Oligohydramnios Due to Placental Dysfunction

Oligohydramnios due to placental dysfunction is reduced amniotic fluid caused by low fetal renal blood flow and urine output in a fetus under chronic hypoxia from placental insufficiency. It is typically found with growth restriction, absent or reversed end diastolic flow, preeclampsia or post term pregnancy. It matters because it marks a fetus at higher risk of stillbirth, acidosis and intrapartum distress.

• Fluid reduces as the fetus redistributes blood flow to the brain.
• Risk factors: preeclampsia, chronic hypertension, antiphospholipid syndrome, smoking, malaria, anaemia, post term pregnancy.
• Fluid may improve slightly with maternal hydration.

Women report reduced fetal movements, and the fundal height is smaller than dates. Hypertension and proteinuria may be present.

• Small abdominal circumference for gestation.
• Little fluid felt around the fetus.
• Differential diagnosis: membrane rupture, isolated oligohydramnios, renal anomaly, constitutionally small fetus, post term placental ageing, ACE inhibitor effect.
• Complications: stillbirth, fetal acidosis, growth restriction, intrapartum distress, caesarean section, neonatal acidosis, neonatal hypoglycaemia.

The approach is Doppler assessment of the fetus and placenta with maternal tests.

• Ultrasound: amniotic fluid index 5 cm or below or deepest vertical pocket below 2 cm with abdominal circumference or estimated weight below the 10th centile; umbilical artery Doppler (raised pulsatility index, absent or reversed end diastolic flow), middle cerebral artery pulsatility index, cerebroplacental ratio, ductus venosus Doppler, uterine artery Doppler.
• Cardiotocography daily to twice weekly.
• Maternal tests: blood pressure, urine protein to creatinine ratio, full blood count, platelets, creatinine, liver enzymes, antiphospholipid antibodies, malaria rapid test, glucose.
• Speculum test for membrane rupture to exclude leakage.

The principle is to treat the maternal cause, give steroids and plan delivery by Doppler stage.

• Supportive: oral water 2 to 3 litres daily; left lateral rest; stop smoking; daily fetal movement counts; admit for absent or reversed end diastolic flow or reduced movements; deliver in a unit with neonatal intensive care.
• Pharmacological: labetalol 200 mg oral every 8 to 12 hours (maximum 2.4 g daily) or nifedipine modified release 30 to 60 mg oral once daily (maximum 120 mg) for blood pressure 140/90 mmHg or more; artemether-lumefantrine 4 tablets (each 20 mg and 120 mg) oral at 0, 8, 24, 36, 48 and 60 hours for malaria; enoxaparin 40 mg subcutaneous daily with aspirin 150 mg oral at night for antiphospholipid syndrome; betamethasone 12 mg IM twice, 24 hours apart, between 24 and 34 weeks and 6 days if delivery is likely; magnesium sulphate 4 g IV over 20 minutes then 1 g per hour until delivery for 24 hours at most before 32 weeks; aspirin 150 mg oral at night from 12 weeks to 36 weeks in the next pregnancy.
• Procedures: delivery at 37 weeks if the umbilical artery Doppler is normal, 34 weeks for absent end diastolic flow, 30 to 32 weeks for reversed flow, and earlier for pathological cardiotocography; caesarean section for abnormal Doppler; induction with misoprostol 25 micrograms vaginal 6-hourly (maximum 4 doses) or a Foley catheter with a 30 mL balloon for normal Doppler with continuous cardiotocography.
• Special groups: severe preeclampsia needs magnesium sulphate 4 g IV over 20 minutes then 1 g per hour for 24 hours after birth and labetalol 20 mg IV then 40 mg, 80 mg and 80 mg at 10 minute intervals (maximum 220 mg) for blood pressure 160/110 mmHg or more.
• Red flags: absent or reversed end diastolic flow, reduced fetal movements, abnormal cardiotocography, anhydramnios, severe hypertension.
• Follow-up: Doppler and amniotic fluid index weekly to twice weekly; cardiotocography twice weekly to daily; newborn glucose check at 2 hours, with glucose below 2.6 mmol/L treated by dextrose 10 percent 2 mL/kg IV over 10 minutes then 80 mL/kg per day.