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.
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 traumapatients 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.
Authors: G R Bernard; A Artigas; K L Brigham; J Carlet; K Falke; L Hudson; M Lamy; J R Legall; A Morris; R Spragg Journal: Am J Respir Crit Care Med Date: 1994-03 Impact factor: 21.405
Authors: Mitchell J Cohen; Michel Carles; Karim Brohi; Carolyn S Calfee; Pamela Rahn; Mariah S Call; Brian B Chesebro; Michael A West; Jean-François Pittet Journal: J Trauma Date: 2010-06
Authors: Sandro B Rizoli; Sandro Scarpelini; Jeannie Callum; Bartolomeu Nascimento; Kenneth G Mann; Ruxandra Pinto; Jan Jansen; Homer C Tien Journal: J Trauma Date: 2011-11
Authors: Michael W Cripps; Matthew E Kutcher; Aaron Daley; Ryan C McCreery; Molly D Greenberg; Leslie M Cachola; Brittney J Redick; Mary F Nelson; Mitchell Jay Cohen Journal: J Trauma Acute Care Surg Date: 2013-08 Impact factor: 3.313
Authors: Benjamin M Howard; Byron Y Miyazawa; Weifeng Dong; Wendy J Cedron; Ryan F Vilardi; Wolfram Ruf; Mitchell Jay Cohen Journal: J Trauma Acute Care Surg Date: 2015-12 Impact factor: 3.313
Authors: Anirban Banerjee; Christopher C Silliman; Ernest E Moore; Monika Dzieciatkowska; Marguerite Kelher; Angela Sauaia; Kenneth Jones; Michael P Chapman; Eduardo Gonzalez; Hunter B Moore; Angelo D'Alessandro; Erik Peltz; Benjamin E Huebner; Peter Einerson; James Chandler; Arsen Ghasabayan; Kirk Hansen Journal: J Trauma Acute Care Surg Date: 2018-06 Impact factor: 3.313
Authors: Donald H Jenkins; Joseph F Rappold; John F Badloe; Olle Berséus; Lorne Blackbourne; Karim H Brohi; Frank K Butler; Andrew P Cap; Mitchell Jay Cohen; Ross Davenport; Marc DePasquale; Heidi Doughty; Elon Glassberg; Tor Hervig; Timothy J Hooper; Rosemary Kozar; Marc Maegele; Ernest E Moore; Alan Murdock; Paul M Ness; Shibani Pati; Todd Rasmussen; Anne Sailliol; Martin A Schreiber; Geir Arne Sunde; Leo M G van de Watering; Kevin R Ward; Richard B Weiskopf; Nathan J White; Geir Strandenes; Philip C Spinella Journal: Shock Date: 2014-05 Impact factor: 3.454
Authors: Julia R Coleman; Ernest E Moore; Michael P Chapman; Anirban Banerjee; Christopher C Silliman; Arsen Ghasabyan; James Chandler; Jason M Samuels; Angela Sauaia Journal: Surgery Date: 2018-06-12 Impact factor: 3.982