Obstetrics and Gynecology

Oligohydramnios

Oligohydramnios: Relatively Reduced Amniotic Fluid Volume

1. What every clinician should know

The degree of oligohydramnios correlates with adverse clinical outcome.Reduced amniotic fluid volume can be subdivided into anhydramnios (complete absence of amniotic fluid), severe oligohydramnios and moderate oligohydramnios. The clinical consequences of oligohydramnios, which can range from stillbirth or perinatal asphyxia due to severe, prolonged umbilical cord compression to intermittent but inconsequential fetal heart rate decelerations during labor, are more frequent in cases of severely decreased amniotic fluid volume.

There are numerous criteria for diagnosing oligohydramnios. A variety of ultrasound diagnostic criteria have been proposed, including subjectively "decreased" volume, absence of a 1 cm or 2 cm vertical fluid pocket, a four quadrant sum of vertical pockets (amniotic fluid index -- AFI) less 5 cm and AFI less than the 5th or 2.5th percentile. All of these criteria have modest predictive power for adverse perinatal outcome but none have adequate specificity for use as a single criterion for mandating delivery.

If oligohydramnios is suspected, increased fetal surveillance should be considered. While the vast majority of cases of oligohydramnios are associated with minimal or no morbidity, a clinically important increase in perinatal mortality, meconium aspiration and requirement for NICU care exists.

If oligohydramnios is diagnosed when delay of delivery is preferred, a trial of maternal hydration may increase amniotic fluid volume. Multiple human and animal studies have demonstrated a link between decreased maternal vascular volume and oligohydramnios. Maternal intravenous infusions have been shown to increase amniotic fluid in selected cases.

2. Diagnosis and differential diagnosis

A. Establishing the diagnosis

Normal amniotic fluid volume. Amniotic fluid volume is estimated using ultrasound to measure vertical pockets of fluid. Fluid pocket measurements must be obtained in the vertical plane, be clear of any fetal or umbilical echoes and at least 1 cm wide. The amniotic fluid index is the sum of the single deepest pockets (SDP) in each of four quadrants of the uterus. An average (50th percentile) value near term for the AFI is approximately 10 cm and for SDP is 4 cm but both the AFI and SDP trend downward significantly toward the EDD - from 12.9 cm (AFI) and 4.8 cm (SDP) at 34 weeks to 8.6 (AFI) and 3.9 cm at 40 weeks (Table I).

table 1.

Percentiles for AFI and MVP

Diagnosing oligohydramnios. While the values for diagnosing oligohydramnios are typically defined as less than 5 cm (AFI) and less than 2 cm (SDP), approximating the fifth percentile for AFI and 2.5th percentile for SDP respectively, the values representing oligohydramnios at 34 weeks (6.4 cm AFI, 2.3 cm SDP) are substantially higher than for 40 weeks (3.7 cm AFI and 2.1 cm). Further, small differences in fluid pocket measurement may either diagnose a patient as having oligohydramnios or "normal" fluid. Since the intraobserver error in measuring AFI is approximately 1 cm, measures in triplicate should be performed before confirming the diagnosis of oligohydramnios.

Use SDP or AFI to diagnose oligohydramnios? A recent systematic review of randomized trials comparing SDP less than 2 cm to AFI less than 5 cm in detecting oligohydramnios reported that using AFI doubled the diagnosis of oligohydramnios without reducing the frequency of neonatal acidosis and NICU care. AFI below 5 cm did identify more cases of cesarean for fetal distress. However, as noted above, the SDP criterion of less than 2 cm is approximately the 2nd percentile while AFI below 5 is the 5th percentile, making AFI twice as likely to identify hydramnios.

The improved sensitivity of AFI in identifying marginal amniotic fluid volumes may be of value in certain clinical circumstances, allowing for more intensive surveillance and initiation of delivery procedures in selected high risk pregnancies. On the other hand, use of SDP will reduce the use of labor induction in otherwise low risk pregnancies. As discussed below, rather than using a single, strict cutoff for "normal" amniotic fluid, the relative degree of fluid reduction should be integrated with the larger clinical picture.

