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Treatment of almost all medical conditions has been affected by the COVID-19 pandemic. NICE has issued rapid update guidelines in relation to many of these. This guidance is changing frequently. Please visit https://www.nice.org.uk/covid-19 to see if there is temporary guidance issued by NICE in relation to the management of this condition, which may vary from the information given below.

Synonym: hydramnios

Polyhydramnios is defined as an abnormally large volume of amniotic fluid. It is known to be associated with adverse pregnancy outcomes and may raise suspicion of a problem with the pregnancy. Greater deviations from the norm are more strongly associated with abnormality.

Physiologically, the volume of fluid increases with gestation to a maximum at 36-37 weeks. It has a number of purposes, including protecting the fetus from trauma and infection, allowing lung development and facilitating the development and movement of the limb and other skeletal parts.

Mechanisms affecting amniotic fluid volume include:

  • Fetal swallowing. By term, the fetus swallows 210-760 ml of amniotic fluid per day. Conditions which cause a problem with swallowing are a common cause of polyhydramnios - for example, atresia of the upper gastrointestinal tract, fetal hypoxia, neuromuscular disorders or brain abnormalities.
  • Fetal urination. This is the main source of amniotic fluid in the second half of pregnancy - there is almost no amniotic fluid in cases of renal agenesis or fetal urinary tract obstruction. The fetus responds to changes by adjusting the amount of urination, thereby contributing to amniotic volume regulation. By term, urinary output is around 700-900 ml per day. Increases in fetal urination - for example, due to fetal anaemia and the subsequent increased cardiac output - may be a cause of increased amniotic fluid volume.
  • Secretions of fetal lung fluid and fetal oral and nasal cavities.
  • Absorption via intramembranous and transmembranous pathways. This includes movement of fluid between the fetal blood and placenta and across intrauterine membranes such as the amnion and chorion.

Conditions which affect any of these mechanisms may result in abnormal quantities of amniotic fluid; either polyhydramnios (too much) or oligohydramnios (too little).


Causes are numerous and include:

  • Idiopathic (the most common; no cause identified - around 50% of cases).
  • Congenital anomalies and genetic disorders. 8-24% of cases. Anomalies may be isolated or due to a genetic disorder (see below). Includes conditions such as:
    • Oesophageal or duodenal atresia.
    • Cardiovascular defects.
    • Microcephaly or anencephaly.
    • Neural tube defects.
    • Renal defects, including Bartter's syndrome (a rare inherited defect in the loop of Henle of the renal tubule).
  • Genetic disorders as referred to above include:
    • Trisomy 21, 18 and 13.
    • Pena-Shokeir syndrome (contractures of the joints (arthrogryposis), growth problems, underdeveloped lungs, facial deformities).
    • Beckwith-Wiedemann syndrome (overgrowth disorder).
  • Maternal diabetes. 5-26% of cases.
  • Multiple pregnancy. 8-10% of cases.
  • Fetal anaemia. 1-11% of cases.
  • Congenital infections (eg, toxoplasmosis, parvovirus, rubella, cytomegalovirus).
  • Hydrops fetalis (excessive fluid in one or more fetal compartment - eg, the pleural or abdominal space - common in rhesus haemolytic disease).
  • Maternal substance abuse.
  • Maternal metabolic abnormalities such as hypercalcaemia.[2]

There are few recent studies but polyhydramnios is said to affect 0.2-1.6% of all pregnancies. Rates are much higher in pregnancies for women with diabetes or gestational diabetes.

Where polyhydramnios is mild, an underlying abnormality is found in only 17%, whereas in moderate-to-severe polyhydramnios, this figure rises to 91%. There is also an association with increasing maternal age and with fetal macrosomia.[4]

The condition is suspected when antenatal examination reveals a uterus that is large for dates. Fetal parts may be difficult to palpate. It may be picked up on clinical or ultrasound examination.

When not diagnosed on routine antenatal examination, it may present with excessive maternal breathlessness, early onset of labour or rupture of membranes, cord prolapse, or abnormal fetal presentation.

Occasionally, the uterus enlarges rapidly. This is known as acute polyhydramnios and is most common in twin pregnancies. In such cases, abnormal connecting blood vessels in the twin placenta result in unequal distribution of blood flow (twin-to-twin transfusion syndrome).[5]The twin receiving the larger amount of blood supply is known as the recipient twin and the twin receiving the smaller amount is known as the donor. The recipient twin produces a large amount of urine and is surrounded by excessive amniotic fluid.

When the uterus appears large for dates on clinical examination, ultrasound scans usually rule out the alternative diagnoses including:

  • Multiple pregnancy
  • Fetal macrosomia
  • Abruptio placenta which may cause rapidly expanding uterine size due to the development of intrauterine haematoma. This is usually an easy differential diagnosis to make, as pain is a predominant feature.
  • Chorioangioma - this is a benign lesion of the placenta due to excess capillary formation in the absence of villus differentiation. It may cause a 'large-for-dates' uterus per se, or be associated with polyhydramnios.


Experienced operators can detect polyhydramnios subjectively.

There are two methods used to quantify amniotic fluid volume:

  • Amniotic fluid index (AFI) or four-quadrant method: the uterine cavity is divided into four quadrants or pockets. The largest vertical pocket in each quadrant is measured in centimetres and the total volume is calculated by adding the four together. A total of more than 24 cm defines polyhydramnios.
  • Single deepest pocket (SDP) method: the deepest pocket is measured vertically. A measurement under 2 cm defines oligohydramnios and where it is over 8 cm there is polyhydramnios.

