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. Inadequate volume of amniotic fluid, oligohydramnios , results in poor development of the lung tissue and can lead to fetal death.
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' 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' GI tract can lead to polyhydramnios.
Oligohydramnios occurs in 4% of pregnancies, and polyhydramnios occurs in 1% of pregnancies.
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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. The PMR increased to 4.12 deaths per 1000 patients with polyhydramnios and 56.5 deaths per 1000 patients with oligohydramnios.
Preterm labor and delivery occurs in approximately 26% of mothers with polyhydramnios. Other complications include premature rupture of the membranes (PROM), abruptio placenta, malpresentation, cesarean delivery, and postpartum hemorrhage. 
Studies show an increased risk of associated fetal anomalies in more severe forms of polyhydramnios. In a series in 1990, 20% of cases of polyhydramnios involved associated fetal anomalies, including problems of the GI system (40%), CNS (26%), cardiovascular system (22%), or genitourinary system (13%).  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.
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.
No age variables are recognized.
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