In rare instances, the volume of amnionic fluid may fall far below the normal limits and occasionally be reduced to only a few milliliters. In general, oligohydramnios developing early in pregnancy is less common and frequently has a poor prognosis. By contrast, in pregnancies that continue beyond term, diminished fluid volume may be found often. Marks and Divon (1992) found oligohydramnios—defined as an AFI of 5 cm or less—in 12 percent of 511 pregnancies of 41 weeks or greater. In 121 women studied longitudinally, there was a mean decrease of 25 percent per week in the AFI beyond 41 weeks. Gagnon and colleagues (2002) found that chronic severe placental insufficiency caused a reduction in amnionic fluid volume not attributable to reduced fetal urine production. The risk of cord compression, and in turn fetal distress, is increased with diminished fluid in all labors, but especially in postterm pregnancy (Grubb and Paul, 1992; Leveno and colleagues, 1984).
A number of varied conditions have been associated with diminished amnionic fluid, and some are listed in Table 21-3. Oligohydramnios almost always is evident when there is either obstruction of the fetal urinary tract or renal agenesis. Therefore, anuria almost certainly has an etiological role in such cases. A chronic leak from a defect in the fetal membranes may reduce the volume of fluid appreciably, but most often labor soon ensues. Exposure to angiotensin-converting enzyme inhibitors has been associated with oligohydramnios (see Chap. 14, Angiotensin-Converting Enzyme [ACE] Inhibitors and Angiotensin-Receptor Blockers).
Table 21-3. Conditions Associated with Oligohydramnios |Favorite Table|Download (.pdf)
Table 21-3. Conditions Associated with Oligohydramnios
Prostaglandin synthase inhibitors
Angiotensin-converting enzyme inhibitors
From 15 to 25 percent of cases of oligohydramnios are associated with the fetal anomalies shown in Table 21-4. Diminished fluid decreases the accuracy of sonographic imaging. For example, Pryde and co-workers (2000) were able to visualize fetal structures in only half of women referred for midtrimester oligohydramnios. After amnioinfusion, they were able to visualize 77 percent of routinely imaged structures. Identification of associated anomalies increased from 12 to 31 percent of fetuses.
Table 21-4. Congenital Anomalies Associated with Oligohydramnios |Favorite Table|Download (.pdf)
Table 21-4. Congenital Anomalies Associated with Oligohydramnios
Amnionic band syndrome
Cardiac: Fallot tetralogy, septal defects
Central nervous system: holoprosencephaly, meningocoele, encephalocoele, microcephaly
Chromosomal abnormalities: triploidy, trisomy 18, Turner syndrome
Genitourinary: renal agenesis, renal dysplasia, urethral obstruction, bladder exstrophy, Meckel-Gruber syndrome, ureteropelvic junction obstruction, prune-belly syndrome
Skeletal: sirenomelia, sacral agenesis, absent radius, facial clefting
TRAP (twin reverse arterial perfusion) sequence
VACTERL (vertebral, anal, cardiac, tracheo-esophageal, renal, limb) association
Fetal outcome is generally poor with early-onset oligohydramnios. Shenker and colleagues (1991) described 80 pregnancies in which only half of the fetuses survived. Mercer and Brown (1986) described 34 midtrimester pregnancies complicated by oligohydramnios defined by the absence of amnionic fluid pockets greater than 1 cm. Nine fetuses—a fourth—had anomalies, and 10 of the 25 who were phenotypically normal either aborted spontaneously or were stillborn because of severe maternal hypertension, restricted fetal growth, or placental abruption. Of the 14 liveborn infants, 8 were preterm and 7 died. The six infants who were delivered at term did well. Garmel and co-workers (1997) observed that appropriately grown fetuses associated with oligohydramnios prior to 37 weeks had a threefold increase in preterm birth but not of later growth restriction or fetal death.
