Antepartum Haemorrhage

Overview & Definition

Antepartum haemorrhage (APH) is defined by RCOG Green-top Guideline No. 63 as bleeding from or into the genital tract from 24+0 weeks of pregnancy and prior to the birth of the baby.^[21] Bleeding before this gestation is classified as a threatened or inevitable miscarriage, which has a different cause, prognosis, and management pathway. Some textbooks and historical systems use a 20- or 28-week cut-off, so the exact threshold should be stated in any exam answer; 24+0 weeks is the RCOG operational definition.^[21]

APH matters because it complicates 3 to 5% of pregnancies and is a leading cause of perinatal and maternal mortality worldwide.^[21] Two placental causes — placental abruption and vasa praevia — can kill the fetus within minutes and the mother within hours. The clinical skill it tests is triage: every woman who bleeds in the third trimester must be assumed to have a praevia until ultrasound proves otherwise, must be resuscitated in parallel with assessment, and must be delivered when there is maternal or fetal compromise.^[1]

The praevia-versus-abruption clinical contrast — painless vs painful, bright vs dark, relaxed vs woody uterus, mother vs fetus compromised — is one of the highest-yield discriminator pairs in all of obstetrics, and examiners return to it in MCQ, SAQ, viva, and OSCE alike. Around it sits a smaller, equally examinable third player, vasa praevia, plus the surgical emergencies uterine rupture and placenta accreta spectrum, and the broader non-placental causes that must be excluded by a speculum examination once praevia is ruled out.^[2]

Classification

APH is classified in two complementary ways — by cause and by severity. ^[1]

By cause (the examiner's framework): ^[1]

By severity (drives the resuscitate-vs-expectant decision): ^[1]

^[21]

Placenta praevia itself is graded twice over. The traditional 4-grade system (Macafee–Johnson, based on the relationship of the placenta to the internal os) is still asked in vivas: Grade I low-lying (placenta in lower segment but not reaching the os); Grade II marginal (placenta reaches the edge of the os but does not cover it); Grade III partial (placenta covers the internal os asymmetrically); Grade IV complete (placenta covers the os symmetrically, central). The modern two-category system used in clinical practice collapses these into minor praevia (placental edge more than 2 cm from the internal os) and major praevia (placental edge covering or within 2 cm of the os). In Bhide's transvaginal-ultrasound cohort the caesarean rate was 90% when the edge lay 0.1 to 2.0 cm from the os but fell to 37% beyond 2 cm, and Vergani found over two-thirds of women with an edge beyond 10 mm deliver vaginally without excess haemorrhage — hence the 2 cm working rule.^[7][8]

Enlarge

Epidemiology & Risk Factors

APH complicates about 3 to 5% of pregnancies and is a leading cause of perinatal and maternal mortality worldwide.^[21] RCOG notes that placenta praevia and placental abruption are the most important causes, not the most common; unexplained APH is frequent after local and placental causes are excluded.^[21]

Risk factors for placenta praevia: previous caesarean section (dose-response with the number of scars, which also drives accreta), multiparity, advanced maternal age (over 35), multiple gestation, IVF/intracytoplasmic sperm injection, smoking, prior uterine surgery (myomectomy, curettage), and a previously affected pregnancy.^[3]

Risk factors for placental abruption were quantified in the Chen 2025 systematic review and meta-analysis of 54 observational studies:^[2] the strongest pregnancy-complication association was placenta previa (AOR 7.31, 95% CI 4.78–11.19) and the strongest maternal-baseline association was previous placental abruption (AOR 2.72, 95% CI 2.16–3.42). Other independent factors in that review include maternal age ≥35 years, smoking, alcohol, marijuana, multiple pregnancy, parity ≥3, anaemia (Hb <11 g/dL), previous caesarean, previous miscarriage or stillbirth, assisted reproduction, preterm PROM, pre-eclampsia, small-for-gestational-age, polyhydramnios, and gestational hypertension.^[2] Green-top 63 additionally lists abdominal trauma (accidental or domestic violence) and cocaine or amphetamine misuse.^[21]

Risk factors for vasa praevia: velamentous cord insertion (62% of cases in the Australian cohort) and a low-lying placenta (60%) dominate, with bilobed or succenturiate-lobed placenta, marginal cord insertion and IVF pregnancy the other classic associations — 95% of affected women had at least one of these risk factors.^[5][10]

Pathophysiology

The three placental causes of APH have distinct mechanisms, and examiners reward the candidate who can explain why each produces its characteristic clinical picture. ^[1]

Enlarge

Placenta praevia. In the third trimester the lower uterine segment progressively forms, lengthens, and thins, and the cervix effaces and begins to dilate. The placenta is inelastic and cannot stretch with this thinning tissue, so the placental edge shears away from the underlying decidua. The torn decidual sinus vessels bleed — and because the blood has a short, direct path through the cervix and vagina, it is fresh, bright-red, and painless. The lower segment is poorly contractile, so it cannot compress the bleeding vessels (unlike the fundus postpartum), which is why praevia bleeding tends to be recurrent and to escalate.^[3] Because the praevia mass sits low in the pelvis, the presenting part cannot engage, producing the classic unstable, transverse, or breech lie that is the bedside clue.

Placental abruption. The initiating event is a rupture of a maternal decidual spiral artery, producing a haematoma at the decidua–placental interface. As the retroplacental clot expands, it progressively strips the placenta off the uterine wall, shearing further vessels and destroying placental tissue. The patient perceives this as a sudden, constant, severe pain; the uterus is irritated into hypertonus and is tender and tense, woody-hard on palpation. The blood may track down and escape through the cervix (revealed abruption, the more common form) or be retained behind the placenta (concealed abruption). Concealed abruption is the more dangerous form: the separation is more extensive, the myometrium becomes infiltrated with extravasated blood producing the purplish, copper-bruised Couvelaire uterus (uteroplacental apoplexy), and the patient may go into shock disproportionate to the visible blood loss.^[2] Couvelaire uterus is contracted but atonic — after delivery it fails to retract and is a cause of postpartum haemorrhage.