B. Causes of oligohydramnios

Four major causes of oligohydramnios are recognized:

  1. Idiopathic.

  2. Ruptured membranes.

  3. Urinary tract anomaly or obstruction.

  4. Placental insufficiency.

Before assigning the category of "idiopathic" to a case of apparent oligohydramnios, care must be taken in clinical measurements and reference to normal values. According to studies utilizing direct or dye-dilution methods, there is a wide range of normal amniotic fluid volume: at term, average amniotic fluid volume is approximately 700 ml, with a relatively wide range of from 300 ml to 1200 ml (10-90th percentiles). Further, there is a strong negative influence of gestational age on volume. Thus reference to gestational age specific tables is recommended.

With regard to excluding the other causes, a methodical clinical and sonographic examination is necessary. Excluding ruptured membranes may be challenging in the preterm period, requiring repetitive vaginal examinations. Detailed sonography should be directed to exclusion of renal anomalies/agenesis and demonstration of bladder emptying. Placental insufficiency leads to oligohydramnios by reducing fetal vascular volume and therefore fetal urinary flow. In order to assign a case of oligohydramnios to placental insufficiency, significant fetal growth deficiency should be present as well as, typically, abnormal fetal umbilical artery Doppler characteristics (increased resistance index, S/D ratio).

3. Management

Antepartum management of first and second trimester oligohydramnios

Options to correct amniotic fluid volume and thus reduce the morbidities associated with prolonged premature rupture of membranes (PROM), including extremity deformations and pulmonary hypoplasia, are extremely limited. Renal agenesis should be considered lethal as should bilateral multicystic displastic kidneys when severe oligohydramnios (SDP less than 2 cm) is diagnosed before 22 weeks. Small studies of intrauterine saline infusion have yielded conflicting results regarding improved outcome in such cases.

For the fetus with lower urinary tract obstruction (LUTO) due to posterior urethral valves, in utero surgery (cystoscopy or vesico-amniotic shunting) to relieve the stricture has been shown to improve survival and to decrease neonatal morbidity in selected cases by allowing fetal urine to drain into the amniotic space and sustain both renal and pulmonary development. If considered, this procedure should be performed in a referral center.

Triaging cases for potential in utero intervention is based on assessing residual amniotic fluid and the appearance of the fetal kidneys; AFI less than 5 cm and the finding of ultrasound features of renal dysplasia are poor prognostic signs. The former practice of serially sampling fetal urinary electrolytes has been shown to be poorly predictive. It must be emphasized that long term outcome of infants treated in utero has been poor, with a disappointingly high incidence of renal failure requiring dialysis.

With early severe oligohydramnios resulting from PROM, the prognosis is very guarded, largely because bacterial entry into the lower uterine segment leads to chorioamnionitis and delivery, typically in the 23-28 week time frame when intact survival is less than 30%. In rare cases, expectant management can be associated with "sealing" of the leak; however, there is no evidence that bed rest or reverse Trendelenberg position restores amniotic fluid volume despite the fact that this is commonly prescribed.

Limited studies utilizing transabdominal or transcervical amnioinfusion to increase amniotic fluid volume have been performed with some indication of benefit; however, these studies are methodologically flawed and thus amnioinfusion for PROM is presently investigational only. Detailed counseling of women regarding the dismal but not uniformly fatal perinatal outcome of pregnancies with severe and sustained oligohydramnios following previable PROM is essential.

Antepartum management of third trimester oligohydramnios

Severe oligohydramnios occurring after 28 weeks of gestation does not lead to clinically important pulmonary hypoplasia or limb deformities. However, owing to the increased risk of umbilical cord compression, the risk of fetal death and perinatal asphyxia are increased, especially when FGR is present. Fetal intolerance of labor, evidenced by severe fetal heart rate decelerations, is common and consequently rates of meconium passage, operative delivery and perinatal asphyxia are elevated. Typically, the risk of these calamities increases as pregnancy advances.

Thus, these cases require intensive biophysical surveillance in order to choose the timing of delivery judiciously. If fetal growth parameters have dropped below the 10th percentile and AFI is below 5 cm, evaluation for delivery should be entertained, especially if 34 weeks of gestation has been achieved. Before 34 weeks, pregnancy is generally managed expectantly with intensive surveillance until growth arrest or reversal of velocity in the umbilical artery or notching of the ductus venosus is detected on Doppler interrogation.

