During normal pregnancy, there is a dynamic balance between the production and absorption of amniotic fluid. An imbalance in this process can lead to abnormal amniotic fluid volume. Abnormalities in the amniotic fluid volume can not only indicate potential maternal-fetal complications but also pose direct risks to perinatal safety.
Polyhydramnios
Polyhydramnios refers to an excessive accumulation of amniotic fluid during pregnancy, with a total volume exceeding 2,000 mL. The incidence is approximately 0.5%–1%. When the volume increases rapidly within a few days, it is termed acute polyhydramnios. When the volume increases gradually over several weeks, it is classified as chronic polyhydramnios.
Etiology
Around one-third of cases are of unknown cause and are classified as idiopathic polyhydramnios. Significant polyhydramnios may be associated with fetal structural abnormalities, maternal pregnancy complications, or other related conditions.
Fetal Disorders
Fetal disorders include structural abnormalities, fetal tumors, neuromuscular developmental disorders, metabolic diseases, and chromosomal or genetic abnormalities. Significant polyhydramnios is often associated with fetal structural abnormalities, most commonly involving the nervous system and gastrointestinal tract. Nervous system abnormalities include conditions such as anencephaly and spina bifida, which are neural tube defects. Neural tube defects may result in increased cerebrospinal fluid leakage, choroid plexus proliferation, increased exudates, and decreased antidiuretic hormone, leading to polyuria. Swallowing dysfunction due to central nervous system abnormalities, such as the absence of the swallowing reflex, may increase amniotic fluid production while reducing its absorption. Gastrointestinal tract abnormalities, such as esophageal or duodenal atresia, prevent fetal swallowing of amniotic fluid, leading to its accumulation and polyhydramnios. Other causes include fetal abdominal wall defects, diaphragmatic hernia, cardiac structural abnormalities, congenital cystic adenomatous malformation of the lungs, sacrococcygeal teratoma, and metabolic diseases like congenital hyperaldosteronism (Bartter syndrome). Polyhydramnios may also be associated with chromosomal anomalies such as trisomy 18, trisomy 21, and trisomy 13, which can impair fetal swallowing and result in fluid accumulation.
Multiple Gestation
The incidence of polyhydramnios with twin pregnancies is approximately 10%, which is ten times higher than that of singleton pregnancies. Monochorionic twin pregnancies exhibit a higher incidence of polyhydramnios and may be complicated by twin-to-twin transfusion syndrome. In such cases, the recipient twin experiences increased blood volume and urinary output, leading to polyhydramnios.
Placental and Umbilical Cord Abnormalities
Polyhydramnios is associated with 15%–30% of cases where the diameter of a placental chorangioma exceeds 1 cm. Giant placentas and velamentous cord insertions can also lead to polyhydramnios.
Pregnancy Complications
The incidence of polyhydramnios ranges from 13%–36% in pregnancies complicated by gestational diabetes. Maternal hyperglycemia elevates fetal blood glucose levels, leading to osmotic diuresis and increased transudation across the placenta and fetal membranes, thereby causing polyhydramnios. Maternal-fetal Rh incompatibility, fetal immune hydrops, and villous edema of the placenta may impair fluid exchange, resulting in polyhydramnios.
Clinical Manifestations and Diagnosis
Clinical Manifestations
Acute Polyhydramnios
Acute polyhydramnios is relatively rare and often occurs between 20 and 24 weeks of gestation. Amniotic fluid volume increases rapidly, causing significant uterine enlargement within a few days. Increased abdominal pressure leads to a range of compressive symptoms. Pregnant women may experience abdominal pain and discomfort, restricted mobility, and distress. Elevated diaphragms result in thoracic compression, causing dyspnea, cyanosis, and an inability to lie flat. On examination, the abdominal skin appears tight and shiny. In severe cases, the skin may become thin and subcutaneous veins prominently visible. Significant uterine enlargement compresses the inferior vena cava, impairing venous return and resulting in edema or varicose veins in the lower limbs and external genitalia. The uterus is markedly larger than expected for the gestational age, and excessive abdominal distension makes identifying fetal positions difficult. Fetal heart tones may be faint or absent due to high intrauterine tension.
