Manage postpartum haemorrhage using current FIGO and SA evidence

In one line

Postpartum haemorrhage is the leading direct cause of avoidable maternal death in South Africa, and the work is not naming the four T's but running an early-triggered, time-critical, choreographed bundle — detect objectively, give tranexamic acid early, and escalate through a planned refractory ladder before the woman decompensates. This chapter assumes the Intermediate PPH groundwork (the four T's, active third-stage management, the opening drill) and concentrates on current evidence, controversy and critical-care escalation.

Assessment

The decisive diagnostic move is objective, early detection rather than visual estimation, which systematically under-reads loss by roughly half.

• Trigger thresholds (SA NDoH 2024, aligning with WHO/E-MOTIVE): diagnose and act at measured loss ≥500 mL, or clinical diagnosis — and in the E-MOTIVE trial the commonest real-world trigger was ≥300 mL plus at least one abnormal vital sign. Use a calibrated under-buttock drape; weigh swabs and linen (1 g ≈ 1 mL).
• Read the physiology, not the number. SA guidance flags HR >110, systolic BP <100, or shock index (HR÷SBP) >0.9 as warning signs — note SA uses >0.9, lower than the ≥1 commonly taught, because the antenatally anaemic, pre-eclamptic (Early-onset severe pre-eclampsia) or HIV-affected SA parturient decompensates with far less reserve.
• Work the four T's at the bedside (tone → trauma → tissue → thrombin) while resuscitating in parallel. A well-contracted uterus with ongoing bleeding redirects you to trauma or tissue.
• Investigations: FBC, coagulation screen with fibrinogen, U&E, crossmatch — and repeat during ongoing loss. A falling fibrinogen (broadly <2 g/L) is the strongest laboratory predictor of progression to severe PPH. Viscoelastic testing (ROTEM/TEG) guides factor replacement where available but is not assumed at district level.

Anaemia is now framed as a cause, not merely a vulnerability: WOMAN-2 and the SA guideline both foreground antenatal anaemia correction as primary prevention. Antenatal optimisation links to contraception and inter-pregnancy spacing in high-risk women (Contraception in high risk women).

The advanced assessment — physiology, scoring, and where the numbers mislead

The critical move is to read the trajectory of compensated shock before decompensation, because the pregnant cardiovascular system hides loss until it collapses suddenly. Two bedside heuristics do most of the work, and both have to be read with their limits in mind:

• The shock index (HR÷SBP). A normal pregnant value sits around 0.7–0.9. SA practice triggers at >0.9 rather than the ≥1.0 used in trauma, and the literature supports this lower bar: an SI ≥1.0 carries a positive likelihood ratio of roughly 3 for needing massive transfusion, but waiting for 1.0 in an already-anaemic woman cedes the early window. The single most useful property of SI is that it is better than either HR or SBP alone — it catches the woman whose pulse has climbed to 115 while her systolic is still a reassuring 105. Pair it with serum lactate where available (a lactate >4 mmol/L sharpens the prediction).
• The "rule of 30". A ~30% loss of blood volume is signalled by a fall of ~30 mmHg in systolic BP, a rise of ~30 bpm in pulse, a fall of ~30% in haematocrit/Hb, and a urine output <30 mL/h. The trap is the lag: in pregnancy, the ~40% plasma-volume expansion means a woman can lose 1000–1500 mL before any of these "30s" move, then crash. So the rule defines moderate–severe shock; it does not define early PPH. A normal BP in a bleeding woman is compensation, not safety.

Where these mislead the unwary:

• The young, fit parturient maintains a normal BP on intense vasoconstriction until ~30–40% loss is gone, then decompensates precipitously. Tachycardia and narrowed pulse pressure precede hypotension — do not be reassured by a "normal" systolic.
• The pre-eclamptic (Early-onset severe pre-eclampsia) is the inverse trap: she is intravascularly contracted, runs a "normal" or high BP that masks substantial loss, tolerates haemorrhage poorly, and on top of that is at high risk of iatrogenic pulmonary oedema if over-resuscitated. Her "normal" BP during PPH is doubly deceptive.
• The woman on a beta-blocker (e.g. labetalol) has a blunted tachycardic response — the SI is falsely reassuring. The same applies to high spinal/epidural block, which abolishes the compensatory tachycardia and can produce profound hypotension from a moderate bleed.
• Concealed loss breaks every haemodynamic rule: a broad-ligament or vaginal/vulval haematoma, a ruptured uterus (Uterine rupture), or atony hidden behind a packed cavity or a contracted lower segment can exsanguinate into spaces the eye never sees. Shock out of proportion to visible loss is the cardinal sign — re-examine, scan the abdomen, and consider the cavity and the broad ligament.

