title: Coagulation system changes associated with susceptibility to infection in trauma patients.
abstract: BACKGROUND
  Infection following trauma is associated with increased morbidity and mortality and is common following severe hemorrhage. There is a strong interaction between the coagulation and immunity. The objective of this study was to establish if there was an association between changes in coagulation status after hemorrhage and the subsequent incidence of infection.
  
  
  METHODS
  Prospective cohort study of adult injured patients presenting to a major trauma center during a 2-year period. Blood was drawn at 24 hours following admission and analyzed using functional thromboelastography testing and laboratory defined tests of coagulation and blood count. Patients were followed up for infectious episodes while in the hospital using Center for Disease Control definitions.
  
  
  RESULTS
  A total of 158 patients were recruited; 71 (45%) developed infection and were older (44 years vs. 32 years, p = 0.01) and more severely injured (Injury Severity Score [ISS], 25 vs.10; p < 0.01). White blood cell counts at 24 hours were normal, and there was no difference between groups (both 9.6 × 10/(9)L). Protein C was lower in those with infection (70.2 IU/dL vs. 83.3 IU/dL, p = 0.02), with a dose-dependent increase in infection as levels of protein C decreased. Plasmin activation at 24 hours was also strongly associated with infection plasmin-antiplasmin (infection vs. no infection, 6,156 μg/L vs. 3,324 μg/L, p = 0.03). The infection cohort had overall 12% lower procoagulant levels (varied between factor VIII 6.4% and factor II 16.2%).
  
  
  CONCLUSIONS
  There is a strong association between the status of the coagulation system after 24 hours and the development of infection following trauma. Improved early coagulation management may decrease infection rates in this patient group.
  
  
  METHODS
  Prognostic prospective study, level III.
authors.affiliation: Department of Trauma Sciences, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom. Elaine.cole@bartsandthelondon.nhs.uk
authors.forename: Elaine
authors.initials: E
authors.lastname: Cole
authors.forename: Ross
authors.initials: R
authors.lastname: Davenport
authors.forename: Henry
authors.initials: H
authors.lastname: De'Ath
authors.forename: Henry
authors.initials: H
authors.lastname: De-Ath
authors.forename: Joanna
authors.initials: J
authors.lastname: Manson
authors.forename: Thomas
authors.initials: T
authors.lastname: Brockamp
authors.forename: Karim
authors.initials: K
authors.lastname: Brohi
mesh_terms: D000328:Adult; D000933:Antifibrinolytic Agents / Q000097:blood; D001772:Blood Cell Count; D001777:Blood Coagulation; D001779:Blood Coagulation Factors / Q000032:analysis; D004198:Disease Susceptibility; D005341:Fibrinolysin / Q000032:analysis; D005342:Fibrinolysis; D006801:Humans; D007239:Infections / Q000097:blood* / Q000209:etiology / Q000276:immunology; D007902:Length of Stay; D011486:Protein C / Q000032:analysis; D012720:Severity of Illness Index; D013916:Thrombelastography; D014947:Wounds and Injuries / Q000097:blood / Q000150:complications*
chemical_list: D000933:Antifibrinolytic Agents; D001779:Blood Coagulation Factors; D011486:Protein C; D005341:Fibrinolysin