Oligohydramnios is a decrease in the volume of amniotic fluid. The diagnosis of oligohydramnios is most frequently made by ultrasound examination. Oligohydramnios was initially defined as a subjective decrease in amniotic fluid volume resulting in fetal crowding as compared with normal values (Crowley et al., 1984). Objective sonographic estimation of amniotic fluid volume involves measuring different dimensions of amniotic fluid pockets. Various definitions of oligohydramnios exist. Oligohydramnios has been defined as a maximal vertical pocket (MVP) of less than 1 cm, but has also been defined as a MVP of less than 2 cm (Manning et al., 1981; Chamberlain et al., 1984). A semiquantitative four-quadrant technique, known as the amniotic fluid index (AFI), is also widely used. Oligohydramnios can be defined as an AFI of less than 5 cm, but has also been defined as an AFI of less than 8 cm (Phelan et al., 1987; Moore, 1993).

Amniotic fluid volume is the result of a balance between inflow and outflow to and from the amniotic cavity. In the first half of pregnancy, the majority of amniotic fluid is a result of active transport of sodium and chloride across the amniotic membrane and fetal skin, with water moving passively in response (Brace and Resnik, 1999). In the second half of pregnancy, the majority of amniotic fluid is a result of fetal micturition (Underwood et al., 2005). Another major source of amniotic fluid is secretion from the respiratory tract. The average amniotic fluid volume is 30 mL at 10 weeks of gestation, rising to 780 mL at 32 to 35 weeks, after which time a natural decrease in volume occurs (Brace and Resnik, 1999). The amniotic fluid volume is not stagnant, but is completely turned over at least once daily. Fetal urine first appears at 8 to 10 weeks of gestation and reaches a production rate of 700 to 900 mL/d near term (Brace and Resnik, 1999).

Oligohydramnios can occur as a result of decreased urinary production or excretion, or can be a result of fluid loss, such as with premature rupture of membranes. Causes of oligohydramnios include ruptured membranes, placental insufficiency, fetal anomalies, medication use by the mother, abnormalities associated with multiple gestations, chromosomal abnormalities, and idiopathic (Garmel et al., 1997). In the second trimester, premature rupture of membranes accounts for 50% of all cases of oligohydramnios; fetal anomalies, 15%; abruption, 7%; abnormalities associated with multiple gestations, 5%; intrauterine growth restriction, 18%; and idiopathic causes, 5% (Shenker et al., 1991). The presence of oligohydramnios in a twin gestation may be due to twin-to-twin transfusion syndrome, intrauterine growth restriction of one twin, or intrauterine fetal death.

Premature rupture of membranes may be suggested with the sonographic appearance of oligohydramnios and an appropriately grown, structurally normal fetus. A sterile speculum examination demonstrating the absence of pooling following a negative phenaphthazine (nitrazine) test will usually rule out rupture of membranes. Occult rupture of membranes may occur, and amniocentesis with indigocarmine dye infusion may be necessary in some cases to rule out membrane rupture as a causative factor of oligohydramnios. Significant oligohydramnios occurring prior to 22 weeks of gestation is associated with a poor prognosis, most likely because of a high likelihood of pulmonary hypoplasia and also because of a high incidence of associated congenital malformations.

Medication use by the mother, such as prostaglandin synthetase inhibitors and angiotensin-converting enzyme inhibitors, has been reported to cause oligohydramnios. Indomethacin is used to treat preterm labor and can result in oligohydramnios, although this is usually reversible following discontinuation of the drug (Kirshon et al., 1991). Oligohydramnios, prolonged neonatal anuria, and ossification defects in the neonatal skull have been reported with in utero exposure to angiotensin-converting enzyme inhibitors (Cunniff et al., 1990; Barr and Cohen, 1991). The use of angiotensin-converting enzyme inhibitors is absolutely contraindicated during pregnancy. It is interesting to note that oligohydramnios is diagnosed more frequently in pregnancies delivered in the summer months suggesting that maternal dehydration may contribute to this finding (Varner et al., 2005).

Because of differing definitions, the reported incidence of oligohydramnios varies from 0.5% to 8% of all pregnancies (McCurdy and Seeds, 1993; Phelan et al., 1987). When an MVP of less than 2 cm is used as a cutoff, the incidence of oligohydramnios is 3% of all pregnancies (Chamberlain et al., 1984). When an AFI of less than 5 cm is used, the incidence of oligohydramnios is 8% (Phelan et al., 1987). Norms for amniotic fluid volume across gestation were established in one report of sonographic amniotic fluid measurements in 791 patients (Moore and Cayle, 1990). The 5th centile for AFI at term was approximately 7 cm. Interobserver variability may account for some of the variations in quoted incidences of oligohydramnios; however, interobserver and intraobserver variability have been reported as reliable and reproducible (Halperin et al., 1985; Moore and Cayle, 1990).