Disseminated intravascular coagulation in abruption. Abruption is one of the leading obstetric triggers of disseminated intravascular coagulation (DIC): the disrupted placenta and decidua release thromboplastin-rich tissue factor into the maternal circulation, igniting systemic coagulation. Platelets, fibrinogen and clotting factors are consumed faster than the liver and bone marrow can replace them, and secondary fibrinolysis is activated — a consumptive coagulopathy that converts a surgical bleed into a haematological one. The classic laboratory picture is prolonged PT and APTT, thrombocytopenia, low fibrinogen and raised D-dimer. A pregnancy-specific DIC score built on fibrinogen concentration, the PT difference, and platelet count has 88% sensitivity and 96% specificity at a cut-off of ≥26 points.^[11] Treatment is two-pronged: deliver — emptying the uterus removes the trigger — and correct the haemostatic problem, which can be guided by point-of-care testing adjusted for pregnancy.^[11] Green-top 63’s massive-haemorrhage appendix (from Green-top 52) gives cryoprecipitate if fibrinogen is <1 g/L.^[21] A single POC case report of massive obstetric bleeding after abruption titrated replacement to keep fibrinogen above 200 mg/dL; that is case-level practice, not a Green-top 63 target.^[12]

Vasa praevia. In velamentous cord insertion or with a bilobed/succenturiate-lobed placenta, some fetal vessels run unprotected through the chorionic membranes (no Wharton's jelly) on their way between cord and placenta. When these vessels traverse the membranes over the internal cervical os, they are termed vasa praevia. They are fetal vessels, carrying fetal (not maternal) blood at fetal blood pressure, so the catastrophic event is rupture of the membranes — spontaneous or artificial — which tears the vessels and the fetus bleeds directly into the amniotic fluid and vagina. Because the fetal circulating volume is small, even modest loss is a major haemorrhage for the fetus: rupture typically produces a sudden fetal heart rate abnormality (sinusoidal pattern, then bradycardia) at the very moment the membranes rupture, while the mother stays haemodynamically normal because no maternal blood has been lost. Population data confirm the stakes — in the Australian cohort, all 58 prenatally diagnosed cases were delivered by caesarean with no perinatal deaths, whereas of the five cases diagnosed only at birth there were two perinatal deaths (case fatality 40%).^[5]

Placenta accreta spectrum. Normally the decidua basalis forms a plane of cleavage (Nitabuch's layer) that allows the placenta to separate cleanly at the third stage. When the decidua is deficient — most often beneath a previous caesarean scar where a low anterior placenta has implanted — the chorionic villi invade directly into the myometrium without that cleavage plane. Invasion limited to the inner myometrium is placenta accreta, deeper into the myometrium is placenta increta, and penetration through the serosa to the bladder or broad ligament is placenta percreta. At attempted placental separation the placenta fails to come away, and catastrophic haemorrhage ensues from the uncontrolled open maternal sinus bed.^[4]

Uterine rupture. A full-thickness disruption of the uterine wall — almost always through a previous classical or lower-segment scar, but occasionally de novo after trauma, oxytocin hyperstimulation, or grand multiparity. The fetus and placenta may extrude into the peritoneal cavity, the presenting part recoils (loss of station), contractions characteristically cease as the uterine muscle retracts, and the mother develops haemoperitoneum and shock with referred shoulder-tip pain from diaphragmatic irritation. ^[1]

Clinical Presentation

The clinical presentation is defined by the underlying cause, and the praevia-vs-abruption-vs-vasa praevia contrast is the spine of the assessment. ^[1]

^[1]

Placenta praevia presents with painless, causeless, bright-red, recurrent vaginal bleeding. The bleeding is fresh because the blood has a short transit; it stops spontaneously (the clot tamponades the venous oozing) and then recurs, often more heavily each time. The uterus is soft, relaxed, and non-tender; the lie is often transverse or oblique and the head fails to engage because the praevia sits in the way; fetal heart tones are normal unless there has been major maternal exsanguination. A warning bleed is the small first episode; a major bleed follows days to weeks later.^[3]

Placental abruption presents with the sudden onset of constant, severe abdominal or low back pain (described as a tearing or crushing pain that does not radiate in waves like a contraction). The uterus is tender, tense, and woody-hard with poorly relaxing hypertonus between contractions; the fundus may be high if there is concealed blood or a retroplacental clot. Vaginal bleeding, when present, is dark red (it has been in contact with the clot and is partially defibrinated). Fetal distress (recurrent late or variable decelerations, bradycardia) or intrauterine death is common. Maternal shock is disproportionate to the visible blood loss in concealed abruption — Green-top 63 notes that bleeding from the introitus may not represent the total blood lost (for example in a concealed placental abruption) and to assess for signs of clinical shock.^[21]

Atypical presentations of abruption are deliberately tested: a concealed abruption with no visible bleeding that presents as preterm labour or unexplained fetal distress; a constant backache that the patient (and the candidate) mistakes for musculoskeletal pain; a patient who does not yet look shocked despite extensive placental separation; or rupture of membranes with blood-stained liquor. Abruption is fundamentally a clinical diagnosis — ultrasound is poor at seeing a fresh retroplacental clot, and a normal ultrasound does not exclude it.^[2]

Vasa praevia presents at the moment of membrane rupture (spontaneous or artificial amniotomy) with painless vaginal bleeding of fresh or dark blood mixed with amniotic fluid, accompanied by rapid onset fetal heart rate abnormalities — classically a sinusoidal pattern (reflecting fetal anaemia and hypoxia) or sudden bradycardia. The mother is haemodynamically normal because only fetal blood has been lost — this is the cardinal clue.^[5]

