Oligohydramnios is a decrease in the volume of amniotic fluid, with the diagnosis usually being made using ultrasound.
Causes of oligohydramnios include ruptured membranes, placental insufficiency, fetal anomalies, maternal injestion of medications, complications of a multiple gestation, chromosomal abnormalities, and idiopathic.
Significant oligohydramnios occurring prior to 22 weeks of gestation is associated with a poor prognosis because of a high likelihood of pulmonary hypoplasia and associated malformations.
Once oligohydramnios is diagnosed, a careful maternal history should be obtained and a physical examination should be performed to evaluate for preterm premature rupture of membranes.
Whenever a diagnosis of oligohydramnios is made, a careful sonographic anatomical survey should be performed to evaluate for fetal anomalies such as features of urinary tract obstruction or renal malformation.
Amnioinfusion may assist sonographic visualization of the fetus when severe oligohydramnios is diagnosed in the midtrimester.
Management of oligohydramnios secondary to preterm premature rupture of membranes depends on the gestational age and on the fetal and maternal status.
Long-term outcome will depend on gestational age at diagnosis, etiology of the problem, and gestational age at delivery.
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).
Prenatal ultrasound image at 20 weeks from pregnancy with severe oligohydramnios demonstrating fetal dolicocephaly. (Courtesy of Prenatal Diagnosis Center, Women and Infants’ Hospital.)
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.
ANTENATAL NATURAL HISTORY
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).
Severely constricted fetus with oligohydramnios due to bladder agenesis and a single dysplastic kidney. (Courtesy of Dr. Joseph Semple.)
The finding of significant oligohydramnios in the second trimester is associated with very high perinatal mortality (Barss et al., 1984; Bhutani et al., 1986; D’Alton et al., 1992). The combination of second trimester oligohydramnios and elevated maternal serum α -fetoprotein (MSAFP) has an extremely poor prognosis. In one report of 21 patients with midtrimester oligohydramnios and elevated MSAFP, only one infant survived (Dyer et al., 1987). Causes of perinatal loss in the setting of second trimester oligohydramnios include lethal congenital abnormalities, pulmonary hypoplasia, severe prematurity, and neonatal sepsis. Oligohydramnios in cases of chronic abruption appears to be an end-stage manifestation of severe uteroplacental insufficiency and is associated with a high incidence of intrauterine fetal death (Shenker et al., 1991).
Second trimester oligohydramnios following preterm premature rupture of membranes (PPROM) carries a poor prognosis, with up to a 60% fetal loss rate, due mostly to pulmonary hypoplasia (Bhutani et al., 1986; D’Alton et al., 1992). Sequelae of PPROM that contribute to the poor outcome include chorioamnionIt is, amnion nodosum (Figure 125-3), neonatal sepsis, neonatal pneumonia, placental abruption, and cord prolapse (Gonen et al., 1989). Neonatal outcome following PPROM can be improved by the routine administration of antibiotics, such as ampicillin and erythromycin (Mercer et al., 1997).
Gross (panel A) and microscopic (panel B) appearances of amnion nodosum in a fetus with oligohydramnios.
The combination of oligohydramnios and fetal growth restriction is associated with significantly increased perinatal morbidity and mortality rates (Hill et al., 1983; Chamberlain et al., 1984; Seeds, 1984). The perinatal mortality rate ranges from 10% to 19% in these situations (Chamberlain et al., 1984). Close fetal surveillance is indicated to avoid antenatal deterioration of fetal status, and elective premature delivery may be needed.
Postmature pregnancies have increased rates of perinatal morbidity and mortality (Beischer et al., 1969). The finding of oligohydramnios in a pregnancy beyond 41 weeks of gestation identifies a subset of patients who are at significantly increased risk for adverse outcomes. There is a significantly higher risk of abnormal fetal testing, presence of fetal heart rate decelerations during labor, meconium staining, cesarean delivery for nonreassuring fetal testing, and depressed 1 - and 5-minute Apgar scores (Rutherford et al., 1987; Sarno et al., 1990; Robson et al., 1992).
