Polyhydramnios and Oligohydramnios

Updated: Sep 20, 2017
  • Author: Brian S Carter, MD, FAAP; Chief Editor: Dharmendra J Nimavat, MD, FAAP  more...
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The amniotic fluid that bathes the fetus is necessary for its proper growth and development. It cushions the fetus from physical trauma, permits fetal lung growth, and provides a barrier against infection. Normal amniotic fluid volume varies. The average volume increases with gestational age, peaking at 800-1000 mL, which coincides with 36-37 weeks' gestation. An abnormally high level of amniotic fluid, polyhydramnios, alerts the clinician to possible fetal anomalies. An inadequate volume of amniotic fluid, oligohydramnios , results in poor development of the lung tissue and can lead to fetal death.

Polyhydramnios occurs in 1% of pregnancies, [1]  whereas oligohydramnios occurs in about 11% of pregnancies. [2]  No age variables are recognized.

In pregnancies affected by polyhydramnios, approximately 20% of neonates are born with a congenital anomaly of some type; therefore, the delivery of these newborns in a tertiary care setting is preferred. This article presents the causes, outcomes, and treatments of polyhydramnios and oligohydramnios, as well as their effects on the developing fetus and neonate.



Rupture of the membranes is the most common cause of oligohydramnios. However, because the amniotic fluid is primarily fetal urine in the latter half of the pregnancy, the absence of fetal urine production or a blockage in the fetus's urinary tract can also result in oligohydramnios. Fetal swallowing, which occurs physiologically, reduces the amount of fluid, and an absence of swallowing or a blockage of the fetus's gastrointestinal tract can lead to polyhydramnios.

A near term fetus produces 500-1200 mL of urine and swallows between 210 and 790 mL of amniotic fluid per day. [3]




The underlying cause of the excessive amniotic fluid volume is obvious in some clinical conditions and is not completely understood in others. Causes include the following:

  • Twin gestation with twin-to-twin transfusion syndrome (increased amniotic fluid in the recipient twin and decreased amniotic fluid in the donor) or multiple gestations
  • Fetal anomalies, including esophageal atresia (usually associated with a tracheoesophageal fistula), tracheal agenesis, duodenal atresia, and other intestinal atresias
  • Central nervous system abnormalities and neuromuscular diseases that cause swallowing dysfunction
  • Congenital cardiac-rhythm anomalies associated with hydrops, fetal-to-maternal hemorrhage, and parvovirus infection
  • Poorly controlled maternal diabetes mellitus (Oligohydramnios may also be seen if severe vascular disease is present.)
  • Chromosomal abnormalities, most commonly trisomy 21, followed by trisomy 18 and trisomy 13.
  • Fetal akinesia syndrome with absence of swallowing

In a study by Kollmann et al of 860 singleton pregnancies complicated by polyhydramnios, 68.8% of the polyhydramnios cases were idiopathic, whereas maternal diabetes was found in 19.8% of cases; congenital anomalies, in 8.5%; and a positive TORCH (toxoplasmosis, other [such as syphilis, varicella-zoster, parvovirus B19], rubella, cytomegalovirus, herpes infection) serology, in 2.9%. [4]


Causes of oligohydramnios include the following:

  • Fetal urinary tract anomalies, such as renal agenesis, polycystic kidneys, or any urinary obstructive lesion (eg, posterior urethral valves [5] )
  • Premature rupture of membranes and chronic leakage of the amniotic fluid;  chorioamnionitis is an additional important maternal complication from oligohydramnios due to rupture of the membranes, which has an incidence of 21-74%. The earlier chorioamnionitis occurs in pregnancy, the greater the fetal risk of bronchopulmonary dysplasia, neurologic complications, pulmonary hypoplasia, and, in severe cases, respiratory failure in the neonate.
  • Placental insufficiency, as seen in pregnancy-induced hypertension, maternal diabetes, or postmaturity syndrome when the pregnancy extends beyond 42 weeks' gestation
  • Maternal use of prostaglandin synthase inhibitors or angiotensin-converting enzyme


If polyhydramnios is not associated with any other findings, the prognosis is usually good. According Desmedt et al, there is a 61% perinatal mortality in polyhydramnios associated with a fetal or placental malformation. [6]  About 20% of infants with polyhydramnios have some type of an anomaly; in these cases, the prognosis depends on the severity of the anomaly. Yefet et al reported that even with normal detailed prenatal ultrasonographic evaluation, polyhydramnios (amniotic fluid index [AFI] >24 cm) is associated with an increased rate of fetal malformations, genetic syndromes, neurologic disorders, and developmental delay, conditions that may only be diagnosed postnatally. [1]

In a study of 163 women with idiopathic polyhydramnios, resolution was more likely when it was diagnosed early in pregnancy and when the AFI was low. [7] When idiopathic polyhydramnios persisted across the pregnancy, there was an increased risk of macrosomia and preterm delivery.

