Polyhydramnios

The overdistended uterus bleeds - Polyhydramnios is a recognized risk factor for uterine atony, and atony causes 70% to 80% of postpartum hemorrhage. Type and screen at a minimum, uterotonics ready, and expect to keep them running after the placenta is out.

Maternal dyspnea is mechanical - Severe polyhydramnios physically resists diaphragmatic movement, giving breathlessness, a tight abdomen, and lower extremity swelling. Sitting her up for neuraxial placement is more comfortable than lying flat, and supine positioning may not be tolerated at all.

Look for maternal diabetes - Gestational diabetes is one of the common maternal causes, working through fetal osmotic diuresis. Review the glucose tolerance screen, get a point-of-care glucose, and plan for a macrosomic fetus.

Cord prolapse and malpresentation - Excess fluid lets the fetus sit in an abnormal lie, and preterm labor or PROM with a non-vertex presentation can drop the cord. That is a crash cesarean with no warning — know before it happens whether you are extending an epidural or inducing.

Plan on a cesarean - Labor dystocia and macrosomia frequently drive operative delivery, and delivery is recommended at a tertiary care center for these patients.

Amnioreduction has a downside - Reductive amniocentesis and indomethacin are reserved for severe symptomatic polyhydramnios. Sudden uterine decompression is itself a recognized precipitant of placental abruption, so a large-volume drain is not a benign procedure.

TTTS in monochorionic twins - The recipient develops polyhydramnios and polycythemia while the donor develops oligohydramnios and severe anemia; it affects 8% to 10% of monochorionic diamniotic pregnancies. Fetoscopic laser photocoagulation of the communicating vessels is the definitive treatment for severe disease and has been managed under epidural anesthesia.

Fetal surveillance drives timing - Antepartum ultrasound for amniotic fluid index or single deepest vertical pocket plus fetal anatomy. Severity matters: an underlying disease or congenital anomaly is identified in 91% of severe cases, and perinatal mortality roughly doubles compared with normal fluid volumes.

Polyhydramnios is a pathologic excess of amniotic fluid — a single deepest vertical pocket over 8 cm, or an amniotic fluid index of 25 cm or more. It complicates 1% to 2% of pregnancies. Amniotic fluid comes mainly from fetal urine and is cleared mainly by fetal swallowing; the fetus makes 500 to 1200 mL of urine and swallows 210 to 760 mL daily, so anything that raises output or blocks swallowing tips the balance.

Maternal hyperglycemia drives fetal osmotic diuresis. From the fetal side, a swallowing defect is the most common cause, along with neuromuscular disease, aneuploidy, congenital infection, and the recipient twin in twin-twin transfusion syndrome (TTTS). Roughly 60% to 70% of cases are idiopathic and about 20% involve a congenital anomaly.