NDLI: Acute coagulopathy of trauma: hypoperfusion induces systemic anticoagulation and hyperfibrinolysis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brohi, Karim Cohen, Mitchell J. Ganter, Michael T. Schultz, Marcus J. Levi, Marcel Mackersie, Robert C. Pittet, Jean-François
Description	Country affiliation: United kingdom Author Affiliation: Brohi K ( Department of Surgery, The Royal London Hospital, London, United Kingdom.)
Abstract	BACKGROUND: Coagulopathy is present at admission in 25% of trauma patients, is associated with shock and a 5-fold increase in mortality. The coagulopathy has recently been associated with systemic activation of the protein C pathway. This study was designed to characterize the thrombotic, coagulant and fibrinolytic derangements of trauma-induced shock. METHODS: This was a prospective cohort study of major trauma patients admitted to a single trauma center. Blood was drawn within 10 minutes of arrival for analysis of partial thromboplastin and prothrombin times, prothrombin fragments 1 + 2 (PF1 + 2), fibrinogen, factor VII, thrombomodulin, protein C, plasminogen activator inhibitor-1 (PAI-1), thrombin activatable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (tPA), and D-dimers. Base deficit was used as a measure of tissue hypoperfusion. RESULTS: Two hundred eight patients were studied. Systemic hypoperfusion was associated with anticoagulation and hyperfibrinolysis. Coagulation was activated and thrombin generation was related to injury severity, but acidosis did not affect Factor VII or PF1 + 2 levels. Hypoperfusion-induced increase in soluble thrombomodulin levels was associated with reduced fibrinogen utilization, reduction in protein C and an increase in TAFI. Hypoperfusion also resulted in hyperfibrinolysis, with raised tPA and D-Dimers, associated with the observed reduction in PAI-1 and not alterations in TAFI. CONCLUSIONS: Acute coagulopathy of trauma is associated with systemic hypoperfusion and is characterized by anticoagulation and hyperfibrinolysis. There was no evidence of coagulation factor loss or dysfunction at this time point. Soluble thrombomodulin levels correlate with thrombomodulin activity. Thrombin binding to thrombomodulin contributes to hyperfibrinolysis via activated protein C consumption of PAI-1.
File Format	HTM / HTML
ISSN	00225282
Issue Number	5
Volume Number	64
e-ISSN	15298809
Journal	The Journal of Trauma: Injury, Infection, and Critical Care
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2008-05-01
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Prospective Studies Complications Wounds And Injuries Humans Blood Coagulation Factors Isolation & Purification Trauma Centers Disseminated Intravascular Coagulation Protein C Metabolism Fibrinolysis Discipline Traumatology Blood Journal Article Injury Severity Score Etiology Classification
Content Type	Text
Resource Type	Article
Subject	Surgery Critical Care and Intensive Care Medicine

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