Longitudinal plasma samples were prospectively collected from 251 critically-injured trauma patients at a single Level 1 Trauma Center on arrival and at 2, 3, 4, 6, 12, 24, 48, 72, 96, and 120 hours after admission to a Level I urban trauma intensive care unit (ICU).
Our methodology for collection of whole blood for viscoelastic testing has been described previously (17 (link)). Briefly, admission samples were collected via initial placement of a 16G or larger peripheral intravenous line; subsequent samples were collected via indwelling arterial catheters. Standard laboratory vacuum-sealed tubes containing 3.2% (0.109 mol/L) sodium citrate were used for all draws. After a waiver of consent was applied for initial blood draws, informed consent was obtained from all patients, as approved by the University of California Committee on Human Research. A total of 603 samples were analyzed on 251 patients. Demographics, resuscitation data, clinical laboratory results, and outcomes were collected in parallel. Point-of-care thromboelastography (TEG) was performed to assess viscoelastic properties of clot formation with the TEG 5000 (Haemonetics; Niles, Il) immediately after sample collection. One mL of citrated whole blood was added to a manufacturer-standardized vial containing the clotting activator kaolin and mixed. Following this, 340 uL was transferred from the kaolin vial to the TEG cup, warmed to 37°C, and recalcified with 20 uL of 0.2 mol/L CaCl2. For the FF TEG, 500 uL of citrated blood was added to the FF vial (kaolin + glycoprotein IIb/IIIa antagonist) and mixed; 340 uL was then transferred to the TEG cup, and warmed and recalcified as above. In parallel, plasma fibrinogen concentration was assayed by the von Clauss method (11 (link)) and plasma-based standard coagulation measures were performed. Platelet contribution to clot strength was calculated as MATEG−MAFF=MAplatelets. Percentage contributions of FF (%MAFF) and platelets (%MAplatelets) were calculated as each respective MA divided by the overall kaolin TEG MA. Coagulopathy was defined by admission INR>=1.3. Thrombocytopenia was defined by platelets <= 200. Multi-organ failure was defined using the Denver Postinjury Multiple Organ Failure Score (18 (link)–20 (link)).
Data are presented as mean (SD), median (interquartile range), or percentage; univariate comparisons were made using Student’s t test for normally distributed data, Wilcoxon rank sum or Kruskal Wallis testing for skewed data, and Fisher’s exact test for proportions. Intergroup comparisons between multiple groups were only judged significant when corrected for multiple comparisons using a standard Bonferroni correction. Linear regression was used to assess correlations between prospectively collected TEG values and laboratory values. Cox proportional hazards regression was used to identify predictors of mortality. An [alpha] = 0.05 was considered significant. All analysis was performed by the authors using Stata version 12 (StataCorp, College Station, TX).
Our methodology for collection of whole blood for viscoelastic testing has been described previously (17 (link)). Briefly, admission samples were collected via initial placement of a 16G or larger peripheral intravenous line; subsequent samples were collected via indwelling arterial catheters. Standard laboratory vacuum-sealed tubes containing 3.2% (0.109 mol/L) sodium citrate were used for all draws. After a waiver of consent was applied for initial blood draws, informed consent was obtained from all patients, as approved by the University of California Committee on Human Research. A total of 603 samples were analyzed on 251 patients. Demographics, resuscitation data, clinical laboratory results, and outcomes were collected in parallel. Point-of-care thromboelastography (TEG) was performed to assess viscoelastic properties of clot formation with the TEG 5000 (Haemonetics; Niles, Il) immediately after sample collection. One mL of citrated whole blood was added to a manufacturer-standardized vial containing the clotting activator kaolin and mixed. Following this, 340 uL was transferred from the kaolin vial to the TEG cup, warmed to 37°C, and recalcified with 20 uL of 0.2 mol/L CaCl2. For the FF TEG, 500 uL of citrated blood was added to the FF vial (kaolin + glycoprotein IIb/IIIa antagonist) and mixed; 340 uL was then transferred to the TEG cup, and warmed and recalcified as above. In parallel, plasma fibrinogen concentration was assayed by the von Clauss method (11 (link)) and plasma-based standard coagulation measures were performed. Platelet contribution to clot strength was calculated as MATEG−MAFF=MAplatelets. Percentage contributions of FF (%MAFF) and platelets (%MAplatelets) were calculated as each respective MA divided by the overall kaolin TEG MA. Coagulopathy was defined by admission INR>=1.3. Thrombocytopenia was defined by platelets <= 200. Multi-organ failure was defined using the Denver Postinjury Multiple Organ Failure Score (18 (link)–20 (link)).
Data are presented as mean (SD), median (interquartile range), or percentage; univariate comparisons were made using Student’s t test for normally distributed data, Wilcoxon rank sum or Kruskal Wallis testing for skewed data, and Fisher’s exact test for proportions. Intergroup comparisons between multiple groups were only judged significant when corrected for multiple comparisons using a standard Bonferroni correction. Linear regression was used to assess correlations between prospectively collected TEG values and laboratory values. Cox proportional hazards regression was used to identify predictors of mortality. An [alpha] = 0.05 was considered significant. All analysis was performed by the authors using Stata version 12 (StataCorp, College Station, TX).
