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 (pre-eclampsia-early-onset-severe) 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 (pre-eclampsia-early-onset-severe) 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.

Immediate (first minutes)

For atony refractory to oxytocin, SA second-line agents are ergometrine 0.5 mg (contraindicated in hypertension/pre-eclampsia — a critical SA pitfall given the disease burden, see hypertension-in-pregnancy-antihypertensives) and misoprostol 400–600 µg sublingually. Carbetocin (heat-stable) is a long-acting prevention option where the cold chain is unreliable — non-inferior to oxytocin for the ≥500 mL/added-uterotonic outcome in CHAMPION (RR 1.01), though non-inferiority was not met at the ≥1000 mL threshold.

The uterotonic ladder — named agents, exact doses, and how they differ

What matters is the mechanism, the dose, and the contraindication that makes each agent the right or wrong choice in a specific SA woman — not just the list. The agents differ by receptor and by the comorbidity that bans them:

• Oxytocin — synthetic nonapeptide acting on myometrial oxytocin receptors; rapid onset, short half-life, so it is given as a bolus plus an infusion. SA NDoH dose: 10 IU IV slow (not rapid undiluted bolus — that causes vasodilatation, hypotension and tachycardia), then 20 IU in 1 L Ringer's lactate at 125 mL/h. The receptor desensitises with prolonged labour exposure, which is why an oxytocin-augmented labour predicts atony and a poorer response.
• Ergometrine — ergot alkaloid; non-selective smooth-muscle constrictor producing a sustained tetanic contraction. Dose 0.5 mg IM (or slow IV). It is contraindicated in hypertension and pre-eclampsia — it raises systemic vascular resistance and can precipitate a hypertensive crisis or stroke. In the SA context, where hypertensive disease is a top maternal killer, reaching reflexively for ergometrine in a pre-eclamptic woman is a recognised fatal error. Also avoid in significant cardiac disease.
• Misoprostol — prostaglandin E1 analogue; 400–600 µg sublingually for treatment (SA). Heat-stable and needs no cold chain — its true value in a district setting. The trade-off is pyrexia and shivering (dose-related), which can confound the picture; it is slower in onset than IV oxytocin and is a second-line/adjunct, not a substitute for the oxytocin infusion.
• Carbetocin — long-acting oxytocin analogue; a single dose gives a sustained contraction. The heat-stable formulation is a prevention agent (CHAMPION), positioned for SA/LMIC settings where the oxytocin cold chain is unreliable — not a rescue drug for established atony.
• Carboprost (15-methyl PGF2α / "PGF2α") — prostaglandin F2α analogue, given by deep IM or intramyometrial injection, repeatable. It is a recognised next-line uterotonic internationally but is not a standard SA EML first- or second-line agent and is contraindicated in asthma (bronchospasm). Mention it as the international option; name oxytocin → ergometrine → misoprostol as the SA sequence.

The other named drug is tranexamic acid — an antifibrinolytic (lysine analogue blocking plasminogen binding to fibrin), 1 g IV over ~10 min, repeated once after 30 min if bleeding continues or restarts within 24 h. It is an adjunct that addresses the thrombin arm, not a uterotonic, and its evidence is for treatment, not anaemic prophylaxis (see evidence section).

Ongoing — the refractory ladder (SA NDoH 2024)

When uterotonics fail, escalate without dithering:

1. Bimanual compression and aortic compression as physical bridges.
2. Uterine balloon tamponade (UBT) — SA options span the improvised condom/glove-catheter balloon, the Bakri, and the locally made Ellavi balloon. The 2024 guideline newly contrasts UBT with suction tamponade (STUT) devices (e.g. JADA-type), which collapse the cavity rather than distend it — still being evaluated.
3. Non-pneumatic anti-shock garment (NASG) as a temporising first-aid measure to stabilise and buy time during transfer from district to surgical capacity — its place is referral logistics, not definitive control.
4. Laparotomy: uterine compression sutures (e.g. Hayman/B-Lynch), stepwise devascularisation, and peripartum hysterectomy — the definitive step, which must not be delayed once conservative measures have failed in an exsanguinating woman.

The refractory ladder in depth — judgement, sequence, and the decision to stop climbing

The governing skill is time discipline: each rung is a bridge with a stopwatch, and the commonest fatal error in the Saving Mothers enquiries is climbing too slowly. Set a mental clock — if a rung is not controlling loss within minutes, move up, and do not return to drugs once you are at mechanical/surgical control.

