Ana Pedrero Gil: Is Coagulopathy with Fibrinolysis Present in All Obstetric Hemorrhages?
Ana Pedrero Gil, Anesthesiologist at Igualada University Hospital, shared a post on LinkedIn:
“Is Coagulopathy with Fibrinolysis Present in All Obstetric Hemorrhages?
Hemorrhage does not automatically mean coagulopathy, nor does coagulopathy automatically mean fibrinolysis. The two processes are fundamentally distinct and often exist independently, and the data show the majority of postpartum hemorrhage happens with a fully intact and functional hemostatic process.
This distinction is critical for understanding where TXA fits into management — and where it does not. Greater than 70% of postpartum hemorrhage is mechanical in nature, caused by uterine atony, as described in a 2025 Lancet systematic review of 834,707 women.
In this review, genital tract trauma accounted for 17% of hemorrhages, while coagulopathy was the underlying cause of only 2.7%. Coagulopathy is a broad term that encompasses multiple distinct phenotypes.
Which patients with PPH have a biological phenotype most likely to benefit from TXA?
Viewed through a phenotypic framework, the limitations of indiscriminate TXA use become apparent. Importantly, the majority of postpartum hemorrhages, particularly uterine atony or genital tract lacerations, occur in the setting of intact hemostasis.
The appropriateness of TXA depends on the underlying hemostatic disturbance: its use is physiologically rational in plasmin-driven hyperfibrinolysis, less clearly beneficial in dilutional coagulopathy, and potentially inappropriate in thrombin-driven disseminated intravascular coagulation with fibrinolytic suppression.
TXA should therefore be conceptualized as a therapy directed at hyperfibrinolysis when present, rather than as a biologically equivalent intervention across all forms of postpartum hemorrhage.
Trauma and Obstetric Hemorrhage: Key Differences In trauma, systemic hyperfibrinolysis is a well-recognized driver of coagulopathy. In obstetric hemorrhage, clinically significant systemic hyperfibrinolysis (acute obstetric coagulopathy) is uncommon, occurring in approximately 1 per 1000 deliveries, and is largely confined to specific etiologies such as placental abruption and amniotic fluid embolism.
Notably, viscoelastic testing has limited sensitivity for detecting fibrinolytic activation in this setting, as studies have shown that even patients with biochemically confirmed hyperfibrinolysis may have normal ROTEM/TEG profiles.
TXA is valuable in the right patient, for the right indication, and within the right therapeutic window. The central challenge is recognizing that postpartum hemorrhage encompasses multiple hemostatic phenotypes, not all of which are equally responsive to antifibrinolytic therapy.
TXA is most biologically rational when excessive fibrinolysis contributes to bleeding, and less compelling when hemorrhage occurs in the setting of preserved coagulation function.”
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