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IntroductionThe understanding of coagulopathies in trauma has increased interest in thromboelastography (TEG®) and thromboelastometry (ROTEM®), which promptly evaluate the entire clotting process and may guide blood product therapy. Our objective was to review the evidence for their role in diagnosing early coagulopathies, guiding blood transfusion, and reducing mortality in injured patients.MethodsWe considered observational studies and randomized controlled trials (MEDLINE, EMBASE, and Cochrane databases) to February 2014 that examined TEG®/ROTEM® in adult trauma patients. We extracted data on demographics, diagnosis of early coagulopathies, blood transfusion, and mortality. We assessed methodologic quality by using the Newcastle-Ottawa scale (NOS) for observational studies and QUADAS-2 tool for diagnostic accuracy studies.ResultsFifty-five studies (12,489 patients) met inclusion criteria, including 38 prospective cohort studies, 15 retrospective cohort studies, two before-after studies, and no randomized trials. Methodologic quality was moderate (mean NOS score, 6.07; standard deviation, 0.49). With QUADAS-2, only three of 47 studies (6.4%) had a low risk of bias in all domains (patient selection, index test, reference standard and flow and timing); 37 of 47 studies (78.8%) had low concerns regarding applicability. Studies investigated TEG®/ROTEM® for diagnosis of early coagulopathies (n = 40) or for associations with blood-product transfusion (n = 25) or mortality (n = 24). Most (n = 52) were single-center studies. Techniques examined included rapid TEG® (n =12), ROTEM® (n = 18), TEG® (n = 23), or both TEG® and rapid TEG® (n = 2). Many TEG®/ROTEM® measurements were associated with early coagulopathies, including some (hypercoagulability, hyperfibrinolysis, platelet dysfunction) not assessed by routine screening coagulation tests. Standard measures of diagnostic accuracy were inconsistently reported. Many abnormalities predicted the need for massive transfusion and death, but predictive performance was not consistently superior to routine tests. One observational study suggested that a ROTEM®-based transfusion algorithm reduced blood-product transfusion, but TEG®/ROTEM®-based resuscitation was not associated with lower mortality in most studies.ConclusionsLimited evidence from observational data suggest that TEG®/ROTEM® tests diagnose early trauma coagulopathy and may predict blood-product transfusion and mortality in trauma. Effects on blood-product transfusion, mortality, and other patient-important outcomes remain unproven in randomized trials.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0518-9) contains supplementary material, which is available to authorized users.

First, the mechanism of injury should be considered when deciding if a patient with a TAWH needs an urgent laparotomy. Clinically apparent anterior TAWHs appear to have a high rate of associated injuries requiring urgent laparotomy. Finally, occult TAWHs diagnosed only by computed tomography may not require urgent laparotomy or hernia repair.

Cryoprecipitate, originally developed as a therapy for patients with antihaemophilic factor deficiency, or haemophilia A, has been in use for almost 50 yr. However, cryoprecipitate is no longer administered according to its original purpose, and is now most commonly used to replenish fibrinogen levels in patients with acquired coagulopathy, such as in clinical settings with haemorrhage including cardiac surgery, trauma, liver transplantation (LT), or obstetric haemorrhage. Cryoprecipitate is a pooled product that does not undergo pathogen inactivation, and its administration has been associated with a number of adverse events, particularly transmission of blood-borne pathogens and transfusion-related acute lung injury. As a result of these safety concerns, along with emerging availability of alternative fibrinogen preparations, cryoprecipitate has been withdrawn from use in a number of European countries. Compared with the plasma from which it is prepared, cryoprecipitate contains a high concentration of coagulation factor VIII, coagulation factor XIII, and fibrinogen. Cryoprecipitate is usually licensed by regulatory authorities for the treatment of hypofibrinogenaemia, and recommended for supplementation when plasma fibrinogen levels decrease below 1 g litre−1; however, this threshold is empiric and is not based on solid clinical evidence. Consequently, there is uncertainty over the appropriate dosing and optimal administration of cryoprecipitate, with some guidelines from professional societies to guide clinical practice. Randomized, controlled trials are needed to determine the clinical efficacy of cryoprecipitate, compared with the efficacy of alternative preparations. These trials will allow the development of evidence-based guidelines in order to inform physicians and guide clinical practice.