• Tamponade test. Inflate a balloon (Bakri/Ellavi/condom-catheter, typically 250–500 mL warmed saline). A positive test (bleeding stops) predicts that laparotomy is avoidable and buys time for resuscitation and transfer; a negative test (bleeding continues around or through the device) is itself the trigger to go to theatre — do not sit watching a failing balloon. Document the inflation volume and the per-vaginam loss after inflation. UBT works for atony and lower-segment/placental-bed bleeding; it does not fix a laceration or a coagulopathy, so a "failed balloon" should prompt you to re-ask which T.
• Suction tamponade (STUT/JADA-type) collapses the cavity with low-level vacuum and apposes the walls — mechanistically the opposite of a distending balloon. The PEARLE study reported high treatment success overall (lower after caesarean than vaginal birth). It is newer and not yet a guaranteed district resource in SA; the 2024 guideline contrasts it with UBT rather than replacing it. Know the concept (collapse vs distend) and that the evidence base is observational/single-arm, not a head-to-head RCT versus balloon.
• NASG is honestly framed in the trial evidence: the cluster-randomised data (Miller; Zambia/Zimbabwe) did not show a statistically significant mortality reduction when applied before transport, so its role is temporising during stabilisation and referral, not a definitive haemostatic device. Apply it to buy minutes while you arrange theatre or transfer a district patient to surgical capacity — and remove it in a controlled, segment-by-segment fashion once the woman is stable and bleeding is controlled.
• At laparotomy, the sequence is conservative-before-radical but with a hard ceiling: compression suture (B-Lynch/Hayman — and the suture must be combined with a uterus that responds to compression, so test bimanual compression first), then stepwise devascularisation (bilateral uterine artery ligation → utero-ovarian → internal iliac, the last being technically demanding and best left to those who can do it fast). Internal iliac ligation is not a manoeuvre to attempt for the first time on an exsanguinating woman if hysterectomy will be faster in your hands. Bleeding from a low placental-bed/PAS site is often not controlled by these uterine-preserving steps.
• The decision to stop climbing — peripartum hysterectomy. The governing principle from the SA enquiries: a slightly early hysterectomy saves a life; a late one loses it. The judgement call is to commit to hysterectomy before the woman is coagulopathic, acidotic and hypothermic (the lethal triad), not after — because operating on a woman already in DIC turns the hysterectomy itself into a source of uncontrollable bleeding. In PAS and in failed conservative control of atony, do not let attachment to fertility delay the definitive step in an exsanguinating woman. Subtotal hysterectomy is faster and adequate for fundal/corporeal atony; total hysterectomy is needed when the bleeding source is the lower segment/cervix (PAS, placenta praevia bed). Pelvic packing and damage-control closure with a planned relook is a legitimate last resort when coagulopathy makes definitive haemostasis impossible.

Massive transfusion & coagulopathy — the haematological arm

In ongoing major loss, activate the massive transfusion protocol early rather than chasing the lab. The key points:

• Empirical ratio while waiting for results. Until lab-guided, give a balanced ratio approximating 1:1:1 (red cells : FFP : platelets) — the principle borrowed from trauma resuscitation — but transition to targeted, fibrinogen-led replacement as soon as near-patient or lab numbers arrive, because obstetric coagulopathy is fibrinogen-dominant and over-transfusing plasma/platelets blindly has its own harms.
• Fibrinogen is the priority factor. It falls first and fastest in PPH; a level <2 g/L in active PPH is ominous and predicts progression. Where fibrinogen concentrate is unavailable (most SA settings), cryoprecipitate is the replacement — and SA guidance emphasises early fibrinogen in massive PPH specifically. But note the OBS2 caveat (below): replace when fibrinogen is genuinely low, not empirically in every bleeder.
• Correct the conditions clotting needs. Keep the woman warm (hypothermia is an enzymatic clotting failure), correct acidosis and ionised hypocalcaemia (citrate in stored blood chelates calcium — give calcium during massive transfusion), and avoid dilutional coagulopathy from large-volume crystalloid (cap crystalloid, move to blood early). This is the lethal triad — hypothermia, acidosis, coagulopathy — and preventing it is more important than any single product.
• Viscoelastic testing (ROTEM/TEG) lets you target the deficient component (a FIBTEM A5 indexes fibrinogen) and reduce blood-product waste where available — but it is not assumed at district level, where the answer is clinical massive-transfusion-protocol activation plus early cryoprecipitate.

Long-term

Anaemia correction, debrief, VTE risk reassessment after major transfusion, and counselling on recurrence risk and future delivery planning — especially in placenta accreta spectrum, where the next pregnancy is a planned-delivery problem, not a labour-ward surprise.

