AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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. 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.

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' 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.

Frequency

United States

Oligohydramnios occurs in 4% of pregnancies, and polyhydramnios occurs in 1% of pregnancies.

Mortality/Morbidity

• Chamberlin used ultrasonography to evaluate the perinatal mortality rate (PMR) in 7562 patients with high-risk pregnancies.¹ 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%).² 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.

Age

No age variables are recognized.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Physical

• Amniotic fluid
• • The volume of the amniotic fluid is evaluated by visually dividing the mother's abdomen into 4 quadrants. The largest vertical pocket of fluid is measured in centimeters. The total volume is calculated by multiplying this value by 4.
  • Polyhydramnios is usually defined as an amniotic fluid index (AFI) of more than 24 cm or a single pocket of fluid at least 8 cm in depth that results in an amniotic fluid volume of more than 2000 mL.
  • Oligohydramnios is sonographically defined as an AFI less than 7 cm or the absence of a fluid pocket 2-3 cm in depth.
• Polyhydramnios
• • Visual inspection may reveal a rapidly enlarging uterus in the pregnant mother.
  • Multiple gestations are associated with polyhydramnios.
  • Fetal abnormalities associated with polyhydramnios include neonatal macrosomia, fetal or neonatal hydrops with anasarca, ascites, pleural or pericardial effusions, and GI tract obstruction (eg, duodenal atresia, tracheoesophageal fistula).
  • Skeletal malformations can also occur; these include congenital hip dislocation, clubfoot, and limb reduction defect.
  • Abnormalities in fetal movement are suggestive of primary neurologic abnormalities or are in association with a genetic syndrome, such as polyploidy.
• Oligohydramnios
• • When the oligohydramnios is associated with renal agenesis or dysgenesis, symptoms include a marked deformation of the fetus due to of intrauterine constraint (Potter syndrome).
  • Obstructive uropathies cause similar deformations, including external compression with a flattened facies and epicanthal folds, hypertelorism, low-set ears, a mongoloid slant of the palpebral fissure, a crease below the lower lip, and micrognathia. Thoracic compression may also occur.
  • Oligohydramnios adversely affects fetal lung development, resulting in pulmonary hypoplasia that typically leads to death from severe respiratory insufficiency. Other fetal deformations include bowed legs, clubbed feet, a single umbilical artery, GI atresias, and a narrow chest secondary to external compression. Infants are typically small for their stated gestational age (SGA). When an abdominal mass is found on examination of the infant in this clinical setting, it often represents multicystic-dysplastic kidney, enlarged urinary bladder, or prune-belly syndrome.

Causes

• 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
  • CNS 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
• Oligohydramnios
• • Fetal urinary tract anomalies, such as renal agenesis, polycystic kidneys, or any urinary obstructive lesion (eg, posterior urethral valves)
  • PROM 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 (BPD), neurologic complications, pulmonary hypoplasia, and, in severe cases, respiratory failure in the neonate.
  • Placental insufficiency, as seen in pregnancy-induced hypertension (PIH), maternal diabetes, or postmaturity syndrome when the pregnancy extends beyond 42 weeks' gestation
  • Maternal use of prostaglandin synthase inhibitors or ACE inhibitors

WORKUP

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

If premature delivery is anticipated with either oligohydramnios or polyhydramnios, the amniotic fluid lamellar body count, lecithin-sphingomyelin (L:S) ratio, and phosphatidylglycerol (PG) concentration are helpful in determining the maturity of the fetal lungs and, therefore, in assessing the likelihood of respiratory distress syndrome.

• Polyhydramnios
• • Glucose tolerance test for mothers with suspected type 2 diabetes mellitus
  • Fetal hydrops testing: If fetal hydrops is present, immunologic and fetal infection need to be investigated. This should include screening for maternal antibodies to D, C, Kell, Duffy, and Kidd antigens to determine maternal antibody production against the fetal red blood cells. Infections of the fetus include cytomegalovirus (CMV), toxoplasmosis, syphilis, and parvovirus B19. The investigation should include the following:
  • • Venereal Disease Research Laboratories (VDRL) test to screen for syphilis
    • Immunoglobulin G (IgG) and immunoglobulin M (IgM) titers to evaluate for exposure to rubella, CMV, toxoplasmosis and parvovirus
    • A test for congenital viruses in the amniotic fluid using the polymerase chain reaction
  • Kleihauer-Betke test to evaluate fetal-maternal hemorrhage
  • Hemoglobin Bart in patients of Asian descent (who may be heterozygous for alpha-thalassemia)
  • Fetal karyotyping for trisomy 21, 13, and 18
• Oligohydramnios
• • Test for systemic lupus erythematosus, which causes immune-mediated infarcts in the placenta and placental insufficiency.  
  • Evaluate for PIH and hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. Test for elevated blood pressure, proteinuria, elevated uric acid, increased liver function test results, and low platelet count.

