Placental Infarction

Placental infarction is ischaemic necrosis of a region of chorionic villi, caused by interruption of maternal blood supply through the spiral arteries. Acute infarcts appear as wedge shaped, firm, dark red areas based on the maternal surface. Older infarcts become tan, grey and then white.

Small peripheral infarcts at term occur in about 25 percent of normal placentas and are harmless.

Large, central, multiple or early infarcts reflect maternal vascular malperfusion. They are associated with pre-eclampsia, chronic hypertension, fetal growth restriction, placental abruption, antiphospholipid syndrome, inherited thrombophilia, sickle cell disease, cocaine use and smoking.

The clinical effect depends on the proportion of placental parenchyma lost. When more than 15 to 20 percent of villous tissue is involved there is risk of fetal growth restriction and stillbirth.

• Not usually clinically evident during pregnancy; diagnosis is histological after delivery.
• Antenatal signs, when infarction is extensive: fetal growth restriction, oligohydramnios, abnormal umbilical or uterine artery Doppler, pre-eclampsia, and reduced fetal movements.
• Ultrasound may show hypoechoic or heterogeneous placental areas, usually non-specific; placental thickening with lakes and calcifications is common in advanced disease.
• Associated placental findings: retroplacental haematoma, decidual vasculopathy, accelerated villous maturation, distal villous hypoplasia and increased syncytial knots.
• Complications: stillbirth, preterm delivery for fetal or maternal indications, neonatal hypoxic ischaemic encephalopathy, and recurrent pregnancy loss.

• Placental examination and histopathology after delivery: villous ghost outlines, loss of nuclear staining and intervillous collapse in recent infarcts, with fibrosis in older ones; the percentage of parenchyma involved and the presence of maternal vascular malperfusion pattern are recorded.
• Antenatal diagnosis relies on serial growth and Doppler abnormalities: estimated fetal weight below the 10th centile or falling growth velocity, raised umbilical artery pulsatility index, reduced cerebroplacental ratio, oligohydramnios and abnormal uterine artery Doppler. Infarcts themselves are not reliably visualised.
• Maternal investigation after a significant infarction or fetal loss: blood pressure, urine protein, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin and anti-beta-2-glycoprotein I IgG and IgM, repeated at 12 weeks), inherited thrombophilia screen when personal or family venous thrombosis is present, sickle cell status, and drug screen where relevant.

• In pregnancy, perform serial growth scans every 2 weeks with umbilical and middle cerebral artery Doppler, amniotic fluid measurement, computerised cardiotocography, and maternal blood pressure and urine protein surveillance.
• Timing of delivery: 37 weeks if Doppler is normal, 36 to 37 weeks if umbilical pulsatility index is raised, 34 weeks for absent end diastolic flow, and 30 to 32 weeks for reversed end diastolic flow. Deliver immediately for abnormal ductus venosus flow or a pathological trace.
• Aspirin 75 to 150 mg nightly from before 16 weeks until 36 weeks in the next pregnancy.
• Antiphospholipid syndrome: aspirin plus enoxaparin 40 mg subcutaneously daily antenatally and for 6 weeks postpartum; if previous thrombosis, therapeutic enoxaparin (1 mg/kg twice daily) throughout.
• Heparin is not routinely indicated for unexplained infarction or thrombophilia without thrombosis or antiphospholipid syndrome.
• Treat hypertension (labetalol, nifedipine), smoking and drug cessation, optimise sickle cell care and glycaemic control.
• Antenatal corticosteroids and magnesium sulphate before preterm delivery as indicated.
• After a stillbirth with infarction, perform thorough investigation, offer bereavement support, and plan the next pregnancy with preconception review, early aspirin, growth surveillance from 24 weeks and delivery planning by 37 to 39 weeks.
• Counsel on recurrence: significant maternal vascular malperfusion recurs in 10 to 25 percent.