Abstract
Amniotic fluid is necessary for normal development of the fetal respiratory, gastrointestinal, urinary, and musculoskeletal systems. Oligohydramnios, a reduced amount of amniotic fluid, complicates 0.5% to 8% of pregnancies. When oligohydramnios is suspected, prompt evaluation should be carried out. Prognosis depends largely upon the etiology and gestational age at the time of diagnosis. In this chapter, we review etiologies of oligohydramnios, current quantitative diagnostic modalities, and management and treatment options.
Keywords
oligohydramnios, amniotic fluid index, AFI, single deepest pocket, SDP
Disease
Definition
The definition of oligohydramnios varies. It may be described subjectively, but accuracy is dependent on operator experience and gestational age; precise objective measurement requires invasive study and is difficult to assess clinically. In practice, the amniotic fluid volume is usually approximated by semiquantitative sonographic measures: amniotic fluid index (AFI), single deepest vertical fluid pocket (SDP), or assessment of a single pocket (e.g., 2 × 2 cm). Techniques are described later.
Amniotic fluid volume changes throughout pregnancy, increasingly linearly until the early third trimester and then remaining constant until term. Oligohydramnios is most often defined as AFI ≤ 5 cm or SDP ≤ 2 cm, but has been defined in gestational age–specific percentile charts as less than or equal to third percentile or less than or equal to fifth percentile. In a study of almost 300 women with dye-determined amniotic fluid volumes, there was no difference in oligohydramnios detection using absolute cutoffs of AFI or SDP versus gestational age–specific values. Comparison of the sensitivities and specificities of AFI versus SDP in 11 studies suggested that the SDP may be the better descriptor of oligohydramnios; the predictive accuracy of SDP was identical to AFI and SDP correlated better with tests such as biophysical profile and Doppler assessment. A metaanalysis of four randomized clinical trials ( n = 3125) comparing perinatal outcomes of pregnancies with oligohydramnios based on AFI versus SDP found no difference in the primary outcome (neonatal intensive care unit admission), or in Apgar scores or umbilical artery pH less than 7.1, although use of AFI resulted in more frequent induction of labor and cesarean delivery for fetal distress. A recent multicenter randomized controlled trial including 1052 women with term singleton pregnancies also showed that use of the AFI method increased the rate of diagnosis of oligohydramnios and labor induction for oligohydramnios without improving perinatal outcome. These findings suggest that SDP may be the preferable method, especially in a low-risk population.
Prevalence and Epidemiology
Oligohydramnios complicates 0.5% to 8% of pregnancies, and management and prognosis depend on gestational age and associated obstetric complications. Outcomes are worse with earlier or more severe oligohydramnios (e.g., anhydramnios) ( Fig. 120.1 ). Etiologies include preterm premature rupture of membranes (PPROM) ( Fig. 120.2 ), fetal abnormalities (especially of the genitourinary tract), and placental insufficiency ( Fig. 120.3 ). In a retrospective review of 128 second-trimester (13–24 weeks, n = 128) and 122 third-trimester (25–42 weeks, n = 122) fetuses with oligohydramnios, the former were more likely to be anomalous and less likely to have unexplained oligohydramnios, whereas the reverse was true of third-trimester fetuses. Specifically, among second-trimester fetuses, 50.7% were complicated by anomalies, 33.6% by PPROM, 7% by abruption, 5% by growth restriction, and only 4% were unexplained. In contrast, third-trimester fetuses were most likely to have unexplained oligohydramnios (52.5%), with anomalies noted in 22.1%, growth restriction in 20.5%, PPROM in 3.3%, and placental abruption in 1.6%. Accordingly, only 10.2% of second-trimester fetuses survived compared with 85.3% of third-trimester fetuses.
Pulmonary hypoplasia is the primary cause of mortality in pregnancies complicated by second-trimester oligohydramnios. Because amniotic fluid is required for the normal development and expansion of the pulmonary system, lack of adequate fluid at critical stages of lung development is associated with poor outcome. Pulmonary hypoplasia is more likely with oligohydramnios during or before 16–24 weeks’ gestation, the canalicular phase of lung development, when the terminal sacs are developing, compared with later in gestation, when the terminal sacs are developed, and the primary changes to prepare for eventual gas exchange have occured.
