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• W4206795753 abstract "The March 2021 issue of Shock showcases an impressive collection of comprehensive reviews, clinical, and basic research studies from our colleagues across the globe. The review articles in this month's issue of Shock start off with a critical analysis of the best available evidence on management approaches and therapeutic strategies toward SARS-CoV-2 and the potential synergistic effects of SARS-CoV-2 and influenza virus co-infection. Next the evolution of Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) into its current state-of-the-art usage is comprehensively reviewed. This is followed by a deep dive into the literature behind post-traumatic angiogenesis. The clinical studies in the current issue are largely focused on a better understanding of the dysfunctional clotting cascade after trauma but also extend to clinical predictors of hemorrhage and organ system dysfunction after trauma as well as a very timely study on the fibrinolysis shutdown and thrombosis in SARS-CoV-2 infection. Meanwhile, the basic science aspect of this month's issue encompasses a diverse collection of studies ranging from the cellular mechanisms underlying sepsis-induced acute lung injury, neurologic outcomes in large animal models of hemorrhage and cardiac arrest, new concerns in rodent modeling of traumatic injury, advancing new techniques in the use of REBOA to control hemorrhage, and a new look at metabolic patterns in peripheral immune cells after brain injury. Perhaps even more impressive than the high quality of the studies is that they come from four different continents once again highlighting the global reach of the Shock community and our shared mission to advance the science of injury, inflammation, and sepsis. This month's issue of Shock is kicked off by a well-timed review by Madurska et al. (1), which focuses on the evolution of REBOA for hemorrhage control, highlighting the evidence supporting most up-to-date usage of the technique as well as the controversy surrounding these new applications of REBOA. The final review in this month's issue comes from Pecoraro et al. (2). In this review, the authors take the reader through a comprehensive review on our current understanding of post-traumatic angiogenesis, the cellular mechanisms for neovessel formation, and the potential for developing novel interventions to promote healing after injury. The first clinical study in the March 2021 issue of Shock comes from Hatton et al. (3) and is a single-center cohort study of severely injured patients surviving greater than 24 h. The authors were able to study nearly 500 patients who had serum levels of soluble thrombomodulin (sTM) and syndecan-1 measured as markers of endothelial dysfunction. They found that elevated levels of sTM and syndecan-1 were both associated with higher rates of acute kidney injury (AKI), increased AKI severity, and prolonged duration of AKI. This association between sTM and syndedan-1 with AKI leads the authors to conclude that treatments which stabilize the endothelium may have future promise in the treatment of AKI after severe injury. The next clinical study by Creel-Bulos et al. (4) is a timely study examining the prevalence of fibrinolysis shutdown in critically ill COVID-19-positive patients using rotational thromboelastometry (ROTEM). The authors found that over 50% of these patients met the criteria for fibrinolysis shutdown. Furthermore, almost half of these patients were diagnosed with venous thromboembolic events during theirs course of illness. Although small in size, this study is one of the first to suggest using ROTEM to identify which COVID-19-positive patients may benefit from the use of fibrinolytics. MacArthur et al. (5) stratified trauma patients from a prospective cohort study to assess thrombin generation kinetics into those who required more than three units of packed red blood cells (PRBC), those who received some PRBCs but less than three, and those who received no PRBCs. They found that accelerated thrombin generation was heavily associated with the need for transfusion. This analysis provides evidence that thrombin assays may provide a more dynamic view of clotting as compared with more traditional assays such at PT/INR. In another study on predictors of hemorrhage, Ushida et al. (6) present a multicenter retrospective study of over 30,000 women who delivered vaginally. They assessed the value of the shock index (SI), heart rate divided by systolic blood pressure, to detect postpartum hemorrhage. They found that SI was a better predictor of postpartum hemorrhage than other vital signs alone. The final clinical study by Barea-Mendoza et al. (7) aimed to identify risk factors for both early (<72 h) and late (beyond 72 h) multisystem organ failure (MOF) after trauma from the Spanish Trauma ICU Registry (RETRAUCI). The authors identified nearly 10,000 trauma ICU patients to include in their analysis and used a multivariate analysis to show that early MOF was associated with injury severity score >16, hemodynamic instability, coagulopathy, and AKI. Late MOF was found to be associated with age >65 years, hemodynamic instability, AKI, and nosocomial infection. These data allow the authors to conclude that early MOF was mostly associated with injury severity and hemorrhage-related complications, while late MOF was most heavily associated with advanced age and infection. From a basic science perspective, this month's issue of Shock brings a set of basic science articles that will advance understanding across the entire span of shock-related pathophysiologic conditions, ranging from detailed analysis of the regulatory mechanisms of inflammation to physiologic studies of hemorrhage control and resuscitation. These studies exemplify the research published in Shock, positioned at the interface between basic science and clinical medicine. Two studies described different mechanisms by which LPS can regulate the inflammatory response. The first is through regulation of neutrophil necroptosis. Necroptosis is a highly inflammatory form of cell death characterized by release of intracellular contents that can serve to amplify the acute inflammatory response. In this issue of Shock, a multinational team headed by Dr Fan have elucidated a mechanism by which LPS can downregulate neutrophil necroptosis through a negative feedback pathway mediated by the NFκB pathway (8). These results suggest a pathway for therapeutic regulation of necroptosis, which is particularly important given new data demonstrating a role for necroptotic cell death in lung inflammation during COVID-19. [Signal Transduct Target Ther. 2020 Oct 9;5(1):235. doi: 