Severe Oligohydramnios

Severe oligohydramnios is a marked reduction in amniotic fluid, with a deepest vertical pocket below 1 cm or an amniotic fluid index below 3 cm, and anhydramnios is the near complete absence of fluid. Causes include rupture of membranes, fetal renal or urinary tract anomaly, placental insufficiency with growth restriction, and drugs. It matters because fluid is needed for lung development, so severe disease before 24 weeks causes pulmonary hypoplasia and limb contractures, and the outlook depends on the cause.

• Fetal urine is the main source of fluid after 16 weeks.
• Risk factors: renal agenesis, posterior urethral valves, prolonged membrane rupture, severe preeclampsia, ACE inhibitor use, indomethacin use.
• Bilateral renal agenesis is lethal.

Women often notice reduced fetal movements or leaking fluid, and fundal height is small. Fetal parts are easily palpable, and in prolonged cases the uterus feels tight around the fetus.

• Small fundal height.
• History of watery discharge in membrane rupture.
• Differential diagnosis: membrane rupture, renal agenesis, polycystic or dysplastic kidneys, urethral obstruction, placental insufficiency, twin to twin transfusion donor, ACE inhibitor effect, post term pregnancy.
• Complications: pulmonary hypoplasia, Potter sequence, limb contractures, umbilical cord compression, fetal death, preterm birth, neonatal respiratory failure.

The approach is a detailed scan with tests to confirm membrane rupture.

• Ultrasound: deepest vertical pocket below 1 cm or amniotic fluid index below 3 cm; kidneys, bladder filling over 30 to 60 minutes, ureters, urethra, growth, Doppler, lung and thorax size.
• Speculum examination for pooling and a test for membrane rupture (nitrazine, placental alpha microglobulin 1 or insulin-like growth factor binding protein 1 test).
• Maternal blood pressure, urine protein, full blood count, urea and creatinine, infection tests; drug history.
• Amniocentesis for karyotype and microarray and amnioinfusion by fetal medicine to improve views where available.

The principle is to find the cause, counsel on prognosis and plan delivery by gestation and fetal condition.

• Supportive: refer to a fetal medicine unit; counselling about the outlook before 24 weeks; oral water 2 to 3 litres daily; stop ACE inhibitors, NSAIDs and indomethacin; daily fetal movement counts; deliver in a unit with neonatal intensive care.
• Pharmacological: 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; for membrane rupture amoxicillin 500 mg oral 8-hourly plus erythromycin 250 mg oral 6-hourly for 7 days; labetalol 200 mg oral every 8 to 12 hours (maximum 2.4 g daily) for hypertension; neonatal surfactant (poractant alfa 200 mg/kg endotracheal, then 100 mg/kg) for respiratory distress.
• Procedures: serial amnioinfusion with sodium chloride 0.9 percent 200 to 500 mL by fetal medicine for selected fetuses before 26 weeks with reachable renal function; vesicoamniotic shunt for obstructive uropathy; delivery at 34 to 36 weeks for viable fetuses with severe oligohydramnios and intact function, earlier for growth restriction by Doppler stage; induction of labour or termination for lethal anomalies after counselling; continuous cardiotocography and amnioinfusion in labour.
• Special groups: bilateral renal agenesis or severe bilateral renal disease needs counselling about termination or comfort care; membrane rupture is managed with antibiotics and steroids and delivery by 34 weeks.
• Red flags: anhydramnios, absent bladder, reduced fetal movements, fever, abnormal Doppler, abnormal cardiotocography.
• Follow-up: amniotic fluid index and Doppler twice weekly; cardiotocography daily to twice weekly; newborn renal ultrasound, blood pressure and creatinine; paediatric nephrology review.