Decreased amniotic fluid volume for gestational age is referred to as oligohydramnios. Oligohydramnios is diagnosed based on ultrasound measurements of amniotic fluid volume and can be defined as either:
- Amniotic fluid index (AFI) ≤ 5 cm
- Single deep pocket (SDP) of < 2 cm
Anhydramnios is an extreme case of oligohydramnios with no measurable pockets of amniotic fluid present.
- Incidence rates are highly variable and based on gestational age and associated risk factors.
- Incidence rates based on gestational age:
- Overall incidence in term pregnancies of 37–42 weeks: 4.4%
- More common in pregnancies > 40 weeks: 11%
- Less common in preterm pregnancies of < 37 weeks: < 1%
- Most cases of oligohydramnios are diagnosed in the 3rd trimester of pregnancy with no identifiable cause.
Pathogenesis and Etiology
Normal amniotic fluid production
Amniotic fluid volume is determined by the volume of fluid flowing into and out of the amniotic sac. The main contributors are:
- Fetal urination (primary source of fluid 2nd half of pregnancy)
- Fetal swallowing (removal of amniotic fluid)
- Lung secretions
- Transport of maternal plasma across the fetal membranes as a result of hydrostatic and oncotic forces
Oligohydramnios is a result of decreased fluid production in relation to fluid removal.
- Primarily due to ↓ urine production in the 2nd half of pregnancy
- Abnormalities in the additional factors listed above do not play significant roles in the development of oligohydramnios for the following reasons:
- In general, ↑ swallowing does not occur.
- Lung secretions do not contribute enough to the amniotic fluid volume in the 2nd half of pregnancy to have an impact.
- Transfer of fluid across the amnion is more successful in preventing polyhydramnios (excess amniotic fluid) than oligohydramnios (fluid outflow is easier than inflow).
- ↓ Amniotic fluid volume → compression:
- Abdominal compression (especially in the 2nd trimester) → limits movement of the diaphragm → pulmonary hypoplasia (poor outcome)
- Musculoskeletal deformities (e.g., club foot, arthrogryposis)
- Umbilical cord compression → ↓ tolerance for uterine contractions in labor
Specific etiologies leading to oligohydramnios include:
- Idiopathic (possibly due to alterations in aquaporin channels in the fetal membranes and placenta)
- Prelabor rupture of membranes (PROM) with a “small/slow leak”
- Placental insufficiency: poor oxygenation and nutrient delivery to the fetus, resulting in poor urine production and often intrauterine growth restriction (IUGR):
- Maternal vascular disease:
- Chronic hypertension
- Pregestational diabetes
- Collagen vascular disease
- Placental abnormalities:
- Placental thrombosis
- Chronic partial placental abruption
- Maternal vascular disease:
- Fetal anomalies affecting urine production:
- Polycystic kidney disease
- Renal agenesis
- Obstructive lesions (e.g., posterior urethral valves, urethral atresia)
- Maternal use of certain medications affecting renal blood flow:
- ACE inhibitors
- Prostaglandin synthase inhibitors (e.g., NSAIDs)
- Twin-twin transfusion syndrome:
- Vascular anastomoses between 2 placentas, typically in monochorionic diamniotic twins, resulting in unequal blood flow
- Blood is siphoned from one twin to the other resulting in:
- A growth-restricted “donor twin” with oligohydramnios and at risk for severe anemia
- A “recipient twin” with polyhydramnios and at risk for fetal hydrops (a form of heart failure)
- Other etiologies associated with oligohydramnios:
- Fetal chromosomal abnormalities
- Maternal infections:
- Toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes simplex (TORCH) infections
- Parvovirus B19
- Fetal demise
Clinical Presentation and Diagnosis
- Decreased uterine size for gestational age (measured as the “fundal height” at prenatal visits)
- Decreasing or inconsistent fetal movements
- Complaints of leaking fluid/PROM
- Incidental finding in routine ultrasound examination (frequent)
- History of conditions associated with vascular disease
- Medication use
- History of recent infections
- Fundal heights should be measured at each prenatal visit → poor fundal growth should be investigated further with ultrasound
- Rule out ruptured membranes (speculum exam for pooling, fern test, pH test of vaginal secretions).
- Look for signs of maternal infection (e.g., fever, rashes).
Amniotic fluid can be assessed quantitatively and qualitatively with ultrasound. For diagnosis, quantitative assessment is recommended by measuring AFI and/or SDP.
- Calculation: Divide the uterus into 4 quadrants, measure the largest vertical pocket of fluid in each quadrant, and add the values together.
