Hyperfibrinolysis after major trauma: differential diagnosis of lysis patterns and prognostic value of thrombelastometry.

Department of Anesthesiology and Intensive Care, AUVA Trauma Hospital, Salzburg, Austria.
The Journal of trauma (Impact Factor: 2.35). 08/2009; 67(1):125-31. DOI: 10.1097/TA.0b013e31818b2483
Source: PubMed

ABSTRACT The aim of this study was to diagnose hyperfibrinolysis (HF) and its pattern using thrombelastometry and to correlate the diagnosis with mortality. Furthermore, routine laboratory based and the rotational thrombelastometry analyzer (ROTEM)-derived variables were also correlated with survival.
Severe trauma patients showing HF in ROTEM were consecutively enrolled in the study. Three different HF patterns were compared: fulminant breakdown within 30 minutes, intermediate HF of 30 to 60 minutes, and late HF after 60 minutes. Injury severity score (ISS), hemodynamics, hemoglobin, hematocrit, platelet count (PC), fibrinogen, and ROTEM variables at admission were analyzed. The observed mortality was compared with the predicted trauma and injury severity score mortality.
Thirty-three patients were diagnosed with HF. The mean ISS was 47 +/- 14. Fulminant, intermediate, or late HF (n = 11 each group) resulted in 100%, 91%, or 73% mortality, respectively, with the best prognosis for late HF (p = 0.0031). The actual overall mortality of HF (88%) exceeded the predicted trauma and injury severity score mortality (70%) (p = 0.039). Lower PC (123 +/- 53 vs. 193 +/- 91; p = 0.034), ROTEM prolonged clot formation time [CFT, 359 (140/632) vs. 82 (14/190); p = 0.042], and lower platelet contribution to maximum clot firmness [MCF(EXTEM) - MCF(FIBTEM), 34 (20/40) vs. 46 (40/53); p = 0.026] were associated with increased mortality.
ROTEM-based diagnosis of HF predicted outcome. Further independent predictors of death were combination of HF with hemorrhagic shock, low PC, and prolonged CFT in ROTEM. ROTEM-based point of care testing in the emergency room is thus able to identify prognostic factors such as prolonged CFT and low platelet contribution to clot firmness (MCF(EX) - MCF(FIB)) earlier than standard laboratory-based monitoring.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Over the last 10 years, the management of major haemorrhage in trauma patients has changed radically. This is mainly due to the recognition that many patients who are bleeding when they come in to the emergency department have an established coagulopathy before the haemodilution effects of fluid resuscitation. This has led to the use of new terminology: acute traumatic coagulopathy, acute coagulopathy of trauma shock or trauma-induced coagulopathy. The recognition of acute traumatic coagulopathy is important, because we now understand that its presence is a prognostic indicator, as it is associated with poor clinical outcome. This has driven a change in clinical management, so that the previous approach of maintaining an adequate circulating volume and oxygen carrying capacity before, as a secondary event, dealing with coagulopathy, has changed to haemostatic resuscitation as early as possible. While there is as yet no universally accepted assay or definition, many experts use prolongation of the prothrombin time to indicate that there is, indeed, a coagulopathy. Hypoxia, acidosis and hypothermia and hormonal, immunological and cytokine production, alongside consumption and blood loss, and the dilutional effects of resuscitation may occur to varying extents depending on the type of tissue damaged, the type and extent of injury, predisposing to, or amplifying, activation of coagulation, platelets, fibrinolysis. These are discussed in detail within the article. © 2014 The Association of Anaesthetists of Great Britain and Ireland.
    Anaesthesia 01/2015; 70 Suppl 1:96-e34. · 3.85 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Mortality from trauma remains a global public health challenge, with most preventable deaths due to bleeding. The recognition of acute traumatic coagulopathy as a distinct clinical entity characterized by early coagulation dysfunction, arising prior to medical intervention, has revolutionized trauma management over the last decade. The aim of this article is to review our current understanding of acute traumatic coagulopathy.
    Current Opinion in Critical Care 10/2014; · 3.18 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Trauma is a leading cause of death, with uncontrolled hemorrhage and exsanguination being the primary causes of preventable deaths during the first 24 h following trauma. Death usually occurs quickly, typically within the first 6 h after injury. One out of four patients arriving at the Emergency Department after trauma is already in hemodynamic and hemostatic depletion. This early manifestation of hemostatic depletion is referred to as the coagulopathy of trauma, which may distinguished as: (i) acute traumatic coagulopathy (ATC) and (ii) iatrogenic coagulopathy (IC). The principle drivers of ATC have been characterized by tissue trauma, inflammation, hypoperfusion/shock, and the acute activation of the neurohumoral system. Hypoperfusion leads to an activation of protein C with cleavage of activated factors V and VIII and the inhibition of plasminogen activator inhibitor-1 (PAI-1), with subsequent fibrinolysis. Endothelial damage and activation results in Weibel–Palade body degradation and glycocalyx shedding associated with autoheparinization. In contrast, there is an IC which occurs secondary to uncritical volume therapy, leading to acidosis, hypothermia, and hemodilution. This coagulopathy may, then, be an integral part of the “vicious cycle” when combined with acidosis and hypothermia. The awareness of the specific pathophysiology and of the principle drivers underlying the coagulopathy of trauma by the treating physician is paramount. It has been shown that early recognition prompted by appropriate and aggressive management can correct coagulopathy, control bleeding, reduce blood product use, and improve outcome in severely injured patients. This paper summarizes: (i) the current concepts of the pathogenesis of the coagulopathy of trauma, including ATC and IC, (ii) the current strategies available for the early identification of patients at risk for coagulopathy and ongoing life-threatening hemorrhage after trauma, and (iii) the current and updated European guidelines for the management of bleeding and coagulopathy following major trauma.
    European Journal of Trauma and Emergency Surgery 04/2014; 40(2):113-126. · 0.38 Impact Factor