Imaging Studies

• Prenatal ultrasonography and polyhydramnios
• • Evaluate fetal swallowing. A decrease in fetal deglutition occurs in anencephaly, trisomy 18, trisomy 21, muscular dystrophy, and skeletal dysplasia.
  • Evaluate the fetal anatomy; assess for diaphragmatic hernia, lung masses, and the absence of the stomach bubble (which is associated with esophageal atresia). The double-bubble sign or a dilated duodenum suggests the possibility of duodenal atresia.
  • Test for fetal arrhythmias and malformations that result in cardiac failure and hydrops.
  • An abnormally large abdominal circumference may be observed with ascites and hydrops fetalis.
  • A macrosomic fetus is observed in association with poorly controlled maternal diabetes.
  • Assess the blood flow velocity in the anterior cerebral artery of the fetus for fetal anemia.
• Prenatal ultrasonography and oligohydramnios
• • Perform serial measurements of the AFI during the pregnancy. If the mother is in the third trimester and if the volume is less than 8 cm, suspect oligohydramnios. Levels less than 5 cm indicate significant oligohydramnios.
  • Visualize the fetal kidneys, collecting system, and bladder. If these are normal, suspect the chronic leakage of amniotic fluid or PIH.
  • Assess fetal growth. If PROM or urinary tract anomalies are absent, consider placental insufficiency and IUGR.
  • Uterine artery Doppler study findings may aid in the diagnosis of placental insufficiency.
  • Postnatally, evaluate organ systems likely to be involved on the basis of the pregnancy history and results of other prenatal evaluations. For more information, see Oligohydramnios.

Other Tests

• Testing of the infant is recommended, depending on the results of postnatal evaluation of the infant. Such evaluation may include chromosome testing, testing for evidence of congenital infection, ultrasonography of the genitourinary tract, and appropriate radiologic evaluation of the GI tract. ECG and echocardiography may also be indicated.

Procedures

• Polyhydramnios
• • Reductive amniocentesis may be performed and has contributed to prolonged pregnancy in patients who are severely affected by hydramnios.³ This procedure can reduce the risk of preterm labor, PROM, umbilical cord prolapse, and placental abruption. However, if too much fluid is removed, placental abruption may occur. Other risks of the procedure include infection, bleeding, and trauma to the fetus.
  • Laser ablation of placental vessels may be efficacious in cases of twin-to-twin transfusion syndrome.
• Oligohydramnios
• • The transabdominal instillation of indigo carmine may be used to evaluate for PROM.
  • The transcervical instillation of isotonic sodium chloride solution (ie, amnioinfusion) at the time of delivery reduces the risk of cord compression, fetal distress and meconium dilution. It also reduces the potential need for cesarean delivery.

Histologic Findings

• Examination of the placenta may be helpful in determining the cause of the polyhydramnios or oligohydramnios.

TREATMENT

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The first step is identifying the etiology of the abnormal volume of amniotic fluid. Medical care includes the use of steroids to enhance fetal lung maturity if preterm delivery is anticipated.

• Polyhydramnios
• • Patients with polyhydramnios tend to have a higher incidence of preterm labor secondary to overdistention of the uterus.
  • Schedule weekly or twice weekly perinatal visits and cervical examinations.
  • Place patients on bed rest to decrease the likelihood of preterm labor.
  • Perform serial ultrasonography to determine the AFI and document fetal growth.
  • In cases of polyhydramnios associated with fetal hydrops secondary to fetal anemia, the direct intravascular transfusion of erythrocytes (or infusion into the fetal abdomen) may improve the fetal hematocrit and fetal congestive heart failure, thereby allowing prolongation of the pregnancy and improving survival.
• Oligohydramnios
• • Maternal bed rest and hydration promote the production of amniotic fluid by increasing the maternal intravascular space. Bed rest may also help when PIH is present, allowing prolongation of the pregnancy.
  • Studies show that oral hydration, by having the women drink 2 liters of water, increases the AFI by 30%.