- Normal AFI: > 5 cm and < 24 cm
- Oligohydramnios: ≤ 5 cm
- The vertical dimension of the largest pocket of amniotic fluid excluding the umbilical cord or fetal extremities
- Normal SDP: ≥ 2 cm and < 8 cm
- Oligohydramnios: < 2 cm
If a patient is diagnosed with oligohydramnios, additional testing may be indicated to identify the underlying etiology:
- Ultrasound to assess fetal growth:
- Always indicated
- IUGR points to uteroplacental insufficiency
- Fetal anatomical survey via ultrasound (if not already done) to look for fetal anomalies
- Maternal screening for aneuploidy:
- Several combinations of ultrasound and serum markers exist as screening tests (e.g., the “quad screen”)
- Noninvasive prenatal testing (NIPT): screen for fetal DNA fragments in maternal blood
- Amniocentesis: an invasive sampling of amniotic fluid (contains fetal DNA) to test for genetic anomalies
- If suspicion arises based on the clinical picture, test maternal serum and amniotic fluid for TORCH pathogens.
- No effective long-term treatment for oligohydramnios is available.
- Encourage maternal hydration:
- The goal is to ↑ uteroplacental perfusion.
- Oral hydration is superior to IV hydration.
- Results are typically transient but still may provide some benefits.
- Monitor regularly to ensure continued fetal well-being.
- Monitoring techniques:
- Fetal “kick counting” by the mother: The mother should feel 10 movements in a 2-hour time period at least 1x/day.
- Fetal nonstress test: monitors fetal heart rate and uterine contractions for 20 minutes
- Biophysical profile: an obstetric ultrasound to identify certain types of fetal movements (includes a fluid measurement)
- Once oligohydramnios is diagnosed, a nonstress test and biophysical profile are typically performed 1–2x/week.
- Delivery is typically indicated:
- After 37-weeks gestational age (regardless of etiology)
- At 34-weeks gestational age for patients with preterm prelabor rupture of membranes (PPROM)
- If monitoring is nonreassuring
- Route of delivery:
- Vaginal deliveries are preferred if patients are candidates.
- Patients should be carefully monitored in labor for signs of fetal distress.
- Cesarean or operative vaginal deliveries should be performed for typical obstetric indications, including nonreassuring, intrapartum fetal monitoring.
- Once membranes are ruptured, a thin catheter can be inserted into the uterine cavity and fluid instilled to “refill” the amniotic cavity.
- May be helpful when monitoring indicates fetal stress from repetitive compression of the umbilical cord (e.g., variable decelerations)
- The catheter also serves as an intrauterine pressure catheter (IUPC), which is capable of measuring the strength of uterine contractions (helpful in managing inductions of labor).
- Approximately 200–300 ml of sterile saline is typically instilled.
Prognosis and Complications
The fetal/neonatal prognosis depends on the cause, severity, gestational age at diagnosis, and duration of oligohydramnios.
- Ominous finding typically ending with spontaneous abortion (94%)
- Patients should be counseled regarding the probability and signs of miscarriage.
- Serial ultrasound exams should be done to follow the natural history of the process.
- No treatments are available.
- Pregnancies with borderline or low–normal amniotic fluid volume generally have a good prognosis:
- Obtain serial sonographic examinations to assess the progress of the disease.
- Emphasize maternal hydration and avoidance of NSAIDs.
- True oligohydramnios typically has a poor prognosis.
- Survival rates based on etiology:
- PPROM: 21%
- Placental abruption: 22%
- Idiopathic: 20%
- Congenital anomalies: 1.5%
- Fetal growth restriction: 0%
- Overall survival rate: 10%
- Pulmonary hypoplasia is typically the cause of death because little can be done to support respiration in the infant after delivery.
- Limb contractures are common due to long-standing compression.
- Depending on the clinical situation (e.g., severe oligohydramnios due to an anomaly identified on an 18-week anatomy scan), elective termination may be an appropriate option.
- Typically a better prognosis when diagnosed in the 3rd trimester due to more developed respiratory and renal organs
- Adverse outcomes are related to:
- Umbilical cord compression
- Uteroplacental insufficiency
- Meconium aspiration
- Overall survival rate: > 85%
- Premature birth
- Pulmonary hypoplasia
- Cord compression
- Meconium aspiration
- Deformities due to intraamniotic adhesions or compression:
- Arthrogryposis (contractures of multiple joints)
- Alteration in the shape of the skull
- Torticollis (i.e. wry neck)
- Club foot
- Amputation of the limb
- Compression of fetal organs leading to hypoxic-ischemic encephalopathy (HIE)
- Beloosesky, R., and Ross, M.G. (2021). Oligohydramnios: Etiology, diagnosis, and management. In Barss, V.A. (Ed.), UpToDate. Retrieved June 22, 2021, from https://www.uptodate.com/contents/oligohydramnios-etiology-diagnosis-and-management
- Keilman C., Shanks A.L. (2020). Oligohydramnios. StatPearls. Retrieved June 22, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK562326
- Carter, B.S. (2017). Polyhydramnios and Oligohydramnios Medication. In Nimavat, D.J. (Ed.), MedScape. Retrieved June 22, 2021, from https://reference.medscape.com/article/975821-overview#showall
- Cunningham, F. G., Leveno, K. J., et al. (2010). Williams Obstetrics (23rd ed. Pp.495‒498).