Oligohydramnios Causes, Symptoms, and Treatment

Last updated by Peer reviewed by Dr Colin Tidy
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Oligohydramnios is defined as too little amniotic fluid. There is an association between oligohydramnios and both intrauterine growth restriction and increased perinatal mortality[1]. Normal amniotic fluid volume changes with gestational age and ways of accurately estimating it have changed over the years. Oligohydramnios has been defined as[2]:

  • Amniotic fluid of less than 500 ml at 32-36 weeks of gestation
  • Maximum vertical pocket (MVP) of less than 2 cm from late mid-trimester.
  • Amniotic fluid index (AFI) of less than 5 cm or less than the 5th percentile, from late mid-trimester.

Amniotic fluid volume (AFV) increases throughout most of pregnancy, with a volume of about 30 ml at 10 weeks of gestation and a peak of about 1 L at 34-36 weeks of gestation. AFV decreases towards term, with a mean AFV of 800 ml at 40 weeks.

Amniotic fluid constantly circulates, with an estimated exchange rate as high as 3600 ml/hour. Excretion of urine by the fetus is the major source of amniotic fluid production in the second half of the pregnancy. Fluid secreted by the fetal respiratory tract also contributes to AFV.

Fetal swallowing is the major pathway of amniotic fluid clearance in the last half of gestation. Fetal skin is highly permeable in the first half of pregnancy but becomes keratinised at 22-25 weeks of gestation, significantly reducing transfer.

The mother's fluid balance (and also therefore the fetus') has a major effect on the AFV. Increased maternal fluid intake has been shown to increase the AFV in women with oligohydramnios[3].

Oligohydramnios is secondary to either an excess loss of fluid, or a decrease in fetal urine production or excretion. Oligohydramnios is usually associated with one of the following conditions:

  • Rupture of amniotic membranes (ROM).
  • Congenital absence of functional renal tissue or obstructive uropathy:
    • Conditions that prevent the formation of urine or the entry of urine into the amniotic sac.
    • Fetal urinary tract malformations, including renal agenesis, cystic dysplasia and ureteral atresia.
  • Decreased renal perfusion leading to reduced urine production:
    • As a sequela of hypoxaemia-induced redistribution of fetal cardiac output.
    • In growth-restricted fetuses, chronic hypoxia results in shunting of fetal blood away from the kidneys to more vital organs.
    • Anuria and oliguria lead to oligohydramnios.
  • Post-term gestation:
    • The cause of decreased AFV in post-term pregnancies is unknown.
    • The decreased efficiency of placental function has been proposed as a cause but this has not been confirmed histologically.
    • Decreased fetal renal blood flow and decreased fetal urine production have been demonstrated beyond 42 weeks in pregnancies involving oligohydramnios.

Oligohydramnios is a complication in approximately 4.4% of all pregnancies and severe oligohydramnios is a complication in 0.7% of pregnancies[4, 5]. Oligohydramnios is more common in pregnancies beyond term, as the AFV normally decreases at term. It complicates as many as 12% of pregnancies that last beyond 41 weeks. 

  • Fetal causes include:
  • Placental causes include:
    • Abruption.
    • Twin-to-twin transfusion syndrome (monochorionic twins)[6].
  • Maternal causes include:
  • Drug-induced causes include indometacin and angiotensin-converting enzyme (ACE) inhibitors.
  • Idiopathic.

Test for systemic lupus erythematosus (causes immune-mediated infarcts in the placenta and placental insufficiency). Other maternal risk factors (including hypertension and diabetes) should also be assessed.


The diagnosis is confirmed by ultrasound. It may be discovered incidentally during routine scanning, or noted during antepartum surveillance for other conditions.

  • Suspicion of oligohydramnios may be prompted by discrepancies in sequential fundal height measurements, or by fetal parts that are easily palpated through the maternal abdomen.
  • During ultrasound, normal-appearing fetal kidneys and fluid-filled bladder may be observed to rule out renal agenesis, cystic dysplasia and ureteral obstruction.
  • Fetal growth should be checked to exclude intrauterine growth restriction leading to oliguria. Doppler ultrasound could be used to assess placental insufficiency, if suspected.

