Etiology and management of hypofibrinogenemia in trauma

Rajen Nathwani, Adrian Proumen, Kevin P. Blaine

Research output: Contribution to journalReview articlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)382-387
Number of pages6
JournalCurrent Opinion in Anaesthesiology
Volume36
Issue number3
DOIs
StatePublished - Jun 1 2023

Keywords

  • coagulopathy
  • fibrinogen
  • hypofibrinogenemia
  • trauma

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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