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Abstract Severe trauma-related bleeding is associated with high mortality. Standard coagulation tests provide limited information on the underlying coagulation disorder. Whole-blood viscoelastic tests such as rotational thromboelastometry or thrombelastography offer a more comprehensive insight into the coagulation process in trauma. The results are available within minutes and they provide information about the initiation of coagulation, the speed of clot formation, and the quality and stability of the clot. Viscoelastic tests have the potential to guide coagulation therapy according to the actual needs of each patient, reducing the risks of over- or under-transfusion. The concept of early, individualized and goal-directed therapy is explored in this review and the AUVA Trauma Hospital algorithm for managing trauma-induced coagulopathy is presented.

Abstract Background Hypertonic saline hydroxyethyl starch (HH) has been recommended for first line treatment of hemorrhagic shock. Its effects on coagulation are unclear. We studied in vitro effects of HH dilution on whole blood coagulation and platelet function. Furthermore 7.2% hypertonic saline, 6% hydroxyethylstarch (as ingredients of HH), and 0.9% saline solution (as control) were tested in comparable dilutions to estimate specific component effects of HH on coagulation. Methods The study was designed as experimental non-randomized comparative in vitro study. Following institutional review board approval and informed consent blood samples were taken from 10 healthy volunteers and diluted in vitro with either HH (HyperHaes®, Fresenius Kabi, Germany), hypertonic saline (HT, 7.2% NaCl), hydroxyethylstarch (HS, HAES6%, Fresenius Kabi, Germany) or NaCl 0.9% (ISO) in a proportion of 5%, 10%, 20% and 40%. Coagulation was studied in whole blood by rotation thrombelastometry (ROTEM) after thromboplastin activation without (ExTEM) and with inhibition of thrombocyte function by cytochalasin D (FibTEM), the latter was performed to determine fibrin polymerisation alone. Values are expressed as maximal clot firmness (MCF, [mm]) and clotting time (CT, [s]). Platelet aggregation was determined by impedance aggregrometry (Multiplate) after activation with thrombin receptor-activating peptide 6 (TRAP) and quantified by the area under the aggregation curve (AUC [aggregation units (AU)/min]). Scanning electron microscopy was performed to evaluate HyperHaes induced cell shape changes of thrombocytes. Statistics: 2-way ANOVA for repeated measurements, Bonferroni post hoc test, p < 0.01. Results Dilution impaired whole blood coagulation and thrombocyte aggregation in all dilutions in a dose dependent fashion. In contrast to dilution with ISO and HS, respectively, dilution with HH as well as HT almost abolished coagulation (MCFExTEM from 57.3 ± 4.9 mm (native) to 1.7 ± 2.2 mm (HH 40% dilution; p < 0.0001) and to 6.6 ± 3.4 mm (HT 40% dilution; p < 0.0001) and thrombocyte aggregation (AUC from 1067 ± 234 AU/mm (native) to 14.5 ± 12.5 AU/mm (HH 40% dilution; p < 0.0001) and to 20.4 ± 10.4 AU/min (HT 40% dilution; p < 0.0001) without differences between HH and HT (MCF: p = 0.452; AUC: p = 0.449). Conclusions HH impairs platelet function during in vitro dilution already at 5% dilution. Impairment of whole blood coagulation is significant after 10% dilution or more. This effect can be pinpointed to the platelet function impairing hypertonic saline component and to a lesser extend to fibrin polymerization inhibition by the colloid component or dilution effects. Accordingly, repeated administration and overdosage should be avoided.

Background: The acute coagulopathy of trauma has been identified as a critical determinant of outcomes. Antifibrinolytic agents have recently been demonstrated to improve outcomes. This prospective study was designed to assess coagulopathy in trauma patients using thromboelastography., Study Design: Trauma patients meeting our institution's highest tier of trauma team activation criteria were prospectively enrolled during a 5-month period ending April 1, 2011. Thromboelastography was performed at admission, +1 hour, +2 hours, and +6 hours using citrated blood. Hyperfibrinolysis was defined as estimated percent lysis ≥15%. Patients were followed throughout their hospital course to collect clinical data and outcomes., Results: One hundred and eighteen patients were enrolled (77.1% were male, 51.7% had penetrating trauma, 7.6% had systolic blood pressure <90 mmHg, 47.5% had Injury Severity Score >16, and 23.7% had Glasgow Coma Scale score ≤8). Hyperfibrinolysis was present in 13 patients (11.0%), with a mean time to detection of 13 minutes (range 2 to 60 minutes). By the 6-hour sampling, 8 (61.5%) of the hyperfibrinolytic patients had expired from hemorrhage. Survivors at this point demonstrated correction of coagulopathy, however, 12 patients (92.3%) ultimately expired (75% hemorrhage, 25% head injury). On stepwise logistic regression, hyperfibrinolysis was a strong predictor of early (24 hours) mortality (odds ratio = 25.0; 95% CI, 2.8-221.4; p = 0.004), predicting 53% of early deaths. Compared with patients without hyperfibrinolysis, patients with hyperfibrinolysis had a greater need for massive transfusion (76.9% vs 8.7%; adjusted odds ratio = 19.1; 95% CI, 3.6-101.3; p < 0.001) and had a greater early mortality (69.2% vs 1.9%; adjusted odds ratio = 55.8; 95% CI, 7.2-432.3; p < 0.001) and in-hospital mortality (92.3% vs 9.5%; adjusted odds ratio = 55.5; 95% CI, 4.8-649.7; p = 0.001)., Conclusions: In this prospective analysis, hyperfibrinolysis on thromboelastography developed in approximately 10% of patients and was considerably more likely to require massive transfusion. Hyperfibrinolysis was a strong independent predictor of mortality. Additional evaluation of the role of thromboelastography-directed antifibrinolytic therapies is warranted., (Copyright © 2012 American College of Surgeons. Published by Elsevier Inc. All rights reserved.)