Measurement of AFV

  • The two most commonly used objective methods of determining AFV include measurement of the maximum vertical pocket depth and the summation of the depths of the largest vertical pocket in each quadrant, or the AFI. (The pregnant abdomen is divided into four quadrants by using the umbilicus as a reference point to divide the uterus into upper and lower halves, and by using the linea nigra to divide the uterus into left and right halves.) The four measurements are summed to obtain the AFI in centimetres.
  • Pockets should be free of fetal limbs and the umbilical cord. AFV may be artificially increased if the transducer is not maintained perpendicular to the floor. Excessive pressure on the maternal abdomen with the transducer may lead to an artificially reduced measurement.
  • A meta-analysis of randomised controlled trials has concluded that the MVP measurement during fetal surveillance is a better choice[7]. The use of the AFI increases the rate of diagnosis of oligohydramnios and the rate of induction of labour without any improvement in peripartum outcomes[8].
  • However, there is no evidence that routine measurement and identification of oligohydramnios in normal term pregnancies reduces perinatal mortality[9].

Sterile speculum examination

  • Sterile speculum examination should be performed to check for ROM. Amniotic fluid may pool in the vagina and a ferning pattern may be observed when fluid from the posterior vault is dried and examined under a microscope.
  • Cervical mucus may cause false positive results (as can semen and blood).
  • Nitrazine paper/sticks turn blue. (The amniotic fluid is more alkaline - pH 6.5-7.0 - than normal vaginal discharge - pH 4.5.)

Management of oligohydramnios is based on gestational age. Planned birth in an obstetric unit is recommended[10]. Transfer to a tertiary referral centre may be appropriate if oligohydramnios is severe.

  • Before term:
    • Expectant management is often the most appropriate course of action, depending on maternal and fetal condition.
    • Ongoing antepartum surveillance (including assessment of fetal growth and follow-up monitoring of AFV) is necessary.
    • Continuous fetal heart rate monitoring during labour has been advocated for all pregnancies complicated by oligohydramnios.
  • At term:
    • Delivery is often the most appropriate management.
    • With reassuring fetal testing, delivery may be safely delayed on the basis of the parity, the gestational age, the inducibility of the mother's cervix and the severity of the oligohydramnios.
  • After term:
    • Isolated oligohydramnios in the post-term patient has no greater risk for caesarean delivery and there is insufficient evidence to support induction for women with oligohydramnios[11, 12].

The treatment of maternal dehydration with oral or intravenous rehydration has been shown to increase the AFV by 30%[5].


Increasing the amount of fluid within the amniotic cavity can be accomplished with the use of amnioinfusion. In this process, sodium chloride or Ringer's lactate is infused under ultrasound guidance via a needle inserted through the uterine wall. The current evidence on the safety and efficacy of this procedure means it is only undertaken in the UK under special arrangements that include audit and research[3].

Amnioinfusion can also be undertaken during labour transcervically via an intrauterine catheter. However, the Royal College of Obstetricians and Gynaecologists does not recommend this for women with preterm rupture of membranes.

Vesico-amniotic shunts

Vesico-amniotic shunts may be used to divert fetal urine to the amniotic fluid cavity in women in whom a fetal obstructive uropathy is determined to be the cause of oligohydramnios. Although it is effective in reversing oligohydramnios, its ability to achieve sustainable good renal function in infancy is variable[13]. Pulmonary function cannot be guaranteed with restoration of the AFV. Although an established procedure, there are limited safety and efficacy data and uncertainty regarding selection criteria; hence it is only undertaken in the UK under special arrangements that include audit and research[14].