A diagnosis of oligohydramnios is almost always made on the basis of sonographic findings. Several methods of sonographic amniotic fluid assessment have been described. The subjective assessment of amniotic fluid volume with ultrasound examination was the earliest technique described (Crowley et al., 1984). This method involved the assessment of the relative amount of amniotic fluid present by comparing the amount of echo-free fluid areas in the uterus with the space occupied by the fetus. Disadvantages of this method include the requirement of a trained observer and the lack of a numerical result that can be used to follow a trend in amniotic fluid volume. Studies of interobserver variability for subjective sonographic assessment of amniotic fluid volume found that among experienced observers subjective estimates had good agreement rates and that this was not improved by the use of an arbitrary amniotic fluid volume classification such as vertical pocket depth (Halperin et al., 1985; Goldstein and Filly, 1988).

However, most clinicians today use some form of objective semiquantitative estimate of amniotic fluid volume, based on the MVP or the AFI. The MVP involves surveying the entire uterus and measuring the depth of the deepest pocket of amniotic fluid in centimeters. Only amniotic fluid pockets free of fetal parts and umbilical cord are measured. The criteria for defining oligohydramnios vary, with some suggesting an MVP of less than 1 cm as an appropriate cutoff for oligohydramnios, while others use a cutoff of less than 2 cm to diagnose oligohydramnios (Manning et al., 1981; Chamberlain et al., 1984).

The AFI involves summing the maximum vertical pockets from each of the four quadrants of the uterus. In a report of sonographic AFI measurements in 197 patients, the mean AFI rose from 7 cm at 12 weeks of gestation to 20 cm at 26 weeks gestation, and then plateaued for the remainder of gestation at approximately 16 cm (Phelan et al., 1987). In a cross-sectional study of 791 pregnancies with AFI measurements, an AFI of 7 cm was at the 5th centile at term, and only 1% of all pregnancies had an AFI of less than 5 cm at term (Moore and Cayle, 1990).

It is important to measure the AFI with the patient supine, to orient the transducer in the maternal sagittal plane, to measure the sonographic planes perpendicular to the floor, to measure fluid pockets free from umbilical cord or fetal extremities, and to use the umbilicus and linea nigra as landmarks for dividing the uterus into four quadrants (Phelan et al., 1987).

There is no agreement in the obstetric literature as to which method of sonographic measurement of amniotic fluid volume is best. In one study comparing MVP with AFI, the correlation coefficient was 0.51, and the MVP was associated with a lower sensitivity (Moore, 1990). Others have found good correlation between the MVP and AFI methods, with the MVP being better (Magann et al., 1994). Both MVP and AFI should therefore be considered reasonable methods for quantifying the amniotic fluid volume.

Whenever a diagnosis of oligohydramnios is made, a careful sonographic fetal anatomy survey should be performed to evaluate for fetal abnormalities, such as features of urinary tract obstruction or malformation. Absence of bladder filling following a 1-hour period of observation suggests a urinary tract abnormality. Fetal renal anomalies including renal agenesis (see Chapter 86), urethral obstruction (see Chapter 82), and multicystic kidneys (see Chapter 78) account for 11% of cases of oligohydramnios discovered during the second trimester (Shenker et al., 1991).

If severe oligohydramnios is present at less than 24 weeks of gestation, the possibility of pulmonary hypoplasia should be considered. Numerous sonographic criteria to predict pulmonary hypoplasia have been described. Measurements of chest circumference are highly predictive of pulmonary hypoplasia in patients with either severe oligohydramnios or prolonged premature rupture of membranes (D’Alton et al., 1992). Normal values for fetal thoracic circumference and for the ratio of thoracic circumference to abdominal circumference have been established, and this ratio has been found to remain constant throughout pregnancy (D’Alton et al., 1992). A thoracic to abdominal circumference ratio of less than 0.80 in the setting of severe oligohydramnios in the second trimester is suspicious for pulmonary hypoplasia. Fetal compression, including dolicocephaly and clubfeet, may be apparent (Figure 125-1).

The differential diagnosis for oligohydramnios includes normal pregnancy during the late third trimester, postmaturity, intrauterine growth restriction, premature rupture of membranes, fetal death, fetal renal anomalies(bilateral multicystic dysplastic kidneys, bilateral renal agenesis, bilateral ureteral obstruction, posterior urethral valves, infantile polycystic kidney disease), neural tube defect, chromosomal abnormality, stuck twin, and medication use (such as indomethacin) by the mother.

The antenatal natural history of oligohydramnios depends on the gestational age at diagnosis and the cause of the oligohydramnios. Oligohydramnios accompanies a variety of serious fetal malformations, the most common being fetal renal abnormalities, and the underlying anomaly will dictate the natural history. Cardiac, skeletal, and neurologic malformations, in addition to aneuploidy and a variety of syndromic abnormalities, often coexist with the primary renal abnormality (McCurdy and Seeds, 1993). Bilateral renal agenesis (Potter syndrome) is uniformly lethal because of associated pulmonary hypoplasia and renal failure (Figure 125-2) (see Chapter 86).