INTRODUCTION — Oligohydramnios refers to amniotic fluid volume that is less than expected for gestational age. It is typically diagnosed by ultrasound examination and may be described qualitatively (eg, reduced amniotic fluid volume) or quantitatively (eg, amniotic fluid index ≤5 cm, single deepest pocket <2 cm).

Oligohydramnios may be idiopathic or have a maternal, fetal, or placental cause (table 1). The fetal prognosis depends on several factors, including the underlying cause, the severity (reduced versus no amniotic fluid), and the gestational age at which oligohydramnios occurs. Because an adequate volume of amniotic fluid is critical to normal fetal movement and lung development and for cushioning the fetus and umbilical cord from uterine compression, pregnancies complicated by oligohydramnios from any cause are at risk for fetal deformation, pulmonary hypoplasia, and umbilical cord compression.

Oligohydramnios is associated with an increased risk for fetal or neonatal death, which may be related to the underlying cause of the reduced amniotic fluid volume or due to sequelae of the reduced amniotic fluid volume.

This topic will discuss issues related to oligohydramnios. Methods of amniotic fluid volume assessment are reviewed separately. (See "Assessment of amniotic fluid volume".)

INCIDENCE — Reported rates of oligohydramnios are highly influenced by the gestational age at the time of the ultrasound examination (preterm, term, or postterm), the population studied (low or high risk, screening or indicated ultrasound examination, antepartum or intrapartum), and variations in diagnostic criteria.

Oligohydramnios occurs in <1 percent of preterm pregnancies and is more common in pregnancies that reach term. In a study of 3050 uncomplicated pregnancies with singleton nonanomalous fetuses between 40 and 41.6 weeks of gestation undergoing semi-weekly monitoring of amniotic fluid index (AFI) because they passed their delivery date, oligohydramnios (defined as AFI ≤5 cm) was observed in 11 percent [1]. A study from China reported a 4.4 percent incidence of oligohydramnios at term [2].

PATHOGENESIS — The volume of amniotic fluid reflects the balance between fluid production and movement of fluid out of the amniotic sac. The most common mechanisms for development of oligohydramnios are fetal oliguria/anuria and fluid loss due to rupture of membranes. A reduction in the egress of lung fluid and increased swallowing do not play major roles. Idiopathic cases (ie, idiopathic oligohydramnios) may be due to alterations in the expression of water pores (aquaporin 1, aquaporin 3) in fetal membranes and placenta [3].

Homeostatic mechanisms, such as intramembranous absorption (transfer of amniotic fluid across the amnion into the fetal circulation), work to maintain amniotic fluid volume; however, these mechanisms appear to be more successful in preventing hydramnios than in preventing oligohydramnios. (See "Physiology of amniotic fluid volume regulation".)

ETIOLOGY — Conditions commonly associated with oligohydramnios are listed in the table (table 1). The most likely etiologies of oligohydramnios vary according to severity and the trimester in which they are diagnosed. The majority of women with oligohydramnios or borderline/low normal amniotic fluid volume present in the third trimester and have no identifiable cause.

First trimester — The etiology of first trimester oligohydramnios is often unclear. Reduced amniotic fluid prior to 10 weeks of gestation is rare because gestational sac fluid is primarily derived from the fetal surface of the placenta, transamniotic flow from the maternal compartment, and secretions from the surface of the body of the embryo.

Criteria suggested for determining reduced amniotic fluid at this gestational age have included a difference between mean gestational sac size and crown-rump length that is less than 5 mm or a mean gestational sac diameter/crown-rump length ratio outside the normal range for gestational age [4-8]. This finding has been associated with poor outcome in selected populations [4]. However, the prognostic value of these findings, when applied to large unselected populations, has not been adequately studied [8].

Second trimester — By the beginning of the second trimester, fetal urine begins to enter the amniotic sac, and the fetus begins to swallow amniotic fluid. Therefore, disorders related to the fetal renal/urinary system begin to play a prominent role in the etiology of oligohydramnios (table 2). These anomalies include intrinsic renal disorders (eg, cystic renal disease) and obstructive lesions of the lower urinary tract (eg, posterior urethral valves, urethral atresia). (See "Prenatal sonographic diagnosis of cystic renal disease" and "Clinical presentation and diagnosis of posterior urethral valves" and "Fetal hydronephrosis: Etiology and prenatal management".)