Long-term & postnatal care in depth — PAS, follow-up, recurrence, debrief

• Placenta accreta spectrum (PAS) — the planned-delivery problem. The FIGO 2019 clinical classification grades PAS by depth: Grade 1 (abnormally adherent — accreta, placenta on the myometrial surface without invasion), Grade 2 (increta — invasion into the myometrium), and Grade 3 (percreta — through the serosa: 3a serosa, 3b bladder, 3c other pelvic organs). The decisive point is that PAS in the next pregnancy is diagnosed antenatally (a praevia over a prior caesarean scar mandates a deliberate look for accreta on ultrasound, with MRI as an adjunct) and managed by a planned, scheduled, MDT caesarean–hysterectomy at a tertiary centre with blood, anaesthesia, urology/vascular and ICU on standby — not by attempting placental delivery on the labour ward. Forcibly delivering an accreta placenta is what turns a manageable elective procedure into an exsanguination. Leaving the placenta in situ (expectant/conservative management) is an option only in highly selected, counselled cases at equipped centres. The single biggest modifiable driver of PAS is the rising caesarean rate, which is why every caesarean indication is also a future-haemorrhage decision.
• After major PPH / massive transfusion. Reassess VTE risk — major PPH and transfusion are themselves risk factors, but balance against bleeding before starting pharmacological thromboprophylaxis; use mechanical prophylaxis until haemostasis is secure, then add LMWH. Correct iron deficiency aggressively (IV iron where oral is insufficient or not tolerated) — postpartum anaemia worsens fatigue, depression and the next pregnancy's risk. Screen for and manage Sheehan syndrome in any woman who had profound hypotensive shock (failure of lactation is the early clue; hypopituitarism may present later). Watch for acute kidney injury and renal recovery after a hypotensive insult.
• Recurrence and future-pregnancy planning. Prior PPH raises the risk in the next pregnancy; document the cause, the response, and the procedures done (a uterine compression suture or a balloon used last time changes the next plan). Counsel on inter-pregnancy spacing and contraception (contraception-in-high-risk-women) — and remember that a prior caesarean for PPH compounds future PAS/praevia risk.
• The debrief is part of the medicine. Offer a structured debrief: women who survive a major PPH and a peripartum hysterectomy are at risk of post-traumatic stress and grief over lost fertility; explain what happened in plain language, what it means for future pregnancies, and arrange psychological support. A near-miss is a sentinel event — feed it into the facility's morbidity-and-mortality / maternal near-miss review so the system learns (this is the NCCEMD logic operating at unit level).

The evidence & the controversy

Tranexamic acid — settled for treatment, nuanced for prevention. The WOMAN trial (n=20,060) reduced death due to bleeding (1.5% vs 1.9%; RR 0.81, 95% CI 0.65–1.00, p=0.045), with a stronger signal when given within 3 hours (RR 0.69, 95% CI 0.52–0.91, p=0.008) and no benefit thereafter — but it did not reduce the composite of all-cause death or hysterectomy (RR 0.97), and hysterectomy itself was unchanged (RR 1.02). The point is that TXA reduces bleeding deaths if given early, not the decision to operate. The 2024 IPD meta-analysis (5 trials, 54,404 women) found TXA cut life-threatening bleeding by ~23% (OR 0.77, 95% CI 0.63–0.93), consistent across vaginal/caesarean birth and across anaemic/non-anaemic women, with no clear excess of thromboembolism (OR 0.96) — though it could not exclude a modest increase. Crucially, WOMAN-2 (n=15,068, anaemic women) found prophylactic TXA at cord clamping did not prevent PPH (RR 1.05). So: TXA is for treating clinically diagnosed PPH, not as routine prophylaxis in the anaemic — fix the anaemia instead.

The WOMAN ARR, and why "early" is the whole game (worked NNT). The absolute reduction in death-due-to-bleeding was 1.9% → 1.5% = 0.4%, i.e. an ARR of 0.004. The number needed to treat is therefore NNT = 1/0.004 = 250 across the whole trial population. That looks unimpressive until you remember the time interaction: the benefit was concentrated in the <3-hour window and absent after it. So the defensible appraisal is not "TXA saves few" but "TXA saves when given early, and the trial's modest overall ARR is diluted by women treated late" — which is exactly why the SA/WHO instruction is give it as early as possible, not at some arbitrary blood-loss threshold. The other appraisal point: TXA reduced bleeding deaths but not hysterectomy and not all-cause mortality — it buys survival from the bleed, it does not change the surgical decision tree.

