Hyperfibrinolysis in severe isolated traumatic brain injury may occur without tissue hypoperfusion: a retrospective observational multicentre study

[1]  F. Castellino,et al.  Translational Research in Acute Lung Injury and Pulmonary Fibrosis Early coagulation events induce acute lung injury in a rat model of blunt traumatic brain injury , 2016 .

[2]  S. Kushimoto,et al.  Can Early Aggressive Administration of Fresh Frozen Plasma Improve Outcomes in Patients with Severe Blunt Trauma?—a Report by the Japanese Association for the Surgery of Trauma , 2016, Shock.

[3]  S. Kushimoto,et al.  High D-Dimer Levels Predict a Poor Outcome in Patients with Severe Trauma, Even with High Fibrinogen Levels on Arrival: A Multicenter Retrospective Study , 2016, Shock.

[4]  M. Hayakawa,et al.  Pathophysiology of Trauma-Induced Coagulopathy and Management of Critical Bleeding Requiring Massive Transfusion , 2015, Seminars in Thrombosis & Hemostasis.

[5]  K. Brohi,et al.  Admission biomarkers of trauma-induced secondary cardiac injury predict adverse cardiac events and are associated with plasma catecholamine levels , 2015, The journal of trauma and acute care surgery.

[6]  B. Konkle,et al.  Brain-derived microparticles induce systemic coagulation in a murine model of traumatic brain injury. , 2015, Blood.

[7]  B. Seifert,et al.  Changes in Coagulation in Standard Laboratory Tests and ROTEM in Trauma Patients Between On-Scene and Arrival in the Emergency Department , 2015, Anesthesia and analgesia.

[8]  Michiyasu Suzuki,et al.  Predictors of deterioration indicating a requirement for surgery in mild to moderate traumatic brain injury , 2014, Clinical Neurology and Neurosurgery.

[9]  B. Bellander,et al.  Formation of microparticles in the injured brain of patients with severe isolated traumatic brain injury. , 2014, Journal of neurotrauma.

[10]  A. Akgun,et al.  Predictive value of liver transaminases levels in abdominal trauma. , 2014, The American journal of emergency medicine.

[11]  M. Hayakawa,et al.  Massive Amounts of Tissue Factor Induce Fibrinogenolysis Without Tissue Hypoperfusion in Rats , 2013, Shock.

[12]  J. Thachil,et al.  Differentiating disseminated intravascular coagulation (DIC) with the fibrinolytic phenotype from coagulopathy of trauma and acute coagulopathy of trauma‐shock (COT/ACOTS) , 2013, Journal of thrombosis and haemostasis : JTH.

[13]  S. Stanworth,et al.  The incidence and magnitude of fibrinolytic activation in trauma patients , 2013, Journal of thrombosis and haemostasis : JTH.

[14]  N. Zhang,et al.  Circulating histones are mediators of trauma-associated lung injury. , 2013, American journal of respiratory and critical care medicine.

[15]  M. Maegele Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options , 2013, Transfusion.

[16]  M. Cohen,et al.  Extracellular histone release in response to traumatic injury: Implications for a compensatory role of activated protein C , 2012, The journal of trauma and acute care surgery.

[17]  A. Karakuş,et al.  The relationship of trauma severity and mortality with cardiac enzymes and cytokines at multiple trauma patients. , 2012, Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES.

[18]  M. Cohen,et al.  Criteria for empiric treatment of hyperfibrinolysis after trauma , 2012, The journal of trauma and acute care surgery.

[19]  S. Ostrowski,et al.  Thrombelastography and biomarker profiles in acute coagulopathy of trauma: a prospective study , 2011, Scandinavian journal of trauma, resuscitation and emergency medicine.

[20]  B. Seifert,et al.  Hyperfibrinolysis Diagnosed by Rotational Thromboelastometry (ROTEM®) Is Associated with Higher Mortality in Patients with Severe Trauma , 2011, Anesthesia and analgesia.

[21]  K. Inaba,et al.  Early coagulopathy after isolated severe traumatic brain injury: relationship with hypoperfusion challenged. , 2010, The Journal of trauma.