Consultations

• A specialist in maternal-fetal medicine should be consulted when significant oligohydramnios or polyhydramnios is present, especially when the condition is unexplained, involves hydrops fetalis, or is associated with congenital malformations.
• Genetic counseling may be helpful in cases in which congenital anomalies are identified.
• Consult a neonatologist, pediatric surgeon, pediatric cardiologist, pediatric nephrologist, or other genetics specialists as required to care for the infant.

Diet

• In cases of polyhydramnios in which maternal diabetes is suspected, perform a glucose tolerance test. If the test results are positive, treat the mother with an American Diabetes Association (ADA) diet. Insulin is rarely needed.

MEDICATION

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Most cases of polyhydramnios respond in the first week of treatment with indomethacin.^{4, 5, 6} The approach appears to be highly effective (90-100% in some studies), provided that the cause is not hydrocephalus or a neuromuscular disorder that alters fetal swallowing.

Drug Category: Prostaglandin inhibitors

When administered to pregnant women with polyhydramnios, these drugs can reduce fetal urinary flow, decreasing the volume of amniotic fluid.

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Polyhydramnios: See recommendations for oligohydramnios below.
• Oligohydramnios
• • Consider hospitalizing and thoroughly evaluating the mother in cases diagnosed after 26-33 weeks' gestation.
  • If the fetus does not have an anomaly, delivery should be performed if the biophysical profile is nonreassuring.
  • The instillation of isotonic sodium chloride solution in the second trimester may be of benefit in some patients. Use transabdominal amnioinfusion to instill 400-600 mL, which may improve visualization for ultrasonography and increase volume of the amniotic fluid.
  • In cases associated with postmaturity, review pregnancy dating. If the gestation is truly longer than term, deliver the fetus by means of either induction or cesarean delivery.
  • If meconium is present during labor, administer amnioinfusion therapy to reduce the potential for fetal distress and prenatal aspiration.

Transfer

• Transfer to a tertiary center is indicated when the pregnant woman has a high likelihood of maternal illness, preterm delivery, or infant problems that may require the resources of a tertiary care facility.

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.
• Oligohydramnios
• • The primary complications 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.