E-MOTIVE — the bundle that changed the algorithm. The cluster-randomised E-MOTIVE trial (Kenya, Nigeria, SA, Tanzania) cut the composite of severe PPH, laparotomy for bleeding or death from bleeding by 60% (1.6% vs 4.3%; RR 0.40, 95% CI 0.32–0.50). The mechanism is mostly earlier detection via calibrated drape plus delivering all bundle elements together rather than sequentially. SA was a trial site, and SA implementation work flags the real barrier as the health-system layer — drug/equipment availability and task-sharing — not the clinical content. The appraisal nuance: the dramatic effect size is partly a detection effect (PPH was detected in 93% vs 51%) — the bundle finds and treats the loss the old practice missed — and a cluster-trial caveat (randomisation was at facility level, so secular trends and contamination are the standard threats to validity). The take-home is that the win came from system redesign, which is why SA implementation hinges on logistics, not on teaching obstetricians a new drug.

Fibrinogen replacement — guided, not empiric. The OBS2 RCT showed that infusing fibrinogen concentrate triggered by FIBTEM A5 ≤15 mm did not improve outcomes in unselected PPH — because most bleeding women still have normal fibrinogen early. The defensible position: targeted replacement once fibrinogen is genuinely low (broadly <2 g/L) is rational, but empiric fibrinogen in every PPH is not evidence-based. SA guidance now emphasises near-patient coagulation testing and early fibrinogen in massive PPH — cryoprecipitate where concentrate is unavailable. The apparent tension with "give fibrinogen early in massive PPH" resolves on selection: OBS2 studied unselected bleeders (most of whom had normal fibrinogen), whereas the early-cryoprecipitate advice applies to massive, abruption/AFE-driven PPH where fibrinogen is already crashing. The unifying rule is replace to a measured deficit, do not replace reflexively.

The SA-specific evidence the international texts under-weight. The Saving Mothers / NCCEMD enquiries identify obstetric haemorrhage as a leading cause of avoidable maternal death, and within it, "bleeding during and after caesarean section" has become the largest sub-category — a pattern driven by the rising caesarean rate and by delays in recognising and re-operating on intra-abdominal/lower-segment bleeding. This reframes prevention for SA practice: meticulous caesarean haemostasis, a low threshold for second-look laparotomy, and treating every caesarean as a future-PAS decision matter as much as the labour-ward uterotonic ladder. The intervention pattern in SA near-miss series (second-look laparotomy, hysterectomy, B-Lynch, ICU) tells you where the system actually saves these women.

Landmark trials & key evidence

These are the studies to cite by name, with the numbers. Treatment evidence (WOMAN, E-MOTIVE, the IPD meta-analysis, OBS2) is strong; prevention evidence (WOMAN-2, CHAMPION) reframes what not to do routinely.

Worked viva — how to structure the answer

Examiners give a stem like "a 32-year-old, para 3, vaginal birth 20 minutes ago, estimated 400 mL on the drape but pulse 118, BP 104/68, the uterus feels soft." A high-scoring answer runs:

1. Frame it — "This is primary PPH from atony — a soft uterus with a shock index of ~1.1, so I am already worried about more loss than the 400 mL suggests; the abnormal vitals plus measured loss are themselves the trigger to act."
2. Resuscitate and treat in parallel, declaring the emergency — "I call for help and declare a major obstetric haemorrhage, two large-bore cannulae with FBC/clotting/fibrinogen/crossmatch, tranexamic acid 1 g IV now, uterine massage, oxytocin 10 IU IV slow then 20 IU in 1 L Ringer's at 125 mL/h, empty the bladder, warmed fluids and early blood, and I keep her warm."
3. Work the four T's out loud — "Tone is my leading diagnosis, but I examine for trauma (a contracted uterus that keeps bleeding sends me to look for a tear), check the placenta is complete (tissue), and watch for oozing/low fibrinogen (thrombin)."
4. Escalate the right subtype — "If atony is refractory to uterotonics I go up the ladder without delay: bimanual and aortic compression, a balloon tamponade test, and if that fails, theatre for compression sutures and stepwise devascularisation, committing to hysterectomy before she becomes coagulopathic. In a pre-eclamptic woman I would not give ergometrine."
5. Justify from evidence — "I give TXA early because WOMAN shows the benefit is in the first 3 hours; I run the E-MOTIVE bundle elements together rather than sequentially; I replace fibrinogen to a measured deficit (OBS2), using cryoprecipitate as concentrate is rarely available here."
6. Bring in the SA system — "If I am at a district hospital without surgical/blood capacity, I stabilise — uterotonics, TXA, NASG to buy time — and transfer with an escort continuing the regimen; the Saving Mothers lesson is that delay kills."
7. Close the loop — anaemia correction, VTE reassessment, debrief, and — if PAS or recurrent PPH — a planned tertiary delivery next time, plus contraception and spacing.

