Primary Fibrinolysis Is Integral in the Pathogenesis of the Acute Coagulopathy of Trauma

Acute Coagulopathy of Trauma-Shock

Advanced Trauma and Surgery ◽

10.1007/978-981-10-2425-2_9 ◽

2016 ◽

pp. 137-144

Author(s):

Baiqiang Li ◽

Haichen Sun

Keyword(s):

Acute Coagulopathy Of Trauma

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Hemostasis and Thrombosis in Trauma Patients

Seminars in Thrombosis and Hemostasis ◽

10.1055/s-0034-1398378 ◽

2015 ◽

Vol 41 (01) ◽

pp. 026-034 ◽

Cited By ~ 14

Author(s):

Satoshi Gando

Keyword(s):

Wound Healing ◽

Protein C ◽

Activated Protein C ◽

Fat Embolism ◽

Whole Body ◽

Severe Bleeding ◽

Trauma Patients ◽

Embolism Syndrome ◽

Acute Coagulopathy Of Trauma ◽

Pathological Reaction

Hemostasis and thrombosis in trauma patients consist of physiological hemostasis for wound healing and the pathological reaction of disseminated intravascular coagulation (DIC). Whole body trauma, isolated brain injury, and fat embolism syndrome, if extremely severe, can cause DIC and affect a patient's prognosis. Shock-induced hyperfibrinolysis causes DIC with the fibrinolytic phenotype, contributing to oozing-type severe bleeding. If uncontrolled, this phenotype progresses to thrombotic phenotype at the late stage of trauma, followed by microvascular thrombosis, leading to organ dysfunction. Another type of pathological hemostatic change is acute coagulopathy of trauma shock (ACOTS), which gives rise to activated protein C–mediated systemic hypocoagulation, resulting in bleeding. ACOTS occurs only in trauma associated with shock-induced hypoperfusion and there is nothing to suggest DIC in this phenomenon. This review will provide information about the recent advances in hemostasis and thrombosis in trauma and will clarify the pathogeneses of the pathological processes observed in trauma patients.

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Thrombelastography and biomarker profiles in acute coagulopathy of trauma: a prospective study

Scandinavian Journal of Trauma Resuscitation and Emergency Medicine ◽

10.1186/1757-7241-19-64 ◽

2011 ◽

Vol 19 (1) ◽

pp. 64 ◽

Cited By ~ 62

Author(s):

Sisse R Ostrowski ◽

Anne Sørensen ◽

Claus F Larsen ◽

Pär I Johansson

Keyword(s):

Prospective Study ◽

A Prospective Study ◽

Acute Coagulopathy Of Trauma

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Hemodilution is Not Critical in the Pathogenesis of the Acute Coagulopathy of Trauma

Journal of Surgical Research ◽

10.1016/j.jss.2011.04.047 ◽

2012 ◽

Vol 173 (1) ◽

pp. 26-30 ◽

Cited By ~ 21

Author(s):

Max Valentin Wohlauer ◽

Ernest E. Moore ◽

Nathan M. Droz ◽

Jeffrey Harr ◽

Eduardo Gonzalez ◽

...

Keyword(s):

Acute Coagulopathy Of Trauma

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Mechanistic Determinants of the Acute Coagulopathy of Trauma (ACoT) in Patients Undergoing Emergency Surgery,

Blood ◽

10.1182/blood.v118.21.3319.3319 ◽

2011 ◽

Vol 118 (21) ◽

pp. 3319-3319

Author(s):

Bryan A Cotton ◽

Sherry L Sixta ◽

Charles E Wade ◽

John B Holcomb ◽

Nena Matijevic-Aleksic

Keyword(s):

Primary Outcome ◽

Multivariate Analyses ◽

Conflicts Of Interest ◽

Independent Predictor ◽

Base Deficit ◽

Blunt Injury ◽

Level 1 ◽

Acute Coagulopathy Of Trauma ◽

Level 1 Trauma Center ◽

Emergent Laparotomy

Abstract Abstract 3319 Introduction: Acute coagulopathy of trauma (ACoT) is a highly lethal phenomenon whose mechanisms have yet to be clearly defined. While likely multi-factorial, it has been reported to only occur in the presence of blunt injury. The purpose of this study was to identify variables that might influence or contribute to the early development of ACoT. Methods: Retrospective review of all patients admitted to a Level 1 trauma center 01/2004–12/2009 who underwent emergent laparotomy. Emergent laparotomy was defined as laparotomy performed within two hours of admission. ACoT(+) was defined as arrival INR >= 1.5, while ACoT(−) was defined as arrival INR<1.5. Univariate and multivariate analyses performed. Primary outcome was the identification of those factors predicting the presence of ACoT on admission. Results: 1218 patients were included, 337 (27%) presented with ACoT(+), 881 (73%) did not. The groups had similar demographics and pre-hospital and ED fluids. Arrival base deficit (median 8.5 vs. 4.0) and ISS (25 vs. 16) were higher in ACoT(+) as were intra-operative RBC (median 4 vs. 0 U) and plasma (3 vs. 0 U); all p<0.05. 40% of ACoT(+) patients sustained penetrating injury. Six-hour (12% vs. 1%), 24-hour (15% vs. 1%), and 30-day (23% vs. 4%) mortality were significantly greater in ACoT(+); all p<0.001. Linear regression found INR values independently associated with arrival base deficit (p<0.001) but not ISS. Controlling for age, gender, mechanism of injury, and pre-hospital resuscitation, multiple logistic regression demonstrated that arrival base deficit was an independent predictor of developing ACoT. Conclusion: The current study found ACoT independently associated with metabolic (base deficit), physiologic (blood pressure) and anatomic insults (ISS). Attempts to address ACoT should focus on correcting each of these components. Moreover, contrary to prior data, 40% of ACoT(+) patients sustained penetrating mechanism. Disclosures: No relevant conflicts of interest to declare.

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