Maternal and placental factors, as well as rupture of the fetal membranes (traumatic or nontraumatic), are also common causes of oligohydramnios in the second trimester (table 1).

The etiologies and relative frequencies of midtrimester oligohydramnios were illustrated in a series of 128 fetuses first noted to have severe oligohydramnios/anhydramnios at 13 to 24 weeks of gestation [9]. The following etiologies were observed: fetal anomaly (51 percent), preterm prelabor rupture of membranes (PPROM) (34 percent), placental abruption (7 percent), fetal growth restriction (FGR) (5 percent), and unknown (4 percent). Six of the 65 anomalous fetuses were aneuploid. The pregnancy outcome was generally poor due to fetal or neonatal death or pregnancy termination. (See 'Prognosis' below.)

Third trimester — Oligohydramnios first diagnosed in the third trimester is often associated with PPROM or with uteroplacental insufficiency due to conditions such as preeclampsia or other maternal vascular diseases. Oligohydramnios frequently accompanies fetal growth restriction related to uteroplacental insufficiency. Fetal anomalies and abruptio placentae also play a role at this gestational age. Amniotic fluid volume normally decreases postterm, so oligohydramnios may develop in these pregnancies. In addition, many cases of third trimester oligohydramnios are idiopathic. (Refer to individual topic reviews on these subjects).

There may be an association between pregnancy during the summer season and oligohydramnios, likely related to suboptimal maternal hydration in hot weather [10].

Maternal TORCH (toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex virus) and parvovirus B19 infections that infect the fetus may be associated with second- or third-trimester oligohydramnios, often in association with other evidence of fetal infection [11,12].

CLINICAL MANIFESTATIONS AND DIAGNOSIS

Presentation — Oligohydramnios may be first suspected because the uterine size is less than expected for gestational age or because the patient presents with prelabor rupture of membranes. It may be detected on an ultrasound examination performed to assess amniotic fluid volume in a patient at risk or as an incidental finding on an ultrasound examination performed for another reason.

Diagnosis — There are both objective and subjective ultrasound criteria for diagnosis of oligohydramnios. Use of an objective criterion is generally preferable (either single deepest pocket [SDP] <2 cm or amniotic fluid index [AFI] ≤5 cm); however, subjective suspicion of amniotic fluid volume by experienced examiners has similar sensitivity for diagnosing reduced amniotic fluid volume confirmed by the dye-dilution method, the gold standard for quantifying volume [13].

It appears that the SDP overly diagnoses polyhydramnios, while the AFI overly diagnoses oligohydramnios [14]. Accordingly, one may consider using the SDP in patients with low amniotic fluid volume and the AFI for patients with high amniotic fluid volume, though this approach may not be practical. The diagnostic performance of methods of ultrasound assessment of amniotic fluid is reviewed separately. (See "Assessment of amniotic fluid volume", section on 'Single deepest pocket' and "Assessment of amniotic fluid volume", section on 'Amniotic fluid index' and "Assessment of amniotic fluid volume", section on 'Qualitative assessment'.)

The most extreme end of the oligohydramnios spectrum is anhydramnios, which can be defined as a lack of a measurable AFI or SDP, although a thin echolucent rim may be imaged on the inner aspect of the uterus.

Multiple gestations — SDP <2 cm is also used for diagnosis of oligohydramnios in multiple gestations. (See "Assessment of amniotic fluid volume", section on 'Multifetal pregnancy'.)

POSTDIAGNOSTIC EVALUATION — Our evaluation of pregnancies with oligohydramnios consists of the following:

●A thorough maternal, personal, and family history and a targeted physical examination are performed to look for maternal conditions that may be associated with oligohydramnios (table 1). The effect of maternal medications (eg, prostaglandin synthase inhibitors) may be limited to oligohydramnios, whereas maternal medical disorders often cause a combination of fetal growth restriction and oligohydramnios.

●Prelabor rupture of membranes (PROM) should be ruled out. (See "Preterm prelabor rupture of membranes: Clinical manifestations and diagnosis", section on 'Diagnostic evaluation and diagnosis'.)

●A comprehensive sonographic evaluation with fetal biometry is performed, as well as a search for fetal anomalies (table 2), markers suggestive of aneuploidy (eg, increased nuchal translucency), fetal growth restriction, or placental abnormalities (eg, chronic abruption) that may account for decreased amniotic fluid volume. (See "Sonographic findings associated with fetal aneuploidy" and "Fetal growth restriction: Screening and diagnosis" and "Placental abruption: Pathophysiology, clinical features, diagnosis, and consequences".)

