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Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls
Summary Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐ti...
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Published in: | British journal of haematology 2006-10, Vol.135 (2), p.220-227 |
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container_title | British journal of haematology |
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description | Summary
Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P |
doi_str_mv | 10.1111/j.1365-2141.2006.06281.x |
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Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0·05), VII, X, XI and XII, antithrombin and protein C (P < 0·01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0·001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0·02), decreased peak thrombin (P < 0·02) and delayed time to peak thrombin (P < 0·001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD‐TFA Rotem, septic patients had delayed clot times (P = 0·04) but an increased maximum velocity of clot formation (P < 0·01) and area under the clot elasticity curve (P < 0·01). LD‐TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0·005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.]]></description><identifier>ISSN: 0007-1048</identifier><identifier>EISSN: 1365-2141</identifier><identifier>DOI: 10.1111/j.1365-2141.2006.06281.x</identifier><identifier>PMID: 17010048</identifier><identifier>CODEN: BJHEAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Blood Coagulation Factors - metabolism ; Blood Coagulation Tests - methods ; C-Reactive Protein - metabolism ; global haemostasis ; Hematologic and hematopoietic diseases ; Hemostasis ; Humans ; Medical sciences ; Middle Aged ; Protein C - metabolism ; sepsis ; Systemic Inflammatory Response Syndrome - blood ; Thrombelastography - methods ; Thrombin - biosynthesis ; thrombin generation ; thromboelastography ; Thromboplastin - metabolism ; thrombosis</subject><ispartof>British journal of haematology, 2006-10, Vol.135 (2), p.220-227</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4471-debe696adf921660a5ad5e81e881a7866523a04d2aa44fe43462cd416990f40a3</citedby><cites>FETCH-LOGICAL-c4471-debe696adf921660a5ad5e81e881a7866523a04d2aa44fe43462cd416990f40a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18123988$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17010048$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Collins, Peter W.</creatorcontrib><creatorcontrib>Macchiavello, Luis I.</creatorcontrib><creatorcontrib>Lewis, Sarah J.</creatorcontrib><creatorcontrib>Macartney, Nichola J.</creatorcontrib><creatorcontrib>Saayman, Anton G.</creatorcontrib><creatorcontrib>Luddington, Roger</creatorcontrib><creatorcontrib>Baglin, Trevor</creatorcontrib><creatorcontrib>Findlay, George P.</creatorcontrib><title>Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls</title><title>British journal of haematology</title><addtitle>Br J Haematol</addtitle><description><![CDATA[Summary
Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0·05), VII, X, XI and XII, antithrombin and protein C (P < 0·01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0·001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0·02), decreased peak thrombin (P < 0·02) and delayed time to peak thrombin (P < 0·001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD‐TFA Rotem, septic patients had delayed clot times (P = 0·04) but an increased maximum velocity of clot formation (P < 0·01) and area under the clot elasticity curve (P < 0·01). LD‐TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0·005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Blood Coagulation Factors - metabolism</subject><subject>Blood Coagulation Tests - methods</subject><subject>C-Reactive Protein - metabolism</subject><subject>global haemostasis</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hemostasis</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Protein C - metabolism</subject><subject>sepsis</subject><subject>Systemic Inflammatory Response Syndrome - blood</subject><subject>Thrombelastography - methods</subject><subject>Thrombin - biosynthesis</subject><subject>thrombin generation</subject><subject>thromboelastography</subject><subject>Thromboplastin - metabolism</subject><subject>thrombosis</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqNkMGO1DAMQCMEYoeFX0C5wK3FbtNMeuAAK9gFrcQFzpGnddmM0qYkHXbn70mZEXvFF1vxs5M8ISRCiTne7UusdVNUqLCsAHQJujJYPjwRm3-Np2IDANsCQZkL8SKlPQDW0OBzcYFbQMjnG_Hz2ocdeblwWpIMg7wjHkNaKLkk3SS76BbXkfdH6byXMy2Op0zeu-VOJv7NkXOaVzodpz6GkWUXxpki93IJuZ6WGHx6KZ4N5BO_OudL8ePzp-9XN8Xtt-svVx9ui06pLRY971i3mvqhrVBroIb6hg2yMUhbo3VT1QSqr4iUGljVSlddr1C3LQwKqL4Ub0975xh-HfKn7OhSx97TxOGQrDYtGF1jBs0J7GJIKfJg5-hGikeLYFfJdm9Xl3Z1aVfJ9q9k-5BHX5_vOOxG7h8Hz1Yz8OYMUMruhkhT59IjZ7CqW7Ny70_cvfN8_O8H2I9fb9aq_gPzMJjm</recordid><startdate>200610</startdate><enddate>200610</enddate><creator>Collins, Peter W.