The association between outcome and severity of oligohydramnios was shown in a review of almost 29,000 fetuses at 24 to 34 weeks. Of these, 166 had oligohydramnios (AFI ≤ 5 cm), 204 had “borderline” fluid (5.1–8 cm), and the remainder were normal (8.1–24 cm). Major malformations were present in 25% of fetuses with oligohydramnios compared to 10% with borderline, and 2% with normal fluid. Compared to fetuses with normal fluid, growth restriction was nine times more likely in fetuses with oligohydramnios, and five times more likely in those with borderline fluid. Risks of preterm birth and cesarean section were higher with oligohydramnios and borderline fluid, but morbidity and mortality were not significantly different with borderline fluid if fetal growth was appropriate. The authors concluded that close surveillance or delivery for oligohydramnios is warranted, but recommendations are not clear for borderline fluid.
Etiology and Pathophysiology
Amniotic fluid is necessary for normal development of the fetal respiratory, gastrointestinal, urinary, and musculoskeletal systems. In the early fetal period, transudation across fetal skin and placental surfaces is the main contributor to amniotic fluid. After the skin is keratinized (22–23 weeks’ gestation), the fluid is predominantly produced by fetal urine, with smaller contributions from oral, nasal, tracheal, and pulmonary fluids. Removal of fluid occurs primarily through fetal swallowing.
Reduced fetal urinary excretion from decreased production or genitourinary obstruction can cause oligohydramnios. These conditions can be characterized as prerenal, renal, or postrenal. Prerenal causes include fetal growth restriction ( Chapter 112 ), twin-twin transfusion syndrome ( Chapter 162 ) ( Fig. 120.4 ), and maternal drug ingestion (including the tocolytic indomethacin and other nonsteroidal antiinflammatories). Briefly, placental insufficiency leads to chronic hypoxemia and growth restriction, and the fetus adapts by redistributing blood flow to vital organs such as the brain, heart, and adrenal glands, and away from peripheral organs, such as the kidney. Decreased renal perfusion leads to decreased urine output and oligohydramnios. Maternal ingestion of drugs that affect fetal renal function can cause oligohydramnios. Angiotensin-converting enzyme inhibitors may affect renal development and function when taken in the second and third trimesters because they directly affect the fetal renin-angiotensin system. Other drugs that affect renal function include nonsteroidal antiinflammatory drugs (especially indomethacin) and cocaine.
Renal causes of oligohydramnios include renal agenesis, multicystic dysplastic kidney, and polycystic kidney disease ( Chapter 10 , Chapter 11 , Chapter 15 , Chapter 16 ). Bilateral renal agenesis is lethal because of anhydramnios and subsequent pulmonary hypoplasia.
Postrenal causes of oligohydramnios result from obstructive uropathy, which affects 2.2:10,000 births. Most cases are benign, but perinatal mortality is 90% in fetuses with severe oligohydramnios (anhydramnios) manifesting in the second trimester. Causes include posterior urethral valves, ureteropelvic junction obstruction, urethral atresia, and urethral stenosis ( Figs. 120.5 and 120.6 ). Male fetuses are more commonly affected, but affected female fetuses may have more complex pathologies, such as cloacal anomalies. The prognosis depends on renal function and underlying etiology.
PPROM is a major cause of oligohydramnios and can be spontaneous or iatrogenic from invasive fetal diagnostic or therapeutic procedures. Overall, PPROM occurs in 3% of pregnancies and accounts for one-third of all preterm births. Umbilical cord compression secondary to oligohydramnios can increase perinatal morbidity and mortality. The latency period between PPROM and delivery is associated with severity of oligohydramnios (e.g., anhydramnios is associated with shorter latency). In addition, there is an inverse relationship between degree of oligohydramnios and risk of chorioamnionitis and neonatal sepsis in patients with PPROM.