[22]  A. Sauaia,et al.  Primary Fibrinolysis Is Integral in the Pathogenesis of the Acute Coagulopathy of Trauma , 2010, Annals of surgery.

[23]  W. Junger,et al.  Circulating Mitochondrial DAMPs Cause Inflammatory Responses to Injury , 2009, Nature.

[24]  M. Hayakawa,et al.  Disseminated intravascular coagulation with a fibrinolytic phenotype at an early phase of trauma predicts mortality. , 2009, Thrombosis research.

[25]  H. Schöchl,et al.  Hyperfibrinolysis after major trauma: differential diagnosis of lysis patterns and prognostic value of thrombelastometry. , 2009, The Journal of trauma.

[26]  K. Inaba,et al.  Evaluation of rotation thrombelastography for the diagnosis of hyperfibrinolysis in trauma patients. , 2008, British journal of anaesthesia.

[27]  H. Wada,et al.  Are fibrin-related markers useful for the diagnosis of thrombosis? , 2008, Seminars in thrombosis and hemostasis.

[28]  G. Manley,et al.  Early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein C pathway. , 2007, The Journal of trauma.

[29]  M. Yamakuchi,et al.  Regulation of Weibel-Palade body exocytosis. , 2005, Trends in cardiovascular medicine.

[30]  S. Kushimoto,et al.  Implications of fibrinogenolysis in patients with closed head injury. , 2003, Journal of neurotrauma.

[31]  W. Nieuwenhuizen,et al.  Molecular mechanisms of initiation of fibrinolysis by fibrin , 2003, Thrombosis and Haemostasis.

[32]  P. Meda,et al.  Tissue-type plasminogen activator (t-PA) is stored in Weibel-Palade bodies in human endothelial cells both in vitro and in vivo. , 2002, Blood.

[33]  O. Kemmotsu,et al.  Coagulofibrinolytic changes after isolated head injury are not different from those in trauma patients without head injury. , 1999, The Journal of trauma.

[34]  T. Hayakawa,et al.  Participation of tissue factor and thrombin in posttraumatic systemic inflammatory syndrome. , 1997, Critical care medicine.

[35]  S. Gando,et al.  Posttrauma coagulation and fibrinolysis , 1992, Critical care medicine.

[36]  B. Risberg,et al.  Early activation of humoral proteolytic systems in patients with multiple trauma , 1986, Critical care medicine.

[37]  P. Gildenberg,et al.  Clinicopathological correlations of disseminated intravascular coagulation in patients with head injury. , 1984, Neurosurgery.

[38]  C. Vecht,et al.  DISSEMINATED INTRAVASCULAR COAGULATION AND HEAD INJURY , 1982, The Lancet.

[39]  P. Gildenberg,et al.  Delayed and recurrent intracranial hematomas related to disseminated intravascular clotting and fibrinolysis in head injury. , 1980, Neurosurgery.

[40]  C. Rao,et al.  Predictive value of serum lactate dehydrogenase in head injury. , 1978, Journal of neurology, neurosurgery, and psychiatry.

[41]  H. Poznanska [Lactate dehydrogenase isoenzymes]. , 1966, Polski tygodnik lekarski.

[42]  S. Kushimoto,et al.  The impact of preinjury antithrombotic medication on hemostatic interventions in trauma patients☆,☆☆,★ , 2017, The American journal of emergency medicine.

[43]  Wenqiang Jiang,et al.  Serum enzyme profile characteristics of victims following the Wenchuan earthquake in China , 2009, Clinical chemistry and laboratory medicine.

[44]  R Bellomo,et al.  Strong ions, weak acids and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders. , 2004, British journal of anaesthesia.

[45]  T. Kooistra,et al.  Regulation of endothelial cell t-PA synthesis and release. , 1994, International journal of hematology.

[46]  H. Lang Creatine Kinase Isoenzymes , 1981, Springer Berlin Heidelberg.

[47]  A. S. Relman Lactic acidosis. , 1971, Transactions of the American Clinical and Climatological Association.