  • The prognosis of oligohydramnios varies depending on the underlying aetiology, the gestational age at diagnosis, and the severity of oligohydramnios. Diagnosis of oligohydramnios during the second trimester is more likely to be associated with fetal or maternal anomalies, whereas diagnosis in the third trimester is more likely to be of unexplained origin.
  • The assessment of AFV is important in pregnancies complicated by abnormal fetal growth or intrauterine growth restriction. Oligohydramnios is a frequent finding in pregnancies involving intrauterine growth restriction and is most likely secondary to decreased fetal blood volume, renal blood flow and subsequently fetal urine output. Pregnancies complicated by severe oligohydramnios have been shown to be at increased risk of fetal morbidity.
  • Compared with women with normal AFI, those with isolated oligohydramnios have been found to have significantly higher rates of an infant with meconium aspiration syndrome (relative risk (RR), 2.83; 95% CI, 1.38-5.77), Cesarean delivery for fetal distress (RR, 2.16; 95% CI, 1.64-2.85) and admission to the neonatal intensive care unit (NICU) (RR, 1.71; 95% CI, 1.20-2.42)[16]. Patients with oligohydramnios and comorbidities were more likely to have an infant with low birth weight (RR, 2.35; 95% CI, 1.27-4.34).
  • Potter syndrome[17].
  • Pulmonary hypoplasia.
  • Fetal compression syndrome.
  • Amniotic band syndrome.
  • The risk of fetal infection is increased (by the presence of prolonged ROM).

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Further reading and references

  1. Morris RK, Meller CH, Tamblyn J, et al; Association and prediction of amniotic fluid measurements for adverse pregnancy outcome: systematic review and meta-analysis. BJOG. 2014 May121(6):686-99. doi: 10.1111/1471-0528.12589. Epub 2014 Feb 7.

  2. Moise KJ Jr; Toward consistent terminology: assessment and reporting of amniotic fluid volume. Semin Perinatol. 2013 Oct37(5):370-4. doi: 10.1053/j.semperi.2013.06.016.

  3. Therapeutic amnioinfusion for oligohydramnios during pregnancy (excluding labour); NICE Interventional Procedure Guidance, November 2006

  4. Hou L, Wang X, Hellerstein S, et al; Delivery mode and perinatal outcomes after diagnosis of oligohydramnios at term in China. J Matern Fetal Neonatal Med. 2020 Jul33(14):2408-2414. doi: 10.1080/14767058.2018.1553944. Epub 2018 Dec 13.

  5. Luton D, Alran S, Fourchotte V, et al; Paris heat wave and oligohydramnios. Am J Obstet Gynecol. 2004 Dec191(6):2103-5.

  6. Borse V, Shanks AL; Twin-To-Twin Transfusion Syndrome

  7. Nabhan AF, Abdelmoula YA; Amniotic fluid index versus single deepest vertical pocket: a meta-analysis of randomized controlled trials. Int J Gynaecol Obstet. 2009 Mar104(3):184-8. Epub 2008 Nov 30.

  8. 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. 2008 Jul 16(3):CD006593.

  9. Rossi AC, Prefumo F; Perinatal outcomes of isolated oligohydramnios at term and post-term pregnancy: a systematic review of literature with meta-analysis. Eur J Obstet Gynecol Reprod Biol. 2013 Jul169(2):149-54. doi: 10.1016/j.ejogrb.2013.03.011. Epub 2013 Apr 2.

  10. Intrapartum care for healthy women and babies; NICE Guideline (Dec 2014 - updated Dec 2022)

  11. Verrotti C, Bedocchi L, Piantelli G, et al; Amniotic fluid index versus largest vertical pocket in the prediction of perinatal outcome in post-term pregnancies. Acta Biomed. 200475 Suppl 1:67-70.

  12. Mozurkewich E, Chilimigras J, Koepke E, et al; Indications for induction of labour: a best-evidence review. BJOG. 2009 Apr116(5):626-36. Epub 2009 Feb 4.

  13. Biard JM, Johnson MP, Carr MC, et al; Long-term outcomes in children treated by prenatal vesicoamniotic shunting for lower urinary tract obstruction. Obstet Gynecol. 2005 Sep106(3):503-8.

  14. Fetal vesico-amniotic shunt for lower urinary tract outflow obstruction; NICE Interventional procedures guidance, December 2006

  15. Keilman C, Shanks AL; Oligohydramnios

  16. Rabie N, Magann E, Steelman S, et al; Oligohydramnios in complicated and uncomplicated pregnancy: a systematic review and meta-analysis. Ultrasound Obstet Gynecol. 2017 Apr49(4):442-449. doi: 10.1002/uog.15929.

  17. Bhandari J, Thada PK, Sergent SR; Potter Syndrome