Little information exists on the antenatal natural history of oligohydramnios prior to 37 weeks of gestation in the absence of intrauterine growth restriction, PPROM, or fetal anomalies. In one case–control study of pregnancies with unexplained oligohydramnios, there was a significantly higher incidence of premature delivery but no difference in overall neonatal outcomes (Garmel et al., 1997). Oligohydramnios associated with maternal hypovolemia is associated with a good perinatal outcome and is generally reversible with hydration (Sherer et al., 1990).
Following a diagnosis of oligohydramnios, a careful maternal history should be obtained to evaluate for illnesses such as hypertension or chronic renal disease and to assess for use of medications such as prostaglandin synthetase inhibitors. Physical examination should include a sterile speculum examination to evaluate for pooling of amniotic fluid in the vaginal vault, phenaphthazine (nitrazine) paper analysis, and microscopic examination of a vaginal smear on a slide for the presence of ferning. The presence of oligohydramnios should prompt a thorough sonographic survey of the fetal anatomy. Visualization of the fetal anatomy may be extremely difficult in cases of severe oligohydramnios. Administration of furosemide to the mother has been advocated to improve detection of bilateral renal agenesis (Kurjak et al., 1981). Other authors have suggested that fetuses with severe growth restriction may not respond to furosemide administration secondary to decreased renal perfusion and decreased glomerular filtration rate, and therefore extreme caution should be used with this approach (Goldenberg et al., 1984).
Amnioinfusion may assist sonographic visualization of the fetus in pregnancies complicated by severe oligohydramnios. In one report of 13 pregnancies complicated by severe oligohydramnios, amnioinfusion of warmed normal saline was successfully performed in all patients and fluid for karyotype analysis was successfully obtained in 8 patients (Quetel et al., 1992). The use of amnioinfusion, together with indigocarmine dye instillation, allowed subsequent adequate ultrasound examination in 12 of 13 patients, a correct diagnosis of ruptured membranes in 6 patients, and an antenatal diagnosis of Meckel–Gruber syndrome in one case (Quetel et al., 1992). If a structural fetal anomaly is identified, karyotyping should be performed. In cases of severe oligohydramnios prior to 24 weeks of gestation, termination of pregnancy may be discussed with the patient.
The management of pregnancies with oligohydramnios secondary to PPROM depends on the gestational age at presentation. Ruptured membranes beyond 34 weeks of gestation should be managed by prompt induction of labor to minimize infectious maternal and fetal morbidity. In cases of PPROM at less than 34 weeks of gestation, expectant management is reasonable, provided there is no evidence of intrauterine infection, fetal compromise, or preterm labor. Frequent assessment in the form of daily fetal heart rate monitoring is recommended. Administration of betamethasone to the mother is advocated with PPROM prior to 32 to 34 weeks of gestation to reduce complications of prematurity. Although the evidence for improving neonatal outcome is less clear than with the use of corticosteroids in patients with intact membranes, there is an additional benefit in reduction of the incidence of intraventricular hemorrhage (National Institutes of Health, 1995). In cases of PPROM prior to 34 weeks of gestation, administration of antibiotics to the mother, typically ampicillin and erythromycin for 7 days, has been shown to increase the latency period prior to delivery and improves overall neonatal outcome (Mercer et al., 1997). There is no conclusive evidence to support or (Courtesy of Dr. Joseph Semple.) exclude a benefit from tocolysis in the setting of PPROM. Expectant inpatient management of PPROM is recommended from 24 to 32 weeks of gestation, provided there is reassuring maternal and fetal testing on a daily basis. In cases of PPROM from 32 to 34 weeks of gestation, evaluation of fetal lung maturity may help decide between expectant management and induction of labor.
In cases of fetal growth restriction with oligohydramnios at less than 36 to 37 weeks of gestation, careful fetal assessment is suggested, consisting of nonstress and biophysical testing at least twice weekly. If there is absent end-diastolic flow in the fetal umbilical artery, daily fetal testing is recommended. Delivery is indicated once a gestational age of 36 to 37 weeks is reached or if fetal testing becomes nonreassuring. In cases of oligohydramnios in the presence of an appropriately grown fetus, delivery should be considered once a gestational age of 37 weeks is reached.
