Fibrinogen for the management of critical obstetric hemorrhage

Abstract

Aim: In cases of critical obstetric hemorrhage leading to extreme hypofibrinogenemia, fibrinogen is the marker that indicates the critical severity, and early fibrinogen supplementation centering on hemostatic resuscitation is a vital treatment to stabilize a catastrophic condition. In this review, we investigated the effect of fibrinogen level on hemostasis and what we can do to treat hypofibrinogenemia efficiently and improve patients' outcome.

Methods: We reviewed numerous articles related to hypofibrinogenemia in critical obstetric hemorrhage. Especially, we performed a systematic review on target value of fibrinogen for hemostasis and effectiveness of fibrinogen concentrate. We also reviewed the articles about the methods for early normalization of fibrinogen level such as tranexamic acid, massive transfusion protocol, and point-of-care testing.

Results: The target value of fibrinogen calculated by needs for massive transfusion was 200 mg/dL or 10 mm of A5_FIBTEM . Although fibrinogen concentrate worked poorly on fibrinogen levels within the normal range, it improved the blood fibrinogen levels rapidly when it was administered to critical obstetric hemorrhage patients with serious hypofibrinogenemia. Hence, the volume of FFP transfused could be reduced along with a reduction in the frequency of pulmonary edema due to volume overload.

Conclusion: The patient group for which fibrinogen concentrate works most effectively is cases with severe hypofibrinogenemia. Further research is required in the light of evidence. The essence of the transfusion algorithm in critical obstetric hemorrhage is to approach the target value for obtaining hemostasis, ensure an accurate and prompt grasp of the severity using point-of-care testing, introduce a massive transfusion protocol and use tranexamic acid.

Keywords: coagulopathy; critical obstetrical hemorrhage; disseminated intravascular coagulation; fibrinogen; fibrinogen concentrate; fresh frozen plasma.

Figure 1

Mechanism of onset of coagulopathy in blood vessel due to low reflux. Hypoperfusion of tissues due to massive blood loss increases the production of thrombomodulin in vascular endothelial cells and promotes the activation of Protein C. Protein C irreversibly inhibits factors Va and VIIIa, causing coagulopathy and, at the same time, inhibiting plasminogen activator inhibitor‐1 and promoting the enhancement of the fibrinolytic system.

Figure 2

Massive transfusion protocol.