A National Institutes of Health workshop recommended documenting assessment of the kidneys (presence, size, location, appearance [echogenicity, cysts, urinary tract dilation]), bladder (size and shape), umbilical cord insertion site and vessel number, and fetal sex [15]. (See "Prenatal sonographic diagnosis of cystic renal disease".)

●If fetal anomalies are identified, fetal genetic testing is offered. Trisomy 13 and triploidy are the most common chromosomal abnormalities associated with early oligohydramnios. If no anatomic abnormalities are detected (isolated oligohydramnios), the risk of genetic abnormalities does not appear to be increased above the baseline risk [16]. (See "Prenatal genetic evaluation of the fetus with anomalies or soft markers" and "Sonographic findings associated with fetal aneuploidy".)

●Maternal serum alpha-fetoprotein (MSAFP) is checked. An elevated MSAFP has prognostic significance and can be helpful in counseling [17-20]. Oligohydramnios associated with an elevated second-trimester MSAFP level may be caused by damage to the fetal membranes or placenta, leading to leakage of amniotic fluid from the vagina or transplacental passage of fetal blood into the maternal circulation [21]. The fetus may or may not be anomalous. The combination (elevated MSAFP, decreased amniotic fluid volume) carries an extremely poor prognosis, including fetal growth restriction, fetal death, preterm delivery, and neonatal death [17-20]. In one review of these cases, only 8 of 57 children (14 percent) survived past the neonatal period [22].

●Fetal magnetic resonance imaging (MRI) may be helpful because it is less limited by lack of amniotic fluid than ultrasound. It has been used alone or in combination with amnioinfusion to better define complex fetal anomalies when this information will alter patient care. T1 and T2 imaging is preferable to T3 imaging because the latter can increase the temperature of amniotic fluid [23,24].

●There is no clear role for Doppler studies in the diagnostic evaluation of pregnancies with isolated oligohydramnios. Although at least one study reported arterial blood flow redistribution, others have not observed this finding [25-27].

●Testing maternal serum or amniotic fluid for an infection-related etiology (maternal TORCH [toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex virus] and parvovirus infection) depends on the degree of suspicion (eg, suggestive maternal history and symptoms, other fetal abnormalities on ultrasound) in individual cases. See individual topic reviews on TORCH and parvovirus B19.

STRATEGIES FOR INCREASING AMNIOTIC FLUID VOLUME, WHEN INDICATED — There is no treatment of oligohydramnios that has been proven to be effective long-term. However, short-term improvement of amniotic fluid volume is possible and may be considered under certain circumstances, such as when a fetal anatomic survey is needed.

Amnioinfusion — Amnioinfusion temporarily increases amniotic fluid volume. It has been used in the following settings. The procedure is described separately. (See "Amnioinfusion".)

●To improve detection of fetal anomalies – During the second trimester, oligohydramnios may limit optimal ultrasound assessment of the fetus. In such cases, transabdominal amnioinfusion of approximately 200 milliliters of saline under ultrasound guidance can provide better visualization of fetal anatomy and thus improve diagnostic precision [28-30]. It is a reasonable option when the information obtained is likely to affect pregnancy management.

A review of patients with unexplained midtrimester oligohydramnios who underwent diagnostic antenatal amnioinfusion found that the overall rate of adequate visualization of fetal structures improved from 51 percent before amnioinfusion to 77 percent after amnioinfusion [28]. In fetuses having preinfusion-identified obstructive uropathy, the identification of associated anomalies increased from 12 percent before amnioinfusion to 31 percent after amnioinfusion.

Other studies reported that information obtained at amnioinfusion at a median gestational age of 22 weeks led to a change of etiologic diagnosis in 13 percent of cases [29] and the most common post-amnioinfusion new findings were renal anomalies, rupture of membranes, and growth restriction [30].

●To facilitate cephalic version – Decreased amniotic fluid impedes the success of external cephalic version. Data on use of amnioinfusion for this indication are low quality and discordant but generally suggest that it does not improve success rates. (See "External cephalic version", section on 'Amnioinfusion'.)

●To prevent fetal sequelae of oligohydramnios – (See 'Investigational therapies' below.)