Chronic Polyhydramnios
Chronic polyhydramnios is more common and typically manifests in late pregnancy. Fluid volume increases gradually over several weeks. Symptoms are milder, and pregnant women generally adapt to the condition. Most individuals experience only rapid abdominal enlargement without significant discomfort or, at most, mild compressive symptoms such as chest tightness or shortness of breath, which are tolerable. During prenatal examinations, rapid increases in fundal height and abdominal circumference are observed, exceeding those expected for gestational age. The abdominal wall becomes shiny and thinned. Palpation reveals increased uterine tension and a sense of fluid fluctuation. Identification of fetal positions may be challenging, and fetal heart tones may be faint. During obstetric palpation, when fundal height measurements exceed those consistent with gestational age or when fetal palpation is difficult or the fetus appears to "float," the possibility of polyhydramnios should be considered.
Auxiliary Examinations
Ultrasound Examination
This is an important diagnostic tool that can assess not only amniotic fluid volume but also fetal conditions such as anencephaly, spina bifida, fetal hydrops, and multiple gestations. Diagnostic metrics for abnormal amniotic fluid volume include the deepest vertical pocket (DVP) and the amniotic fluid index (AFI). Normal DVP values range from 2 cm to 8 cm, while normal AFI values range from 8 cm to 25 cm. A DVP ≥ 8 cm or an AFI ≥ 25 cm indicates polyhydramnios. Some authorities suggest using an AFI greater than 3 standard deviations above the mean for the gestational age or above the 97.5th percentile as diagnostic criteria.
Fetal Disease Screening
Chromosomal abnormalities in some fetuses may be associated with polyhydramnios. For pregnant women with polyhydramnios, in addition to using ultrasound to exclude structural abnormalities, fetal cells from amniotic fluid or umbilical cord blood may be analyzed for cytogenetic or molecular genetic testing to detect numerical or structural chromosomal abnormalities, as well as microdeletions or duplications. Doppler ultrasound can assess the peak systolic velocity of the fetal middle cerebral artery to predict fetal anemia if present. PCR testing can help detect infections in the fetus caused by human parvovirus B19, Treponema pallidum (syphilis), Toxoplasma, herpes simplex virus, rubella virus, or cytomegalovirus. However, pregnant women undergoing amniocentesis for polyhydramnios should be informed about the risk of membrane rupture, as excessive amniotic fluid and high intra-amniotic pressure can increase the likelihood of complications such as miscarriage or preterm birth.
Other Tests
Additional assessments include glucose tolerance testing for gestational diabetes and maternal blood typing with antibody titer testing in cases of Rh blood group incompatibility.
Effects on the Mother and Fetus
Effects on the Mother
In most cases, symptoms are mild or absent. Severe or rapidly developing polyhydramnios can cause overdistension of the uterus, leading to high intra-abdominal pressure and compression of neighboring organs, which can produce symptoms resembling abdominal compartment syndrome. In severe instances, maternal cardiac failure may occur. Excessive uterine tension increases the risk of preterm premature rupture of membranes (PPROM), preterm birth, and placental abruption. Overstretching of uterine muscle fibers can result in uterine atony after delivery, significantly increasing the incidence of postpartum hemorrhage.
Effects on the Fetus
Common complications include abnormal fetal presentation, fetal distress, and an increased risk of preterm birth. Rapid outflow of amniotic fluid upon membrane rupture may lead to umbilical cord prolapse. Higher severity of polyhydramnios correlates with increased perinatal mortality. The perinatal mortality rate for severe polyhydramnios in the second trimester exceeds 50%.
Management
Management strategies are based on the presence or absence of fetal structural or genetic abnormalities, gestational age, and the severity of maternal symptoms.
Polyhydramnios in the Presence of Fetal Structural Abnormalities
For severe fetal structural abnormalities, pregnancy termination is advised. In cases of non-severe fetal structural abnormalities, fetal condition, prognosis, and the availability of advanced neonatal surgical interventions should be evaluated in consultation with the pregnant woman and her family to determine the appropriate course of action. For cases involving fetal hemolysis secondary to maternal-fetal blood group incompatibility, intrauterine transfusion may be provided at a fetal medicine center if conditions permit.
