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Updated: Dec 9, 2025

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
Published on: June 4, 2020
Early thromboelastography in acute traumatic coagulopathy: an observational study focusing on pre-hospital trauma
Alessandra Spasiano1, Cristina Barbarino1, Anna Marangone2
1Anesthesiology and Intensive Care Medicine, Department of Medicine, University of Udine, ASUFC Udine, P.le Santa Maria della Misericordia 15, 33100, Udine, Italy.
Background:
Major brain injury and uncontrolled blood loss remain the primary causes of early trauma-related mortality. One-quarter to one-third of trauma patients exhibit trauma-induced coagulopathy (TIC). Thromboelastometry (ROTEM) and thrombelastography (TEG) are valuable alternatives to standard coagulation testing, providing a more comprehensive overview of the coagulation process.
Purpose:
Evaluating thromboelastographic profile, the incidence of fibrinolysis (defined as Ly30 > 3%) in severe trauma patients, and factors influencing pathological coagulation pattern.
Methods:
Prospective observational 2 years cohort study on severe trauma patients assisted by Helicopter Emergency Medical System (HEMS) and Level 1 Trauma Center, in a tertiary referral University Hospital.
Results:
Eighty three patients were enrolled, mean NISS (new injury severity score) 36 (± 13). Mean R value decreased from 7.25 (± 2.6) to 6.19 (± 2.5) min (p < 0.03); 48 (60%) patients had a reduction in R from T0 to T1. In NISS 25-40 and NISS > 40 groups, changes in R value increased their significance (p = 0.04 and p < 0.03, respectively). Pathological TEG was found in 71 (88.8%) patients at T0 and 74 (92.5%) at T1. Hypercoagulation was present in 57 (71.3%) patients at T0, and in 66(82.5%) at T1. 9 (11.3%) patients had hyperfibrinolysis at T0, 7 (8.8%) patients at T1. Prevalence of StO2 < 75% at T0 was greater in patients whose TEG worsened (7 patients, 46.7%) against whose TEG remained stable or improved (8 patients, 17.4%) from T0 to T1 (p = 0.02). 48 (57.8%) patients received < 1000 mL of fluids, while 35 (42.2%) received ≥ 1000 mL. The first group had fewer patients with hypercoagulation (20, 41.6%) than the second (6, 17.6%) at T1 (p < 0.03). No differences were found for same TEG pattern at T0, nor other TEG pattern.
Conclusion:
Our population is representative of a non-hemorrhagic severe injury subgroup. Almost all of our trauma population had coagulation abnormalities immediately after the trauma; pro-coagulant changes were the most represented regardless of the severity of injury. NISS appears to affect only R parameter on TEG. Hyperfibrinolysis has been found in a low percentage of patients. Hypoperfusion parameters do not help to identify patients with ongoing coagulation impairment. Small volume resuscitation and mild hypotermia does not affect coagulation, at least in the early post-traumatic phase.
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