Continuing Education Activity
Oligohydramnios is a disorder of amniotic fluid resulting in decreased amniotic fluid volume for gestational age. Low amniotic fluid volumes can be the result of numerous maternal, fetal, or placental complications and can lead to poor fetal outcomes. This activity will highlight the pathophysiology, etiology, evaluation, and treatment of oligohydramnios, and also review the role of healthcare teams in the assessment and management of this condition.
- Describe the diagnostic workup for oligohydramnios.
- Review the pathophysiology of amniotic fluid production resulting in disorders of amniotic fluid.
- Outline the differential diagnosis for both maternal and fetal causes of oligohydramnios.
- Summarize the etiology-specific management of oligohydramnios.
Oligohydramnios is defined as decreased amniotic fluid volume (AFV) for gestational age. The volume of amniotic fluid changes over gestation, increasing linearly until 34 to 36 weeks gestation, at which point the AFV levels off (approximately 400mL) and remains constant until term. The AFV then begins to decrease steadily after 40 weeks gestation, leading to reduced volume in post-term gestations. This pattern allows for clinical assessment of AFV throughout pregnancy using fundal height measurements and ultrasound evaluation.
Amniotic fluid disorders should be included in the differential diagnosis whenever there is a discrepancy between the fundal height measurement and gestational age. Discrepancies should prompt an amniotic fluid assessment by ultrasound.
Transabdominal ultrasound evaluation of AFV includes the use of either the maximum vertical pocket (MVP) or the amniotic fluid index (AFI) depending on the institution. The sonographer systematically scans the abdomen and obtains an image that demonstrates the maximum vertical pocket - the deepest pocket of amniotic fluid that does not include fetal umbilical cord or body parts. The measurement should be made from the 12 o’clock position to the 6 o’clock position. The normal range for MVP is 2-8 cm: a pocket <2cm is considered oligohydramnios in both single and multifetal gestations An MVP > 8 is considered polyhydramnios. The amniotic fluid index (AFI) is an alternative assessment of AFV. The AFI can be determined after 20 weeks of gestation by dividing the uterus into four quadrants through the umbilicus and determining the MVP in each quadrant. The sum of the four maximum vertical pockets is equal to the AFI. An AFI <5cm is consistent with oligohydramnios.
The use of the maximum vertical pocket tends to overly diagnose cases of polyhydramnios, while the use of the AFI tends to underdiagnose cases of oligohydramnios. With this in mind, some institutions opt to use the MVP in gestations with low AFV and use the AFI in cases of high AFV. The MVP should serve to evaluate oligohydramnios in multifetal pregnancies, as you will not be able to measure all four quadrants for each fetus.
The volume of amniotic fluid in the gestational sac is a result of a balance between fluid production and fluid movement out of the sac. In the first 20 weeks, lung secretions, along with hydrostatic and osmotic transport of maternal plasma through the fetal membranes, make up the majority of amniotic fluid production. At around week 16, the fetal kidneys begin to function, and the production of fetal urine steadily increases, taking over the majority of amniotic fluid production until the gestation is at term.
Fetal genitourinary abnormalities can, therefore, result in a diagnosis of oligohydramnios after 16 to 20 weeks gestation. Examples include bladder outlet obstruction, dysplastic kidneys, and renal agenesis. Fetal swallowing and intramembranous absorption, thought to occur by osmotic absorption of fluid directly across the amnion and into fetal blood vessels, are the primary routes of amniotic resorption. Therefore, fetal gastrointestinal anomalies, such as tracheoesophageal fistula (incidence rate of approximately 1 in 3500 live births), can result in excess fluid volume, or polyhydramnios.
Oligohydramnios complicates 4.4% of all pregnancies at term. The incidence of oligohydramnios is less than 1% in preterm pregnancies.
History and Physical
Following ultrasound diagnosis by amniotic fluid assessment, clinical assessment should be focused on determining the etiology.
- History: A thorough maternal and family history is necessary to screen for conditions associated with oligohydramnios: medication use, past medical history, and rupture of membranes.
- Physical Exam: Target physical exam to determine etiology: measure fundal height, speculum examination, tests for ruptured membranes (pH, nitrazine test, rupture of fetal membranes test).
- Ultrasound: Perform a targeted ultrasound assessment for structural abnormalities in the genitourinary tract, assess for fetal growth restriction and markers of aneuploidy, umbilical artery Doppler to assess placental insufficiency .
- Nonstress Tests: Performed at least once per week until delivery.
