Placental Abruption

Summary

Placental abruption is the most common cause of painful antepartum haemorrhage. Diagnosis is clinical; ultrasound cannot reliably exclude it. Immediate maternal stabilization and fetal assessment are priorities. Mode of delivery depends on maternal/fetal status, with emergency caesarean indicated in compromise. Concealed haemorrhage often leads to underestimation of actual blood loss.

Definition

Placental abruption (abruptio placentae) refers to the premature separation of a normally implanted placenta from the uterine wall before delivery of the fetus. It is one of the leading causes of antepartum haemorrhage (APH), which is defined as vaginal bleeding after 24 weeks’ gestation and before delivery. The condition carries significant risks for both mother and fetus, including haemorrhagic shock, disseminated intravascular coagulation (DIC), intrauterine fetal death, and maternal mortality

Pathophysiology

Placental abruption is usually triggered by rupture of maternal vessels in the basal decidua. Accumulated blood dissects the placenta from the uterine wall, forming a retroplacental haematoma. The degree of placental separation determines the severity of maternal bleeding and fetal compromise.

• Revealed abruption: blood tracks between membranes and cervix, presenting as vaginal bleeding.

• Concealed abruption: blood is retained within the uterus, causing uterine distension, shock, and Couvelaire uterus (extravasation of blood into myometrium).

• Mixed abruption: features of both types

Risk Factors

• Previous placental abruption (strongest predictor)

• Hypertensive disorders: pre-eclampsia, chronic hypertension, renal disease, SLE, antiphospholipid syndrome

• Mechanical factors: trauma, sudden uterine decompression (e.g. rupture of membranes in polyhydramnios), multiple pregnancy, uterine myomas

• Lifestyle: smoking, alcohol, cocaine

• Increased maternal age and parity

• Premature rupture of membranes

• First-trimester bleeding with intrauterine haematoma

• Thrombophilias

Clinical Features

• Classical triad: painful vaginal bleeding, uterine tenderness, and increased uterine tone (“woody” uterus).

• Other symptoms: abdominal/back pain, reduced fetal movements, uterine contractions, or silent concealed bleeding with sudden intrauterine fetal demise.

• Examination findings: tender rigid uterus, signs of shock (out of proportion to visible blood loss), abnormal lie/presentation, decreased fetal heart rate variability or absent fetal heart activity.

Diagnosis

Diagnosis is primarily clinical. Ultrasound may show a retroplacental haematoma but has low sensitivity (2–25%) and cannot reliably exclude abruption.

• History & examination: quantify bleeding, assess pain, evaluate risk factors, exclude placenta praevia by ultrasound before vaginal examination.

• Maternal investigations: FBC, coagulation profile, renal/liver function, blood group and cross-match, Kleihauer test (if Rh-negative).

• Fetal assessment: cardiotocography (≥26 weeks) or fetal heart auscultation if <26 weeks.

Differential Diagnoses

• Placenta praevia – painless vaginal bleeding, confirmed on ultrasound.

• Vasa praevia – fetal vessel rupture after membrane rupture; presents with vaginal bleeding + fetal distress.

• Marginal placental bleed – small peripheral abruption, minimal compromise.

• Uterine rupture – typically in labour with history of uterine surgery.

• Local causes – cervical ectropion, polyps, malignancy, vaginal/cervical infection.

Management

Initial management follows ABCDE resuscitation:

• Admission, oxygen, IV access with two large-bore cannulas.

• Blood tests and cross-match, blood products available.

• Continuous maternal and fetal monitoring.

• Anti-D administration within 72 hours for Rh-negative women.

Definitive management depends on severity, gestational age, and maternal/fetal condition:

• Emergency caesarean section – indicated if there is maternal or fetal compromise.

• Vaginal delivery (preferable) – if mother is stable, cervix favourable, and no contraindication; amniotomy and oxytocin may accelerate labour.

• Conservative management – possible in mild/partial abruption with maternal/fetal stability and preterm gestation, with close in-hospital monitoring.

Complications

Maternal:

• Hypovolaemic shock

• DIC (due to tissue factor release from decidua)

• Acute renal failure

• Postpartum haemorrhage

• Sheehan’s syndrome (pituitary infarction after massive haemorrhage)

• Amniotic fluid embolism

• Uterine rupture (rare, severe cases)

Fetal:

• Hypoxia and growth restriction

• Preterm delivery

• Intrauterine fetal death