Thrombelastography-identified coagulopathy is associated with increased morbidity and mortality after traumatic brain injury
Department of Surgery, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd., Mail Code L-223, Portland, OR 97239-3098, USA. American journal of surgery
(Impact Factor: 2.29).
03/2012; 203(5):584-8. DOI: 10.1016/j.amjsurg.2011.12.011
The purpose of this study was to determine the relationship between coagulopathy and outcome after traumatic brain injury.
Patients admitted with a traumatic brain injury were enrolled prospectively and admission blood samples were obtained for kaolin-activated thrombelastogram and standard coagulation assays. Demographic and clinical data were obtained for analysis.
Sixty-nine patients were included in the analysis. A total of 8.7% of subjects showed hypocoagulability based on a prolonged time to clot formation (R time, > 9 min). The mortality rate was significantly higher in subjects with a prolonged R time at admission (50.0% vs 11.7%). Patients with a prolonged R time also had significantly fewer intensive care unit-free days (8 vs 27 d), hospital-free days (5 vs 24 d), and increased incidence of neurosurgical intervention (83.3% vs 34.9%).
Hypocoagulability as shown by thrombelastography after traumatic brain injury is associated with worse outcomes and an increased incidence of neurosurgical intervention.
Available from: Eiichi Suehiro
- "Since this monitoring is able to be performed at bedside and repeatedly, we can observe a state of coagulopathy in real time. These values were associated with the clinical outcome in TBI patients  . In another report, tranexamic acid was administered as antifibrinolytic therapy for the acute phase of trauma expected to cause massive hemorrhage in adults . "
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ABSTRACT: Careful course observation is necessary for cases of mild to moderate traumatic brain injury even when disturbed consciousness is mild on admission. This is because delayed enlargement of hematoma and progression of cerebral swelling may occur and result in an emergency craniotomy. Here, we investigated coagulopathy and abnormal fibrinolysis as a predictive factor of “deterioration requiring surgery” in mild to moderate traumatic brain injury.Patients and methodsSixty-one patients with mild to moderate (Glasgow Coma Scale (GCS) score 9–15) traumatic brain injury were admitted between June 2009 and October 2010. There were 54 subjects in the study, excluding those treated with oral antiplatelet agents and anticoagulants. Patients were classified into those with deterioration requiring surgery [op(+)] or those without deterioration requiring surgery [op(−)]. This was based on whether surgical treatment was performed for hematoma expansion, and exacerbated consciousness level within 3 days after admission. Age, GCS score on admission and blood test findings (platelet count, PT-INR, APTT, fibrinogen, FDP, and d-dimer) on admission were compared.ResultsThe op(+) and op(−) groups comprised 7 (13.0%) and 47 patients (87.0%), respectively. Platelet counts (24.8 vs 18.5 × 104/μl) were decreased, and PT-INR (1.0 vs 1.2) was higher in the op(+) group. Specially, APTT (28.6 vs 39.1 s), FDP (28.9 vs 112.9 μg/ml), and d-dimer (17.3 vs 69.6 μg/ml) values were significantly higher in the op(+) group.Conclusions
Coagulopathy and abnormal fibrinolysis, which are measurable in routine medical practice, is associated with deterioration requiring surgery in mild to moderate traumatic brain injury, indicating that careful course observation is necessary.
Available from: Mark L Ryan
- "It is important to note that this study does not address the "acute coagulopathy of trauma", the dysegulated coagulation process that occurs in patients with high injury severity, prolonged hemorrhage , and/or massive transfusion. Hypocoagulability, as measured by prolongation of TEG R and K times along with decreased α and MA values, has been associated with the need for massive transfusion, morbidity, and mortality   . Recently Vogel et al. described this phenomenon in critically injured pediatric trauma patients, showing significant correlation between altered TEG and the need for lifesaving interventions, blood product transfusion, and overall mortality . "
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Coagulation changes in pediatric trauma patients are not well defined. To fill this gap, we tested the hypothesis that trauma evokes a hypercoagulable response.
A prospective observational study was conducted in hospitalized patients (age 8 months to 14 years) admitted for trauma or elective surgery. Informed consent was obtained from the parents and informed assent was obtained in patients 7 years of age or older. Coagulation changes were evaluated on fresh whole blood using thromboelastography (TEG) and on stored plasma using assays for special clotting factors.
Forty three patients (22 trauma, median injury severity score = 9; and 21 uninjured controls) were evaluated. With trauma vs control, prothrombin time (PT) was higher by about 10% (p < 0.001), but activated partial thromboplastin time was not altered. TEG clotting time (R; p = 0.005)) and fibrin cross-linking were markedly accelerated (K time, alpha angle; p < 0.001) relative to the control patients. D-Dimer, Prothrombin Fragment 1 + 2, and Plasminogen Activator Inhibitor-1 were all elevated, whereas Protein S activity was reduced (all p < 0.01). Importantly, a large fraction of TEG values and clotting factor assays in the pediatric control group were outside the published reference ranges for adults.
A hypercoagulable state is associated with minor trauma in children. More work is needed to determine the functional significance of these changes and to establish normal pediatric reference ranges.
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ABSTRACT: Prehospital management affects long-term outcome of patients with severe traumatic brain injury (TBI). This article reviews the current concepts and ongoing controversies of prehospital treatment of severe TBI.
Prehospital management focuses on the prevention of secondary brain injury and rapid transport to a neurotrauma center for definitive diagnosis and life- as well as brain-saving emergency treatment such as decompressive craniotomy. There is a broad consensus that adequate airway management, prevention of hypoxia, hypocapnia or hypercapnia, prevention of hypotension and control of hemorrhage represent preclinical therapeutic modalities that may contribute to improved survival in severe TBI. The precise role of prehospital endotracheal intubation, osmotic agents and early therapeutic hypothermia needs to be clarified in the context of time required for transportation, local infrastructure, geographical factors and availability of experienced emergency teams.
Prehospital management of TBI remains challenging. There are no universal objectives suitable to all patients. Randomized, controlled clinical trials are necessary for developing optimal protocols for paramedic and physician emergency medical teams.
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