Evaluate and manage a patient presenting with postpartum haemorrhage (PPH)

Clinical overview

Postpartum haemorrhage is the single largest direct cause of maternal death in South Africa and worldwide, and the most reliably preventable one. The Saving Mothers reports (NCCEMD) have consistently ranked obstetric haemorrhage among the top contributors to maternal mortality in South Africa, alongside hypertension and non-pregnancy-related infections (predominantly HIV-associated). Critically, a large proportion of haemorrhage deaths are judged avoidable — the woman bled, the response was late, disorganised, or under-resourced, and she died of something we know exactly how to stop. Your job as a registrar is to convert that knowledge into a fast, choreographed, escalating response, every single time.

The classic definition is blood loss ≥500 mL after vaginal birth or ≥1000 mL after caesarean, with severe (or major) PPH usually taken as ≥1000 mL or any loss causing haemodynamic compromise. The 2025 WHO/FIGO/ICM consolidated guideline shifts the trigger earlier: diagnose and act on measured blood loss ≥300 mL with abnormal haemodynamics (pulse >100, shock index >1, systolic BP <100 or diastolic BP <60 mmHg), OR ≥500 mL — whichever comes first, with the greatest vigilance in the first 2 hours. The point is to stop waiting for the old 500 mL mark. These thresholds are clinically useful but treacherous: visual estimation systematically under-reads blood loss, a healthy young woman compensates until she suddenly does not, and the antenatally anaemic patient — extremely common in South African practice — tolerates far less. Treat the trajectory and the physiology, not a number on a swab. PPH is timed: primary PPH occurs within 24 hours of birth (overwhelmingly atonic), secondary PPH from 24 hours to 6 (or 12) weeks (usually retained products or endometritis). This chapter is weighted to the verb — evaluate and manage — so the emphasis is on a structured assessment and a relentless, escalating drill. Closely linked are Antepartum haemorrhage, Uterine rupture, Shock management and Resuscitation in pregnancy.

Core knowledge

The four T's — causes by frequency

Almost all PPH fits one (or more) of four mechanisms. Memorise them in order of frequency because that order drives your initial actions.

Tone dominates. The contracted myometrium mechanically occludes the spiral arteries supplying the placental bed — the "living ligatures." Anything that prevents sustained contraction causes atony: an over-distended uterus (multiple pregnancy, polyhydramnios, macrosomia — see Macrosomia and Multiple pregnancy), prolonged or augmented labour with an exhausted myometrium, chorioamnionitis, tocolytics, retained tissue, high parity, and uterine fibroids (Fibroids).

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Figure J12.1 — The 4 T bedside source finder for primary postpartum haemorrhage, linking clues to first-line targets while resuscitation runs.

Risk factors and why they matter

Antenatal and intrapartum risk factors should raise your guard and your preparation — IV access, group-and-save, delivery in an appropriate level of care — but they do not predict the individual: a majority of PPH occurs in women with no identified risk factor, which is exactly why active management of the third stage of labour is given to everyone. Key flags include previous PPH, previous caesarean (placenta praevia/accreta risk — Antepartum haemorrhage), grand multiparity, anaemia, prolonged third stage, instrumental delivery (Instrumental delivery), and pre-eclampsia/HELLP (Pre eclampsia and HELLP, which also brings thrombocytopenia and impaired coagulation).

Placenta accreta spectrum

In a woman with placenta praevia overlying a previous caesarean scar, suspect placenta accreta spectrum (PAS) — abnormally adherent or invasive placentation. With rising caesarean rates in South Africa this is an increasing cause of catastrophic, often torrential, PPH and peripartum hysterectomy. Where antenatal imaging raises the suspicion, the woman should be delivered in a setting with blood-bank, anaesthetic and surgical capacity — a planning problem, not a labour-ward surprise.

Physiology of compensation

At term, uterine blood flow approaches ~500–700 mL/min, so atony empties a circulation fast. A healthy parturient maintains blood pressure by vasoconstriction and tachycardia until roughly 30–40% of blood volume is lost, then decompensates abruptly. The anaemic, pre-eclamptic, or septic woman has far less reserve. Hypothermia, acidosis and coagulopathy form the "lethal triad" that perpetuates bleeding once massive haemorrhage is established — which is why early, warmed, balanced resuscitation and early tranexamic acid matter so much.