Studies show that as the severity of polyhydramnios increases, the likelihood of determining the etiology increases. In cases of mild polyhydramnios, the likelihood of finding a significant problem is only about 16.5%; this should be communicated to the parents. 

In the setting of oligohydramnios with renal agenesis, mortality is 100%. Milder forms of renal dysplasia or obstructive uropathy can be associated with a mild to severe degree of pulmonary hypoplasia and long-term renal failure. In cases of pulmonary hypoplasia, the effectiveness of many treatments such as the administration of surfactant, high-frequency ventilation, and nitric oxide has not been established. The prognosis in these cases is related to the volume of amniotic fluid and the gestational age at which oligohydramnios develops.

Borderline oligohydramnios (AFI 5.1-8 cm) does not appear to be a risk factor for adverse perinatal outcomes in uncomplicated, late preterm pregnancies. [8]


When Chamberlin used ultrasonography to evaluate the perinatal mortality rate (PMR) in 7562 patients with high-risk pregnancies, the PMR of patients with normal fluid volumes was 1.97 deaths per 1000 patients. [9]  However, the PMR increased to 4.12 deaths per 1000 patients with polyhydramnios and 56.5 deaths per 1000 patients with oligohydramnios.

In twin gestation with twin-to-twin transfusion, polyhydramnios may occur in the recipient twin, and oligohydramnios may occur in the donor. This complication is associated with high morbidity and mortality rates.


Idiopathic polyhydramnios appears to increase the risk of prolonged first stage of labour, nonvertex presentation, and cesarean delivery. [10] Preterm labor and delivery occurs in approximately 26% of mothers with polyhydramnios. Other complications include premature rupture of the membranes (PROM), abruptio placenta, malpresentation, and postpartum hemorrhage. [11]

Studies show an increased risk of associated fetal anomalies in more severe forms of polyhydramnios. In a series, 20% of cases of polyhydramnios involved associated fetal anomalies, including problems of the gastrointestinal system (40%), central nervous system (26%), cardiovascular system (22%), or genitourinary system (13%). [12]  Among these cases of polyhydramnios, multiple gestations occurred in 7.5%, 5% were due to maternal diabetes, and the remaining 8.5% were due to other causes. However, at least 50% of the patients had no associated risk factors.


The mortality rate in oligohydramnios is high. The lack of amniotic fluid allows compression of the fetal abdomen, which limits movement of its diaphragm. In addition to chest wall fixation, the lack of amniotic fluid flowing in and out of the fetal lung leads to pulmonary hypoplasia.

Oligohydramnios is also associated with meconium staining of the amniotic fluid, fetal heart conduction abnormalities, umbilical cord compression, poor tolerance of labor, lower Apgar scores, and fetal acidosis. In cases of intrauterine growth restriction (IUGR), the degree of oligohydramnios is often proportional to growth restriction, is frequently reflective of the extent of placental dysfunction, and is associated with a corresponding increase in the PMR.

Maternal body mass index (BMI) does not appear to be associated with oligohydramnios in late gestation. [13]  However, there is an increased risk of primary cesarean delivery with increasing maternal BMI.



Risks and complications of amnioinfusion include amniotic fluid embolism, maternal respiratory distress, increased maternal uterine tone, and transient fetal respiratory distress. An increase in the risk of maternal or fetal infection is not substantiated.

Risks of amniocentesis include fetal loss (1-2%). Other complications are placental abruption, preterm labor, fetal-maternal hemorrhage, maternal Rh sensitization, and fetal pneumothorax. The risk of fetal infection is slightly increased.


The primary complications of oligohydramnios are those related to fetal distress before or during labor. The risk of fetal infection is increased in the presence of prolonged rupture of the membranes.