</creator><creator>Macchiavello, Luis I.</creator><creator>Lewis, Sarah J.</creator><creator>Macartney, Nichola J.</creator><creator>Saayman, Anton G.</creator><creator>Luddington, Roger</creator><creator>Baglin, Trevor</creator><creator>Findlay, George P.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><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>200610</creationdate><title>Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls</title><author>Collins, Peter W. ; Macchiavello, Luis I. ; Lewis, Sarah J. ; Macartney, Nichola J. ; Saayman, Anton G. ; Luddington, Roger ; Baglin, Trevor ; Findlay, George P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4471-debe696adf921660a5ad5e81e881a7866523a04d2aa44fe43462cd416990f40a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Blood Coagulation Factors - metabolism</topic><topic>Blood Coagulation Tests - methods</topic><topic>C-Reactive Protein - metabolism</topic><topic>global haemostasis</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hemostasis</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Protein C - metabolism</topic><topic>sepsis</topic><topic>Systemic Inflammatory Response Syndrome - blood</topic><topic>Thrombelastography - methods</topic><topic>Thrombin - biosynthesis</topic><topic>thrombin generation</topic><topic>thromboelastography</topic><topic>Thromboplastin - metabolism</topic><topic>thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Collins, Peter W.</creatorcontrib><creatorcontrib>Macchiavello, Luis I.</creatorcontrib><creatorcontrib>Lewis, Sarah J.</creatorcontrib><creatorcontrib>Macartney, Nichola J.</creatorcontrib><creatorcontrib>Saayman, Anton G.</creatorcontrib><creatorcontrib>Luddington, Roger</creatorcontrib><creatorcontrib>Baglin, Trevor</creatorcontrib><creatorcontrib>Findlay, George P.</creatorcontrib><collection>Pascal-Francis</collection><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>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Collins, Peter W.</au><au>Macchiavello, Luis I.</au><au>Lewis, Sarah J.</au><au>Macartney, Nichola J.</au><au>Saayman, Anton G.</au><au>Luddington, Roger</au><au>Baglin, Trevor</au><au>Findlay, George P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2006-10</date><risdate>2006</risdate><volume>135</volume><issue>2</issue><spage>220</spage><epage>227</epage><pages>220-227</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><coden>BJHEAL</coden><abstract><![CDATA[Summary
Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0·05), VII, X, XI and XII, antithrombin and protein C (P < 0·01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0·001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0·02), decreased peak thrombin (P < 0·02) and delayed time to peak thrombin (P < 0·001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD‐TFA Rotem, septic patients had delayed clot times (P = 0·04) but an increased maximum velocity of clot formation (P < 0·01) and area under the clot elasticity curve (P < 0·01). LD‐TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0·005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.]]></abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>17010048</pmid><doi>10.1111/j.1365-2141.2006.06281.x</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Aged, 80 and over Biological and medical sciences Blood Coagulation Factors - metabolism Blood Coagulation Tests - methods C-Reactive Protein - metabolism global haemostasis Hematologic and hematopoietic diseases Hemostasis Humans Medical sciences Middle Aged Protein C - metabolism sepsis Systemic Inflammatory Response Syndrome - blood Thrombelastography - methods Thrombin - biosynthesis thrombin generation thromboelastography Thromboplastin - metabolism thrombosis |
title | Global tests of haemostasis in critically ill patients with severe sepsis syndrome compared to controls |
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