Uterine rupture presents as sudden, severe, tearing abdominal pain during labour (or rarely antenatally after trauma), cessation of previously painful contractions (the uterus has retracted away from the defect), loss of the presenting part (the head that was engaged recoils), fetal bradycardia, vaginal bleeding, and maternal shock with shoulder-tip pain from haemoperitoneum. A rupture may also present more insidiously as scar tenderness, persistent tachycardia, or non-reassuring CTG in a woman labouring after a previous caesarean.^[1]

Local (non-placental) causes present with lighter bleeding, often post-coital or after a vaginal examination, and a normal fetus and uterus. Cervical ectropion (common in pregnancy and with the pill), cervical polyp, cervicitis, vulval varicosities, or — importantly — cervical cancer must be considered. Even when a local cause is suspected, praevia must be excluded by ultrasound before any speculum or digital examination, and any visible cervical lesion must be referred for biopsy. ^[1]

A 'show' (the blood-tinged mucus plug expelled at the onset of labour) is mucus mixed with a small amount of blood and is not a true APH — but a candidate must be able to distinguish it, and any heavier bleeding in labour must be managed as possible praevia or abruption until proven otherwise. ^[1]

Differential Diagnosis

The differential of APH is the list of causes above, and the task is to distinguish them rather than enumerate them. ^[1]

The can't-miss mimic is vasa praevia masquerading as a normal third-trimester bleed — missing a prenatal diagnosis converts pooled perinatal survival from 98.6% to 72.1% (25-fold higher odds of perinatal death; hypoxic morbidity 50-fold higher). The classic examiner's trap is attributing fetal distress in an abruption to "prematurity" and delaying delivery: the perinatal mortality of abruption is dominated by delay, not by the bleed itself.^[10]

Clinical & Bedside Assessment

The focused assessment of APH runs in parallel with resuscitation (the two do not happen in sequence). The history establishes onset, volume (in sanitary pads or clots), colour, pain, relation to ROM, fetal movements, trauma, drug use (cocaine, anticoagulants), obstetric history (gestational age, parity, previous scars, previous abruption or praevia), and risk factors. ^[1]

Abdominal examination is the bedside discriminator: ^[1]

^[1]

A speculum examination can identify cervical dilatation or a lower genital tract cause (Green-top 63). It is used after ultrasound has excluded praevia — never digital until then.^[21]

Assess shock clinically. Green-top 63 emphasises that visible loss often underestimates total loss (especially concealed abruption) and that the presence of fetal or maternal shock defines massive haemorrhage even before volume is known.^[21] Tachycardia, cool peripheries, and a falling urine output are treated as hypovolaemia; do not wait for a low haemoglobin.^[21]

Named signs and manoeuvres. The woody-hard uterus of concealed abruption feels like a board — the fundus is tender, the uterus does not relax between Braxton-Hicks, and the patient winces on light palpation. A high fundus for dates suggests concealed blood or a retroplacental clot. Loss of station of the presenting part during labour signals uterine rupture. The Apt test (see Investigations) is the bedside laboratory test that confirms fetal blood in suspected vasa praevia. ^[1]

Investigations

Investigations in APH serve four purposes: to localise the placenta (praevia), to identify vasa praevia, to support (not exclude) abruption, to diagnose accreta antenatally, and to prepare for delivery and transfusion. ^[1]

Bloods (every APH): ^[1]

• Full blood count — haemoglobin, haematocrit, platelets (thrombocytopenia in DIC); note that Hb at presentation underestimates the loss because haemodilution takes hours.
• Group and save for minor APH; cross-match blood according to the severity of bleeding for major APH; activate the massive haemorrhage protocol if shock.
• Coagulation screen — PT, APTT, fibrinogen and D-dimer: these are the core of the pregnancy-specific DIC work-up. Green-top 63’s appendix gives cryoprecipitate if fibrinogen is <1 g/L; do not treat a “normal” non-pregnant fibrinogen as reassuring in late pregnancy without obstetric context.^[21][11]
• Urea and electrolytes, liver function tests — baseline and to detect pre-eclampsia/HELLP as a comorbidity.
• Blood gas — base deficit and lactate quantify shock severity.
• Kleihauer-Betke test or flow cytometry — to size the fetomaternal haemorrhage in RhD-negative mothers (to adjust anti-D dosing) and after maternal trauma. ^{[19] [1]}

Ultrasound — localise the placenta. The single most important diagnostic step. Transabdominal ultrasound is performed first; if the placenta is low or the view is unclear, transvaginal ultrasound (TVS) is performed — it is safe in praevia (it does not provoke bleeding) and is more accurate because the internal os is seen directly. The placental edge is measured relative to the internal os: major praevia if the placenta covers or lies within 2 cm; minor praevia if it is more than 2 cm from the os (and vaginal delivery is usually feasible).^[3] A praevia diagnosed at the 20-week anomaly scan commonly resolves (the lower segment forms and the placenta appears to 'migrate' away from the os), so the diagnosis is confirmed by a repeat third-trimester scan if the placenta remains low (timing per Green-top 27a / unit protocol).

