Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations

Background: Acute traumatic coagulopathy (ATC) is an impairment of hemostasis that occurs early after injury and is associated with a 4‐fold higher mortality, increased transfusion requirements and organ failure. Objectives: The purpose of the present study was to develop a clinically relevant defin...

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Veröffentlicht in:Journal of thrombosis and haemostasis 2010-09, Vol.8 (9), p.1919-1925
Hauptverfasser: FRITH, D., GOSLINGS, J. C., GAARDER, C., MAEGELE, M., COHEN, M. J., ALLARD, S., JOHANSSON, P. I., STANWORTH, S., THIEMERMANN, C., BROHI, K.
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container_end_page 1925
container_issue 9
container_start_page 1919
container_title Journal of thrombosis and haemostasis
container_volume 8
creator FRITH, D.
GOSLINGS, J. C.
GAARDER, C.
MAEGELE, M.
COHEN, M. J.
ALLARD, S.
JOHANSSON, P. I.
STANWORTH, S.
THIEMERMANN, C.
BROHI, K.
description Background: Acute traumatic coagulopathy (ATC) is an impairment of hemostasis that occurs early after injury and is associated with a 4‐fold higher mortality, increased transfusion requirements and organ failure. Objectives: The purpose of the present study was to develop a clinically relevant definition of ATC and understand the etiology of this endogenous coagulopathy. Patients/methods: We conducted a retrospective cohort study of trauma patients admitted to five international trauma centers and corroborated our findings in a novel rat model of ATC. Coagulation status on emergency department arrival was correlated with trauma and shock severity, mortality and transfusion requirements. 3646 complete records were available for analysis. Results: Patients arriving with a prothrombin time ratio (PTr) > 1.2 had significantly higher mortality and transfusion requirements than patients with a normal PTr (mortality: 22.7% vs. 7.0%; P 
doi_str_mv 10.1111/j.1538-7836.2010.03945.x
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C. ; GAARDER, C. ; MAEGELE, M. ; COHEN, M. J. ; ALLARD, S. ; JOHANSSON, P. I. ; STANWORTH, S. ; THIEMERMANN, C. ; BROHI, K.</creator><creatorcontrib>FRITH, D. ; GOSLINGS, J. C. ; GAARDER, C. ; MAEGELE, M. ; COHEN, M. J. ; ALLARD, S. ; JOHANSSON, P. I. ; STANWORTH, S. ; THIEMERMANN, C. ; BROHI, K.</creatorcontrib><description>Background: Acute traumatic coagulopathy (ATC) is an impairment of hemostasis that occurs early after injury and is associated with a 4‐fold higher mortality, increased transfusion requirements and organ failure. Objectives: The purpose of the present study was to develop a clinically relevant definition of ATC and understand the etiology of this endogenous coagulopathy. Patients/methods: We conducted a retrospective cohort study of trauma patients admitted to five international trauma centers and corroborated our findings in a novel rat model of ATC. Coagulation status on emergency department arrival was correlated with trauma and shock severity, mortality and transfusion requirements. 3646 complete records were available for analysis. Results: Patients arriving with a prothrombin time ratio (PTr) &gt; 1.2 had significantly higher mortality and transfusion requirements than patients with a normal PTr (mortality: 22.7% vs. 7.0%; P &lt; 0.001. Packed red blood cells: 3.5 vs. 1.2 units; P &lt; 0.001. Fresh frozen plasma: 2.1 vs. 0.8 units; P &lt; 0.001). The severity of ATC correlated strongly with the combined degree of injury and shock. The rat model controlled for exogenously induced coagulopathy and mirrored the clinical findings. Significant coagulopathy developed only in animals subjected to both trauma and hemorrhagic shock (PTr: 1.30. APTTr: 1.36; both P &lt; 0.001 compared with sham controls). Conclusions: ATC develops endogenously in response to a combination of tissue damage and shock. It is associated with increased mortality and transfusion requirements in a dose‐dependent manner. When defined by standard clotting times, a PTr &gt; 1.2 should be adopted as a clinically relevant definition of ATC.</description><identifier>ISSN: 1538-7933</identifier><identifier>ISSN: 1538-7836</identifier><identifier>EISSN: 1538-7836</identifier><identifier>DOI: 10.1111/j.1538-7836.2010.03945.x</identifier><identifier>PMID: 20553376</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Animals ; Blood Coagulation ; Blood Coagulation Disorders - etiology ; Blood Transfusion - methods ; coagulopathy ; Cohort Studies ; Disease Models, Animal ; Female ; hemorrhage ; Humans ; Male ; Middle Aged ; rat ; Rats ; Retrospective Studies ; shock ; Shock, Hemorrhagic - diagnosis ; transfusion ; trauma ; Wounds and Injuries - complications</subject><ispartof>Journal of thrombosis and haemostasis, 2010-09, Vol.8 (9), p.1919-1925</ispartof><rights>2010 International Society on Thrombosis and Haemostasis</rights><rights>2010 International Society on Thrombosis and Haemostasis.