Fibrinogen Deficiency and Dysfunction in Postpartum Hemorrhage: Evidence, Thresholds, and Management Across Resource Settings

Pregnancy is characterized by progressive hemostatic adaptation: increased fibrinogen synthesis, enhanced thrombin generation, and reduced fibrinolytic potential together prepare the maternal circulation for delivery-related blood loss. A fall in fibrinogen during pregnancy or the immediate postpartum period therefore does not carry the same meaning as an equivalent value outside of pregnancy. It may instead represent loss of a pregnancy-specific hemostatic reserve. Fibrinogen concentration is consistently associated with the severity of postpartum hemorrhage, but randomized trials have not shown that empirical replacement in all women with early postpartum hemorrhage improves clinical outcomes. This narrative review summarizes current evidence on pregnancy-associated fibrinogen deficiency and dysfunction, with emphasis on pathophysiology, trial findings, fibrinogen thresholds, replacement strategies, congenital fibrinogen disorders, and research gaps. Current data support using fibrinogen as both a severity marker and a selective treatment target, interpreted according to gestational age, bleeding phenotype, placental involvement, and resource setting. Direct evidence generated in low-resource settings is limited; no randomized trial of fibrinogen measurement or replacement has been conducted in such a setting.