01/01/2023
🚦Polyhydramnios
●Polyhydramnios is typically caused by decreased fetal swallowing or increased fetal urination.
The most common etiologies are: fetal malformations and/or genetic disorders, maternal diabetes mellitus, multiple gestation, and fetal anemia. Rare causes include congenital viral infection or Bartter syndrome.
●If there is a subjective impression of polyhydramnios, we suggest that an objective measure such as an amniotic fluid index (AFI) be performed. We use single deepest pocket ≥8 cm or AFI ≥24 cm. Objective indices are standardized and provide a measurement that can be followed on serial examinations, even though sensitivity and positive predictive value (PPV) are suboptimal.
●A comprehensive sonographic evaluation is recommended to determine whether fetal anomalies or fetal hydrops is present. Suggested laboratory evaluations depend upon sonographic findings and may include screening for gestational diabetes, testing for fetomaternal hemorrhage if fetal anemia is suspected, maternal serology to determine exposure to infectious agents (eg, syphilis, parvovirus, cytomegalovirus, toxoplasmosis, rubella), and appropriate tests for hereditary anemias (eg, alpha thalassemia) or metabolic abnormalities.
●We recommend offering karyotype analysis in cases of severe polyhydramnios or if there are associated anatomic anomalies, if knowledge of the karyotype will affect management.
●The outcome of pregnancies complicated by polyhydramnios varies according to the severity and underlying etiology of the excessive fluid accumulation. Possible complications include maternal respiratory compromise, preterm labor, premature rupture of membranes (PROM), fetal malposition, and umbilical cord prolapse and/or postpartum uterine atony.
●We suggest treatment for polyhydramnios in singleton pregnancy only if there is preterm labor or significant maternal discomfort.
●The therapeutic option is determined by the gestational age, degree of discomfort, and sensitivity or contraindication to prostaglandin synthetase inhibitors.
●For severe symptomatic polyhydramnios at less than 32 weeks of gestation, we suggest amnioreduction (to normalize fluid volume) and treatment with indomethacin to maintain normal amniotic fluid volume (AFV). A course of corticosteroids is given prior to amnioreduction because of the increased risk of preterm birth.
●During indomethacin therapy, we monitor AFV at least weekly and titrate the indomethacin dose to AFV changes. We also monitor ductal Doppler flow at 2-7 days intervals, with increased surveillance after 28 weeks of gestation, to look for early evidence of constriction. It may be possible to discontinue indomethacin treatment if polyhydramnios does not recur as the indomethacin is tapered. Indomethacin is discontinued no later than 32 weeks because of the risk of premature ductal constriction.
●For severe symptomatic polyhydramnios between 32-34 weeks of gestation, we suggest amnioreduction. After 34 weeks, we offer amniocentesis for fetal lung maturity and deliver if maturity is confirmed. We suggest not administering indomethacin because of the high risk of premature closure of the ductus arteriosus at this gestational age. However, in select cases, this risk may be outweighed by the risk associated with multiple amniocenteses or prematurity. In these cases, ductal Doppler flow should be followed at least weekly to detect early evidence of constriction.
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