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
- Diabetes mellitus
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.