The other judgement call is subtype recognition at the bedside, because the four T's are not equiprobable and the dominant subtype dictates the management that follows.

Aetiology & subtypes — why the dominant "T" rewrites the plan

This assumes the four-T framework from Intermediate. Each T is best treated as a distinct disease with its own mechanism, its own tell, and its own decisive intervention — while recognising that the four overlap and evolve (atony causes coagulopathy through dilution and consumption; trauma drives atony reflexively; retained tissue prevents retraction).

• Tone (atony, ~70%) — failure of the living ligature. Mechanism: the myometrium fails to clamp the spiral arteries that perfuse the placental bed at term at ~700–800 mL/min. Tell: a soft, "boggy" uterus that firms on massage and re-relaxes. Drivers worth naming because they change prevention: over-distension (multiple pregnancy Multiple pregnancy, polyhydramnios, macrosomia), exhausted myometrium (prolonged or augmented labour, high-parity), chorioamnionitis, tocolytic/halogenated-anaesthetic exposure, and a full bladder. Decisive interventions: uterotonics → mechanical (tamponade) → surgical compression/devascularisation. This is the one subtype that the E-MOTIVE bundle is built to pre-empt.
• Trauma (~20%) — bleeding from a contracted uterus. Mechanism: lacerated genital tract (cervix, vagina, perineum), an extending caesarean angle, or uterine rupture/inversion (Uterine rupture). Tell: brisk bleeding despite a well-contracted fundus. This is the subtype most often missed because reflexive uterotonics do nothing — the management is examination and surgical/anatomical repair, not more oxytocin. A high vaginal/paravaginal haematoma can present as pain and shock with little external loss. Uterine inversion is its own emergency — immediate manual replacement before the ring contracts, with uterine relaxation if needed, and stop the uterotonics until it is back.
• Tissue (~10%) — retained products/placenta. Mechanism: retained cotyledon, succenturiate lobe, or membranes prevent retraction. The advanced end of this subtype is placenta accreta spectrum (PAS) — abnormally adherent/invasive placentation over a prior scar — which is not a labour-ward surprise to be managed reactively but a planned-delivery problem (see long-term section). Tell: incomplete placenta or persistent bleeding after delivery of the placenta; on PAS, a placenta that will not separate over a previous caesarean scar.
• Thrombin (~1% as a primary cause, but the great amplifier) — coagulopathy. Mechanism: dilutional and consumptive coagulopathy in massive PPH; placental abruption (antepartum haemorrhage) and amniotic-fluid embolism as primary consumptive/DIC triggers; pre-existing disease (von Willebrand, thrombocytopenia, anticoagulation); and the haemodilution of large-volume crystalloid. The distinguishing feature of obstetric coagulopathy is that fibrinogen falls first and fastest — a fibrinogen <2 g/L early predicts severe PPH, and abruption/AFE can drop it precipitously. The decisive move is early, fibrinogen-led replacement rather than waiting for a globally deranged clotting screen.

The decisive link is the mechanism → intervention mapping: a contracted uterus that keeps bleeding is not an atony problem and more oxytocin is the wrong answer; a soft uterus that will not respond to escalating uterotonics needs mechanical and surgical control, not a fifth drug; bleeding with a low fibrinogen and oozing from puncture sites is coagulopathy and needs the lab-led ladder. Identifying the dominant T, then choosing the next step from its mechanism, is the structure of the whole response.

Management

Resuscitation and treatment run simultaneously. The SA NDoH 2024 algorithm operationalises the WHO/FIGO bundle as E-MOTIVE: Early detection → Massage, Oxytocic, Tranexamic acid, IV fluids, Examination, Escalation. In October 2025 the WHO, with FIGO and the International Confederation of Midwives, drew the international recommendations into a single Consolidated Guideline on the Prevention, Diagnosis and Treatment of Postpartum Haemorrhage, the current global reference that this SA-operative approach aligns with.

Immediate (first minutes)