Polyhydramnios in the Presence of a Normal Fetus
The underlying cause should be investigated, and the primary condition treated. Prostaglandin synthetase inhibitors such as indomethacin, which have an antidiuretic effect, may be used to reduce fetal urine output and decrease amniotic fluid volume. Ultrasound monitoring of amniotic fluid volume is recommended weekly during treatment. Due to the potential closure of the fetal ductus arteriosus with indomethacin, long-term use should be avoided, and it is contraindicated after 32 weeks of gestation. Indomethacin use solely for reducing amniotic fluid volume is not recommended.
For mild symptoms, maternal rest and a lateral recumbent position may improve uteroplacental circulation. Sedatives may be used if necessary. Weekly ultrasounds help monitor the AFI and fetal growth.
For severe symptoms, transabdominal amniocentesis may be performed to remove an appropriate amount of amniotic fluid to relieve compression symptoms. Amniotic fluid obtained during the procedure may also be used to assess fetal lung maturity if necessary. During amnioreduction, maternal blood pressure, heart rate, respiratory status, and fetal heart rate should be monitored closely. Sedatives and uterine contraction suppressants may be administered if necessary to prevent preterm labor. In certain cases, repeat amnioreduction may occur every 3 to 4 weeks to reduce intra-amniotic pressure.
For polyhydramnios with recurrent fluid accumulation and severe maternal symptoms, if the pregnancy is ≥ 34 weeks and fetal lungs are mature, pregnancy termination may be considered. If fetal lungs are not mature, corticosteroids such as dexamethasone may be administered to promote fetal lung maturity before considering pregnancy termination.
Management During Labor
Attention should be given to the risk of umbilical cord prolapse and placental abruption. If uterine contractions are weak following membrane rupture, oxytocin infusion may be used to strengthen contractions while carefully monitoring labor progress. After delivery of the fetus, uterotonic agents should be administered promptly to prevent postpartum hemorrhage.
Oligohydramnios
Oligohydramnios refers to a condition in which the amniotic fluid volume is less than 300 mL during late pregnancy. The incidence rate ranges from 0.4% to 4%. Oligohydramnios significantly impacts perinatal outcomes and is associated with adverse pregnancy results.
Etiology
Oligohydramnios is primarily associated with reduced production or increased leakage of amniotic fluid. In some cases, the cause is unknown. Common causes include the following:
Fetal Structural Abnormalities
The condition is often related to abnormalities in the fetal urinary system, such as Meckel-Gruber syndrome, Prune-Belly syndrome, renal agenesis (e.g., Potter syndrome), renal tubular dysplasia, ureteral or urethral obstruction, or bladder exstrophy. These may result in oliguria or anuria, leading to reduced amniotic fluid levels. Chromosomal abnormalities, conditions such as omphalocele, diaphragmatic hernia, tetralogy of Fallot, cystic hygroma, microcephaly, hypothyroidism, and other structural defects can also cause oligohydramnios.
Placental Dysfunction
Post-term pregnancy and placental degeneration can result in placental dysfunction with decreased uteroplacental perfusion. Fetal growth restriction and chronic hypoxia provoke fetal blood redistribution to prioritize perfusion to the brain and heart, leading to reduced renal blood flow, decreased urine output, and subsequent oligohydramnios.
Amniotic Membrane Abnormalities
Some cases of oligohydramnios are linked to changes in the permeability of the amniotic membrane, inflammation, or intrauterine infections. Rupture of the membranes and leakage of amniotic fluid exceeding production rates can lead to oligohydramnios.
Maternal Factors
Hypertensive disorders during pregnancy can reduce placental blood flow. Maternal dehydration or hypovolemia increases plasma osmotic pressure, causing a corresponding increase in fetal plasma osmotic pressure and reduced urine formation. Prolonged use of certain medications, such as prostaglandin synthetase inhibitors or angiotensin-converting enzyme inhibitors, which have antidiuretic effects, may result in oligohydramnios. Autoimmune diseases such as systemic lupus erythematosus, Sjögren's syndrome, and antiphospholipid syndrome are also associated with reduced amniotic fluid levels.