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BackgroundThrombelastography is a laboratorial test that measures viscoelastic changes of the entire clotting process. There is growing interest in its clinical use in trauma resuscitation, particularly for managing acute coagulopathy of trauma and assisting decision making concerning transfusion. This review focuses on the clinical use of thrombelastography in trauma, with practical points to consider on its use in civilian and military settings.MethodsA search in the literature using the terms “thrombelastography AND trauma” was performed in PUBMED database. We focused the review on the main clinical aspects of this viscoelastic method in diagnosing and treating patients with acute coagulopathy of trauma during initial resuscitation.ResultsThrombelastography is not a substitute for conventional laboratorial tests such as INR and aPTT but offers additional information and may guide blood transfusion. Thrombelastography can be used as a point of care test but requires multiple daily calibrations, should be performed by trained personnel and its technique requires standardization. While useful partial results may be available in minutes, the whole test may take as long as other conventional tests. The most important data provided by thrombelastography are clot strength and fibrinolysis. Clot strength measure can establish whether the bleeding is due to coagulopathy or not, and is the key information in thrombelastography-based transfusion algorithms. Thrombelastography is among the few tests that diagnose and quantify fibrinolysis and thus guide the use of anti-fibrinolytic drugs and blood products such as cryoprecipitate and fibrinogen concentrate. It may also diagnose platelet dysfunction and hypercoagulability and potentially prevent inappropriate transfusions of hemostatic blood products to non-coagulopathic patients.ConclusionsThrombelastography has characteristics of an ideal coagulation test for use in early trauma resuscitation. It has limitations, but may prove useful as an additional test. Future studies should evaluate its potential to guide blood transfusion and the understanding of the mechanisms of trauma coagulopathy.

Background:Acute coagulopathy after traumatic brain injury (TBI) involves a complex multifactorial hemostatic response that is poorly characterized. Objectives: To examine early posttraumatic alterations in coagulofibrinolytic, endothelial, and inflammatory blood biomarkers in relation to sympathetic nervous system (SNS) activation and 6-month patient outcomes, using multivariate partial least-squares (PLS) analysis.Patients and Methods:A multicenter observational study of 159 adult isolated TBI patients admitted to the emergency department at an urban level I trauma center, was performed. Plasma concentrations of 6 coagulofibrinolytic, 10 vascular endothelial, 19 inflammatory, and 2 catecholamine biomarkers were measured by immunoassay on admission and 24 h postinjury. Neurological outcome at 6 months was assessed using the Extended Glasgow Outcome Scale. PLS-discriminant analysis was used to identify salient biomarker contributions to unfavorable outcome, whereas PLS regression analysis was used to evaluate the covariance between SNS correlates (catecholamines) and biomarkers of coagulopathy, endotheliopathy, and inflammation.Results:Biomarker profiles in patients with an unfavorable outcome displayed procoagulation, hyperfibrinolysis, glycocalyx and endothelial damage, vasculature activation, and inflammation. A strong covariant relationship was evident between catecholamines and biomarkers of coagulopathy, endotheliopathy, and inflammation at both admission and 24 h postinjury.Conclusions:Biomarkers of coagulopathy and endotheliopathy are associated with poor outcome after TBI. Catecholamine levels were highly correlated with endotheliopathy and coagulopathy markers within the first 24 h after injury. Further research is warranted to characterize the pathogenic role of SNS-mediated hemostatic alterations in isolated TBI.

Background Coagulopathic bleeding is a leading cause of in-hospital death after injury. A recently proposed transfusion strategy calls for early and aggressive frozen plasma transfusion to bleeding trauma patients, thus addressing trauma-associated coagulopathy (TAC) by transfusing clotting factors (CF). This strategy may dramatically improve survival of bleeding trauma patients. However, other studies suggest that early TAC occurs by protein C activation and is independent of CF deficiency. The present study investigated whether CF deficiency is associated with early trauma-associated coagulopathy. Methods Prospective observational cohort study of severely traumatized patients (ISS ≥16) admitted shortly after injury, receiving minimal fluids and no prehospital blood. Blood was assayed for CF levels, thromboelastography and routine coagulation tests. Critical CF deficiency was defined as ≤30% activity of any CF. Results Of 110 patients, 22 (20%) had critical CF deficiency: critically low factor V level was evident in all these patients. INR, aPTT and TEG were abnormal in 32%, 36% and 35% respectively of patients with any critically low CF. Patients with critical CF deficiency suffered more severe injuries, were more acidotic, received more blood transfusions and showed a trend towards higher mortality (32% vs. 18% p=.23). Computational modelling showed coagulopathic patients had pronounced delays and quantitative deficits in generating thrombin. Conclusions 20% of all severely injured patients had critical clotting factor deficiency on admission, particularly of factor V. The observed factor V deficit aligns with current understanding of the mechanisms underlying early TAC. Critical deficiency of factor V impairs thrombin generation and profoundly affects hemostasis.