Polyhydramnios (aka Hydramnios)

1. What every clinician should know

Polyhydramnios is typically caused by decreased fetal swallowing or increased fetal urination. It is diagnosed sonographically by an amniotic fluid index (AFI) greater than 24 cm or a single deepest pocket (SDP) greater than 8 cm.

Polyhydramnios is associated with increased risks of adverse pregnancy outcomes such as:

  • Macrosomia

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  • Cesarean delivery for non-reassuring fetal heart rate tracing

  • Stillbirth

The incidence in a general obstetric population ranges from 0.2-1.6%.

The likelihood that polyhydramnios is associated with a distinct identifiable etiology depends upon its severity. While most cases of mild polyhydramnios (SDP 8-11 cm or AFI 24-29 cm) are idiopathic (about 66%), with moderate (SDP 12-15 cm/AFI 30-35 cm) and severe ( SDP > 15 cm/ AFI > 35cm), polyhydramnios the etiology has a greater chance of being related to:

Maternal causes:

  • Pregestational or gestational diabetes mellitus (15% of all cases of polyhydramnios)

  • Isoimmunization

Fetal causes:

  • Congenital anomalies (13% of all cases of polyhdramnios)

    Gastrointestinal obstruction

    CNS abnormalities

    Cystic hygroma

    Nonimmune hydrops

    Sacrococcygeal teratoma


  • Twin-twin transfusion syndrome (5% of all cases of polyhydramnios)

  • Myotonic dystrophy or other neuromuscular syndromes (fewer than 1% of all cases of polyhydramnios)

2. Diagnosis and differential diagnosis

The diagnosis of polyhydramnios is based upon sonographic visualization of increased amniotic fluid volume.

The AFI is the sum of the SDPs from each of four quadrants of the uterus, with polyhydramnios defined as an AFI greater than 24 cm.

When diagnosis of polyhydramnios is made, a comprehensive sonographic evaluation should be performed to determine whether fetal anomalies are present.

It is important to keep in mind that the prevalence of an anomalous infant increases with the severity of polyhydramnios, reaching up to 30% in cases of severe polyhydramnios.

As noted above, the differential diagnosis includes maternal causes (e.g. diabetes mellitus) and fetal causes (such as aneuploidy, anatomic abnormalities or genetic anomalies). Correspondingly, assessment of maternal and familial medical history, gestational diabetes and of the fetus through a targeted sonographic examination should be performed. The results of these assessments will further delineate the value of other laboratory assessments such as invasive prenatal diagnosis (via amniocentesis).

3. Management

It is not clear that any medical intervention improves the outcome of women with polyhydramnios. When a clear-cut etiology is evident, such as maternal diabetes or fetal anemia from isoimmunization, the underlying problem should be addressed.

When polyhydramnios is caused by a congenital anomaly or is idiopathic, treatment is expectant and focused on assuring fetal well being and intervening for maternal complications.

Treatment of polyhydramnios via amnioreduction in singleton pregnancy is warranted only if symptomatic (e.g. significant maternal discomfort). Indomethacin has been used to lessen amniotic fluid in some cases as well, although if this treatment is continued for more than 48 hours, fetal echocardiograms should be performed.

Intrapartum – Cesarean should only be performed for typical obstetric indications. Rupture of membranes may cause cord prolapse or placental abruption due to rapid uterine decompression and observation for these possibilities should be performed.

Postpartum – The clinician should be prepared to deal with postpartum uterine atony, given the increased risk of this complication.

4. Complications

A. Complications related to polyhydramnios
  • Maternal respiratory compromise

  • Premature labor and premature rupture of membranes (12-22%)

  • Fetal malposition (7-20%)

  • Fetal macrosomia (16-24%)

  • Placental abruption (1-5%)

  • Umbilical cord prolapse (1-3%)

  • Cesarean delivery for non-reassuring fetal heart rate tracing (17-44%)

  • Stillbirth (3-9%)

  • Uterine atony (0.5-2%)

B. Complications related to the treatment of polyhydramnios

Amnioreduction: (1-2%)

  • Rupture of membranes

  • Direct fetal injury

  • Infection

Indomethacin: (maternal)

  • Nausea (3-9%)

  • Esophageal reflux (3-9%)

  • Gastritis (<3%)

  • Emesis (<3%)

  • Platelet dysfunction (<1%)

Indomethacin: (fetal) (<1%)

  • Constriction of the ductus arteriosus

5. Prognosis and outcome

The prognosis of polyhydramnios depends on the severity of polyhydramnios as well as the etiology. Most cases of idiopathic mild polyhydramnios resolve spontaneously (75%) with no adverse outcome to the fetus or the mother. In polyhydramnios associated with maternal diabetes, perinatal mortality rate, fetal anomalies rate and aneuploidy rate are not different from the general population. In cases of moderate to severe polyhydramnios not associated with diabetes, there is more than a six times higher risk of perinatal mortality, five times higher risk of delivery of a fetus with growth restriction and a 25 times higher risk of having fetal anomalies.

Recurrence of polyhydramnios in the next pregnancy depends on the etiology of the previous polyhydramnios. No studies have been conducted to conclude on the effect of polyhydramnios on long term maternal health.

6. What is the evidence for specific management and treatment recommendations

Magann, EF, Chauhan, SP. “Sonographic assessment of amniotic fluid: oligohydraminios and polyhydramnios”. Fetal Evidence-Chapter-50. vol. p. 2007. pp. 252-359.

Magann, EF, Chauhan, SP. “A Review of Idiopathic Hydramnios and Pregnancy Outcomes”. Obstetrical & Gynecological Survey. vol. 62. 2007. pp. 795-802.

Maymon, E, Ghezzi, F. “. Isolated hydramnios at term gestation and the occurrence of peripartum complications”. European Journal of Obstetrics, Gynecology, & Reproductive Biology. vol. 77. 1998. pp. 157-61.

Dashe, JS. “Hydramnios: Anomaly prevalence and sonographic Detection”. Obstetrics & Gynecology. vol. 100. 2002. pp. 134-9.

Biggio, JR. “Hydramnios prediction of adverse perinatal outcome”. Obstetrics & Gynecology. vol. 94. 1999. pp. 773-7.

Kuang-Chao, C, Jui-Der, L. “Perinatal outcomes of polyhydramnios without associated congenital fetal anomalies after the gestational age of 20 weeks”. Chang Gung Med J. vol. 28. 2005. pp. 222-8.

Hill, LM, Breckle, R, Thomas, ML, Fries, JK. “Polyhydramnios: ultrasonically detected prevalence and neonatal outcome”. Obstet Gynecol. vol. 69. 1987. pp. 21

Moore, TR. “The Role of amniotic fluid assessment in evaluating fetal well-being”. Clin Perinatology. vol. 38. 2011. pp. 33-46.

Mazor, M. “Polyhydramnios is an independent risk factor for perinatal mortality and intrapartum morbidity in preterm delivery”. Eur J Obstet Gynecol Reprod Biol. vol. 70. 1996. pp. 41-7.