Treatment / Management
In addition to managing the underlying cause, prenatal management includes weekly maximum vertical pocket measurements and nonstress tests, which have demonstrated to decrease the occurrence of unexplained fetal death. Fetal growth should undergo serial assessment. Maternal hydration status also plays a vital role in management, particularly in cases of isolated oligohydramnios in the third trimester.
Although there is some controversy surrounding the timing of delivery in cases of isolated oligohydramnios, the current recommendations support delivery at 37 weeks gestation, assuming membranes remain intact.
Oligohydramnios is associated with many conditions/complications of pregnancy, and the differential breaks down into the following categories: maternal, fetal, placental, and idiopathic.
- Maternal causes: Oligohydramnios has correlations with any medical or obstetric condition leading to uteroplacental insufficiency (8% of all gestations). Possible causes include chronic hypertension, vascular disease, thrombophilia, and preeclampsia. It also correlates with certain drugs (angiotensin-converting enzyme inhibitors, NSAIDs, and cocaine use) and maternal diabetes.
- Fetal causes: Rupture of membranes is the most common cause. Preterm premature rupture of membranes (PPROM) alone accounts for greater than 37% of oligohydramnios cases diagnosed in the second and third trimesters. Genitourinary tract abnormalities (renal agenesis, obstructive nephropathy) are associated with oligohydramnios and occur at an incidence of 3 to 7 per 1000 live births. Post-term pregnancies, fetal growth restriction (5% of the second trimester and 20.5% of third-trimester diagnoses), chromosomal abnormalities (10% of oligohydramnios cases in the second trimester), and fetal demise are also associated with oligohydramnios.
- Placental causes: Placental causes of oligohydramnios include abruption (8.6% of all oligohydramnios cases) and twin-twin transfusion syndrome (oligohydramnios-polyhydramnios sequence).
- Idiopathic/unexplained: The majority of oligohydramnios cases, 50.7% diagnosed in the third trimester, are of unexplained etiology and, typically, associated with better outcomes.
The management and prognosis of oligohydramnios vary greatly depending on the underlying etiology, the gestational age at diagnosis, and the severity of oligohydramnios. Diagnosis of oligohydramnios during the second trimester is more likely to be associated with fetal or maternal anomalies, whereas diagnosis in the third trimester is more likely to be of unexplained origin. In one study, the etiology of oligohydramnios was unexplained in just 4% of second-trimester gestations, whereas 52% of those diagnosed in the third trimester were idiopathic. Only 10.2% of fetuses diagnosed in the second trimester survived, while the survival rate was 85.3% in those diagnosed in the third trimester.
In cases of oligohydramnios diagnosed in the second trimester, pulmonary hypoplasia is the most significant predictor of fetal mortality. The mortality rate of second-trimester oligohydramnios can be as high as 90%, with pulmonary hypoplasia accounting for 87% of those deaths. The most severe pulmonary hypoplasia occurs with oligohydramnios before or during 16 to 24 weeks gestational age, when the terminal sacs of the fetal lung are developing. Low AFV during the second and early third trimester also increases the likelihood of limb contractures and birth defects due to compression of fetal parts.
There are several additional complications to be aware of during the labor course of a gestation complicated by oligohydramnios. These include an increased risk of umbilical cord compression, meconium aspiration, cesarean delivery, fetal heart rate decelerations, and nonreactive fetal tracings. Administration of 1 to 2 liters of oral or intravenous fluids during labor shown to transiently increase AFV and decrease cord compression over the labor course.
Deterrence and Patient Education
Patient education regarding oligohydramnios should focus on the importance of receiving routine prenatal care throughout the course of pregnancy. Regular prenatal care allows the health care team to recognize and diagnose gestational complications, such as oligohydramnios. The clinical care team can then formulate an appropriate follow-up plan to minimize the risk of both the fetal and maternal complications associated with oligohydramnios.
Enhancing Healthcare Team Outcomes
The care and management of patients with amniotic fluid disorders rely on interprofessional communication among several providers to ensure adequate screening, diagnosis, and management of these conditions in the antepartum, partum, and postpartum periods. Obstetricians or clinically trained midwives often detect oligohydramnios during routine prenatal care visits.
Following diagnosis, it is often necessary to consult maternal-fetal medicine specialists and neonatologists who can help to develop an optimal care plan to limit the risk of complications for both the mother and the fetus. The care plans include antepartum management, the timing of delivery, and postpartum care that are each catered to the underlying etiology of oligohydramnios.