Newbould and colleagues (1994) described autopsy findings in 89 infants with the Potter sequence or Potter syndrome (see Chap. 16, Renal Agenesis). Only 3 percent had a normal renal tract; 34 percent had bilateral renal agenesis; 34 percent had bilateral cystic dysplasia; 9 percent had unilateral agenesis with dysplasia; and 10 percent had minor urinary abnormalities.
Otherwise normal infants may suffer the consequences of early-onset severely diminished amnionic fluid. Adhesions between the amnion may entrap fetal parts and cause serious deformities, including amputation. Moreover, because the fetus is subjected to pressure from all sides, musculoskeletal deformities such as clubfoot are observed frequently.
The presence of oligohydramnios markedly increases the fetal risk for pulmonary hyperplasia such as shown in Figure 21-4. Its incidence at birth approximates 1 per 1000 infants, but when amnionic fluid is scant, pulmonary hypoplasia is common (Moessinger and colleagues, 1989). Winn and associates (2000) performed a prospective cohort study in 163 cases of oligohydramnios that followed prematurely ruptured membranes at 15 to 28 weeks. Almost 13 percent of fetuses developed pulmonary hypoplasia. When rupture occurred at earlier gestational ages, hypoplasia was more common. Kilbride and co-workers (1996) studied 115 women with prematurely ruptured membranes before 29 weeks. There ultimately were seven stillbirths and 40 neonatal deaths and a calculated perinatal mortality rate of 409 per 1000. The risk of lethal pulmonary hypoplasia was 20 percent. Adverse outcomes were more likely with earlier rupture as well as duration exceeding 14 days.
Normal-sized lungs (top) are shown in comparison with hypoplastic lungs (bottom) of fetuses at the same gestational age. (Reproduced from BJOG, Vol. 101, Issue X, MJ Newbould, M Lendon, and AJ Barson, Oligohydramnios sequence: The spectrum of renal malformations, 598, 1994, with the permission of the Royal College of Obstetricians and Gynaecologists.)
According to Fox and Badalian (1994) and Lauria and colleagues (1995), there are three possibilities that account for pulmonary hypoplasia. First, thoracic compression may prevent chest wall excursion and lung expansion. Second, lack of fetal breathing movements decreases lung inflow. The third and the most widely accepted model involves a failure to retain intrapulmonary amnionic fluid or an increased outflow with impaired lung growth and development. Albuquerque and colleagues (2002) found a relationship between oligohydramnios and spinal flexion in the human fetus that also may contribute to fetal pulmonary hypoplasia.
Oligohydramnios in Late Pregnancy
Using an amnionic fluid index of less that 5 cm, Casey and co-workers (2000) cited an incidence of oligohydramnios of 2.3 percent in more than 6400 pregnancies undergoing sonography after 34 weeks at Parkland Hospital. They confirmed previous observations that this finding is associated with an increased risk of adverse perinatal outcomes (Table 21-5).
Table 21-5. Pregnancy Outcomes (in percent) in 147 Women with Oligohydramnios at 34 Weeks |Favorite Table|Download (.pdf)
Table 21-5. Pregnancy Outcomes (in percent) in 147 Women with Oligohydramnios at 34 Weeks
Oligohydramniosa (n = 147)
Normal AFI (n = 6276)
Cesarean for FHR
Management of oligohydramnios in late pregnancy depends on the clinical situation. Initially, an evaluation for fetal anomalies and growth is critical. In a pregnancy complicated by oligohydramnios and fetal-growth restriction, close fetal surveillance is important because of associated morbidity. In many cases, evidence for fetal or maternal compromise will override potential complications from preterm delivery. However, oligohydramnios detected before 36 weeks in the presence of normal fetal anatomy and growth may be managed expectantly in conjunction with increased fetal surveillance (see Chap. 15, Antepartum Assessment).
