Oligohydramnios

• Conditions such as preeclampsia, chronic hypertension, collagen vascular disease, nephropathy, and thrombophilia cause uteroplacental insufficiency. These conditions decrease the blood flow to vital organs such as the placenta which supplies blood, oxygen, and nutrients to the developing fetus. Decreased blood flow to the fetus causes impaired urine production which leads to reduced amniotic fluid and oligohydramnios.
• Medications such as angiotensin converting enzyme inhibitors (lisinopril), prostaglandin synthetase inhibitors (NSAIDs, anti-inflammatory steroids), and trastuzumab decrease blood flow to the kidneys of the fetus. When the fetal kidneys are not able to produce adequate amounts of urine, this leads to reduced amniotic fluid or oligohydramnios.
• Maternal dehydration, especially in the hotter summer months
• Infections such as the TORCH infections (toxoplasma gondii, rubella, cytomegalovirus, herpes simplex virus) and parvovirus B19

• Chromosomal abnormalities such as Down Syndrome which are associated with gastrointestinal abnormalities
• Congenital abnormalities such as renal agenesis and cystic renal disease are associated with impaired urine production, and posterior urethral valves or urethral atresia which are associated with obstruction of the lower urinary tract
• Intrauterine demise
• Post-term pregnancy
• Rupture of membranes
• intrauterine growth restriction (IUGR) associated with placental insufficiency
• amnion nodosum; failure of secretion by the cells of the amnion covering the placenta

• Placental abruption
• Twin-twin transfusion
• Placental thrombosis or infarction

The volume of amniotic fluid typically increases until 36 weeks and starts decreasing after 40 weeks in post-term gestations.[3] For this reason, discrepancies between fundal height measurements and gestational age can be a clinical indication of amniotic fluid abnormality and should be evaluated by ultrasound. Other common clinical presentations include fetal malpresentation, undue prominence of fetal parts, premature rupture of membranes, and reduced amount of amniotic fluid.

Diagnosis of oligohydramnios is made by conducting a transabdominal ultrasound of the abdomen. There are two methods that can be used to make the diagnosis. The first is by using an amniotic fluid index (AFI). In this method, the sonographer measures the amniotic fluid in each of the four quadrants of the abdomen (right upper quadrant, left upper quadrant, right lower quadrant, left lower quadrant) and adds the values together. For reference, a normal AFI is 5-25 cm. An AFI <5 cm is considered oligohydramnios and an AFI >25 cm is considered polyhydramnios. Randomized control trials have shown that use of AFI can cause an increased number of false positive diagnosis of oligohydramnios and recommend using the measurement of a single deepest pocket (SDP) of amniotic fluid to diagnose oligohydramnios instead.[1]

To calculate a single deepest pocket, the sonographer scans each of the four quadrants of the abdomen looking for the deepest pocket of amniotic fluid that does not include any fetal body parts or an umbilical cord. It is measured from the 12 o'clock position to the 6 o'clock position. For reference, a normal SDP is 2-8 cm. A SDP <2 cm is considered oligohydramnios and a SDP >8 cm is considered polyhydramnios. The use of a SDP for diagnosis of oligohydramnios is associated with less false positives and thus less unnecessary interventions without an increase in adverse perinatal outcomes.[1]

In a multiple gestation pregnancy, measuring a single deepest pocket is the most accurate determination of adequate amniotic fluid levels.[2]

There is no way to permanently increase the volume of amniotic fluid, but it can be temporarily increased to allow for a complete anatomy scan of the fetus on ultrasound.

One way to achieve this is through an amnioinfusion, which is the insertion of 200mL of saline into the amniotic sac. One study showed an improvement in fetal structure visibility by 26% (51% to 77% before and after the infusion respectively). There is also some low quality data that may indicate a potential benefit of amnioinfusion is to facilitate external cephalic version.[2] Amnioinfusion can be used during labor to prevent umbilical cord compression. There is uncertainty about the procedure's safety and efficacy, and it is recommended that it should only be performed in centers specializing in invasive fetal medicine and in the context of a multidisciplinary team.[5]

One to two liters of oral hydration can temporarily increase amniotic fluid in dehydrated patients with isolated oligohydramnios.[6]

Other investigational therapies may also be useful such as desmopressin, tissue sealants, or sildenafil citrate. These methods are less commonly used and are experimental.[4]

In case of congenital lower urinary tract obstruction, fetal surgery seems to improve survival, according to a randomized yet small study.[7]

Patients who are preterm are managed in the outpatient setting with weekly or biweekly testing to monitor for accurate fetal growth and decrease chances of unexpected fetal death. This includes a weekly non-stress test (NST) and single deepest pocket (SDP) assessment which is also referred to as the modified BPP.[1] Sonographic fetal growth exams may also be indicated.

Idiopathic, uncomplicated, and persistent oligohydramnios can be delivered at 36 0/7 weeks - 37 6/7 weeks of gestation or at diagnosis if diagnosis is later.[1]

Complications may include cord compression, musculoskeletal abnormalities such as facial distortion and clubfoot, pulmonary hypoplasia and intrauterine growth restriction. Amnion nodosum is frequently also present (nodules on the fetal surface of the amnion).[8]

The use of oligohydramnios as a predictor of gestational complications is controversial.[9][10]

Potter syndrome is a condition caused by oligohydramnios. Affected fetuses develop pulmonary hypoplasia, limb deformities, and characteristic facies. Bilateral agenesis of the fetal kidneys is the most common cause due to the lack of fetal urine.