Purpose of review Recent therapeutic and observational studies have demonstrated improved survival with better management of haemostasis early after injury. This review delineates our current understanding of the clinical importance, aetiology and pathophysiology of acute traumatic coagulopathy (ATC). Recent findings Trauma causes an acute disruption of the equilibrium between all components of haemostasis (coagulation, anticoagulation, fibrinolysis, platelets and endothelium). In patients with a combination of severe tissue damage and systemic hypoperfusion, this will progress rapidly to an endogenous coagulopathy that is independently associated with worse outcomes. New discoveries of the interactions between neurohormonal, vascular, and coagulation systems are beginning to explain how this haemostatic impairment develops and offer novel targets for therapeutic manipulation. Routine coagulation screening tests are ineffective for diagnosing ATC and guiding resuscitation in real-time. Viscoelastic coagulation tests (such as ROTEM or TEG) have emerged as practical, rapid and sensitive diagnostic modalities. Their role in therapeutic targeting requires further validation. Summary Conventional concepts of traumatic coagulopathy as a late occurring condition in response to iatrogenic haemodilution are redundant. ATC is an endogenous impairment of haemostasis that begins at the moment of injury. Further outcome improvements are possible with better understanding of the process by which this coagulopathy develops and how it may be inhibited.

Acute traumatic coagulopathy.

The appropriate strategy for trauma-induced coagulopathy management is under debate. We report the treatment of major trauma using mainly coagulation factor concentrates. This retrospective analysis included trauma patients who received ≥ 5 units of red blood cell concentrate within 24 hours. Coagulation management was guided by thromboelastometry (ROTEM®). Fibrinogen concentrate was given as first-line haemostatic therapy when maximum clot firmness (MCF) measured by FibTEM (fibrin-based test) was 1.5 times normal. Lack of improvement in EXTEM MCF after fibrinogen concentrate administration was an indication for platelet concentrate. The observed mortality was compared with the mortality predicted by the trauma injury severity score (TRISS) and by the revised injury severity classification (RISC) score. Of 131 patients included, 128 received fibrinogen concentrate as first-line therapy, 98 additionally received PCC, while 3 patients with recent coumarin intake received only PCC. Twelve patients received FFP and 29 received platelet concentrate. The observed mortality was 24.4%, lower than the TRISS mortality of 33.7% (P = 0.032) and the RISC mortality of 28.7% (P > 0.05). After excluding 17 patients with traumatic brain injury, the difference in mortality was 14% observed versus 27.8% predicted by TRISS (P = 0.0018) and 24.3% predicted by RISC (P = 0.014). ROTEM®-guided haemostatic therapy, with fibrinogen concentrate as first-line haemostatic therapy and additional PCC, was goal-directed and fast. A favourable survival rate was observed. Prospective, randomized trials to investigate this therapeutic alternative further appear warranted.

https://epub.ub.uni-muenchen.de/23300/1/cc8948.pdf

Goal-directed coagulation management of major trauma patients using thromboelastometry (ROTEM)-guided administration of fibrinogen concentrate and prothrombin complex concentrate

patients with acute traumatic coagulopathy, with 29% falsenegative results. In acute traumatic coagulopathy, the rotational thromboelastometry clot amplitude at 5 mins was diminished by 42%, and this persisted throughout clot maturation. Rotational thromboelastometry clotting time was not significantly prolonged. Clot amplitude at a 5-min threshold of 1.2, p < .001). Conclusions: In trauma hemorrhage, prothrombin time ratio is not rapidly available from the laboratory and point-of-care devices can be inaccurate. Acute traumatic coagulopathy is functionally characterized by a reduction in clot strength. With a threshold of clot amplitude at 5 mins of <35 mm, rotational thromboelastometry can identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion. (Crit Care Med 2011; 39:2652‐2658)

/pdf/functional-definition-and-characterization-of-acute-1ievdpf6d2.pdf

Functional definition and characterization of acute traumatic coagulopathy.

Introduction
Thromboelastometry (TEM)-guided haemostatic therapy with fibrinogen concentrate and prothrombin complex concentrate (PCC) in trauma patients may reduce the need for transfusion of red blood cells (RBC) or platelet concentrate, compared with fresh frozen plasma (FFP)-based haemostatic therapy.

/pdf/transfusion-in-trauma-thromboelastometry-guided-coagulation-2sfgyaeryo.pdf

Transfusion in trauma: thromboelastometry-guided coagulation factor concentrate-based therapy versus standard fresh frozen plasma-based therapy

Objective:Injury and shock lead to alterations in conventional coagulation tests (CCTs). Recently, rapid thrombelastography (r-TEG) has become recognized as a comprehensive assessment of coagulation abnormalities. We have previously shown that admission r-TEG results are available faster than CCTs a

Admission Rapid Thrombelastography Can Replace Conventional Coagulation Tests in the Emergency Department: Experience With 1974 Consecutive Trauma Patients

Background: Bleeding is a major cause of death in patients with traumatic injuries. Recently, thrombelastograph (TEG) has been suggested as an additional means of evaluating coagulation in trauma patients. We hypothesized that TEG data would aid in defining the coagulopathy of trauma in patients with penetrating traumatic injuries. Methods: A retrospective study was performed of patients (n = 44) with penetrating injuries admitted to a combat support hospital during a 2-month period in 2004. Recorded data included standard laboratory data, TEG parameters, and blood product use in the first 24 hours after admission. Values were compared with clinically accepted ranges and those obtained from the Haemoscope Corporation. Results: At admission, International Normalization Ratio, prothrombin time, and partial thromboplastin time were increased in 39% (≥1.5), 31% (>16 seconds), and 37% (>40 seconds) of patients, respectively, suggesting hypocoagulation, but these variables did not correlate with the use of blood products (p > 0.05). TEG values obtained within 24 hours of admission (6 hours ± 5.7 hours; median of 4.5 hours) demonstrated hypocoagulation based on delayed propagation of the clot (increased K time and reduced α-angle) and decreased clot strength (reduced maximal amplitude [MA]). MA correlated (r = 0.57, p < 0.01) with blood product use as well as platelet count (r = 0.61, p < 0.01). Patients with reduced MA (n = 23) used more blood products and had reduced platelet counts and hematocrit. Conclusion: Thrombelastography was a more accurate indicator of blood product requirements in our patient population than prothrombin time, partial thromboplastin time, and International Normalization Ratio. Thrombelastography enhanced by platelet count and hematocrit can guide blood transfusion requirements.

A Reduction in Clot Formation Rate and Strength Assessed by Thrombelastography Is Indicative of Transfusion Requirements in Patients With Penetrating Injuries

Kimberly A. Smith

Papers

A Reduction in Clot Formation Rate and Strength Assessed by Thrombelastography Is Indicative of Transfusion Requirements in Patients With Penetrating Injuries