Clinical Manifestations and Diagnosis
Clinical Manifestations
The symptoms of oligohydramnios are often nonspecific. Fetal growth restriction is commonly observed, and pregnant women may feel that their abdominal size is smaller compared to others at the same gestational age. Discomfort during fetal movements may occur. Placental dysfunction often manifests in reduced fetal movements. Physical examination may reveal that uterine height and abdominal circumference are smaller than expected for gestational age, especially when fetal growth restriction is present. The uterus may feel tightly wrapped around the fetus and may be sensitive, with stimuli easily triggering uterine contractions. During labor, contractions may be intense but poorly coordinated. Membrane rupture may result in the leakage of clear or bloody fluid, or pregnant women may notice dampness in their underwear. Vaginal examination may reveal limited visibility of the anterior amniotic sac, tight adhesion of the membranes to the presenting fetal part, and minimal fluid leakage following artificial membrane rupture.
Auxiliary Examinations
Ultrasound Examination
Ultrasound is the most critical diagnostic tool for oligohydramnios. During late pregnancy, a DVP ≤ 2 cm indicates oligohydramnios, while a DVP ≤ 1 cm denotes severe oligohydramnios. An AFI ≤ 5 cm is diagnostic of oligohydramnios. Ultrasound can also help identify fetal growth restriction and abnormalities such as renal agenesis, renal dysplasia, or urinary obstruction.
Electronic Fetal Monitoring
Fetuses with oligohydramnios often exhibit reduced placental reserve. Non-stress tests (NST) may show a non-reactive pattern. During labor, uterine contractions may exacerbate umbilical cord compression, resulting in fetal heart rate decelerations such as variable or late decelerations.
Fetal Chromosomal Analysis
Cells obtained from amniotic fluid or umbilical cord blood may undergo cytogenetic or molecular genetic testing to identify chromosomal abnormalities, including numerical or structural anomalies, and microdeletions or duplications. Sampling is more challenging during oligohydramnios, and risks and possible failures should be disclosed.
Effects on the Mother and Fetus
Effects on the Fetus
Perinatal mortality rates increase significantly in cases of oligohydramnios. Mild oligohydramnios increases perinatal mortality by 13 times, while severe oligohydramnios increases mortality by 47 times. Causes of death include fetal hypoxia and structural abnormalities. Early pregnancy oligohydramnios may lead to fetal adhesions to the membranes, resulting in structural anomalies such as limb shortening. In mid-to-late pregnancy, external uterine pressure directly impacts the fetus, causing musculoskeletal deformities such as torticollis, scoliosis, or abnormalities of the hands and feet. Oligohydramnios secondary to congenital renal agenesis may result in Potter syndrome, characterized by pulmonary hypoplasia, epicanthal folds, flat nasal bridges, low-set ears, and limb abnormalities, with a poor prognosis. Most affected infants die shortly after birth. Oligohydramnios is often associated with fetal growth restriction and may even result in intrauterine fetal death.
Effects on the Mother
Increased rates of operative delivery and labor induction are commonly observed in cases of oligohydramnios.
Management
Management decisions depend on whether fetal abnormalities are present and the gestational age.
Oligohydramnios with Severe Lethal Fetal Structural Abnormalities
Pregnancy should be terminated promptly if the fetus is diagnosed with severe lethal structural abnormalities. Structural abnormalities may be confirmed through ultrasound, while chromosomal abnormalities require invasive prenatal diagnostic techniques. After evaluation and discussion with the pregnant woman and her family, termination of pregnancy is appropriate if fetal viability is determined to be impossible.
Oligohydramnios with a Normal Fetus
The cause should be identified and addressed. Regular monitoring of the intrauterine condition of the fetus should include fetal movement counts, biophysical profiling, ultrasound assessments of amniotic fluid volume, and measurement of umbilical artery Doppler parameters such as the systolic-to-diastolic (S/D) ratio, along with electronic fetal monitoring.
Pregnancy Termination
During term gestation, if the fetus is viable outside the womb, pregnancy termination may be warranted. In cases of placental dysfunction, fetal distress, or severe meconium-stained amniotic fluid with poor prospects for rapid delivery, cesarean section may be used to improve perinatal survival rates. If the fetus has good reserve function and no significant intrauterine hypoxia, vaginal delivery with close monitoring of labor progression and fetal heart rate changes may be considered. Oligohydramnios caused by preterm premature rupture of membranes should be managed accordingly.
Close Observation
In cases of preterm pregnancy where fetal lungs are immature, treatment should focus on addressing the underlying cause and extending gestation as much as possible. Appropriate management should depend on gestational age and the intrauterine condition of the fetus, with pregnancy termination considered when necessary.