Epidemiology


Etiology

  • Typically idiopathic (∼ 70% of cases)
  • Fetal anomalies
    • Gastrointestinal (e.g., esophageal atresia, duodenal atresia and stenosis): reduced swallowing and absorption of amniotic fluid
    • CNS: anencephaly (leads to impaired swallowing of amniotic fluid, leakage of cerebrospinal fluid, and increased urination due to lack of fetal ADH), meningomyelocele (impaired fetal swallowing, due to Chiari II malformation)
    • Pulmonary: cystic lung malformations
    • Multiple pregnancy: twin-to-twin transfusion syndrome
  • Maternal conditions
    • Diabetes mellitus
      • Increased maternal glucose levels increase fetal glucose levels as well, resulting in polyuria.
    • Rh incompatibility

Pathophysiology


Clinical features


Diagnostics

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Treatment

  • First-line / Conservative Management:
    • Mild / Asymptomatic: Expectant management; treat underlying maternal cause (e.g., strict glycemic control in GDM).
    • Antenatal Surveillance: Weekly to twice-weekly NST / BPP starting at 32–34 weeks GA for moderate-to-severe cases.
  • Second-line / Symptomatic Management:
    • Therapeutic Amnioreduction: Indicated for severe maternal respiratory compromise or preterm labor symptoms.
    • Indomethacin (decreases fetal urine output via renal vasoconstriction):
      • Only used if GA < 32 weeks (avoids premature closure of the ductus arteriosus and oligohydramnios).
  • Delivery Planning:
    • Idiopathic/Mild: Deliver at 39w0d–39w6d.
    • Severe/Refractory: Deliver at 34w0d–37w6d based on maternal-fetal status.
    • Intrapartum Precaution: Avoid sudden/rapid artificial rupture of membranes (AROM) to prevent rapid decompression.