Ultrasound — vasa praevia. Transvaginal ultrasound with colour and pulsed-wave Doppler is the diagnostic test: it demonstrates fetal vessels crossing the internal os, with the characteristic arterial waveform matching the fetal heart rate. Whether to screen universally remains debated, but targeted screening of high-risk women (velamentous cord insertion, low-lying placenta, bilobed or succenturiate placenta, IVF pregnancy — at least one risk factor was present in 95% of Australian cases) is the established practice, and the payoff is large: pooled perinatal survival is 98.6% with a prenatal diagnosis versus 72.1% without, with a 25-fold higher odds of perinatal death when the diagnosis is missed.^[5][10]

Apt test (Singer test). A bedside chemical test on vaginal blood that distinguishes fetal from maternal blood. The blood is mixed with sodium hydroxide (an alkali): adult haemoglobin denatures and turns brown/pinkish-brown, whereas fetal haemoglobin (which resists alkali denaturation) stays pink. A pink result = fetal blood = vasa praevia until proven otherwise. Modern alternatives include the Kleihauer-Betke test and flow cytometry on the vaginal blood. ^[1]

Ultrasound and MRI — placenta accreta spectrum. Ultrasound features of accreta include: loss of the normal retroplacental 'clear space' (sonolucent zone), placental lacunae (swiss-cheese appearance), myometrial thinning to under 1 mm, bladder wall interruption (loss of the hyperechoic bladder–uterine interface), and increased vascularity on colour Doppler (abnormal placental bed vascularity). MRI is used as an adjunct for suspected deep invasion (increta, percreta) and to map the anatomy pre-operatively, particularly the relationship to the bladder.^[3][4]

Placental abruption is a clinical diagnosis — ultrasound is insensitive for an acute retroplacental clot. A normal ultrasound does not exclude abruption. When seen, a retroplacental clot appears as a heterogeneous, hyperechoic then hypoechoic mass behind the placenta that compresses the placenta; an elevated fundal height and a tender uterus are more reliable than the scan.^[2]

Continuous cardiotocography (CTG) is mandatory in any APH of concern. Recurrent late decelerations, bradycardia, reduced variability, or a sinusoidal pattern suggest abruption or vasa praevia. A sinusoidal pattern (smooth, undulating baseline with normal variability absent) in the context of bleeding at ROM is vasa praevia until proven otherwise.^[5]

Management — Resuscitation

Enlarge

^[1]

Resuscitation and assessment run in parallel, not in sequence. The aim is to restore circulating volume, correct coagulopathy, monitor the fetus, and prepare for delivery while the obstetric team gathers. ^[1]

^{[1] [13]}

Fluid resuscitation (Green-top 63 appendix, from Green-top 52): for haemorrhage up to 1000 mL without shock — one 14-gauge cannula and crystalloid. For massive haemorrhage (>1000 mL or clinical shock) — oxygen 10–15 L/min, two 14-gauge cannulae, left lateral tilt, keep warm, and until blood arrives infuse up to 3.5 L warmed crystalloid (Hartmann’s 2 L and/or colloid 1–2 L) as rapidly as required.^[21] Give cryoprecipitate if fibrinogen is <1 g/L in that appendix.^[21] Keep the patient warm — hypothermia and acidosis worsen coagulopathy.

Anti-D immunoglobulin: Green-top 63 states that in the non-sensitised RhD-negative woman, for all events after 20+0 weeks, at least 500 iu anti-D Ig should be given, followed by a test to identify FMH greater than 4 mL red cells, with additional anti-D as required. The Kleihauer test is used to quantify FMH so the dose can be gauged.^[21] Recurrent bleeds need further anti-D on a national schedule (Green-top 22 is cited by GTG 63; BCSH is a related haematology guideline).^[19]

Tranexamic acid 1 g intravenously, with one repeat dose if bleeding continues after 30 minutes, is the antifibrinolytic regimen validated by the WOMAN trial in over 20,000 women with postpartum haemorrhage: death due to bleeding fell from 1.9% to 1.5% (RR 0.81), with the benefit concentrated in women treated within 3 hours (RR 0.69) and no excess of thromboembolic events. There is no comparable randomised evidence in antepartum haemorrhage — use in major APH with coagulopathy is an extrapolation from these PPH data.^[13]

Corticosteroids for fetal lung maturation. Green-top 63 recommends a single course of antenatal corticosteroids between 24+0 and 34+6 weeks for women at risk of preterm birth (spotting from a likely lower-genital-tract cause, where imminent delivery is unlikely, is less clearly benefited).^[21] The later ALPS trial randomly assigned women at 34+0 to 36+5 weeks at high risk of late-preterm birth to two injections of betamethasone 24 hours apart or placebo: the neonatal composite of respiratory treatment or death within 72 hours fell from 14.4% to 11.6% (RR 0.80), with more neonatal hypoglycaemia (24.0% vs 15.0%).^[16] ALPS milligram strength is not stated in the PubMed abstract; do not invent 12 mg from memory.

Magnesium sulphate for fetal neuroprotection. In the NICHD BEAM trial, women at imminent risk of delivery between 24 and 31 weeks received magnesium sulphate as a 6 g intravenous bolus then 2 g per hour, or placebo. The primary composite of stillbirth, infant death, or moderate/severe CP was not significantly different (11.3% vs 11.7%, RR 0.97); among survivors, moderate or severe CP fell from 3.5% to 1.9% (RR 0.55).^[14] A meta-analysis of trials before 34 weeks found CP RR 0.69 without an overall paediatric mortality difference.^[15]

