22/10/2017 Polyhydramnios and Oligohydramnios: Background, Pathophysiology, Etiology

Polyhydramnios and Oligohydramnios

Updated: Sep 20, 2017
Author: Brian S Carter, MD, FAAP; Chief Editor: Dharmendra J Nimavat, MD, FAAP more...

OVERVIEW

Background
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.

Pathophysiology
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]

Etiology
Polyhydramnios
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

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22/10/2017 Polyhydramnios and Oligohydramnios: Background, Pathophysiology, Etiology

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]

Oligohydramnios
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

Prognosis
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.

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22/10/2017 Polyhydramnios and Oligohydramnios: Background, Pathophysiology, Etiology

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]

Morbidity/mortality
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.

Polyhydramnios

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.

Oligohydramnios

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.

Complications

Polyhydramnios

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.

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22/10/2017 Polyhydramnios and Oligohydramnios: Background, Pathophysiology, Etiology

Oligohydramnios

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.

Clinical Presentation

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