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      Acute coagulopathy in trauma: with or without shock? That is the question

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          Abstract

          In an interesting and original article in a recent issue of Critical Care, Oshiro and colleagues describe the profile of acute coagulopathy of trauma-shock (ACOTS) using viscoelastic techniques [1]. The authors, in light of their results, demonstrate the hypothesis that ACOTS is a type of disseminated intravascular coagulation (DIC) with a fibrinolytic profile. However, we would like to highlight some aspects we consider to be of interest. It has caught our attention that, fulfilling national laws, patients were not subjected to fluid resuscitation during transport to the hospital. We understand that aggressive fluid resuscitation is deleterious to the patient and induces the possibility of dilutional coagulopathy [2]–[4]. However, despite the absence of strong evidence in this respect, current guidelines recommend its administration in patients with hemodynamic compromise after trauma but during the prehospital phase [4,5]. In this regard, we think the submission of information related to the hemodynamic status of patients during this phase or at hospital admission would have been interesting. It is widely known that trauma hypotension induces hyperfibrinolysis increase, which finally promotes ACOTS. Therefore, the lack of such data prevents us from knowing, from a physiological point of view, whether the increase of DIC profile with hyperfibrinolytic character was enhanced by these motifs [2]. Regardless of these observations, we consider that the study presents important evidence for understanding the ACOTS in trauma patients, and this is one of the major challenges to overcome during the management of these patients. Author’s response Satoshi Gando We appreciate the interest of Egea-Guerrero and colleagues in our article regarding DIC in trauma [1]. We agree that the patient’s hemodynamic status during transport and at hospital admission is important. Although we did not collect data for hemodynamic parameters, we presented direct evidence of hypoperfusion based on the lactate levels in the subjects who developed DIC. Our previous study demonstrated that DIC occurs during the early phase of trauma independently of lactate levels [6]. Trauma itself can cause DIC, whereas hypoperfusion accelerates DIC via release of tissue plasminogen activator from endothelial cells, resulting in the fibrinolytic phenotype. ACOTS has recently attracted much attention in the field of trauma. However, many questions have been raised, as indicated in ‘ACOTS: with or without shock? That is the question’. The definition of ACOTS requires the inclusion of shock-induced hypoperfusion, increased activated protein C (APC) level, APC-mediated thrombin shutoff and plasminogen activator inhibitor-1 (PAI-1) inhibition in the circulation, the presence of normal endothelial cells that can newly express endothelial thrombomodulin, and soluble thrombomodulin with full domains and 100% activity. However, the APC levels did not increase in ACOTS patients and no differences have been reported in thrombin generation or the PAI-1 levels between ACOTS patients and control subjects [7]. Therefore, ‘ACOTS: reality or myth? That is the question’ would also be considered a suitable title. Regardless of whether ACOTS is a reality or a myth, the points raised in their letter are very important for trauma management. Abbreviations ACOTS: Acute coagulopathy of trauma-shock; APC: Activated protein C; DIC: Disseminated intravascular coagulation; PAI-1: Plasminogen activator inhibitor-1. Competing interests The authors declare that they have no competing interests.

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          Most cited references 6

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          Management of bleeding and coagulopathy following major trauma: an updated European guideline

          Introduction Evidence-based recommendations are needed to guide the acute management of the bleeding trauma patient. When these recommendations are implemented patient outcomes may be improved. Methods The multidisciplinary Task Force for Advanced Bleeding Care in Trauma was formed in 2005 with the aim of developing a guideline for the management of bleeding following severe injury. This document represents an updated version of the guideline published by the group in 2007 and updated in 2010. Recommendations were formulated using a nominal group process, the Grading of Recommendations Assessment, Development and Evaluation (GRADE) hierarchy of evidence and based on a systematic review of published literature. Results Key changes encompassed in this version of the guideline include new recommendations on the appropriate use of vasopressors and inotropic agents, and reflect an awareness of the growing number of patients in the population at large treated with antiplatelet agents and/or oral anticoagulants. The current guideline also includes recommendations and a discussion of thromboprophylactic strategies for all patients following traumatic injury. The most significant addition is a new section that discusses the need for every institution to develop, implement and adhere to an evidence-based clinical protocol to manage traumatically injured patients. The remaining recommendations have been re-evaluated and graded based on literature published since the last edition of the guideline. Consideration was also given to changes in clinical practice that have taken place during this time period as a result of both new evidence and changes in the general availability of relevant agents and technologies. Conclusions A comprehensive, multidisciplinary approach to trauma care and mechanisms with which to ensure that established protocols are consistently implemented will ensure a uniform and high standard of care across Europe and beyond. Please see related letter by Morel et al http://ccforum.com/content/17/4/442
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            Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis.

