Abstract

Background: Post-partum haemorrhage (PPH) remains the leading cause of maternal mortality worldwide, yet the pathophysiological processes that transform normal Post-partum bleeding into a lifethreatening coagulopathic state are incompletely understood. This review integrates biochemical and biophysical perspectives on PPHrelated mortality, focusing on molecular coagulopathy, uterine biomechanics, and hemodynamic collapse. Methods: We conducted a narrative synthesis of peerreviewed literature from PubMed, Scopus, and WHO databases (2015–2025), emphasizing mechanistic studies, clinical trials, and global burden data. Key outcomes included prevalence of PPH, coagulopathy biomarkers, hemodynamic parameters, and mortality reduction strategies. Results: Globally, PPH affects 9.97% of deliveries (95% CI: 6.90–13.04%), with severe PPH in 4.52% (95% CI: 2.47–6.57%). Biochemically, acute obstetric coagulopathy (AOC) is driven by dysregulated plasmin generation causing hyperfibrinolysis, leading to fibrinogen and factor V cleavage. Biophysical mechanisms center on uterine atony responsible for 70–80% of PPH where failure of myometrial contraction prevents mechanical compression of spiral arteries. Hemodynamic derangements include a 36fold increase in Ddimer and rapid depletion of factor XIII. Tranexamic acid, administered within three hours, reduces bleedingrelated mortality by onethird. Conclusions: PPH mortality is a consequence of interacting biochemical coagulopathy and biophysical uterine failure. Early detection using objective blood loss measurement and prompt implementation of the MOTIVE bundle (massage, oxytocin, tranexamic acid, intravenous fluids, vaginal examination, escalation) are critical. Future research should focus on pointofcare viscoelastic testing and genotypeguided prophylaxis.

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