Maternal hydration — In cases of isolated oligohydramnios in which delivery is not indicated, oral hydration with one to two liters of water can transiently increase amniotic fluid volume and may have some benefit, particularly in hypovolemic patients. This approach is easier and safer than intravenous fluid administration or amnioinfusion. Hydration with water appears to reduce maternal plasma osmolality and sodium concentration, resulting in osmotically driven maternal to fetal water flux; it also improves uteroplacental perfusion.

A 2015 systematic review and meta-analysis of the efficacy of maternal hydration strategies for improving amniotic fluid volume found that maternal hydration was most effective in pregnancies with isolated oligohydramnios and that hypotonic solutions were more effective than isotonic fluids [31]. Whether maternal hydration improved clinical outcome in pregnancies with isolated oligohydramnios was unclear because of heterogeneity in patient selection, sonographic diagnostic criteria, hydration protocols, and outcome assessment.

A prospective study not included in the analysis provided an example of the potential effect of maternal hydration. In this study, 10 women with third trimester oligohydramnios (amniotic fluid index [AFI] <5 cm) and 10 women with normal amniotic fluid volume were asked to consume two liters of water over two hours [32]. In women with oligohydramnios, hydration increased mean AFI by 3.2 cm (95% CI 1.1-5.3) but had no effect on AFI in women with normal amniotic fluid volume.

Investigational therapies — Investigational approaches to increase amniotic fluid volume have explored novel treatments.

●Hydration and DDAVP – The combined use of oral water ingestion and desmopressin (DDAVP) markedly and transiently increases amniotic fluid volume [33,34]. This effect is attributed to both of maternal hydration and antidiuresis, and thus maternal plasma hypoosmolality. Use of DDAVP for this indication should be considered experimental, and used only under approved research protocols.

●Tissue sealants – A variety of tissue sealants (eg, fibrin glue, gelatin sponge, amniopatch) have shown some success in stopping leakage from ruptured membranes in case reports. Neither the safety nor the efficacy of these sealants has been established. (See "Prelabor rupture of membranes before and at the limit of viability", section on 'Repair of leaks'.)

●Hydration and sildenafil citrate – In a pilot trial of women with idiopathic oligohydramnios diagnosed after 30 weeks of gestation, administration of sildenafil citrate 25 mg thrice daily and one liter of intravenous hydration (IV) followed by oral hydration significantly increased the AFI compared with IV and oral hydration alone [35]. The sildenafil group also delivered later (38.3 versus 36.0 weeks of gestation), had a lower rate of cesarean delivery (28 versus 73 percent), and a lower rate of neonatal intensive care unit admission (11 versus 41 percent). However, a multicenter Dutch trial (STRIDER) of sildenafil for treatment of poor prognosis early onset growth restriction using the same dose [36] was halted early because of higher than expected rates of lung disease and death of newborns in the intervention group [37]. At the time the trial was closed, use of sildenafil did not result in any benefits.

The populations differed between the two trials (idiopathic oligohydramnios versus poor prognosis growth restriction), which might account for some of the differences in outcome. Although the idiopathic oligohydramnios trial demonstrated neonatal benefits in the sildenafil group versus the hydration-only group, we believe the STRIDER trial results are striking. Until more data are available about the postnatal effects of antenatal administration of sildenafil and the mechanism for the adverse postnatal effects is understood, the use of sildenafil in pregnancy should be restricted to carefully designed clinical trials monitored by data and safety monitoring boards.

●Amnioinfusion – Serial transabdominal amnioinfusions have been used with some success in research studies to improve fetal outcome in pregnancies with idiopathic oligohydramnios [38], early oligohydramnios due to preterm prelabor rupture of membranes [39], and oligohydramnios due to renal anomalies. (See "Renal agenesis: Prenatal diagnosis", section on 'Pregnancy outcome and obstetric management'.)

●Vesicoamniotic shunt or amnioport – In fetuses with oligohydramnios due to lower urinary tract obstruction, shunting has been used with some success as an investigative approach to increase amniotic fluid volume and prevent adverse pulmonary, orthopedic, and renal sequelae. (See "Renal agenesis: Prenatal diagnosis", section on 'Pregnancy outcome and obstetric management' and "Management of posterior urethral valves", section on 'Prenatal intervention'.)

PROGNOSIS — The fetal/neonatal prognosis depends on the cause, severity, gestational age at onset, and duration of oligohydramnios. In fetuses with renal anomalies, the type of extra-renal anomalies, if present, also affects prognosis.

