovascular strategy to achieve precision aortic flow regulation, termed Endovascular Variable Aortic Control (EVAC). Methods Following instrumentation, 5 Yorkshire-cross swine were subjected to controlled 25% hemorrhage, followed by precision low volume aortic flow regulation using a commercially available compliant balloon catheter pre-positioned in the descending thoracic aorta, connected to a custom, wireless syringe pump. Closed-loop feedback algorithms based on streaming physiologic data were used to determine balloon volume changes. Results The EVAC syringe pump was highly effective at maintaining precise aortic flow throughout the 45-minute intervention period during steady state conditions as well as during rapid fluid administration. Aortic flow and distal mean arterial pressure remained stable during EVAC, despite changing proximal hemodynamics. Balloon volume was dynamic, averaging over 500 changes during intervention, with a mean volume change of 6.7 uL and a maximal change of 100 uL. Conclusion The EVAC syringe pump is capable of achieving aortic flow regulation with high precision, beyond what is achievable with manual control. This serves as a model for future device design, enabling as-of-yet unachievable clinical therapies for hemorrhage and shock states. Future technological development is required to fully translate this into clinical use. Level of Evidence – Level V Study Type – Translational Science Keywords – EVAC, P-REBOA, REBOA, automation, hemorrhage

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.

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.

Background: Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an emergent technology for the treatment of non-compressible torso hemorrhage (NCTH). While aortic occlusion (AO) above the site of hemorrhage provides hemostasis and time for surgical intervention, ischemia-reperfusion injury to the kidneys is a known complication. We aimed to report the incidence and factors associated with acute kidney injury (AKI) following AO in patients with NCTH or in similar porcine models. Methods: We searched Pubmed (MEDLINE), Embase, Scopus, and ProQuest Dissertations & Theses from inception to July 2017. We included original studies of trauma patients with NCTH treated with REBOA, or similar porcine studies that included renal parameters, excluding case reports and case series. After duplicate removal, full texts of studies retrieved via the search strategy were evaluated by two authors. Renal parameters (e.g., creatinine concentration, urine output, histopathology) were extracted. Quality of the evidence and risk of bias were assessed. Results: Twelve out of 2,100 records were included (3 trauma patients, 9 porcine studies). While 1/3 human reports described AO in Zone 1, all swine publications reported Zone 1. All human studies reported renal damage. There were nonetheless inconsistencies in definitions used. Evidence of AKI was reported in 3/9 swine studies. Conclusions: Consistent reporting of AKI incidence is lacking from human clinical studies of AO in NCTH trauma patients. While comorbidities in trauma patients may contribute to AKI, animal models support the association between AO and AKI. As REBOA is growing in popularity as a therapy for NCTH, further studies determining factors associated with the AKI are needed.