Exam traps & red flags

• Giving ergometrine in a hypertensive/pre-eclamptic woman — a high-frequency SA failure; it can precipitate a hypertensive crisis.
• Reaching for a fifth uterotonic when the uterus is well-contracted — a firm fundus that keeps bleeding is trauma or tissue, not atony; examine the genital tract and check the placenta rather than escalating drugs.
• Waiting for 500 mL or for the BP to fall. A rising pulse and a shock index >0.9 precede hypotension; treat the trajectory. Remember the "rule of 30" lag — a normal BP is compensation, not safety.
• Being reassured by a normal BP on a beta-blocker or in a pre-eclamptic — the tachycardic response is blunted and the intravascular volume is already contracted; both mask the true loss.
• Watching a failing balloon. A negative tamponade test (bleeding around/through the device) is itself the trigger for theatre — do not sit and observe.
• Empiric fibrinogen/FFP "because she's bleeding" — OBS2 says guide it; early empiric factor replacement in an unselected woman is the wrong answer that looks thorough. But in massive abruption/AFE-driven PPH, fibrinogen is already crashing — replace early there.
• Routine prophylactic TXA in anaemic women — WOMAN-2 negative; correct anaemia antenatally instead.
• Delaying hysterectomy in placenta accreta spectrum or a failed conservative ladder — a slightly early hysterectomy saves a life; a late one loses it. Operating once she is in the lethal triad (hypothermia, acidosis, coagulopathy) makes the hysterectomy itself a bleeding source.
• Managing an accreta reactively on the labour ward — PAS is an antenatal diagnosis and a planned tertiary caesarean-hysterectomy; forcibly delivering the placenta causes the exsanguination.
• Missing concealed loss — broad-ligament/vaginal haematoma, uterine rupture, or atony hidden by a packed cavity; shock out of proportion to visible loss is the tell.
• Forgetting the caesarean. In SA, "bleeding during and after caesarean section" is the largest haemorrhage sub-cause — keep a low threshold for second-look laparotomy.
• Visual estimation as your only quantification — it under-reads by ~50%; weigh and use a calibrated drape.

Evidence anchors

• WHO recommendations on assessment of postpartum blood loss and a treatment bundle for PPH (2023)
• E-MOTIVE trial — Early detection and treatment of PPH, NEJM 2023
• FIGO recommendations on the management of PPH, 2022 (Escobar et al.)
• FIGO classification for the clinical diagnosis of placenta accreta spectrum disorders, IJGO 2019 (Jauniaux et al.)
• WOMAN trial — early tranexamic acid in PPH, Lancet 2017
• WOMAN-2 trial — TXA in women with moderate/severe anaemia, Lancet 2024
• Tranexamic acid for postpartum bleeding — IPD meta-analysis, Lancet 2024
• OBS2 — viscoelastometric-guided fibrinogen concentrate in PPH, BJA 2017
• CHAMPION — heat-stable carbetocin vs oxytocin to prevent PPH after vaginal birth, NEJM 2018
• PEARLE — intrauterine vacuum-induced haemorrhage-control (JADA) device for PPH, Obstet Gynecol 2020
• NASG cluster-randomised trial — first-aid device for obstetric haemorrhage, PLoS One 2013 (Miller et al.)
• CRASH-2 — early tranexamic acid in bleeding trauma (the precedent to WOMAN), Lancet 2010 (Shakur et al.)
• SA NDoH Guidelines for Maternity Care in South Africa — PPH update, March 2024 (Fawcus; doses: oxytocin 10 IU IV + 20 IU in 1 L Ringer's at 125 mL/h; TXA 1 g IV; ergometrine 0.5 mg; misoprostol 400–600 µg SL; UBT/STUT; NASG)
• FIGO Safe Motherhood Committee — non-pneumatic anti-shock garment as a temporising measure (IJGO, 2015)
• NCCEMD Saving Mothers reports — obstetric haemorrhage among the leading causes of avoidable maternal death in South Africa; "bleeding during and after caesarean section" the largest haemorrhage sub-cause