First trimester — Reduced amniotic fluid volume in the first trimester is an ominous finding; the pregnancy usually aborts. In one series, 15 of 16 patients (94 percent) with a normal fetal heart rate and small sac noted on first-trimester sonogram went on to spontaneously abort compared with only 4 of 52 control patients (8 percent) with normal sac size [4]. (See "Pregnancy loss (miscarriage): Ultrasound diagnosis".)

We counsel these patients regarding the poor prognosis and inform them of the signs of miscarriage. Serial sonographic examinations are helpful for following the natural history of the process (eg, worsening oligohydramnios, embryonic/fetal demise, or [rarely] resolution).

Second trimester — In the second trimester, prognosis and management depend upon the underlying etiology and the magnitude of amniotic fluid reduction.

●Borderline/low normal amniotic fluid volume – Pregnancies with borderline/low normal amniotic fluid volume generally have a good prognosis [18,40-42]. Serial sonographic examinations every one to two weeks are helpful for following the natural history of the process, which may remain stable, resolve, or progress to development of oligohydramnios and/or fetal growth restriction.

●Oligohydramnios – In the second trimester, oligohydramnios often ends in fetal or neonatal death [9,43]. In the large series described above (128 fetuses first noted to have oligohydramnios at 13 to 24 weeks of gestation), survival was reported in 9/43 (21 percent) fetuses with PPROM, 2/9 (22 percent) fetuses with abruption, 1/5 (20 percent) idiopathic cases, 1/65 (1.5 percent) fetuses with congenital anomalies, and 0/6 fetuses with fetal growth restriction [9]. Many of these women chose pregnancy termination because of the poor prognosis.

Before terminating a pregnancy, parents should receive multidisciplinary counseling, when appropriate, regarding the suspected etiology of oligohydramnios, further evaluation, short- and long-term prognosis, and their options (eg, termination, continuation of pregnancy, palliative neonatal care, aggressive neonatal care). Consultation with a pediatric nephrologist is particularly important when oligohydramnios is due to renal disorders as dialysis and future renal transplant may be options in some cases [44,45].

In ongoing pregnancies, the risks for and potential sequelae of cord compression, preterm birth, and neonatal abnormalities should be discussed. Cord compression can lead to asphyxia and fetal demise. Preterm delivery, either spontaneous or indicated by maternal or fetal complications, occurs in more than 50 percent of cases of oligohydramnios and is associated with increased morbidity and mortality [17-19,29,40,46,47]. Neonatal abnormalities as a result of development in a severely low amniotic fluid environment may be structural or functional and include skeletal deformations, contractures, and pulmonary hypoplasia. (See "Prelabor rupture of membranes before and at the limit of viability", section on 'Musculoskeletal development' and "Prelabor rupture of membranes before and at the limit of viability", section on 'Pulmonary hypoplasia'.)

An exception to the poor prognosis described above is oligohydramnios related to second-trimester amniocentesis. In these cases, the membranes often "reseal," amniotic fluid reaccumulates, and pregnancy outcome is normal (see "Diagnostic amniocentesis", section on 'Leakage of amniotic fluid'). There are few reports of the occurrence of oligohydramnios after chorionic villus sampling; outcomes have been mixed [48,49]. (See "Chorionic villus sampling".)

Third trimester — There appears to be an inverse relationship between amniotic fluid volume in the third trimester and adverse pregnancy outcome. Adverse outcomes are related to umbilical cord compression, uteroplacental insufficiency, and meconium aspiration. In particular, uteroplacental insufficiency and cord compression are associated with fetal heart rate abnormalities that result in cesarean delivery and low Apgar scores [9,50-53]. The duration of oligohydramnios is also a prognostic factor. Patients who present with idiopathic oligohydramnios at an earlier gestational age are at increased risk for adverse perinatal outcomes compared with those presenting later in gestation [9,54].

Potential types and frequencies of adverse outcomes are illustrated by the following studies:

●In a study including over 28,000 pregnancies that underwent ultrasound examination between 24 and 34 weeks of gestation, major malformations were more common in pregnancies with oligohydramnios (amniotic fluid index [AFI] ≤5 cm) and borderline AFI (5 to 8 cm) than in those with normal fluid: major malformations were present in 25, 10, and 2 percent of fetuses, respectively [42]. Among nonanomalous fetuses, complications that occurred more often in pregnancies with oligohydramnios and borderline AFI included preterm birth: 62, 37, and 8 percent, respectively; cesarean delivery for nonreassuring fetal status: 9, 9, and 4 percent, respectively; and birth weight below the third percentile: 37, 21, and 4 percent, respectively.