The outcomes of pregnancies with intrapartum oligohydramnios are conflicting. Chauhan and associates (1999) performed meta-analysis of 18 studies comprising more than 10,500 pregnancies in which the intrapartum AFI was less than 5 cm. Compared with controls whose index was greater than 5 cm, women with oligohydramnios had a significantly increased 2.2-fold risk for cesarean delivery for fetal distress and a 5.2-fold increased risk for a 5-minute Apgar score of less than 7. Cord compression during labor is common with oligohydramnios. Baron and colleagues (1995) reported a 50-percent increase in variable decelerations during labor and a sevenfold increased cesarean delivery rate in these women. Divon and associates (1995) studied 638 women with a postterm pregnancy in labor and observed that only those whose amnionic fluid index was 5 cm or less had fetal heart rate decelerations and meconium. Interestingly, Chauhan and colleagues (1995) showed that diminished amnionic fluid index increased the cesarean delivery rate only in women whose labor attendants were made aware of the findings!
Conversely, using the RADIUS trial database, Zhang and colleagues (2004) reported that oligohydramnios of this degree was not associated with adverse perinatal outcomes. Similarly, Magann and co-workers (1999) did not find that associated oligohydramnios increased risks for intrapartum complications. Casey and co-workers (2000) showed a 25-percent increase in nonreassuring fetal heart rate patterns when women with oligohydramnios were compared with normal controls. Despite this, the cesarean delivery rate for pregnancies with this finding increased only from 3 to 5 percent (see Table 21-5).
Numerous studies have evaluated whether intrapartum amnioinfusion may prevent fetal morbidity from meconium-stained fluid—often associated with oligohydramnios. Pierce and colleagues (2000) performed meta-analysis of 13 such studies of more than 1900 women. They found that amnioinfusion resulted in significantly decreased adverse outcomes that included meconium beneath the cords (OR 0.18), meconium aspiration syndrome (OR 0.30), neonatal acidemia (OR 0.42), and cesarean delivery rate (0.74). Conversely, Spong and associates (1994) found no benefits when they compared therapeutic with prophylactic amnioinfusion for meconium. Indeed, meconium aspiration syndrome occurred only in the group undergoing therapeutic amnioinfusion. Surprisingly, only 16 percent of the group randomized to expectant therapy ultimately required amnioinfusion for variable fetal heart rate decelerations. These findings are in agreement with reviews of outcomes before and after amnioinfusion protocols were implemented (De Meeus, 1997; Rogers, 1996; Usta, 1995, and all their colleagues).
Fraser and associates (2005) reported results from a 56-center, 13-country international trial of amnioinfusion in 1998 women at term in labor and with thick meconium. They found that amnioinfusion did not reduce the risk of meconium aspiration syndrome, cesarean delivery, or other major indicators of maternal or neonatal morbidity. The incidence of perinatal death or meconium aspiration syndrome was not significantly different—4.5 versus 3.4 percent in the amnioinfused women compared with controls. Finally, Xu and colleagues (2007) recently performed a meta-analysis of 12 trials that included more than 4000 women randomly assigned to amnioinfusion versus no treatment. When outcomes in 1999 women undergoing amnioinfusion were compared with those in 2031 control women, there was no evidence that amnioinfusion reduced the risk of meconium aspiration syndrome (RR 0.59, 95% CI 0.28–1.25), 5-minute Apgar score <7 (RR 0.9, 95% CI 0.58–1.41), or cesarean delivery (RR 0.89, 95% CI 0.73–1.1).
Finally, a number of maternal deaths have been associated with amnioinfusion in pregnancies complicated by thick meconium-stained fluid (Dibble and Elliot, 1992; Maher and colleagues, 1994). In at least seven of these cases, rapid labor was thought to play a major role (Dorairajan and Soundararaghavan, 2005).
Taken together, these results suggest that routine prophylactic amnioinfusion for labors complicated by meconium-stained amnionic fluid is not warranted. Indeed, the American College of Obstetricians and Gynecologists (2006) concluded that routine prophylactic amnioinfusion for this reason is not recommended. The College, however, concluded that amnioinfusion is a reasonable approach in the treatment of repetitive variable decelerations, regardless of amnionic fluid meconium status. Amnioinfusion is discussed in greater detail in Chapter 29 (Amnioinfusion), and the technique is described in Chapter 18 (Prophylactic Amnioinfusion for Variable Decelerations).