Distinct coagulation-fibrinolysis profiles in traumatic and upper gastrointestinal hemorrhagic shock: Clinical relevance of tPA/PAI-1 complex in traumatic hemorrhagic shock.

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.