An increased tendency in fibrinogen activity and its association with a hypo-fibrinolytic state in early stages after injury in patients without acute traumatic coagulopathy (ATC)

S He,M Blombäck,F Boström,J Svensson,A Östlund,H Wallen

doi:10.1007/s11239-018-1642-1

Abstract

Acute traumatic coagulopathy (ATC) diagnosed by prolongation of APTT and/or PT/INR involves alterations in platelet activity, coagulation and fibrinolysis. However, data showing the haemostatic situation in injured patients without ATC are scarce. To assess whether haemostatic impairment is also present in injured patients without ATC, ten injured patients without ATC and ten normal individuals were examined. The patients were sampled on arrival at the emergency department 0, 2, 12 h after surgical or other intervention. Thrombin generation, fibrin formation and fibrin proteolysis were determined via several laboratory methods, using tissue factor as the coagulation trigger. Thrombograms demonstrated that trauma accelerated both thrombin generation and decay. In the presence of unaffected peak thrombin levels, these two contradictory effects cancelled each other out, leading to the global endogenous thrombin potential (ETP) remaining normal. Under the mediation of normal ETP, fibrin network permeability (Ks) kept the reference levels in the two groups of subjects. Fibrinogen (FBG) activity (Clauss) rose with time from 0 to 2 h and 12 h, which significantly slowed down Clot Lysis Potential as determined by an in vitro method with exogenous t-PA. Summary: the main haemostatic impairment in the present patients concerned an increased tendency in FBG activity. Since an increase in FBG is a biomarker of acute inflammation and also predicts greater fibrin production which down-regulates fibrinolysis, we suggest that during early stages after injury, patients without ATC may suffer from worsening inflammation and confront enhancement of thrombosis risk due to dysfunction of fibrinolysis.

Highlights

Major traumas bring a variety of disorders to haemostatic function, thereby increasing the risk of haemorrhage soon after injury, and/or thrombosis later [1, 2]
When trauma patients arrive at emergency departments, values of INR > 1.5 or APTT > 1.5 times normal are used to identify early coagulation deficiencies, termed acute traumatic coagulopathy (ATC)
In the whole observation period, FBG activity remained within the reference range (2.0–4.2 g/L)

Summary

Introduction

Major traumas bring a variety of disorders to haemostatic function, thereby increasing the risk of haemorrhage soon after injury, and/or thrombosis later [1, 2]. When trauma patients arrive at emergency departments, values of INR > 1.5 or APTT > 1.5 times normal are used to identify early coagulation deficiencies, termed acute traumatic coagulopathy (ATC). Developed knowledge of the coagulation cascade [5] has prompted clinicians and researchers into consideration that APTT and/or PT/INR (as signals of time-to-start of detectable fibrin) cannot fully characterize dynamic impairments in the global haemostatic system caused by trauma and may result in inadequate guidance in emergency management. In recent years, numerous investigations have been focused on assessment of how ATC alters the overall haemostasis potential, including platelet activity,. Accumulated findings support the idea that the pathogenic mechanisms underlying ATC involve interplay between platelet dysfunction, acquired fibrinogen insufficiency, enhancements in endothelial activation, the inflammation response, endogenous anticoagulation and clot lysis by plasmin, etc. Data showing the haemostatic situation in injured patients without ATC are scarce in the literature [6]

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Results

Conclusion