Comparison between point-of-care international normalised ratio, COAST, TICCS and truncated FibAT scores to rule in clinically significant hypofibrinogenaemia in the prehospital setting.

Abstract

Background: Hypofibrinogenaemia on ED arrival and in the prehospital setting has been associated with both increased mortality and increased blood transfusions. The timely administration of fibrinogen-rich products on arrival to hospital is difficult to achieve and there is no clinical benefit with early, in-hospital empirical fibrinogen supplementation.

Methods: This was a prospective study of a convenience sample of adult trauma patients who had blood drawn in the prehospital setting prior to the administration of tranexamic acid. A point-of-care international normalised ratio (PoCINR) was performed at the time of blood draw, and Coagulopathy of Severe Trauma (COAST) score, Trauma Induced Coagulopathy Clinical Score (TICCS) and truncated Fibrinogen on Admission in Trauma (FibAT) score were calculated. Hypofibrinogenaemia was defined as a FibTEM A5<10 or a fibrinogen level ≤1.5 g/L with a clinically important specificity defined as 85%.

Results: A total of 152 patients were included in the primary analysis. The cohort was predominately male (82.9%) with a median age of 35 years (IQR 26-51). The median Injury Severity Score was 17 (IQR 10-25.5) with 18.4% sustaining penetrating trauma and 24.3% receiving prehospital blood transfusions. The area under the receiver operating characteristic curve for hypofibrinogenaemia was PoCINR: 0.63 (95% CI 0.53 to 0.73), FibAT: 0.57 (95% CI 0.47 to 0.67), COAST: 0.47 (95% CI 0.37 to 0.58) and TICCS: 0.50 (95% CI 0.40 to 0.61). A cut-off PoCINR value of ≥1.2, FibAT score ≥4, COAST≥4 and TICCS≥12 all yielded ≥85% specificity in detecting hypofibrinogenaemia.

Conclusions: PoCINR and a truncated FibAT are potential tools for the prehospital detection of hypofibrinogenaemia. Future work should examine the feasibility of PoC devices to test for hypofibrinogenaemia in the prehospital setting and if the use of PoC devices and/or clinical risk stratification tools would result in more rapid fibrinogen replacement.