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4845-22fef44d601867fc1d83f440eb756ea09a36298ca40e9bbb69ead92bbdaaac7c3</citedby><cites>FETCH-LOGICAL-c4845-22fef44d601867fc1d83f440eb756ea09a36298ca40e9bbb69ead92bbdaaac7c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20553376$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FRITH, D.</creatorcontrib><creatorcontrib>GOSLINGS, J. C.</creatorcontrib><creatorcontrib>GAARDER, C.</creatorcontrib><creatorcontrib>MAEGELE, M.</creatorcontrib><creatorcontrib>COHEN, M. J.</creatorcontrib><creatorcontrib>ALLARD, S.</creatorcontrib><creatorcontrib>JOHANSSON, P. I.</creatorcontrib><creatorcontrib>STANWORTH, S.</creatorcontrib><creatorcontrib>THIEMERMANN, C.</creatorcontrib><creatorcontrib>BROHI, K.</creatorcontrib><title>Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations</title><title>Journal of thrombosis and haemostasis</title><addtitle>J Thromb Haemost</addtitle><description>Background: Acute traumatic coagulopathy (ATC) is an impairment of hemostasis that occurs early after injury and is associated with a 4‐fold higher mortality, increased transfusion requirements and organ failure. Objectives: The purpose of the present study was to develop a clinically relevant definition of ATC and understand the etiology of this endogenous coagulopathy. Patients/methods: We conducted a retrospective cohort study of trauma patients admitted to five international trauma centers and corroborated our findings in a novel rat model of ATC. Coagulation status on emergency department arrival was correlated with trauma and shock severity, mortality and transfusion requirements. 3646 complete records were available for analysis. Results: Patients arriving with a prothrombin time ratio (PTr) &gt; 1.2 had significantly higher mortality and transfusion requirements than patients with a normal PTr (mortality: 22.7% vs. 7.0%; P &lt; 0.001. Packed red blood cells: 3.5 vs. 1.2 units; P &lt; 0.001. Fresh frozen plasma: 2.1 vs. 0.8 units; P &lt; 0.001). The severity of ATC correlated strongly with the combined degree of injury and shock. The rat model controlled for exogenously induced coagulopathy and mirrored the clinical findings. Significant coagulopathy developed only in animals subjected to both trauma and hemorrhagic shock (PTr: 1.30. APTTr: 1.36; both P &lt; 0.001 compared with sham controls). Conclusions: ATC develops endogenously in response to a combination of tissue damage and shock. It is associated with increased mortality and transfusion requirements in a dose‐dependent manner. When defined by standard clotting times, a PTr &gt; 1.2 should be adopted as a clinically relevant definition of ATC.</description><subject>Adult</subject><subject>Animals</subject><subject>Blood Coagulation</subject><subject>Blood Coagulation Disorders - etiology</subject><subject>Blood Transfusion - methods</subject><subject>coagulopathy</subject><subject>Cohort Studies</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>hemorrhage</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>rat</subject><subject>Rats</subject><subject>Retrospective Studies</subject><subject>shock</subject><subject>Shock, Hemorrhagic - diagnosis</subject><subject>transfusion</subject><subject>trauma</subject><subject>Wounds and Injuries - complications</subject><issn>1538-7933</issn><issn>1538-7836</issn><issn>1538-7836</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtOwzAQRS0EoqXwCyg7VglOnDgOEgtUHgVVYlPWZuJMiqu8iJPS_j1OS7vGG8-M770eHUIcn3q-Pbcrz4-YcGPBuBdQO6UsCSNvc0LGx4fTQ50wNiIXxqwo9ZMooOdkFNAoYizmY_L5iLmudKfryoEqc7JWr7E1Tp07oPoOna6FvoROK0fVsOyLuoHua3vnqMLaFBQ7F24abHWJVWcHulqj6fQShlBzSc5yKAxe_d0T8vH8tJjO3Pn7y-v0Ye6qUISRGwQ55mGYceoLHufKzwSzPcU0jjgCTYDxIBEK7ChJ05QnCFkSpGkGACpWbEJu9rlNW3_3dgFZaqOwKKDCujcy5kEYC858qxR7pWprY1rMZWN3h3YrfSoHvHIlB3JyoCgHvHKHV26s9frvkz4tMTsaDzyt4H4v-NEFbv8dLN8Ws6Fiv1hfi8M</recordid><startdate>201009</startdate><enddate>201009</enddate><creator>FRITH, D.</creator><creator>GOSLINGS, J. C.</creator><creator>GAARDER, C.</creator><creator>MAEGELE, M.</creator><creator>COHEN, M. J.</creator><creator>ALLARD, S.</creator><creator>JOHANSSON, P. I.</creator><creator>STANWORTH, S.</creator><creator>THIEMERMANN, C.