Placental Insufficiency

Placental insufficiency is failure of the placenta to deliver adequate oxygen and nutrients to the fetus and remove waste, producing fetal growth restriction, oligohydramnios and, in severe cases, hypoxaemia, acidaemia and stillbirth. The usual substrate is abnormal trophoblast invasion and spiral artery remodelling in early pregnancy, which is the same defect underlying pre-eclampsia, so the two frequently coexist.

Other contributors are maternal vascular disease (chronic hypertension, diabetes with vasculopathy, renal disease, antiphospholipid syndrome, thrombophilia), smoking, cocaine, chronic anaemia, high altitude, placental infarction, chronic abruption, chronic histiocytic intervillositis, and abnormal placental or cord structure.

Fetal growth restriction is defined as estimated fetal weight or abdominal circumference below the 3rd centile, or below the 10th centile with abnormal Doppler indices. Early onset disease (before 32 weeks) is dominated by placental pathology with severe Doppler abnormality and high pre-eclampsia rates; late onset disease is milder, with brain sparing and a subtle fall in growth velocity.

• Often silent. Symphysis fundal height lags by more than 3 cm or plots below the 10th centile on a customised chart; reduced fetal movements are a presenting complaint.
• Risk markers: maternal hypertension, previous growth restricted baby or stillbirth, low pregnancy associated plasma protein A in the first trimester, raised uterine artery pulsatility index at 20 to 24 weeks, unexplained raised maternal serum alpha fetoprotein or hCG, bleeding in early pregnancy.
• Ultrasound: small fetus with preserved head circumference early then asymmetry (head-to-abdomen ratio increased), oligohydramnios, small or thick placenta with calcification, and in advanced disease absent growth.
• Doppler progression: raised umbilical artery pulsatility index, then absent end diastolic flow, then reversed end diastolic flow; middle cerebral artery vasodilation (brain sparing; cerebroplacental ratio below the 5th centile); then ductus venosus a-wave absent or reversed and abnormal short term variation on computerised cardiotocography, which signal imminent acidaemia.
• Neonatal consequences: hypoglycaemia, hypothermia, polycythaemia, necrotising enterocolitis in preterm infants, neurodevelopmental impairment, and long term cardiometabolic risk.

• Serial biometry every 2 weeks (abdominal circumference, head circumference, femur length, estimated fetal weight) with growth velocity assessment, with amniotic fluid (deepest vertical pocket or index) at each scan.
• Umbilical artery Doppler at every surveillance visit; middle cerebral artery Doppler and cerebroplacental ratio; uterine artery Doppler; ductus venosus Doppler in early onset disease.
• Cardiotocography with computerised short term variation (concerning below 3.5 ms at 29 to 32 weeks gestation, below 4.5 ms later).
• Aetiological workup in early severe cases: detailed anomaly scan, karyotype or microarray, CMV and toxoplasma and syphilis serology, maternal antiphospholipid antibodies, and placental histology after delivery.
• Maternal assessment: blood pressure, urinalysis, renal and liver function, platelet count, to exclude coexisting pre-eclampsia.

No treatment restores placental function; management is optimising maternal factors, surveillance and timing delivery to balance fetal hypoxaemia against prematurity.

• Prevention in women at high risk (previous pre-eclampsia or growth restriction, chronic hypertension, diabetes, renal disease, antiphospholipid syndrome, multiple moderate risk factors): aspirin 75 to 150 mg orally nightly, started before 16 weeks and continued until 36 weeks. Calcium 1.5 to 2 g daily if dietary intake is low.
• Stop smoking and cocaine; treat hypertension (labetalol 100 to 400 mg orally every 8 to 12 hours, nifedipine modified release 30 to 90 mg daily), optimise glycaemic control, treat anaemia.
• Antiphospholipid syndrome with previous obstetric morbidity: add prophylactic low-molecular-weight heparin (enoxaparin 40 mg subcutaneously daily) to aspirin.
• Sildenafil, heparin and bed rest do not improve outcome and are not recommended.
• Surveillance frequency by severity: normal umbilical Doppler, weekly to fortnightly Doppler and growth; abnormal umbilical pulsatility index, twice weekly; absent end diastolic flow, daily to alternate day with ductus venosus and computerised cardiotocography; reversed end diastolic flow, inpatient with at least daily monitoring.
• Antenatal corticosteroids for any delivery before 34 weeks: betamethasone 12 mg intramuscularly, two doses 24 hours apart. Magnesium sulphate 4 g intravenous loading over 20 to 30 minutes then 1 g/hour for neuroprotection when delivery is before 30 to 32 weeks.
• Delivery timing, based on Doppler findings and gestation: late onset disease with normal umbilical Doppler, deliver at 37 weeks; abnormal umbilical pulsatility index or low cerebroplacental ratio, 36 to 37 weeks; absent end diastolic flow, 34 weeks; reversed end diastolic flow, 30 to 32 weeks; abnormal ductus venosus or computerised short term variation below threshold, deliver at once regardless of gestation after steroid cover where time permits; spontaneous late decelerations or abnormal fetal heart rate trace, deliver immediately.
• Mode: caesarean section is usual with absent or reversed end diastolic flow or abnormal ductus venosus; induction with continuous fetal monitoring may be considered with isolated mildly abnormal late onset findings.
• Neonatal team present; early feeding and glucose monitoring; cord blood gases; placental histology sent.
• Counselling for future pregnancy: aspirin, early uterine artery Doppler, serial growth scans; recurrence risk is about 20 percent.