When amnionic luid volume becomes abnormally decreased in the late second or in the third trimester, it is very often associated with fetal-growth restriction, with a placental abnormality, or with a maternal complication such as preeclampsia or vascular disease (Table 11-4). The underlying cause in such cases is frequently uteroplacental insuiciency, which can impair fetal growth and reduce fetal urine output. Exposure to selected medications has also been linked with oligohydramnios as discussed subsequently. Investigation of third-trimester oligohydramnios generally includes evaluation for ruptured membranes and sonography to assess fetal growth. Umbilical artery Doppler studies are recommended if growth restriction is identiied (Chap. 10, p. 213). Oligohydramnios is commonly encountered in lateterm and postterm pregnancies (Chap. 43, p. 837). Magann and coworkers (1997) found that amnionic luid volume decreased by approximately 8 percent per week beyond 40 weeks.
By approximately 18 weeks, the fetal kidneys are the main contributor to amnionic luid volume. Selected renal abnormalities that lead to absent fetal urine production include bilateral renal agenesis, bilateral multicystic dysplastic kidney, unilateral renal agenesis with contralateral multicystic dysplastic kidney, and the infantile form of autosomal recessive poycystic kidney dis ease. Urinary abnormalities may also result in oligohydramnios because of fetal bladder outlet obstruction. Examples of this are posterior urethral valves, urethral atresia or stenosis, or the megacystis microcolon intestinal hypoperistalsis syndrome. Complex fetal genitourinary abnormalities such as persistent cloaca and sirenomelia similarly may result in a lack of amnionic luid. Many of these renal and urinary abnormalities are discussed and depicted in Chapter 10 (p. 208). If no amnionic luid is visible beyond the mid-second trimester due to a genitourinary etiology, the prognosis is extremely poor unless fetal therapy is an option. Fetuses with bladder-outlet obstruction may be candidates for vesicoamnionic shunt placement (Chap. 16, p. 325).
Oligohydramnios has been associated with exposure to drugs that block the renin-angiotensin system. These include angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers, and nonsteroidal antiinlammatory drugs (NSAIDs). When taken in the second or third trimester, ACE inhibitors and angiotensin-receptor blockers may create fetal hypotension, renal hypoperfusion, and renal ischemia, with subsequent anuric renal failure (Bullo, 2012; Guron, 2000). Fetal skull bone hypoplasia and limb contractures have also been described (Schaefer, 2003). NSAIDs can be associated with fetal ductus arteriosus constriction and with lower fetal urine production. In neonates, their use may result in acute and chronic renal insuiciency (Fanos, 2011). These agents are discussed in Chapter 12 (p. 241).
Oligohydramnios is associated with adverse pregnancy outcomes. Casey and colleagues (2000) found that an AFI �5 em
TABLE 11-4. Pregnancy Outcomes in Women Diagnosed with Oligohydramnios between 24 and 34 Weeks' Gestation
AFI �5 em AFI 8 to 24 em Factor (n = 166) (n = 28,1s85) P Value
Major malformation 42 (25) 634 (2) <.00l1 1) <.001