</creator><creator>BROHI, K.</creator><general>Blackwell Publishing Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201009</creationdate><title>Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations</title><author>FRITH, D. ; GOSLINGS, J. C. ; GAARDER, C. ; MAEGELE, M. ; COHEN, M. J. ; ALLARD, S. ; JOHANSSON, P. I. ; STANWORTH, S. ; THIEMERMANN, C. ; BROHI, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4845-22fef44d601867fc1d83f440eb756ea09a36298ca40e9bbb69ead92bbdaaac7c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Animals</topic><topic>Blood Coagulation</topic><topic>Blood Coagulation Disorders - etiology</topic><topic>Blood Transfusion - methods</topic><topic>coagulopathy</topic><topic>Cohort Studies</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>hemorrhage</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>rat</topic><topic>Rats</topic><topic>Retrospective Studies</topic><topic>shock</topic><topic>Shock, Hemorrhagic - diagnosis</topic><topic>transfusion</topic><topic>trauma</topic><topic>Wounds and Injuries - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FRITH, D.</creatorcontrib><creatorcontrib>GOSLINGS, J. C.</creatorcontrib><creatorcontrib>GAARDER, C.</creatorcontrib><creatorcontrib>MAEGELE, M.</creatorcontrib><creatorcontrib>COHEN, M. J.</creatorcontrib><creatorcontrib>ALLARD, S.</creatorcontrib><creatorcontrib>JOHANSSON, P. I.</creatorcontrib><creatorcontrib>STANWORTH, S.</creatorcontrib><creatorcontrib>THIEMERMANN, C.</creatorcontrib><creatorcontrib>BROHI, K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of thrombosis and haemostasis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FRITH, D.</au><au>GOSLINGS, J. C.</au><au>GAARDER, C.</au><au>MAEGELE, M.</au><au>COHEN, M. J.</au><au>ALLARD, S.</au><au>JOHANSSON, P. I.</au><au>STANWORTH, S.</au><au>THIEMERMANN, C.</au><au>BROHI, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations</atitle><jtitle>Journal of thrombosis and haemostasis</jtitle><addtitle>J Thromb Haemost</addtitle><date>2010-09</date><risdate>2010</risdate><volume>8</volume><issue>9</issue><spage>1919</spage><epage>1925</epage><pages>1919-1925</pages><issn>1538-7933</issn><issn>1538-7836</issn><eissn>1538-7836</eissn><abstract>Background: Acute traumatic coagulopathy (ATC) is an impairment of hemostasis that occurs early after injury and is associated with a 4‐fold higher mortality, increased transfusion requirements and organ failure. Objectives: The purpose of the present study was to develop a clinically relevant definition of ATC and understand the etiology of this endogenous coagulopathy. Patients/methods: We conducted a retrospective cohort study of trauma patients admitted to five international trauma centers and corroborated our findings in a novel rat model of ATC. Coagulation status on emergency department arrival was correlated with trauma and shock severity, mortality and transfusion requirements. 3646 complete records were available for analysis. Results: Patients arriving with a prothrombin time ratio (PTr) &gt; 1.2 had significantly higher mortality and transfusion requirements than patients with a normal PTr (mortality: 22.7% vs. 7.0%; P &lt; 0.001. Packed red blood cells: 3.5 vs. 1.2 units; P &lt; 0.001. Fresh frozen plasma: 2.1 vs. 0.8 units; P &lt; 0.001). The severity of ATC correlated strongly with the combined degree of injury and shock. The rat model controlled for exogenously induced coagulopathy and mirrored the clinical findings. Significant coagulopathy developed only in animals subjected to both trauma and hemorrhagic shock (PTr: 1.30. APTTr: 1.36; both P &lt; 0.001 compared with sham controls). Conclusions: ATC develops endogenously in response to a combination of tissue damage and shock. It is associated with increased mortality and transfusion requirements in a dose‐dependent manner. When defined by standard clotting times, a PTr &gt; 1.2 should be adopted as a clinically relevant definition of ATC.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20553376</pmid><doi>10.1111/j.1538-7836.2010.03945.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Adult
Animals
Blood Coagulation
Blood Coagulation Disorders - etiology
Blood Transfusion - methods
coagulopathy
Cohort Studies
Disease Models, Animal
Female
hemorrhage
Humans
Male
Middle Aged
rat
Rats
Retrospective Studies
shock
Shock, Hemorrhagic - diagnosis
transfusion
trauma
Wounds and Injuries - complications
title Definition and drivers of acute traumatic coagulopathy: clinical and experimental investigations
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