The location of delivery will depend on the cause of the oligohydramnios and the gestational age at diagnosis. If a congenital abnormality is present, delivery at a tertiary care center where appropriately trained personnel are available is recommended. In patients with PPROM, delivery location will depend on the gestational age. For patients at less than 32 weeks of gestation, delivery should occur in a tertiary care center with a neonatal intensive care unit. The mode of delivery should be based on usual obstetric practices; there is no indication to alter the mode of delivery based solely on the presence of oligohydramnios or PPROM. However, there is an increased incidence of cesarean delivery in pregnancies complicated by oligohydramnios, regardless of cause. For this reason, elective cesarean delivery may be reasonable in the setting of significant oligohydramnios with an unfavorable cervix. The significance of oligohydramnios as an isolated finding in the management of labor is difficult to ascertain. In one retrospective case–control study, the frequency of nonreassuring fetal testing, meconium staining, cesarean delivery, and admission to the neonatal intensive care unit were not significantly different when 65 women with oligohydramnios in the absence of IUGR, PPROM, or fetal anomalies were compared with 122 controls matched by indication for sonography (Garmel et al., 1997).
The management of pregnancy complicated by oligohydramnios secondary to PPROM at previable gestational ages (less than 24 weeks) should be individualized. The option of pregnancy termination should be discussed because of the risks of maternal infectious morbidity and the high likelihood of poor perinatal outcome. When expectant management is selected in such cases, inpatient hospitalization is generally not recommended after the initial evaluation, as active fetal intervention is not generally an option. Expectant management should include bed rest at home, daily monitoring of maternal temperature, and observation for the development of regular contractions. In 10% of such patients, leakage of amniotic fluid stops because of membrane resealing, amniotic fluid reaccumulates, and perinatal outcome is significantly improved (Johnson et al., 1990).
Amnioinfusion has been described to reduce the incidence of pulmonary hypoplasia in patients with severe oligohydramnios who are remote from term (Nakayama et al., 1983; Hansmann et al., 1991). However, this treatment remains experimental. The instillation of an isotonic antibiotic solution via the cervix has been used for treating patients with PPROM, but should also be considered experimental (Ogita et al., 1984). Amnioinfusion has also been described for patients with PPROM (Garzetti et al., 1997; Locatelli et al., 2000, Tranquilli et al., 2005). Because of the invasive nature of such approaches and the possibility for adverse maternal and perinatal outcomes, appropriately controlled clinical trials are necessary before these techniques can be recommended.
Another potential intervention for midtrimester PPROM is attempting to correct the defect. It is hoped that this treatment can increase the latency time to delivery, restore amniotic fluid volume to decrease the risk for lung hypoplasia as well as limb and muscular contracture defects, and decrease infectious morbidity.
Amniotic membrane patching has been suggested in carefully selected patients without evidence of intramniotic infection and confirmed PPROM. Transabdominal intra-amniotic injection of platelets and cryoprecipitate has been used as a therapy for midtrimester PPROM. In a preliminary study, Quintero et al. treated 7 patients with iatrogenic PPROM (all cases of PPROM occurred following an invasive procedure such as amniocentesis or fetoscopy) diagnosed between 16 and 24 weeks of gestation with an amniopatch (Quintero et al., 1999). For the amniopatch, an amniocentesis was performed with a 22-gauge needle and platelets were administered followed by cryoprecipitate. Two mililiters of indigo carmine was then instilled to aid in documentation of amniotic fluid leakage. Intravenous antibiotics were then given for one week. Three pregnancies progressed well. The amniotic fluid re-accumulated and there was no further leakage. Two patients had unexplained intrauterine fetal demise despite resealing. One patient resealed but continued to have oligohydramnios secondary to fetal bladder outlet obstruction, and one patient had a miscarriage secondary to twin-to-twin transfusion syndrome despite resealing. This study demonstrates that, although experimental, an amniopatch with platelets and cryoprecipitate might be a promising therapy for iatrogenic cases of PPROM.
