Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Research Abstract Details 

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Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Abstract Text:

Karim Brohi,Mitchell J Cohen,Michael T Ganter,Michael A Matthay,Robert C Mackersie, Pittet,

OBJECTIVES: Coagulopathy following major trauma is conventionally attributed to activation and consumption of coagulation factors. Recent studies have identified an acute coagulopathy present on admission that is independent of injury severity. We hypothesized that early coagulopathy is due to tissue hypoperfusion, and investigated derangements in coagulation associated with this. 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, fibrinogen, thrombomodulin, protein C, plasminogen activator inhibitor-1, and D-dimers. Base deficit (BD) was used as a measure of tissue hypoperfusion. RESULTS: A total of 208 patients were enrolled. Patients without tissue hypoperfusion were not coagulopathic, irrespective of the amount of thrombin generated. Prolongation of the partial thromboplastin and prothrombin times was only observed with an increased BD. An increasing BD was associated with high soluble thrombomodulin and low protein C levels. Low protein C levels were associated with prolongation of the partial thromboplastin and prothrombin times and hyperfibrinolysis with low levels of plasminogen activator inhibitor-1 and high D-dimer levels. High thrombomodulin and low protein C levels were significantly associated with increased mortality, blood transfusion requirements, acute renal injury, and reduced ventilator-free days. CONCLUSIONS: Early traumatic coagulopathy occurs only in the presence of tissue hypoperfusion and appears to occur without significant consumption of coagulation factors. Alterations in the thrombomodulin-protein C pathway are consistent with activated protein C activation and systemic anticoagulation. Admission plasma thrombomodulin and protein C levels are predictive of clinical outcomes following major trauma.

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Publishing Authors By Initials

K Brohi,MJ Cohen,MT Ganter,MA Matthay,RC Mackersie,JF Pittet,

For similar disorders of environmental origin: wounds and injuries research abstracts see: disorders of environmental origin: wounds and injuries research

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Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Annals of surgery

VOLUME: 245

Page Numbers: 812-8

Journal Abbreviation:

ISSN: 0003-4932

DAY: 3

MONTH: May

YEAR: 2007

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372354

Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Keywords Mesh Terms:

KEYWORDS: Wounds and Injuries

MESH TERMS: complications

Chemical & Substance for Abstract: Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Information

Substance Name: Thrombomodulin

Registry Number: 0

Grant and Affiliation Information for Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway?

AFFILIATION: Department of Surgery, University of California at San Francisco, San Francisco, CA, USA. karim@trauma.org

Country: United States

AGENCY: United States NIGMS

GRANT: R01 GM 62188

ACRONYM: GM

MEDLINETA: Ann Surg

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