Antepartum Haemorrhage

Overview & Definition

Antepartum haemorrhage (APH) is defined as vaginal bleeding from the genital tract occurring after 24 weeks of gestation and until the birth of the baby.[1] The 24-week cut-off is the lower threshold of fetal viability in most settings; 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, but 24 weeks is the operational definition used by RCOG and most modern guidelines.[3]

APH matters because it is common (3 to 5% of pregnancies), it is a leading reason for emergency antenatal admission, and two of its 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]

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]

Epidemiology & Risk Factors

APH affects about 3 to 5% of pregnancies and is the commonest reason for emergency antenatal admission in obstetrics. The three placental causes together account for roughly half of all cases; the remainder are local causes and the substantial unexplained group.[1]

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:[2] the strongest independent associations were placenta praevia (adjusted OR about 7.3) and previous abruption (adjusted OR about 2.7), with hypertensive disorders of pregnancy (pre-eclampsia, gestational or chronic hypertension), cigarette smoking (dose-dependent and the key modifiable exposure), cocaine use, advanced maternal age, multiparity, preterm pre-labour rupture of membranes, chorioamnionitis, polyhydramnios, short umbilical cord, thrombophilias (factor V Leiden, antithrombin deficiency, antiphospholipid syndrome), and intrauterine growth restriction also implicated.

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]

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, and a pregnancy-specific DIC score built on fibrinogen concentration, the PT difference and platelet count improves early diagnosis (88% sensitivity, 96% specificity at the validated cut-off).[11] Treatment is two-pronged: deliver — emptying the uterus removes the trigger — and replace haemostatic components guided by point-of-care testing adjusted for pregnancy; during massive obstetric haemorrhage, transfusion should keep fibrinogen above 200 mg/dL (2 g/L).[11][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]

Placenta praevia presents with painless, causeless, bright-red, recurrent vaginal bleeding, typically after 28 weeks and most commonly around 30 to 34 weeks as the lower segment forms. 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 — the concealed retroplacental clot can hold 1 to 2 L of blood that never reaches the perineum.[2]

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 it converts a 95% survival (antenatally diagnosed) into a 50%-or-worse mortality. 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.[2]

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]

A speculum examination is used (after ultrasound) to assess the cervix and vagina for a local cause, to visualise the source of bleeding, and to take swabs — but never digital. The speculum may be left in place to observe ongoing loss. [1]

Assess shock in four quadrants. The young pregnant woman compensates remarkably: tachycardia, tachypnoea, and a narrowed pulse pressure (the diastolic rises with sympathetic drive) appear before hypotension. Hypotension is a late, pre-terminal sign — by the time the systolic drops, more than 30 to 40% of the blood volume is already lost. Cool peripheries, delayed capillary refill, anxiety, and oliguria signal decompensated shock. [1]

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, and during ongoing obstetric haemorrhage transfusion should keep fibrinogen above 200 mg/dL (2 g/L).[11][12]
• 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 scan at 32 weeks (and again at 36 if still low).

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

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]

Fluid resuscitation: warm isotonic crystalloid titrated to response in shocked patients, with early escalation to the massive-transfusion pathway — red cells, fresh-frozen plasma, platelets and cryoprecipitate guided by point-of-care coagulation testing. The fibrinogen concentration is the critical coagulation target in obstetric haemorrhage: keep it above 200 mg/dL (2 g/L) during ongoing bleeding with DIC, because a low fibrinogen is an early marker of consumptive coagulopathy in pregnancy.[11][12] Keep the patient warm — hypothermia and acidosis worsen coagulopathy.

Anti-D immunoglobulin should be given to every RhD-negative, non-sensitised woman after a potentially sensitising event such as APH — even small bleeds can cause fetomaternal haemorrhage — as soon as possible after the bleed, with repeat dosing for recurrent events. Testing to size any fetomaternal haemorrhage (Kleihauer-Betke test or flow cytometry) is used to adjust the dose, because a large fetal bleed requires additional anti-D; dose, timing and testing schedules follow national haematology guidance such as the BCSH anti-D 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. The ALPS trial randomly assigned women at risk of delivery in the late preterm window (34+0 to 36+6 weeks) 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 less severe respiratory complications, less surfactant use and more neonatal hypoglycaemia (24% vs 15%).[16] This late-preterm evidence complements the long-standing practice of antenatal corticosteroids for women at risk of earlier delivery, whenever the mother is stable enough to wait.