Management — Definitive & Stepwise

Definitive management is dictated by the cause and the gestational age and condition of mother and fetus. ^[1] Placenta praevia. The principle is no digital vaginal examination and caesarean delivery when the placenta covers the os or lies within 2 cm of it — planned caesarean before labour (timing follows local protocol and RCOG Green-top 27a).^[3] A praevia with the placental edge more than 2 cm from the os may be offered a trial of vaginal delivery: in Bhide's TVS cohort the caesarean rate was 90% with an edge of 0.1 to 2.0 cm but only 37% beyond 2 cm, and Vergani found more than two-thirds of women with an edge beyond 10 mm deliver vaginally without increased haemorrhage.^[7][8] When the fetus is immature and bleeding has settled, Green-top 63 supports remaining in hospital at least until bleeding stops if the loss was heavier than spotting; spotting that has settled with reassuring tests may go home with safety-netting.^[21] Do not perform digital VE until praevia is excluded. Give corticosteroids 24+0–34+6 if preterm birth is likely, and anti-D after 20+0 as above.^[21] Named “Macafee–Johnson” bed-rest bundles are historical teaching labels, not Green-top 63 text. Placental abruption. The principle is resuscitate, correct coagulopathy, and deliver — delivery is the definitive treatment because it removes the DIC trigger: management of obstetric DIC demands prompt attention to the underlying condition, including delivery of the patient, alongside correction of the haemostatic problem.^[11] Vaginal delivery (amniotomy plus oxytocin infusion to augment) is appropriate if the fetus is dead (intrauterine death), or the fetus and mother are stable and vaginal delivery is achievable in a reasonable time; the dead fetus still needs prompt delivery because the retained dead placenta perpetuates DIC. Emergency caesarean section is performed if the fetus is alive with compromise, or if vaginal delivery is not feasible or would be unsafe (e.g. severe pre-eclampsia, prior classical scar).^[2] Correct coagulopathy before and during surgery with cryoprecipitate, FFP and platelets — operating on uncorrected coagulopathy courts disaster. The uterus may be Couvelaire and atonic — be ready for postpartum haemorrhage (see uterotonic ladder below). Vasa praevia. Planned caesarean section before the membranes rupture — the rationale of prenatal diagnosis is exactly this: in the Australian cohort, all 58 prenatally diagnosed women were delivered by caesarean before rupture of membranes with no perinatal deaths, while undiagnosed cases suffered a 40% case fatality.^[5] Emergency caesarean if presenting with acute bleeding at ROM and a live fetus. The Apt test confirms fetal blood. If the fetus is already dead, the mode of delivery follows obstetric indications. Placenta accreta spectrum. Multidisciplinary planned caesarean delivery in a centre of excellence — outcomes are improved when delivery occurs in centres with multidisciplinary expertise and experience (maternal-fetal medicine, gynaecologic oncology, vascular, trauma and urologic surgery, transfusion medicine, intensive care, neonatology, interventional radiology and anaesthesia).^[4] In the Jauniaux–Bhide meta-analysis of previa with prior caesareans, 90.9% of accreta cases were diagnosed prenatally by ultrasound and caesarean hysterectomy was performed in 89.7% of cases with detailed management data.^[9] Options are elective caesarean–hysterectomy (the traditional definitive procedure, leaving the placenta in situ within the removed uterus) or conservative management (delivering the baby and leaving the placenta in situ to involute over months, accepting the risk of infection, delayed haemorrhage and delayed hysterectomy), supported by a massive haemorrhage protocol.

Uterine rupture. Immediate laparotomy under general anaesthesia. The fetus is delivered, the rupture is repaired if feasible, or hysterectomy is performed if the tear is irreparable or bleeding is uncontrollable. Aggressive blood and clotting-factor replacement is essential. Neonatal resuscitation is anticipated. ^[1] The uterotonic and surgical ladder for refractory bleeding at caesarean (accreta, atonic Couvelaire uterus, or concurrent PPH) — effectiveness rankings below are from the Cochrane network meta-analysis of uterotonics: ^[17]

1. Uterine massage and bimanual compression.
2. Oxytocin — the standard first-line uterotonic and the WHO reference comparator in the Cochrane network meta-analysis of 140 trials.^[17]
3. Ergometrine plus oxytocin (fixed combination) — the most effective regimen for preventing PPH of at least 500 mL (RR 0.69 vs oxytocin) and at least 1000 mL (RR 0.77), but with more vomiting (RR 3.10) and hypertension (RR 1.77) — avoid in hypertension/pre-eclampsia.^[17]
4. Carbetocin — comparable effectiveness (RR 0.72 for PPH of at least 500 mL) with the most favourable side-effect profile among the top-ranked agents.^[17]
5. Misoprostol plus oxytocin — effective (RR 0.73) but with more fever (RR 3.18); misoprostol alone remains useful where IV therapy is unavailable.^[17]
6. Tranexamic acid 1 g IV (repeat once after 30 minutes) — reduces death from bleeding in postpartum haemorrhage when given early.^[13]
7. Uterine balloon tamponade (e.g. Bakri balloon) and compression sutures (B-Lynch, Cho).
8. Stepwise vessel ligation — uterine artery devascularisation, then bilateral internal iliac (hypogastric) artery ligation.
9. Emergency hysterectomy — the life-saving last resort. In a systematic review of 981 emergency peripartum hysterectomies for uncontrolled bleeding, maternal mortality was 2.6% and morbidity 56%, with the highest risk in multiparous women with previous or current caesarean delivery and abnormal placentation — do not delay in the exsanguinating patient.^[20]

Specific Subtypes & Scenarios

Minor / unexplained APH. After excluding praevia, abruption (clinically), vasa praevia (in high-risk cases), and local causes by speculum, a residual 'unexplained' bleed is the commonest single label. It is not benign: it behaves like a mild abruption with higher rates of intrauterine growth restriction, preterm birth, and stillbirth, so the rest of the pregnancy warrants enhanced surveillance (growth scans, umbilical artery Doppler, weekly CTG or reduced fetal movements review, and patient warning about recurrent bleeding).^[2]

APH with a viable fetus vs a previable fetus. Management is modified by gestational age. Under 34+6 weeks with a stable mother and fetus, offer corticosteroids if preterm birth is likely and there is no immediate indication to deliver.^[21] Deliver for maternal or fetal compromise at any gestation. Before 24+0 weeks the bleed is classified as a threatened miscarriage by the RCOG APH definition.^[21]

