He Zhang, Rong Zhang, Xiao-Jie Zhang, Tao Shang, Hui-Zhen Kang, Ze-Xin Xie, Yong Tian
THS exhibits a distinct coagulation-fibrinolysis phenotype characterized by concurrent activation of thrombin and plasmin generation compared with UGIB-HS. The altered tPA/PAI-1 complex profile may reflect etiology-specific regulation of balance between fibrinolytic activation and endogenous regulatory responses and provides complementary prognostic information for early risk stratification in THS.
OBJECTIVES: To define distinct coagulation-fibrinolysis phenotypes in traumatic hemorrhagic shock (THS) compared with upper gastrointestinal bleeding-associated hemorrhagic shock (UGIB-HS), and to explore whether the tissue plasminogen activator/plasminogen activator inhibitor-1 complex (tPA/PAI-1 complex) provides insight into etiology-specific fibrinolytic regulation and early bleeding-related risk in THS.
METHODS: This retrospective observational study included 216 patients with blunt THS, 30 patients with UGIB-HS, and 30 blunt trauma controls without shock. Admission levels of tPA/PAI-1 complex, thrombin-antithrombin complex (TAT), plasmin-α2-antiplasmin complex (PIC), fibrinogen, lactate, Injury Severity Score (ISS), and Sequential Organ Failure Assessment (SOFA) score were analyzed. Multivariable logistic regression and receiver operating characteristic (ROC) analyses were performed.
RESULTS: Compared with UGIB-HS, THS showed markedly higher TAT and PIC levels (>9-fold and >8-fold, respectively), lower fibrinogen levels, and lower tPA/PAI-1 complex concentrations (14.43 ± 3.79 vs. 15.16 ± 3.25 ng/mL, P = 0.003). Compared with trauma controls, THS patients exhibited increased tPA/PAI-1 complex, TAT, and PIC levels (all P < 0.0001). In THS, tPA/PAI-1 complex correlated positively with TAT, PIC, ISS, and SOFA score, and negatively with fibrinogen (all P < 0.001). After adjustment for age, lactate, ISS, and fibrinogen, tPA/PAI-1 complex remained independently associated with bleeding-related adverse outcomes (OR 1.368, 95% CI 1.216-1.561), with a multivariable model AUC of 0.878 (95% CI 0.834-0.923).
CONCLUSIONS: THS exhibits a distinct coagulation-fibrinolysis phenotype characterized by concurrent activation of thrombin and plasmin generation compared with UGIB-HS. The altered tPA/PAI-1 complex profile may reflect etiology-specific regulation of balance between fibrinolytic activation and endogenous regulatory responses and provides complementary prognostic information for early risk stratification in THS.