title: Hypercoagulability after burn injury.
abstract: BACKGROUND
  Hypercoagulability is a homeostatic response to trauma, but relatively little information is available about coagulation changes after burn injury. Therefore, we tested the hypothesis that burn patients are hypercoagulable at admission and/or during recovery.
  
  
  METHODS
  A prospective observational trial was conducted at an American Burn Association verified Burn Center. Thromboelastography (TEG) was performed on blood drawn from indwelling catheters upon admission and weekly for those who remained hospitalized. Routine and special coagulation tests were performed on stored samples. Data are expressed as median (interquartile range).
  
  
  RESULTS
  Twenty-four patients (88% male) were enrolled, with a median age of 49 (20) years and a median total body surface area burn of 29% (23%); 21 experienced thermal burns (4 inhalational injuries), and 3 had electrical burns. There were no significant differences in TEG or coagulation assays between patients with thermal versus electrical burn injury, but there were significant differences between men versus women and between those with or without inhalational injury. Sixteen patients had repeat samples 1 week after intensive care unit admission. The repeat TEG was more hypercoagulable (all p < 0.05). Fibrinogen and natural anticoagulation proteins (protein C, protein S, and antithrombin III) were also increased (all p < 0.05). Two patients (8%) developed venous thromboembolism (VTE); TEG reaction time, fibrinogen, and partial thromboplastin time were decreased (all p < 0.05) at admission compared with those with no VTE. All changes occurred despite pharmacologic thromboprophylaxis. There was no significant correlation between TEG and total body surface area or between TEG and fluid balance.
  
  
  CONCLUSIONS
  In general, burn patients have normal coagulation parameters at admission but become hypercoagulable during recovery. However, those who are hypercoagulable at admission may have an increased risk of VTE. Additional monitoring and/or thromboprophylaxis may be indicated.
  
  
  METHODS
  Epidemiologic/prognostic study, level III.
authors.affiliation: Division of Trauma, the Dewitt-Daughtry Family Department of Surgery, University of Miami Miller School of Medicine and Ryder Trauma Center, Miami, Florida 33136, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Van Haren
authors.forename: Chad M
authors.initials: CM
authors.lastname: Thorson
authors.forename: Evan J
authors.initials: EJ
authors.lastname: Valle
authors.forename: Alexander M
authors.initials: AM
authors.lastname: Busko
authors.forename: Gerardo A
authors.initials: GA
authors.lastname: Guarch
authors.forename: David M
authors.initials: DM
authors.lastname: Andrews
authors.forename: Louis R
authors.initials: LR
authors.lastname: Pizano
authors.forename: Carl I
authors.initials: CI
authors.lastname: Schulman
authors.forename: Nicholas
authors.initials: N
authors.lastname: Namias
authors.forename: Kenneth G
authors.initials: KG
authors.lastname: Proctor
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D001780:Blood Coagulation Tests; D002053:Burn Units; D002056:Burns / Q000097:blood* / Q000150:complications; D015331:Cohort Studies; D005260:Female; D006801:Humans; D015994:Incidence; D015601:Injury Severity Score; D008297:Male; D008875:Middle Aged; D010314:Partial Thromboplastin Time; D011379:Prognosis; D011446:Prospective Studies; D018570:Risk Assessment; D012737:Sex Factors; D016019:Survival Analysis; D013916:Thrombelastography / Q000379:methods; D013923:Thromboembolism / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D019851:Thrombophilia / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology