Oligohydramnios

Etiology

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.[6] 

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.[4]

Epidemiology

Oligohydramnios complicates 4.4% of all pregnancies at term. The incidence of oligohydramnios is less than 1% in preterm pregnancies.[7]

History and Physical

Following ultrasound diagnosis by amniotic fluid assessment, clinical assessment should be focused on the following to determine 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.[4]
• 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).[8]

Evaluation

The evaluation of oligohydramnios includes the following:

• 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.[5]
• Nonstress Tests: Performed at least once per week until delivery.[9]

Treatment / Management

In addition to managing the underlying cause, prenatal management includes weekly maximum vertical pocket measurements and nonstress tests, which have been 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.[10] 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.[11](A1)

Differential Diagnosis

Oligohydramnios is associated with many conditions/complications of pregnancy, and the differential breaks down into the following categories: maternal, fetal, placental, and idiopathic.[4]

• 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.[4]
• 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.[12]
• Placental causes: Placental causes of oligohydramnios include abruption (8.6% of all oligohydramnios cases) and twin-twin transfusion syndrome (oligohydramnios-polyhydramnios sequence).[12]
• Idiopathic/unexplained: The majority of oligohydramnios cases, 50.7% diagnosed in the third trimester, are of unexplained etiology and typically associated with better outcomes.[12]

Prognosis

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.[12]

 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 of 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.[12]

Complications

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.[1] 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.[10]