Prognosis

• Polyhydramnios
• • If the condition is not associated with any other findings, the prognosis is usually good.
  • According Desmedt et al, the PMR in polyhydramnios associated with a fetal or placental malformation was 61%.⁷
  • As mentioned in Background and Mortality/Morbidity 20% of infants with polyhydramnios have some anomaly; in these cases, the prognosis depends on the severity of the anomaly.
  • 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.
• Oligohydramnios
• • In renal agenesis, the mortality rate is 100%.
  • Milder forms of renal dysplasia or obstructive uropathy can be associated with 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.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to perform ultrasonography in a pregnancy complicated by either polyhydramnios or oligohydramnios to investigate associated or contributory fetal anomalies
• The underlying anomalies may determine the outcome of the fetus, as well as the treatment and outcome of the neonate. As appropriate, specialists should be consulted, and the patient should be transferred in a timely fashion to optimize the outcome of the pregnancy and to reduce the risk of perinatal mortality.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Chamberlain PF, Manning FA, Morrison I, et al. Ultrasound evaluation of amniotic fluid volume. II. The relationship of increased amniotic fluid volume to perinatal outcome. Am J Obstet Gynecol. Oct 1 1984;150(3):250-4. [Medline].
2. Ben-Chetrit A, Hochner-Celnikier D, Ron M, Yagel S. Hydramnios in the third trimester of pregnancy: a change in the distribution of accompanying fetal anomalies as a result of early ultrasonographic prenatal diagnosis. Am J Obstet Gynecol. May 1990;162(5):1344-5. [Medline].
3. Abdel-Fattah SA, Carroll SG, Kyle PM, Soothill PW. Amnioreduction: how much to drain?. Fetal Diagn Ther. Sep-Oct 1999;14(5):279-82. [Medline].
4. Cabrol D, Jannet D, Pannier E. Treatment of symptomatic polyhydramnios with indomethacin. Eur J Obstet Gynecol Reprod Biol. May 1996;66(1):11-5. [Medline].
5. Kramer WB, Van den Veyver IB, Kirshon B. Treatment of polyhydramnios with indomethacin. Clin Perinatol. Sep 1994;21(3):615-30. [Medline].
6. Mamopoulos M, Assimakopoulos E, Reece EA, et al. Maternal indomethacin therapy in the treatment of polyhydramnios. Am J Obstet Gynecol. May 1990;162(5):1225-9. [Medline].
7. Desmedt EJ, Henry OA, Beischer NA. Polyhydramnios and associated maternal and fetal complications in singleton pregnancies. Br J Obstet Gynaecol. Dec 1990;97(12):1115-22. [Medline].
8. Biggio JR Jr, Wenstrom KD, Dubard MB, Cliver SP. Hydramnios prediction of adverse perinatal outcome. Obstet Gynecol. Nov 1999;94(5 Pt 1):773-7. [Medline].
9. Brace RA, Resnik R. Dynamics and disorders of amniotic fluid. In: Creasy RK, Resnik R, eds. Maternal-Fetal Medicine. 4^th ed. 1999:632-43.
10. Fanaroff AA, Martin RJ. Diseases of the fetus and infant. In: Neonatal-Perinatal Medicine. 6^th ed. 1997:315-9.
11. Harrison MR, Golbus MS, Filly RA. Prenatal diagnosis and treatment. In: The Unborn Patient. 2^nd ed. 1990:139-49.
12. Hill LM, Breckle R, Thomas ML, Fries JK. Polyhydramnios: ultrasonically detected prevalence and neonatal outcome. Obstet Gynecol. Jan 1987;69(1):21-5. [Medline].
13. Jones KL. Oligohydramnios sequence. In: Smith's Recognizable Patterns of Human Malformation. 5^th ed. 1997.
14. Kilpatrick SE. Histologic prognostication in soft tissue sarcomas: grading versus subtyping or both? A comprehensive review of the literature with proposed practical guidelines. Ann Diagn Pathol. Feb 1999;3(1):48-61. [Medline].
15. Macri CJ, Schrimmer DB, Leung A, et al. Prophylactic amnioinfusion improves outcome of pregnancy complicated by thick meconium and oligohydramnios. Am J Obstet Gynecol. Jul 1992;167(1):117-21. [Medline].
16. Morales WJ, Talley T. Premature rupture of membranes at <25 weeks: a management dilemma. Am J Obstet Gynecol. Feb 1993;168(2):503-7. [Medline].
17. Phelan JP, Ahn MO, Smith CV, et al. Amniotic fluid index measurements during pregnancy. J Reprod Med. Aug 1987;32(8):601-4. [Medline].
18. Pitt C, Sanchez-Ramos L, Kaunitz AM, Gaudier F. Prophylactic amnioinfusion for intrapartum oligohydramnios: a meta- analysis of randomized controlled trials. Obstet Gynecol. Nov 2000;96(5 Pt 2):861-6. [Medline].
19. Rib DM, Sherer DM, Woods JR Jr. Maternal and neonatal outcome associated with prolonged premature rupture of membranes below 26 weeks' gestation. Am J Perinatol. Sep 1993;10(5):369-73. [Medline].
20. Schumacher B, Moise KJ Jr. Fetal transfusion for red blood cell alloimmunization in pregnancy. Obstet Gynecol. Jul 1996;88(1):137-50. [Medline].
21. Vergani P, Ghidini A, Locatelli A, et al. Risk factors for pulmonary hypoplasia in second-trimester premature rupture of membranes. Am J Obstet Gynecol. May 1994;170(5 Pt 1):1359-64. [Medline].
22. Xiao ZH, Andre P, Lacaze-Masmonteil T, et al. Outcome of premature infants delivered after prolonged premature rupture of membranes before 25 weeks of gestation. Eur J Obstet Gynecol Reprod Biol. May 2000;90(1):67-71. [Medline].

Article Last Updated: Feb 14, 2008