Etiology and management of hypofibrinogenemia in trauma

Abstract

Purpose of reviewFibrin polymerization is essential for stable clot formation in trauma, and hypofibrinogenemia reduces hemostasis in trauma. This review considers fibrinogen biology, the changes that fibrinogen undergoes after major trauma, and current evidence for lab testing and treatment.Recent findingsFibrinogen is a polypeptide that is converted to fibrin by the action of thrombin. During trauma, fibrinogen levels are consumed and reduce within the first few hours because of consumption, dilution, and fibrinolysis. Fibrinogen levels usually rebound within 48 hours of injury and can contribute to thrombotic events. The Clauss fibrinogen assay is the gold standard test for fibrinogen levels, although viscoelastic hemostatic assays are often used when a lab delay is anticipated. An evidence-based threshold for fibrinogen replacement is not well established in the literature, but expert opinion recommends maintaining a level above 150 mg/dl.SummaryHypofibrinogenemia is an important cause of nonanatomic bleeding in trauma. Despite multiple pathologic causes, the cornerstone of treatment remains fibrinogen replacement with cryoprecipitate or fibrinogen concentrates.

Hemostatic effect of fibrinogen concentrate on traumatic massive hemorrhage: a propensity score matching study

“… 4 Hence, there is consensus that fibrinogen concentrate (FC) needs to be administered to hemorrhaging patients once hypofibrinogenemia is documented by standard laboratory test (SLT) or viscoelastic hemostatic assay (VHA), although the triggering serum level varies by guideline. 5 Therefore, administering FC can also be a rational therapeutic option for managing TIC. 6 …”