●In a 2016 meta-analysis of 12 studies including approximately 36,000 women at term of which 2414 (6.7 percent) had isolated oligohydramnios, women with oligohydramnios had significantly higher rates of labor induction, cesarean delivery, low Apgar scores and neonatal intensive care unit admission than those with normal amniotic fluid volume [55].

●In a retrospective study including over 4000 pregnancies with isolated oligohydramnios, total neurologic and gastrointestinal morbidity-related hospitalizations in the pediatric period were significantly more common as compared with pregnancies with normal amniotic fluid volume [56].

PRENATAL CARE — Specific pregnancy complications associated with oligohydramnios are managed as appropriate for the condition. (Refer to individual topic reviews on specific chromosomal and congenital anomalies, midtrimester PPROM, maternal medical disorders, preeclampsia, abruptio placenta, etc).

Given the potential high risk of adverse outcome, we deliver patients with oligohydramnios who are at term. (See 'Timing of delivery' below.)

In ambulatory patients, we perform a nonstress test (NST) and single deepest pocket (SDP; or a biophysical profile) once or twice weekly until delivery, depending upon the maternal and fetal condition. Combined use of the NST and SDP is associated with a low rate of unexpected fetal death [57-59]. We also obtain serial sonographic examinations to monitor fetal growth.

Patients with oligohydramnios newly diagnosed early in the third trimester may be hospitalized to undergo evaluation of possible causes (see 'Postdiagnostic evaluation' above), daily NSTs, and maternal hydration in an attempt to increase amniotic fluid volume. (See 'Maternal hydration' above.)

Although the role of Doppler velocimetry in managing fetal growth restriction is well established, its use in assessment or management of idiopathic oligohydramnios has not been validated.

TIMING OF DELIVERY

Our approach — The indications for delivery in women with oligohydramnios attributable to a specific condition (eg, preeclampsia, premature rupture of membranes, fetal growth restriction, congenital anomaly, postterm pregnancy, etc) are discussed separately in topic reviews on these disorders.

Our indications for delivery in patients with idiopathic oligohydramnios include, but are not limited to, nonreassuring fetal testing or reaching 36+0 to 37+6 weeks of gestation regardless of the cervical Bishop score [60]. Although induction increases the risk of cesarean delivery [61,62], there is insufficient evidence to assure us that perinatal outcome with continued conservative management of oligohydramnios at term is comparable to that with delivery, even in the presence of an appropriately grown, noncompromised fetus and absence of maternal disease. Use of cervical ripening agents is an option for patients with an unfavorable cervix [63].

Alternatively, the patient can be followed with serial nonstress testing and biophysical profiles until she is at full term (≥39 weeks). The risks and benefits of various management plans should be discussed with the patient, so she can make an informed decision.

Evidence — In a meta-analysis that stratified controlled studies of women with oligohydramnios into two groups of high risk (oligohydramnios plus comorbid condition) versus low risk (isolated oligohydramnios), high-risk patients were more likely to have an infant with low birth weight (relative risk 2.35, 95% CI 1.27-4.34), but rates of five minute Apgar score <7, neonatal intensive care unit admission, meconium-stained amniotic fluid, and cesarean delivery for fetal distress were similar for both groups [53]. Stillbirth rates were too low to analyze. Although the authors concluded that management of patients with oligohydramnios should be dictated by the comorbid condition and not the presence of oligohydramnios alone, we believe oligohydramnios management should be similar in both low- and high-risk pregnancies.

Timing of delivery in pregnancies complicated by idiopathic oligohydramnios is controversial [64]. Only one small, randomized trial has evaluated outcomes with intervention versus expectant management. In this trial, 54 pregnancies beyond 40 weeks of gestation with isolated oligohydramnios were randomly assigned to either induction of labor or expectant management [65]. No differences were found for any important maternal or neonatal outcome.

Observational studies have reported conflicting results. In one retrospective series, the corrected perinatal mortality rate in structurally normal fetuses with oligohydramnios was significantly lower when delivery was initiated upon diagnosis (in gestations of at least 28 weeks) than with conservative management (18 versus 90 per 1000 births) [66]; this suggests that intervention is indicated. However, the groups came from different institutions and time periods, so they may not have been comparable.

