Evaluation of Trauma-Induced Coagulopathy by Systematic Insights Into Pathophysiology and Advances in Emergency Resuscitation

TL;DR

This paper reviews how trauma-induced coagulopathy develops and how emergency resuscitation can be improved to save lives.

Contribution

The study systematically identifies key mechanisms of TIC and highlights potential biomarkers for diagnosis and treatment.

Findings

Three main mechanisms contribute to TIC: disrupted fibrinolysis, impaired platelet function, and damaged vessel walls.

Coagulation abnormalities like hypofibrinogenemia and elevated activated protein C are linked to worse patient outcomes.

Fibrinogen, thrombin, and activated protein C are suggested as diagnostic markers for TIC.

Abstract

Trauma-induced coagulopathy (TIC) exists as a fatal complication that develops from severe injuries and substantially increases patient mortality. Effective knowledge of TIC pathophysiology, together with optimized resuscitation strategies, is fundamental for enhancing patient outcomes. This review system examined TIC mechanisms through an analysis of present-day intervention methods. This systematic research with meta-analysis covered PubMed, Scopus, and Web of Science, together with Google Scholar databases, to review TIC pathophysiology and resuscitation practices. The inclusion of observational and experimental designs occurred by using predetermined selection criteria. Two independent researchers collected data from studies that received quality assessments through the Newcastle-Ottawa Scale (version 2011), along with the Cochrane Risk of Bias Tool (version 2) evaluation. The GRADE (Grading of Recommendations Assessment, Development, and Evaluation) approach served as the method for evaluating evidence certainty. The analyzed studies amounted to 11 after meeting the established criteria. Three major mechanisms led to TIC development, including disrupted fibrinolysis function, impaired platelet functioning, and damaged vessel walls. Six studies submitted for meta-analysis demonstrated that coagulation abnormalities, including hypofibrinogenemia and elevated activated protein C, result in adverse outcomes with a pooled HR of 6.3 (95% CI: 3.04-13.05, p < 0.05). The compound variation (I² = 69%) across data points appeared from differences between measurements and experimental conditions used in the studies. This review presents fibrinogen together with thrombin and activated protein C as diagnostic markers for TIC while supporting the use of protocol-based resuscitation. Future research requires several hospitals to participate in trials to establish new treatment protocols and establish uniform biomarker testing procedures in clinical settings.

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