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 loading bolus followed by a constant 2 g per hour infusion, or placebo: moderate or severe cerebral palsy among survivors fell from 3.5% to 1.9% (RR 0.55).[14] A meta-analysis of trials in women at risk of delivery before 34 weeks confirms the cerebral palsy reduction (RR 0.69) without an overall 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 per unit protocol and RCOG Green-top 27a, commonly around 36 to 37 weeks, to avoid an emergency presentation with the cervix dilating and the praevia edge shearing).[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] The Macafee–Johnson expectant regimen is used when the fetus is immature and bleeding has settled: inpatient bed rest, cross-matched blood held at all times, no vaginal examination, serial growth and wellbeing scans, and corticosteroids — to gain gestational age, balancing the risk of a catastrophic recurrent bleed against the risk of prematurity. Anti-D is given to RhD-negative mothers after each bleed.[19] 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 weeks with a stable mother and fetus, the aim is to gain gestational age (corticosteroids, expectant inpatient care, careful monitoring) — the Macafee–Johnson regimen for praevia, inpatient observation for abruption that has settled. At 34 weeks and beyond, or with compromise at any gestation, deliver. Before 24 weeks the bleed is classified and managed as a threatened miscarriage.[3]

APH with trauma (road traffic accident, fall, domestic violence). Direct abdominal trauma carries a significant risk of abruption (from shearing forces or seat-belt injury) and rarely of uterine rupture. Assess the mother (ABCDE), then the fetus (CTG for 4 to 6 hours minimum, or 24 hours if any abnormality); perform a Kleihauer-Betke test to size fetomaternal haemorrhage (especially in Rh-negative women); ultrasound for placenta, fetal wellbeing, and retroplacental clot. Deliver for maternal or fetal compromise, non-reassuring CTG, or major abruption. Domestic violence screening is mandatory — APH may be its presentation.[6]

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. Abruption often presents as preterm labour (the retroplacental clot irritates the uterus). Tocolysis is generally contraindicated in significant abruption (it may mask the diagnosis and worsen the bleed) — the management is delivery, not tocolysis. Steroids for fetal lung maturation are given if time allows. [1]

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]

Recurrence and next pregnancy: previous abruption is among the strongest predictors of recurrence — adjusted OR about 2.7 in the Chen meta-analysis — and accreta risk climbs with each caesarean (4.1% after one, 13.3% after two or more in previa).[2][9] For women at risk of recurrent placental disease, antiplatelet prophylaxis with low-dose aspirin reduces pre-eclampsia (RR 0.81) and fetal or 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]

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 a formal accreta assessment by ultrasound at 32 weeks, with MRI if sonographic features are present, and planned delivery at 34 to 36 weeks in a centre of excellence with multidisciplinary input and consent for possible hysterectomy.[4]

Pre-eclampsia or chronic hypertension. These women are at elevated risk of abruption — hypertensive disorders of pregnancy are independent risk factors — although the strongest associations in the Chen meta-analysis were coexisting placenta praevia (adjusted OR about 7.3) and previous abruption (adjusted OR about 2.7).[2] Optimise blood pressure, offer antiplatelet prophylaxis with 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 in the Cochrane meta-analysis of 51 trials),[18] and counsel them to report abdominal pain or bleeding urgently with a low threshold to admit and assess.

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. Refusal of blood products markedly increases maternal mortality from major APH. Management must include early multidisciplinary discussion, a documented management plan, cell salvage (often acceptable), tranexamic acid, erythropoietin, iron, and explicit consent about which components are and are not acceptable. Mortality rises about 6-fold if blood is refused in a major bleed.[1]

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 24 weeks to birth. Below 24 weeks it is threatened miscarriage.[1]
• 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, cross-match, FBC/coagulation/fibrinogen, continuous CTG, anti-D to RhD-negative, tranexamic acid 1 g IV early if major bleeding,[13] betamethasone if preterm and stable,[16] magnesium sulphate for neuroprotection before very preterm delivery.[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]
• Macafee–Johnson regimen: expectant inpatient care (bed rest, cross-matched blood at all times, no VE, serial scans) for immature praevia with settled bleeding to gain gestational age.
• 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 vaginal bleeding from the genital tract from 24 weeks of gestation until the birth of the baby. 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, often abnormal lie — diagnosed by transvaginal ultrasound, never digital vaginal examination until praevia excluded, caesarean if major), 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; risks hypertension/pre-eclampsia, previous abruption, trauma, smoking, cocaine; resuscitate and deliver), and vasa praevia (fetal vessels running over the membranes across the internal os — painless bleeding at rupture of membranes with sudden fetal compromise

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.