Manifestations of Disease
Clinical Presentation
Oligohydramnios is typically an incidental finding on routine ultrasound (US) examination. It should be suspected clinically when the fundal height is less than expected for dates, or if the patient complains of vaginal leaking of fluid. Common tests for rupture of membranes include sterile speculum examination (for fluid that is nitrazine positive and shows ferning) or tests that detect a protein marker of amniotic fluid in the vagina. If tests are equivocal, rupture of membranes can be diagnosed via US-guided amnioinfusion of indigo carmine dye followed by observation of leakage of blue fluid through the cervix. Indigo carmine has been used in the “amnio-dye test” to confirm ruptured membranes in the past; however, widespread shortages in the availability of this agent and the absence of a suitable substitute have made this test impractical.
Imaging Technique and Findings
Ultrasound.
US has been used for semiquantitative measures of amniotic fluid using tools such as AFI, SDP, or assessment of a single pocket (e.g., 2 × 2 cm). The patient lies supine, and the transducer is kept in the maternal sagittal plane, perpendicular to the maternal coronal plane. AFI is the sum of the deepest vertical pocket of fluid, excluding fetal parts and umbilical cord, in four quadrants between the maternal midline vertically and a transverse line halfway between the pubic symphysis and uterine fundus. SDP is a measure of the single deepest pocket of fluid.
A careful fetal structural survey is warranted in the case of oligohydramnios, even with a previous normal anatomic survey, because of the possibility of a previously unrecognized anomaly, especially renal. One pitfall in bilateral renal agenesis is that the adrenal glands may assume a discoid shape and move laterally and inferiorly, mimicking kidneys. One distinguishing feature of renal agenesis is absence of a bladder. Color or power Doppler US can be used to identify the renal arteries, distinguishing kidneys from adrenal glands (see Chapter 11 ). Multicystic dysplastic kidney disease, a congenital renal condition with severely disorganized tubules, glomeruli, and ducts with cystic lesions in the collecting tubules, on US shows multiple noncommunicating cysts of varied sizes starting at the periphery of the affected kidneys with echogenic renal parenchyma between the cysts. Amniotic fluid may be normal in unilateral cases (see Chapter 15 ).
Prenatal renal impairment may result from polycystic kidney disease, in which cysts form in normally developing kidneys, making them appear cystic and echogenic upon US. There are two forms: autosomal dominant and autosomal recessive. The latter manifests as large hyperechogenic kidneys and oligohydramnios, and can be lethal (see Chapter 16 ). In contrast, autosomal dominant polycystic kidney disease manifests later in life and typically is not found on prenatal US, although cyst formation begins in utero.
Oligohydramnios may result from various forms of renal obstruction, and US detects fetal obstructive uropathy with a sensitivity of 95% and specificity of 80%. Findings suggestive of obstruction are dilation of the renal pelvis and calyces, increased renal echogenicity, and bladder distention. When obstructive uropathy is suspected, detailed assessment should include evaluation of dilation (hydronephrosis, hydroureter), renal parenchyma (echogenicity), renal size, and bladder size. In the case of bilateral hydronephrosis, a small or absent bladder suggests ureteropelvic obstruction, whereas a large bladder suggests bladder outlet obstruction. Posterior urethral valves should be suspected if the “keyhole” sign is present (enlarged bladder with dilatation of proximal urethra) ( Chapters 12 and 14 ).
Severe oligohydramnios may result in deformation syndromes such as craniofacial deformities and limb defects, although detection is often because inadequate fluid results in a poor acoustic window. The fetus may have Potter facies, a “silk stocking effect,” with flattened nose and low-set, flattened, enlarged external auricles. There may be positional deformation of the hands and feet with flexion contractures of the elbows, knees, and feet. Transvaginal US scan may assist in evaluating extremities.
In the fetus with suspected placental insufficiency-related oligohydramnios, especially if growth restriction is also present, Doppler evaluation is indicated ( Chapter 110 ).
Magnetic Resonance Imaging.
If oligohydramnios makes US visualization suboptimal, magnetic resonance imaging (MRI) may be helpful. This may be a useful complementary tool in fetal urinary tract anomalies diagnosed on US (see Fig. 120.6 ).
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