APH with trauma (road traffic accident, fall, domestic violence). Green-top 63 lists abdominal trauma (accidental and domestic violence) among abruption risk factors.^[21] Resuscitate the mother, monitor the fetus (CTG once the mother is stable or resuscitation has started), and send a Kleihauer in RhD-negative women to gauge anti-D.^[21] A fixed “4 to 6 hour CTG” rule is not in Green-top 63 and is not used here. Deliver for maternal or fetal compromise or major abruption. Ask about domestic violence — APH may be its presentation.^[21]

The pregnant woman on anticoagulation. A woman on therapeutic low-molecular-weight heparin (e.g. for a mechanical heart valve or thrombophilia) presenting with APH is balanced between bleeding (the presenting problem) and thrombosis (the indication). Withhold the next LMWH dose, consider protamine sulphate for partial reversal of recently administered LMWH (dosing per haematology protocol), and involve haematology; once bleeding is controlled, restart prophylactic LMWH as soon as safe. Warfarin is reversed with vitamin K and prothrombin complex concentrate. ^[1]

APH with preterm labour. Green-top 63: tocolysis should not be used to delay delivery in major APH, haemodynamic instability, or fetal compromise; a senior obstetrician should decide if tocolysis is ever used (for example to complete steroids or allow transfer in a selected stable preterm woman).^[21] Offer corticosteroids 24+0 to 34+6 if preterm birth is likely and delivery is not immediate.^[21]

Complications & Pitfalls

Maternal complications of APH: haemorrhagic shock, disseminated intravascular coagulation, acute kidney injury (acute tubular or cortical necrosis from prolonged hypotension), Sheehan syndrome (anterior pituitary infarction from profound hypovolaemia — failure to lactate, amenorrhoea, secondary hypothyroidism and adrenal insufficiency), postpartum haemorrhage (from atonic Couvelaire uterus or accreta), peripartum hysterectomy and loss of fertility, infection (chorioamnionitis, wound infection), thromboembolism (the hypercoagulable state plus immobility), psychological trauma, and Rh sensitisation in the unprotected mother.^[1]

Fetal and neonatal complications: prematurity (iatrogenic and spontaneous), intrauterine growth restriction, hypoxic ischaemic encephalopathy, intrauterine death, fetal anaemia and exsanguination (vasa praevia), birth asphyxia, and neonatal coagulopathy.^[2]

Couvelaire uterus (uteroplacental apoplexy). In concealed abruption the blood extravasates through the myometrium to the serosa, giving a purplish, copper-bruised appearance. The muscle is contracted but functionally atonic — after delivery it fails to retract and is a cause of refractory postpartum haemorrhage, often forcing hysterectomy. ^[1]

^[1]

Recurrence and next pregnancy: previous abruption AOR 2.72 (Chen); after two prior abruptions Green-top 63 cites 19–25% recurrence.^[2][21] Accreta risk with previa/low-lying placenta: 4.1% after one caesarean, 13.3% after two or more.^[9] Antiplatelet prophylaxis in women at risk of pre-eclampsia: PE RR 0.81, fetal/neonatal death RR 0.84.^[18]

Prognosis & Disposition

Maternal outcome is determined by the cause, severity, gestational age, presence of coagulopathy, and the speed of resuscitation and delivery. In well-resourced settings with prompt care, maternal mortality is low; in low-resource settings with delayed access, APH remains a leading direct cause of maternal death.^[1] Perinatal outcome by cause: ^[1]

^[10]

Disposition: a woman with major APH is managed in a tertiary obstetric unit with on-site theatre, haematology, neonatology, and (for accreta) interventional radiology. After a minor, settled, explained bleed, she may be discharged with a clear safety-net: return immediately for recurrent or heavier bleeding, abdominal pain, reduced fetal movements, rupture of membranes, or fever; anti-D follow-up; and a plan for enhanced antenatal surveillance.^[3]

Follow-up: review at the next antenatal visit; arrange growth scans and Doppler for unexplained APH (which behaves like a mild abruption); address modifiable risk factors (smoking cessation, blood pressure optimisation); offer psychological support; counsel on future pregnancy (risk of recurrence, the role of aspirin, surveillance for praevia/accreta, mode of future delivery). ^[1]

Special Populations

Previous caesarean scar plus low/anterior placenta (placenta accreta spectrum). The highest-risk constellation in modern obstetrics. A woman with one or more previous caesareans and a low anterior placenta should have formal antenatal accreta assessment and planned delivery in a centre of excellence with multidisciplinary expertise and consent for possible hysterectomy.^[4]

Pre-eclampsia or chronic hypertension. Chen 2025 lists pre-eclampsia and gestational hypertension among independent pregnancy-complication risk factors for abruption, but the largest AORs in that review were placenta previa (7.31) and previous abruption (2.72) — do not teach hypertension as “the strongest” risk factor.^[2] Offer antiplatelet prophylaxis with low-dose aspirin in women at risk of pre-eclampsia (Cochrane 51 trials: pre-eclampsia RR 0.81, preterm birth RR 0.93, fetal or neonatal death RR 0.84).^[18] Counsel them to report abdominal pain or bleeding urgently.

IVF, multiple pregnancy, and high-risk placental anatomy. These women are at elevated risk of praevia and vasa praevia. Routine transvaginal ultrasound with colour Doppler at the 20-week anomaly scan (with targeted screening in those with a low placenta, bilobed placenta, or velamentous cord insertion) is the standard of care.^[5]

Anticoagulated woman. See Specific Subtypes: withhold the next dose, consider reversal, balance bleeding against thrombosis, involve haematology early. ^[1]

Previable fetus (under 24 weeks). Bleeding is classified as threatened miscarriage (or ectopic until intrauterine pregnancy confirmed); management is expectant with anti-D to Rh-negative women. The 24-week cut-off is regional (some settings use 20 or 28 weeks); state the definition you are using.^[3]

Jehovah's Witness patient. Green-top 63 does not give a specific refusal-of-transfusion protocol; it points to CMACE/RCOG guidance on declining blood products and to surgical/anaesthetic Jehovah’s Witness codes of practice.^[21] Plan early with the woman: which components are acceptable, cell salvage, and a documented haemorrhage plan. Do not quote an unsourced fold-increase in mortality.

