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Liver Injury as a Risk Factor for Post-traumatic Venous Thromboembolism.

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Liver injury (LI) in severely injured patients independently predicts pulmonary embolism (PE), but not deep venous thrombosis (DVT). This finding suggests LI may contribute to PE development through unique mechanisms.

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Area of Science:

  • Trauma Surgery
  • Vascular Surgery
  • Critical Care Medicine

Background:

  • Venous thromboembolism (VTE) is a significant cause of death in severely injured patients.
  • Current VTE risk stratification and prophylaxis methods are insufficient, indicating a gap in understanding VTE risk factors.
  • The liver's crucial role in coagulation prompted investigation into liver injury (LI) as a potential VTE risk factor.

Purpose of the Study:

  • To determine if liver injury (LI) is independently associated with an increased risk of VTE in severely injured patients.
  • To differentiate the association of LI with pulmonary embolism (PE) versus deep venous thrombosis (DVT).

Main Methods:

  • Retrospective review of the American College of Surgeons TQIP database (2017-2021).
  • Inclusion criteria: Severely injured patients (max abdominal Abbreviated Injury Score ≥ 4) with or without LI.
  • Exclusion criteria: Transfers, burns, all-cause mortality, patients < 18 years.
  • Logistic regression analysis was used to assess the independent effect of LI on PE and DVT development, controlling for confounders.

Main Results:

  • The study analyzed 44,506 patients; 18,642 (41.9%) had LI, 1,736 (3.9%) had DVT, and 890 (2.0%) had PE.
  • After adjusting for confounders, LI was independently associated with PE (aOR 1.279, 95% CI 1.088-1.504).
  • LI was not independently associated with DVT (aOR 1.011, 95% CI 0.897-1.140).

Conclusions:

  • Liver injury is an independent predictor of pulmonary embolism (PE) in severely injured patients.
  • LI is not associated with deep venous thrombosis (DVT), suggesting PE may arise from local liver-related prothrombotic mechanisms.
  • Further research is needed to elucidate the mechanisms (e.g., portal vein coagulation, endothelial injury, blood stasis) and consider LI in VTE risk stratification.