            Coagulopathy is present at admission in 25% of trauma patients, is associated with shock and a 5-fold increase in mortality. The coagulopathy has recently been associated with systemic activation of the protein C pathway. This study was designed to characterize the thrombotic, coagulant and fibrinolytic derangements of trauma-induced shock. This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1 + 2 (PF1 + 2), fibrinogen, factor VII, thrombomodulin, protein C, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), and D-dimers. Base deficit was used as a measure of tissue hypoperfusion. Two hundred eight patients were studied. Systemic hypoperfusion was associated with anticoagulation and hyperfibrinolysis. Coagulation was activated and thrombin generation was related to injury severity, but acidosis did not affect Factor VII or PF1 + 2 levels. Hypoperfusion-induced increase in soluble thrombomodulin levels was associated with reduced fibrinogen utilization, reduction in protein C and an increase in TAFI. Hypoperfusion also resulted in hyperfibrinolysis, with raised tPA and D-Dimers, associated with the observed reduction in PAI-1 and not alterations in TAFI. Acute coagulopathy of trauma is associated with systemic hypoperfusion and is characterized by anticoagulation and hyperfibrinolysis. There was no evidence of coagulation factor loss or dysfunction at this time point. Soluble thrombomodulin levels correlate with thrombomodulin activity. Thrombin binding to thrombomodulin contributes to hyperfibrinolysis via activated protein C consumption of PAI-1.
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              Liberal versus restricted fluid resuscitation strategies in trauma patients: a systematic review and meta-analysis of randomized controlled trials and observational studies*.

              Hemorrhage is responsible for most deaths that occur during the first few hours after trauma. Animal models of trauma have shown that restricting fluid administration can reduce the risk of death; however, studies in patients are difficult to conduct due to logistical and ethical problems. To maximize the value of the existing evidence, we performed a meta-analysis to compare liberal versus restricted fluid resuscitation strategies in trauma patients. Medline and Embase were systemically searched from inception to February 2013. We selected randomized controlled trials and observational studies that compared different fluid administration strategies in trauma patients. There were no restrictions for language, population, or publication year. Four randomized controlled trials and seven observational studies were identified from 1,106 references. One of the randomized controlled trials suffered from a high protocol violation rate and was excluded from the final analysis. The quantitative synthesis indicated that liberal fluid resuscitation strategies might be associated with higher mortality than restricted fluid strategies, both in randomized controlled trials (risk ratio, 1.25; 95% CI, 1.01-1.55; three trials; I(2), 0) and observational studies (odds ratio, 1.14; 95% CI, 1.01-1.28; seven studies; I(2), 21.4%). When only adjusted odds ratios were pooled for observational studies, odds for mortality with liberal fluid resuscitation strategies increased (odds ratio, 1.19; 95% CI, 1.02-1.38; six studies; I(2), 26.3%). Current evidence indicates that initial liberal fluid resuscitation strategies may be associated with higher mortality in injured patients. However, available studies are subject to a high risk of selection bias and clinical heterogeneity. This result should be interpreted with great caution.
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                Author and article information

                Contributors
                Journal
                Crit Care
                Crit Care
                Critical Care
                BioMed Central
                1364-8535
                1466-609X
                2014
                19 June 2014
                : 18
                : 3
                : 437
                Affiliations
                [1 ]NeuroCritical Care Unit, Virgen del Rocío University Hospital, IBiS/CSIC/University of Seville, Avda. Manuel Siurot s/n 41013, Seville, Spain
                Article
                cc13931
                10.1186/cc13931
                4075411
                Copyright © 2014 Egea-Guerrero et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Categories
                Letter

                Emergency medicine & Trauma

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