Most studies have reported no increased risk of fetal acidosis and generally good outcomes in pregnancies with isolated oligohydramnios (AFI <5 cm) in the third trimester (ie, appropriately grown nonanomalous fetus, reassuring fetal heart rate pattern, no maternal disease) when compared with controls with normal amniotic fluid volumes [52,61,62,67-75]. Importantly, most studies examining the benefits of AFI assessments instituted scheduled antenatal testing for these patients, suggesting that oligohydramnios may precede fetal compromise [68]. Alternatively, this may be related, in part, to the low sensitivity and specificity of AFI for uteroplacental insufficiency, especially in the absence of other indicators of impaired placental perfusion, such as fetal growth restriction, preeclampsia, fetal abnormalities, postterm pregnancy, or abruption [76,77].

FETAL ASSESSMENT DURING LABOR — Neither amniotic fluid index nor single deepest pocket performed on admission to the labor unit accurately predicts the risk of peripartum complications [78-80]. We recommend obtaining a short electronic fetal heart rate recording upon admission of patients in labor to help determine whether the fetal heart rate should be monitored continuously or whether intermittent monitoring is likely to be sufficient. If the fetal heart rate is not reactive or fetal heart rate decelerations are present, then we recommend continuous electronic fetal heart rate monitoring during labor. We also consider transcervical amnioinfusion for patients with oligohydramnios and variable fetal heart rate decelerations in labor. (See "Intrapartum category I, II, and III fetal heart rate tracings: Management", section on 'Variable decelerations without loss of variability or accelerations'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Oligohydramnios and polyhydramnios".)

SUMMARY AND RECOMMENDATIONS

●Oligohydramnios refers to amniotic fluid volume that is less than expected for gestational age. It is typically diagnosed by ultrasound examination and may be described qualitatively or quantitatively (eg, amniotic fluid index [AFI] ≤5 cm; single deepest pocket <2 cm). (See 'Clinical manifestations and diagnosis' above.)

●Conditions commonly associated with oligohydramnios are listed in the table (table 1). The most likely etiologies of oligohydramnios vary according to the trimester in which it is diagnosed. The majority of women with oligohydramnios present in the third trimester and have no identifiable cause. (See 'Etiology' above.)

●Maternal history and physical examination and a comprehensive sonographic evaluation are recommended for all pregnancies with oligohydramnios. Use of additional tests (eg, karyotype, instillation of dye, testing for an infection-related etiology) depends upon individual clinical circumstances. (See 'Postdiagnostic evaluation' above.)

●There is no effective long-term treatment of oligohydramnios. In idiopathic oligohydramnios, maternal treatment with intravenous isotonic solution, oral hydration, or amnioinfusion can lead to short-term improvement. These procedures may be useful under certain circumstances, such as to facilitate diagnostic ultrasound evaluation when the fetal anatomic survey is suboptimal. (See 'Strategies for increasing amniotic fluid volume, when indicated' above.)

●Reduced amniotic fluid in the first trimester appears to be an ominous finding. We counsel these patients regarding the poor prognosis, discuss the signs of miscarriage, and follow the pregnancy with serial ultrasound examinations to determine its course. (See 'First trimester' above.)

●The prognosis and management of second trimester oligohydramnios depend upon the underlying etiology and severity of oligohydramnios. Pregnancies with borderline/low normal amniotic fluid volume generally have a good prognosis. Anhydramnios diagnosed at this time may induce anatomical and functional fetal abnormalities and often results in fetal or neonatal death.

We initially perform a fetal structural survey to rule out a fetal malformation since serious abnormalities may influence future management. Serial sonographic examinations to monitor amniotic fluid volume, fetal growth, and fetal well-being are performed until delivery. (See 'Second trimester' above.)

●Some studies have shown an inverse relationship between amniotic fluid volume in the third trimester and the incidence of adverse pregnancy outcome. Adverse outcomes are related to umbilical cord compression, uteroplacental insufficiency, and meconium aspiration. Given the potential high risk of adverse outcome, we perform a nonstress test and AFI (or biophysical profile) once or twice weekly until delivery. (See 'Third trimester' above.)

●For women with idiopathic oligohydramnios, we suggest delivery at 36+0 to 37+6 weeks of gestation rather than expectant management (Grade 2C). Although induction of an unfavorable cervix may increase the length of labor, there is insufficient evidence to assure us that perinatal outcome with continued conservative management of oligohydramnios at term is comparable to that with delivery. (See 'Timing of delivery' above.)