With more moderate degrees of oligohydramnios (AFI 3-5 cm) and with normal fetal growth, systematic reviews of randomized trials of both intravenous and oral maternal hydration have demonstrated increased AFI and fetal urinary flow. Intravenous infusions are less effective than oral hydration. At least 2 hours should be allowed after 2 L of hydration before remeasuring amniotic fluid volume in order to maximize the likelihood of observing a beneficial effect.

Intrapartum management of oligohydramnios

Since reduced amniotic fluid is the putative cause of severe variable fetal heart rate decelerations in labor, it would seem logical that infusing fluid retrograde into the uterus would reduce these and thereby improve outcome. Typical clinical protocols involve recognition of significant FHR variable decelerations, placement of an intrauterine catheter and bolusing 200-500 ml physiologic saline followed by a continuous infusion at 100 ml/hour.

A recent systematic review of randomized trials concluded that meconium aspiration, cesarean section, maternal endometritis and perinatal morbidity were reduced by approximately half. However, caution in use of amnioinfusion with severe FHR variables should be taken, as the time taken to arrange and conduct the intrauterine saline infusion may prolong fetal exposure to umbilical cord compressions and actually degrade fetal condition.

4. Complications

First and second trimester oligohydramnios

Severe reduction in amniotic fluid volume in this period is usually associated with premature rupture of membranes (PROM) or absence/obstruction of fetal urinary flow (renal agenesis, bladder outlet obstruction). PROM occurring prior to 20 weeks, termed previable rupture of membranes, typically leads to advancing maternal chorioamnionitis, periviable delivery (23-27 weeks) and the morbidities of extreme prematurity for the neonate. Perinatal survival rates are approximately 50%.

In cases of severe first or second trimester oligohydramnios arising from chronic PROM or urinary obstruction, fetal gross body activity and breathing movements can be inhibited by the lack of amniotic fluid. This may lead to limb deformities and pulmonary hypoplasia. While the orthopedic abnormalities can be managed postnatally, pulmonary hypoplasia has a high degree of lethality in the early neonatal period. Unfortunately, prediction of pulmonary hypoplasia antenatally using sonographic parameters of thoracic area, circumference and other measures has poor sensitivity and specificity.

Third trimester oligohydramnios

Third trimester oligohydramnios may evolve as part of the sequence of progressive placental insufficiency which evolves from increasingly severe fetal growth restriction accompanied by reduced fetal renal perfusion and urinary flow which can lead to decreases in amniotic fluid volume. When oligohydramnios appears in this setting, reductions in fetal oxygen delivery are also frequent, significantly increasing the risk of in utero fetal death or perinatal asphyxia. Conversely, a small for dates fetus with normal amniotic fluid suggests an intrinsic growth problem such as chromosomal anomaly or TORCH infection. In cases of FGR complicated by oligohydramnios, intensive fetal surveillance is indicated, which may include hospitalization, twice weekly Doppler and biophysical testing and administration of antenatal corticosteroids.

Term and post-term oligohydramnios

Declining amniotic fluid volume is a normal finding in the term and post-term period and indeed may be physiologic as the fetus reduces intra- and extravascular fluid in anticipation of extrauterine life. On the other hand, abnormally low amniotic fluid volume may occur as a consequence of placental senescence, which in turn is associated with rising risk of fetal demise, meconium passage and perinatal asphyxia in the post-term period. Thus the task for the clinician is to identify the fetus at risk for perinatal morbidity and avoid the risks of labor induction in the others, as labor induction itself increases not only the risks of maternal morbidity (e.g. operative delivery) but also the risk of fetal and newborn sepsis.

5. Prognosis and outcome

Severe first and second trimester oligohydramnios

Previable PROM. Latency (the time from membrane rupture until delivery) is proportional to the residual AFI, with higher AFI having better prognosis. Median latency is 30 days but the range is wide. Among those expectantly managed, the incidence of chorioamnionitis is 70-90%. The mean gestational age at delivery is 23-25 weeks with a very wide range, neonatal survival is 30-50% but morbidity in the newborns (intraventricular hemorrhage, cerebral palsy) is high. Although small randomized trials suggest improvement in these outcomes with prophylactic amnioinfusion, this should be considered investigational.

