Hyperfibrinolysis in trauma-induced coagulopathy: exploring the role of inflammatory cytokines

Hyperfibrinolysis is the excessive fibrinolytic activity observed in severely injured patients with trauma-induced coagulopathy (TIC). Previous studies suggest that inflammatory cytokines initiate inflammatory responses triggered by trauma and could impact on the coagulation cascade; however, the association between inflammatory cytokines and the development of hyperfibrinolysis has not been fully evaluated.

The aim of this study was to identify the characteristics of the inflammatory cytokines dynamics in TIC, particularly hyperfibrinolysis.

This is a secondary analysis of the Pragmatic, Randomized Optimal Platelet and Plasma Ratios trial. Study patients were stratified into the hyperfibrinolysis and nonhyperfibrinolysis groups using thromboelastography LY30 values and plasmin-antiplasmin complex. Serial values of inflammatory cytokine level (0-24 hours postadmission) were compared between the hyperfibrinolysis and nonhyperfibrinolysis groups. Subgroup analysis investigated the cytokines comparing patients with traumatic brain injury with hyperfibrinolysis and those without hyperfibrinolysis.

A total of 477 patients were included (hyperfibrinolysis, 45; nonhyperfibrinolysis, 432). The levels of interleukin (IL)-6, interleukin 1 receptor antagonist (IL-1Ra), and major vault protein (MVP)-1 were significantly higher in the hyperfibrinolysis group than those in the nonhyperfibrinolysis group across the time points within 24 hours after presentation. The level of platelet-derived growth factor subunit B (PDGF-B) upon arrival was significantly higher in the hyperfibrinolysis group. The IL-6, IL-1Ra, and MVP-1 levels peaked at 4 hours postadmission and PDGF-B peaked upon arrival and downtrended thereafter.

The current study revealed that IL-6, IL-1Ra, and MVP-1 levels trended upward for 4 hours postadmission and PDGF-B peaked upon arrival and downtrended thereafter in severely injured patients with hyperfibrinolysis.