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: 2.96).
08/2009; 67(1):125-31. DOI: 10.1097/TA.0b013e31818b2483
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.
Available from: Timothy Pohlman
- "HF in hemorrhaging patients, if determined by viscoelastic assay, can be categorized as fulminant, intermediate, or late, resulting in 100%, 91%, or 73% mortality, respectively . Progressive hemodilution during resuscitation can decreases endogenous antifibrinolytic proteins including PAI-1, α 2 -antiplasmin and thrombin-activatable fibrinolysis inhibitor (TAFI), and contribute to the hyperfibrinolytic propensity associated with severe hemorrhage  .Bothfibrin and fibrinogen degradation products in excess contribute to coagulopathy in bleeding patients by interfering with fibrin polymerization and clot stability , and by blocking ADP-induced platelet aggregation . Also this bleeding diathesis is potentiated by diminished hepatic clearance of degradation products due to pre-existing liver disease, and hypoxic injury to the liver (shock liver). "
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ABSTRACT: The early recognition and management of hemorrhage shock are among the most difficult tasks challenging the clinician during primary assessment of the acutely bleeding patient. Often with little time, within a chaotic setting, and without sufficient clinical data, a decision must be reached to begin transfusion of blood components in massive amounts. The practice of massive transfusion has advanced considerably and is now a more complete and, arguably, more effective process. This new therapeutic paradigm, referred to as damage control resuscitation (DCR), differs considerably in many important respects from previous management strategies for catastrophic blood loss. We review several important elements of DCR including immediate correction of specific coagulopathies induced by hemorrhage and management of several extreme homeostatic imbalances that may appear in the aftermath of resuscitation. We also emphasize that the foremost objective in managing exsanguinating hemorrhage is always expedient and definitive control of the source of bleeding.
Copyright © 2015. Published by Elsevier Ltd.
Available from: Herbert Schöchl
- "Animal studies have revealed that hypothermia decreases fibrinogen synthesis and acidosis increases fibrinogen breakdown ; both of these conditions are common in trauma. Low plasma fibrinogen concentration has also been reported with hyperfibrinolysis (HF), another common occurrence in trauma [7,31-33]. This may be related to the fact that plasmin not only dissolves fibrin but (at high levels) also cleaves fibrinogen (hyperfibrinogenolysis) . "
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ABSTRACT: Low plasma fibrinogen concentration is a predictor of poor outcome in major trauma patients. The role of fibrinogen concentrate for rapidly increasing fibrinogen plasma levels in severe trauma is not well defined.
In this retrospective study we included severe trauma patients treated with fibrinogen concentrate alone (FC group), fibrinogen concentrate with prothrombin complex concentrate (FC--PCC group) or fibrinogen concentrate with PCC and fresh frozen plasma (FC--PCC--FFP group). PCC was generally administered as the second step of intraoperative therapy, while FFP was only administered as a third step. All patients received >=1 g fibrinogen concentrate within 24 hours. Plasma fibrinogen concentration and ROTEM parameters upon emergency room (ER) admission, intensive care unit (ICU) admission, and after 24 hours were analysed.
Among 157 patients fulfilling the inclusion criteria, 83% were male; mean age was 44 years and median injury severity score (ISS) was 29. Standard coagulation tests reflected increasing severity of coagulopathy with increasing complexity of haemostatic therapy (highest severity in the FC--PCC--FFP group; p < 0.0001). Total 24-hour fibrinogen concentrate dose also increased with complexity of haemostatic therapy. Plasma fibrinogen concentration was maintained, with no significant difference between ER admission and ICU admission in all patient groups. FIBTEM clot firmness at 10 minutes (CA10) was similarly maintained, albeit with a small increase in the FC--PCC group. Fibrinogen concentration and FIBTEM CA10 were within the normal range in all groups at 24 hours. The ratio of fibrinogen concentrate to red blood cells (g:U) ranged between 0.7:1.0 and 1.0:1.0.
Fibrinogen concentrate therapy maintained fibrinogen concentration and FIBTEM CA10 during the initial phase of trauma care until ICU admission. After 24 hours, these parameters were comparable between the three groups and within the normal range for each of them. Further studies are warranted to investigate the effect of fibrinogen concentrate on clinical outcomes.
Available from: Herbert Schöchl
- "In the AUVA Trauma Centre of Salzburg, rapid point-of-care (POC) estimation of fibrin polymerization (that is via the FIBTEM assay on thromboelastometry (ROTEM)) has been established to diagnose fibrinogen deficiencies and to guide fibrinogen substitution in major trauma patients [10,14,15,20-22]. POC blood gas analyses and full blood cell counts are routinely performed in severe trauma patients upon admission to the ER. "
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ABSTRACT: Fibrinogen plays a key role in hemostasis and is the first coagulation factor to reach critical levels in massively bleeding trauma patients. Consequently, rapid estimation of plasma fibrinogen (FIB) is essential upon emergency room (ER) admission, but is not part of routine coagulation monitoring in many centers. We investigated the predictive ability of the laboratory parameters hemoglobin (Hb) and base excess (BE) upon admission, as well as the Injury Severity Score (ISS), to estimate FIB in major trauma patients.
In this retrospective study, major trauma patients (ISS [greater than or equal to]16) with documented FIB analysis upon ER admission were eligible for inclusion. FIB was correlated with Hb, BE and ISS, alone and in combination using, regression analysis.
675 patients were enrolled (median ISS 27). FIB upon admission correlated strongly with Hb, BE and ISS. Multiple regression analysis showed that Hb and BE together predicted FIB (adjusted R2=0.46; loge(FIB) = 3.567 + 0.223.Hb - 0.007.Hb2 + 0.044.BE), and predictive strength increased when ISS was included (adjusted R2=0.51; loge(FIB) = 4.188 + 0.243.Hb - 0.008.Hb2 + 0.036.BE - 0.031.ISS + 0.0003.ISS2). Of all major trauma patients admitted with Hb <12 g/dL, 74% had low (<200 mg/dL) FIB and 54% had critical (<150 mg/dL) FIB. Of patients admitted with Hb <10 g/dL, 89% had low FIB and 73% had critical FIB. These values increased to 93% and 89%, respectively, among patients with an admission Hb <8 g/dL. Sixty-six percent of patients with only a weakly negative BE (<2 mmol/L) showed low FIB. Of patients with BE <6 mmol/L upon admission, 81% had low FIB and 63% had critical FIB. The corresponding values for BE <10 mmol/L were 89% and 78%, respectively.
Upon ER admission, FIB of major trauma patients shows strong correlation with rapidly obtainable, routine laboratory parameters such as Hb and BE. These two parameters might provide an insightful and rapid tool to identify major trauma patients at risk of acquired hypofibrinogenemia. Early calculation of ISS could further increase the ability to predict FIB in these patients. We propose that FIB can be estimated during the initial phase of trauma care based on bedside tests.
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