Acquired hypofibrinogenemia is most frequently caused by hemodilution and consumption of clotting factors. The aggressive replacement of fibrinogen has become one of the core principles of modern management of massive hemorrhage. The best method for determining the patient's fibrinogen level remains controversial, and particularly in acquired dysfibrinogenemia, could have major therapeutic implications depending on which quantification method is chosen. This review introduces the available laboratory and point-of-care methods and discusses the relative advantages and limitations. It also discusses current strategies for the correction of hypofibrinogenemia.
Keywords: Clauss fibrinogen assay; PT-derived fibrinogen; afibrinogenemia; direct oral anticoagulant; dysfibrinogenemia; fibrinogen antigen; functional fibrinogen; gravimetric fibrinogen assay; viscoelastic testing.