Evidence, Guidelines & Regional Differences

The principal guidelines are RCOG Green-top Guideline No. 27a (placenta praevia) and 27b (placenta accreta), updated by Jauniaux and colleagues in 2019;^[3] ACOG Committee Opinion on placenta accreta spectrum in the United States; RANZCOG guidance in Australia and New Zealand; and FOGSI guidance in India. They are broadly concordant but differ in detail:

Landmark evidence: ^[1]

• Silver et al (2015) defined the centre of excellence for placenta accreta: outcomes improve when delivery occurs in centres with multidisciplinary expertise in this increasingly common, highly morbid condition.^[4]
• Jauniaux and Bhide (2017) meta-analysed 14 cohorts (3889 pregnancies) of previa or low-lying placenta with prior caesareans: accreta complicated 4.1% after one caesarean and 13.3% after two or more, 90.9% were diagnosed prenatally by ultrasound, and cesarean hysterectomy was performed in 89.7%.^[9]
• Chen et al (2025) quantified the independent risk factors for placental abruption — strongest for placenta praevia and previous abruption, with hypertensive disorders and smoking the leading modifiable exposures.^[2]
• Zhang et al (2021) meta-analysed 21 studies of vasa praevia: perinatal survival 98.6% with prenatal diagnosis versus 72.1% without (OR for death 25.4; hypoxic morbidity 50-fold higher) — the evidence base for targeted screening.^[10]
• Rouse et al (2008) and Conde-Agudelo and Romero (2009) established magnesium sulphate before very preterm delivery as cerebral palsy prophylaxis (moderate or severe CP 1.9% vs 3.5%, RR 0.55; pooled RR 0.69 before 34 weeks).^[14][15]
• The WOMAN trial (2017) established tranexamic acid 1 g IV early as standard in postpartum haemorrhage (death from bleeding RR 0.81), and its principles are extrapolated to major APH with coagulopathy.^[13]
• Gallos et al (2018) ranked the uterotonics for PPH prevention in a 140-trial network meta-analysis: ergometrine plus oxytocin, carbetocin, and misoprostol plus oxytocin beat oxytocin alone.^[17]

Controversies. Whether to screen universally for vasa praevia (cost-effectiveness debated, but growing consensus for at least targeted screening). The optimal timing of delivery in accreta (balancing iatrogenic prematurity against emergency presentation with bleeding). The role of interventional radiology balloon catheters (helpful but with their own complications). The acceptability and safety of cell salvage in obstetrics (now widely accepted with a separate suction line for amniotic fluid). The conservative (placenta-in-situ) management of accreta — increasingly offered in selected cases but carries real risks of infection, re-bleeding, and delayed hysterectomy. ^[1]

Exam Pearls

• APH = bleeding from or into the genital tract from 24+0 weeks to birth (RCOG GTG 63). Below 24+0 it is threatened miscarriage.^[21]
• Praevia: painless, bright-red, recurrent; soft relaxed uterus; abnormal lie; previous LSCS. Never digital VE until ultrasound excludes praevia. Abruption: painful, woody-hard, dark/concealed, fetal distress, shock disproportionate. Risks HTN/PE, previous, trauma, smoking, cocaine.^[2]
• Vasa praevia: painless bleeding at rupture of membranes + sudden fetal compromise (sinusoidal CTG); mother haemodynamically normal because it is fetal blood. Emergency caesarean. Apt test positive (fetal Hb resists alkali denaturation, stays pink).^[5]
• Concealed abruption = Couvelaire uterus + DIC + shock out of proportion; classical hard board-like abdomen; high fundus.
• Resuscitate every APH: ABC, two large-bore IVs if massive, 4 units cross-matched if major/massive, FBC/coagulation/fibrinogen, continuous CTG, anti-D ≥500 iu after 20+0 plus Kleihauer in RhD-negative women.^[21] TXA 1 g IV is WOMAN-trial PPH evidence (repeat once after 30 minutes if bleeding continues).^[13] Steroids 24+0–34+6 if preterm-birth risk;^[21] BEAM magnesium is 6 g then 2 g/h at 24–31 weeks (primary composite NS; CP 1.9% vs 3.5%).^[14]
• Planned delivery mode: praevia covering the os or edge within 2 cm → caesarean (90% CS rate with edge 0.1–2.0 cm vs 37% beyond 2 cm);^[7] vasa praevia → caesarean before membrane rupture (all 58 prenatally diagnosed Australian cases delivered thus, no deaths);^[5] accreta → multidisciplinary centre of excellence.^[4]
• Accreta: previous LSCS + low/anterior placenta; ultrasound features — loss of retroplacental clear space, placental lacunae, myometrial thinning, bladder wall interruption.^[4]
• Ergometrine: avoid in hypertension/pre-eclampsia (hypertension RR 1.77 in the Cochrane NMA).^[17] Carboprost: avoid in asthma (bronchoconstrictor). Misoprostol: safe in both (but fever RR 3.18).^[17]
• Sheehan syndrome: anterior pituitary infarction from profound hypovolaemic shock — failure to lactate, amenorrhoea, hypothyroidism, adrenal insufficiency.
• Antiplatelet prophylaxis (low-dose aspirin) in women at risk of pre-eclampsia: reduces pre-eclampsia (RR 0.81), preterm birth (RR 0.93) and fetal or neonatal death (RR 0.84).^[18]
• Expectant care (GTG 63): heavier than spotting or ongoing bleeding — remain in hospital at least until bleeding stops; spotting that has settled with reassuring tests may go home.
• Abruption is a clinical diagnosis — ultrasound is insensitive for retroplacental clot; a normal scan does not exclude it. Deliver the live compromised fetus by emergency caesarean; the dead fetus by prompt vaginal delivery (with amniotomy and oxytocin) to stop DIC.
• 2 cm rule: placental edge within 2 cm of internal os at term = caesarean (90% CS rate); more than 2 cm = may trial vaginal (37% CS; two-thirds deliver vaginally beyond 10 mm).^[7][8]