Administration of a cervical plug to retard the loss of fluid from the amniotic cavity is another potential treatment of midtrimester PPROM. In one study, 15 women with PPROM (either iatrogenic or spontaneous) had a gelatin sponge placed within the uterine cavity (O’Brien et al., 2002). The research protocol included hospital admission, amnioinfusion, cerclage placement, antibiotic administration, and perioperative tocolysis. Eight pregnancies (53%) delivered after 24 weeks of gestation, 6 of whom (30%) survived until hospital discharge. There were two intrauterine fetal deaths. The mean gestational age at delivery was 31.8 weeks (range 25–36 weeks). No adverse sequelae were attributed to the gelatin sponge. However, several anatomic abnormalities were diagnosed that were likely to be secondary to decreased amniotic fluid volume. This aggressive interventional protocol may improve outcomes in patients with previable PPROM by reducing the incidence of lethal pulmonary hypoplasia. However, further study is needed, before this approach could be considered mainstream. Several issues must be addressed such as route of applications (transvaginal versus transcervical), whether combinations of plugging agents are more efficacious, which fetuses are likely to benefit, and whether or not maternal complications are associated with this intervention.
Prophylactic amnioinfusion during labor to correct abnormal fluid volumes has not been found to be beneficial unless associated with recurrent variable decelerations.
Fetal intervention by means of vesicoamniotic shunting may be considered in selected fetuses with severe oligohydramnios secondary to bladder outlet obstruction. Benefits of shunting may include a decreased incidence of pulmonary hypoplasia. Prognosis in these cases is related to the duration of exposure of the developing fetal lung to severe oligohydramnios and to the severity of the underlying renal condition. The option of vesicoamniotic shunting in such cases is described in more detail in Chapter 82.
The extent of newborn intervention in cases of oligohydramnios will depend on the gestational age at diagnosis, the gestational age at delivery, and the cause of the oligohydramnios. If a sonographic diagnosis of renal agenesis is certain, no resuscitation of the newborn is indicated. However, if doubt exists about the diagnosis, a neonatologist should be present at delivery to evaluate for features of Potter syndrome and pulmonary hypoplasia. Intubation and mechanical ventilation of the newborn may be considered appropriate until a more definitive diagnosis for severe oligohydramnios is made. Pulmonary air leak may develop secondary to positive pressure ventilation in the setting of pulmonary hypoplasia, which may require the placement of chest tubes.
No surgical treatments have been described.
The long-term outcome will depend on the gestational age at diagnosis, the gestational age at delivery, and the underlying cause of the oligohydramnios. The longest duration of survival reported with a diagnosis of bilateral renal agenesis is 39 days. Severe oligohydramnios may result in the development of arthrogryposis (see Chapter 101). Contractures of previously normal joints may also occur in cases of severe oligohydramnios of long duration. The feet are most commonly involved, typically resulting in positional clubfoot. Compression of the fetus against the uterine wall in the setting of severe oligohydramnios can produce a spectrum of abnormalities. Potter syndrome is characterized by low-set ears, hypertelorism, receding chin, flattened nose, wrinkled skin, and joint contractures.
GENETICS AND RECURRENCE RISK
The recurrence risk of oligohydramnios will depend on the underlying cause. The cause of bilateral renal agenesis is multifactorial. The recurrence risk following delivery of an infant with bilateral renal agenesis and a negative family history is approximately 3% to 4%. In a study of 41 index patients with bilateral renal agenesis, bilateral severe renal dysgenesis, or agenesis of one kidney with dysgenesis of the other, 10 of 111 first-degree relatives were found to have clinically unsuspected renal malformations (Roodhooft et al., 1984). Parents offetuses with oligohydramnios due to renal anomalies should therefore be evaluated by ultrasound examination for renal anomalies.
The recurrence risk for premature rupture of membranes occurring in a future pregnancy is uncertain, but may be as high as 32% (Asrat et al., 1991). Such patients should therefore be considered at high risk for this complication in all future pregnancies.
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