Urinary anomalies. Untreated, neonatal survival is approximately 50%, with a high degree of severe renal impairment among the survivors. Placement of vesico-amniotic shunt improves survival with an odds-ratio of 3-5. However, even among treated subjects end stage renal disease (15-30%), ongoing bladder dysfunction (30-50%) and childhood growth abnormalities are frequent.

Third trimester oligohydramnios

Normally grown fetus. In the fetus at term (37-40 weeks) with normal growth, the effect of oligohydramnios on outcome is modest. Indeed many studies fail to demonstrate a difference in outcome of term pregnancies with normal or low amniotic fluid volume. In pregnancies 41 weeks and beyond, oligohydramnios is associated with moderate increases in meconium stained amniotic fluid, poor fetal tolerance of labor and increased cesarean delivery (odds ratios 1.5-2.0). Accordingly, initiating labor induction at term solely on the basis of an AFI below 5 cm should be approached with caution.

Fetus with FGR. Fetal growth restriction is an independent risk factor for poor perinatal outcome, with odds ratios ranging from 5-20. Although the degree of growth restriction and gestational age are strong predictors of perinatal morbidity, the risks are further multiplied several fold when oligohydramnios is present.

6. What is the evidence for specific management and treatment recommendations

Magann, EF, Sanderson, M, Martin, JN. "The amniotic fluid index, single deepest pocket, and two-diameter pocket in normal human pregnancy". Am J Obstet Gynecol. vol. 182. 2000. pp. 1581-8.

(This paper provides normative data for AFI and SDP.)

Moore, TR, Cayle, JE. "The amniotic fluid index in normal human pregnancy". Am J Obstet Gynecol. vol. 162. 1990. pp. 1168-73.

(This is the original paper describing normal values for the AFI across gestation in normal pregnancy.)

Nabhan, AF, Abdelmoula, YA. "Amniotic fluid index versus single deepest vertical pocket as a screening test for preventing adverse pregnancy outcome". Cochrane Database Syst Rev. vol. 3. 2008. pp. CD006593.

(There is no evidence that labor induction with an AFI less than 5 cm or SDP less than 2 cm is superior in the prevention of poor peripartum outcomes, including: admission to a neonatal intensive care unit; an umbilical artery pH of less than 7.1; the presence of meconium; an Apgar score of less than 7 at five minutes; or caesarean delivery. When the AFI was used, significantly more cases of oligohydramnios were diagnosed [RR 2.39, 95% CI 1.73 to 3.28], and more women had inductions of labor [RR 1.92; 95% CI 1.50 to 2.46] and caesarean delivery for fetal distress [RR 1.46; 95% CI 1.08 to 1.96]).

Hofmeyr, GJ, Gulmezoglu, AM. "Maternal hydration for incrdration with 2L of fluid appears to increase amniotic fluid volume and may be beneficial in theasing amniotic fluid volume in oligohydramnios and normal amniotic fluid volume". Cochrane Database Syst Rev. vol. 1. 2002. pp. CD000134.

(Maternal hye management of oligohydramnios and prevention of oligohydramnios during labour or prior to external cephalic version.)

Hofmeyr, GJ, Essilfie-, AG, Lawrie, TA. "Amnioinfusion for preterm premature rupture of membranes". Cochrane Database of Systematic Reviews. vol. No. 12. 2011.

(There is limited evidence that amnioinfusion following preterm PPROM may be beneficial by preventing infection, lung damage and death of neonates, and by preventing maternal amnionitis. However, current evidence is insufficient to recommend amnioinfusion for routine use in PPROM.)

Hofmeyr, GJ, Lawrie, TA. "Amnioinfusion for potential or suspected umbilical cord compression in labour". Cochrane Database Syst Rev. vol. 1. 2012 Jan18. pp. CD000013.

(The use of amnioinfusion for potential or suspected umbilical cord compression may be of benefit by reducing the frequency of variable FHR decelerations, improving short-term measures of neonatal outcome, reducing maternal postpartum endometritis and lowering the use of caesarean section although there were methodological limitations to the trials reviewed.)
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