10.1038/s41392-020-00334-0. PMID: 33037188]. Dr Wong et al. (9) report a second LPS-mediated regulatory pathway in endothelial cells. In endotoxin-sensitive tissues, ERK activation is a primary downstream pathway of the LPS receptor, TLR4. To define the specific effects of LPS on the endothelia, Dr Wong et al. used a combination of siRNA knockdown and pharmacologic inhibitors to define the role of LPS-induced ERK activation on primary human endothelial cells. They found that ERK activity was associated with increased production of soluble mediators of inflammation including IL-6 and VCAM. However, LPS-induced ERK was also associated with decreased endothelial permeability and maintenance of cell–cell adhesion. Together these results suggest a nuanced immunologic response by the endothelia, releasing soluble mediators to signal the presence of an infection while concomitantly strengthening intercellular interactions to reinforce the endothelial barrier. Two studies in Shock this month evaluate the effects of common analgesia and sedation regimens on outcomes in model of critical illness. A team at the James Cook University in Queensland extend their studies of a small volume resuscitation protocol using Adenosine, Lidocaine and magnesium (ALM) to evaluate the interactions between narcotic Buprenorphine analgesia and ALM resuscitation for hemorrhagic shock (10). Consistent with their extensive past body of work, ALM resuscitation was associated with improved outcomes from hemorrhagic shock. Strikingly, they found that as compared with analgesia with the veterinary NSAID Carprieve, Buprenorphine analgesia was associated with cardiovascular depression and significantly increased mortality. These data suggest that Buprenophrine may have confounding effects on studies of hemodynamics of shock and should be used with caution, and further, that NSAID therapy can provide adequate analgesia with less cardiovascular complications. Along this vein, Dr Shen et al. (11) have evaluated the effects of Dexmedetomidine post-treatment on cardiovascular and neurological outcomes after cardiac arrest in swine. The authors show that after cardiac arrest, Dexmedetomidine treatment was associated with improved outcomes and that a high-dose regimen augmented these salutatory effects. Based on these data, it will be important to pursue clinical studies of Dexmedetomidine as a component of post-arrest treatment regimens. Next, Akama et al. (12) report on temporal changes in group 2 innate lymphoid cells (ILC2s) in a cecal ligation and puncture model of sepsis-induced acute lung injury. ILC2s are now recognized a key cell type in immune regulation and homeostasis in the lung. However, their role in acute lung injury is not well characterized. Akama et al. present data showing that after the induction of sepsis-induced acute lung injury that ILC2s have reduced production of IL-13 and high expression of programmed cell death 1 receptor (PD-1). Furthermore, utilizing IL-33 knockout mice they show that IL-33 regulates IL-13 production in ILC2s possibly through modulation of PD-1 expression and signaling in the injured lung. These data offer new insight into immune homeostasis and response to sepsis-induce acute lung injury. Both Morgan et al. and Necsoiu et al. provide studies that seek to improve acute treatment of hemorrhagic shock (13, 14). With an eye toward the next generation of personalized medicine in critical care, Morgan et al. have assessed the combination of near-infrared spectroscopy and transcranial Doppler ultrasonography as tools for measuring cerebral oxygenation to guide resuscitation during hemorrhagic shock. The authors deploy a primate model of decompensated shock and compare the standard-of-care invasive monitoring to their noninvasive approach, but found only weak-to-moderate concordance between the noninvasive approach and gold-standard invasive monitoring. Although these results do not support a shift away from invasive monitoring, the data do suggest that in resource poor settings, such as prolonged field care, noninvasive monitoring could be a powerful tool to help guide resuscitation and provide personalized care in the field. Necsoiu et al. describe a novel bi-lobed REBOA catheter with both a noncompliant balloon for complete aortic occlusion and a second compliant balloon that allows partial aortic occlusion while maintaining some distal perfusion. They found that partial occlusion is associated with improved survival as compared with full aortic occlusion, while maintaining improved above-balloon perfusion pressures as compared with animals treated with resuscitation alone. The authors note that a partial REBOA reconciles the competing priorities of the hemorrhagic shock patient: maintaining central blood pressure and CNS perfusion, decreasing lower-body MAP to control hemorrhage, and minimizing lower-body warm ischemia time. Lastly, Dr Zink et al. (15) present a methodologically advanced study of the effects of acute brain injury on metabolism. The authors use a large animal (porcine) model of acute subdural hematoma to assess the effects of intracranial blood on circulating leukocyte metabolism. They carefully dissected the metabolic flux within the leukocytes after insult, and although no significant differences were detected in any single metabolite, by integrating the data using principal components factor reduction they were able to detect significant interactions within the metabolic flux, suggesting distinct metabolic phenotypes induced by acute subdural hematoma. Importantly, the authors have utilized a model of hemodynamically stable SAH. Consequently, the alterations in leukocyte metabolism they report are likely a direct result of acute blood in the intracranial space and may shed light on the complications of the frequently encountered minor to moderate intracranial hemorrhage. As a whole, this month's issue of Shock gives the readership a collection of high-quality clinical and basic science studies ranging from hemorrhage control to cellular mechanisms of lung injury to two timely pieces on management approaches and therapeutic strategies toward SARS-CoV-2. Each new study and review article provides the reader with new insights into the biology of injury, inflammation, and infection and brings our international Shock community one step closer to bridging the gap between the science of Shock and improving the care of our injured and infirmed patients across the globe." @default.
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• W4206795753 date "2021-03-01" @default.
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• W4206795753 title "What's New in Shock, March 2021?" @default.
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