Exam application bank (NEET-PG / INICET)

One-line answer

Antepartum haemorrhage (APH) is bleeding from or into the genital tract from 24+0 weeks of pregnancy and prior to the birth of the baby (RCOG Green-top 63). The three placental causes are placenta praevia (low placenta over/near the internal os — classically painless, bright-red, recurrent bleeding, soft relaxed non-tender uterus; never digital vaginal examination until praevia excluded), placental abruption (premature separation of a normally-sited placenta — painful, tense tender woody-hard uterus, dark or concealed bleeding, fetal distress, shock disproportionate to visible loss; Chen: previa AOR 7.31, previous abruption AOR 2.72), and vasa praevia (fetal vessels across the internal os — painless bleeding at rupture of membranes with sudden fetal compromise in a haemodynamically normal mother; Zhang pooled survival 98.6% with prenatal diagnosis versus 72.1% without). ^[21]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. ^[1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. ^[1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. ^[1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. ^[1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. ^[1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Antepartum Haemorrhage.

^[1]

References21ShowHide

1. [1]Young JS, White LM Vaginal Bleeding in Late Pregnancy Emerg Med Clin North Am, 2019.PMID 30940370
2. [2]Chen D, Gao X, Yang T, et al. Independent risk factors for placental abruption: a systematic review and meta-analysis BMC Pregnancy Childbirth, 2025.PMID 40140972
3. [3]Jauniaux E, Alfirevic Z, Bhide AG, et al. Placenta Praevia and Placenta Accreta: Diagnosis and Management: Green-top Guideline No. 27a BJOG, 2019.PMID 30260097
4. [4]Silver RM, Fox KA, Barton JR, et al. Center of excellence for placenta accreta Am J Obstet Gynecol, 2015.PMID 25460838
5. [5]Sullivan EA, Javid N, Duncombe G, et al. Vasa Previa Diagnosis, Clinical Practice, and Outcomes in Australia Obstet Gynecol, 2017.PMID 28796681
6. [6]Wright GL, Friedman A, Ananth CV, et al. Placental Abruption: Temporal Trends, Risk Factors, and Associated Adverse Maternal Outcomes Am J Perinatol, 2026.PMID 40940025
7. [7]Bhide A, Prefumo F, Moore J, et al. Placental edge to internal os distance in the late third trimester and mode of delivery in placenta praevia BJOG, 2003.PMID 14511970
8. [8]Vergani P, Ornaghi S, Pozzi I, et al. Placenta previa: distance to internal os and mode of delivery Am J Obstet Gynecol, 2009.PMID 19631924
9. [9]Jauniaux E, Bhide A Prenatal ultrasound diagnosis and outcome of placenta previa accreta after cesarean delivery: a systematic review and meta-analysis Am J Obstet Gynecol, 2017.PMID 28268196
10. [10]Zhang W, Geris S, Al-Emara N, et al. Perinatal outcome of pregnancies with prenatal diagnosis of vasa previa: systematic review and meta-analysis Ultrasound Obstet Gynecol, 2021.PMID 32735754
11. [11]Erez O, Othman M, Rabinovich A, et al. DIC in Pregnancy - Pathophysiology, Clinical Characteristics, Diagnostic Scores, and Treatments J Blood Med, 2022.PMID 35023983
12. [12]Hikida Y, Sumikura H, Okada H, et al. The value of the portable fibrinogen measuring device-a case report of severe postpartum hemorrhage with obstetric disseminated intravascular coagulation JA Clin Rep, 2021.PMID 33687590
13. [13]WOMAN Trial Collaborators Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial Lancet, 2017.PMID 28456509
14. [14]Rouse DJ, Hirtz DG, Thom E, et al. A randomized, controlled trial of magnesium sulfate for the prevention of cerebral palsy N Engl J Med, 2008.PMID 18753646
15. [15]Conde-Agudelo A, Romero R Antenatal magnesium sulfate for the prevention of cerebral palsy in preterm infants less than 34 weeks' gestation: a systematic review and metaanalysis Am J Obstet Gynecol, 2009.PMID 19482113
16. [16]Gyamfi-Bannerman C, Thom EA, Blackwell SC, et al. Antenatal Betamethasone for Women at Risk for Late Preterm Delivery N Engl J Med, 2016.PMID 26842679
17. [17]Gallos ID, Williams HM, Price MJ, et al. Uterotonic agents for preventing postpartum haemorrhage: a network meta-analysis Cochrane Database Syst Rev, 2018.PMID 29693726
18. [18]Duley L, Henderson-Smart DJ, Knight M, et al. Antiplatelet agents for preventing pre-eclampsia and its complications Cochrane Database Syst Rev, 2004.PMID 14974075
19. [19]Qureshi H, Massey E, Kirwan D, et al. BCSH guideline for the use of anti-D immunoglobulin for the prevention of haemolytic disease of the fetus and newborn Transfus Med, 2014.PMID 25121158
20. [20]Rossi AC, Lee RH, Chmait RH Emergency postpartum hysterectomy for uncontrolled postpartum bleeding: a systematic review Obstet Gynecol, 2010.PMID 20177297
21. [21]Royal College of Obstetricians and Gynaecologists Antepartum Haemorrhage: Green-top Guideline No. 63 RCOG, 2011.Source