By both methods, the measurement can then further define polyhydramnios as mild, moderate or severe. The higher the measurement, the higher the likelihood of fetal abnormality.[6]

Laboratory tests

The following may be helpful in excluding associated diseases:

  • Blood glucose and oral glucose tolerance test.
  • Maternal infection screen.
  • If fetal anaemia or hydrops fetalis is suspected the following may also be appropriate:
    • Screening for maternal antibodies against fetal red blood cells.
    • Screening for cytomegalovirus, syphilis, rubella, toxoplasmosis, parvovirus 19.
    • Genotyping.

Amniocentesis and fetal karyotyping may be considered.

  • Management is undertaken in secondary care. There are no guidelines or large studies to guide management decisions.
  • The first step is to identify if there is an underlying cause.
  • Identified causes are treated as appropriate. Fetal hydrops anaemia is treated with intravascular transfusion. If gestational diabetes is diagnosed, tight glycaemic control should be maintained. This may involve dietary manipulation, oral medication or insulin.[7]
  • Mild polyhydramnios can be simply monitored and treated conservatively.
  • Preterm labour is common due to overdistension of the uterus, and measures should be taken to minimise this complication. This includes regular antenatal checks and inspection of the uterus. Serial ultrasound scans should be carried out to monitor the AFI and fetal growth.
  • Induction of labour should be considered if fetal distress develops. Induction by artificial rupture of the membranes (ARM) should be controlled, performed by an obstetrician and with consent to proceed to lower-segment caesarean section if required.
  • Corticosteroids should be given to the mother antenatally if preterm delivery is imminent or considered.[8]This helps to improve lung maturity.
  • Prostaglandin synthetase inhibitors, particularly indometacin, may be used. This acts at least partly by reducing renal blood flow and reducing fetal urination. It is used usually for a maximum of 48 hours and regimes vary. It is not used in twin-to-twin syndrome or after 32 weeks, as adverse effects outweigh benefits in these cases. The main risk is fetal ductus arteriosus constriction and the risk increases with gestation. Sulindac has also been used but there are no trials to confirm efficacy and safety.
  • Amnioreduction (drainage of amniotic fluid under ultrasound guidance) is also used in cases where indometacin is contra-indicated, in severe polyhydramnios, or in patients who are symptomatic. It is more commonly used in twin-to-twin transfusion syndrome. There are few studies but those that exist suggest it is safe and effective, although serial procedures may be required.[9]
  • Polyhydramnios associated with twin-to-twin syndrome may benefit from laser ablation of the connecting placental vessels.[5]

There is a higher incidence of preterm labour and delivery. Other complications include premature rupture of the membranes, abruptio placenta, malpresentation, postpartum haemorrhage and cord prolapse. There is a higher incidence of caesarean section.

For the mother, the risk of urinary tract infections is increased due to increased pressure on the urinary tract. The mother may have increased dyspnoea due to increased pressure on the diaphragm. There is also a higher risk of hypertension in pregnancy.

Studies of pregnancies associated with polyhydramnios but not congenital malformation showed that polyhydramnios was an independent risk factor for low birth weight, low Apgar scores, fetal death and neonatal mortality.[10, 11]

  • Only 17% of pregnancies with mild polyhydramnios have a significant associated problem. However, an underlying abnormality is associated with 91% of cases of moderate-to-severe polyhydramnios.[3]
  • A poor prognosis is associated with the more severe fetal or placental malformations. The severity of the prognosis is naturally dependent on the severity of the abnormality.
  • The more severe the polyhydramnios, the more likely the chance of finding an underlying cause.[6]
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Further reading and references

  1. Sandlin AT, Chauhan SP, Magann EF; Clinical relevance of sonographically estimated amniotic fluid volume: polyhydramnios. J Ultrasound Med. 2013 May32(5):851-63. doi: 10.7863/ultra.32.5.851.

  2. Shani H, Sivan E, Cassif E, et al; Maternal hypercalcemia as a possible cause of unexplained fetal polyhydramnion: a case series. Am J Obstet Gynecol. 2008 Oct199(4):410.e1-5.

  3. Hamza A, Herr D, Solomayer EF, et al; Polyhydramnios: Causes, Diagnosis and Therapy. Geburtshilfe Frauenheilkd. 2013 Dec73(12):1241-1246.

  4. Mathew M, Saquib S, Rizvi SG; Polyhydramnios. Risk factors and outcome. Saudi Med J. 2008 Feb29(2):256-60.

  5. Rossi AC, D'addario V; Twin-twin transfusion syndrome. Minerva Ginecol. 2009 Apr61(2):153-65.

  6. Pri-Paz S, Khalek N, Fuchs KM, et al; Maximal amniotic fluid index as a prognostic factor in pregnancies complicated by polyhydramnios. Ultrasound Obstet Gynecol. 2012 Jun39(6):648-53. doi: 10.1002/uog.10093.

  7. Diabetes in pregnancy: management of diabetes and its complications from preconception to the postnatal period; NICE Clinical Guideline (February 2015 - last updated Dec 2020)

  8. Crowther CA, McKinlay CJ, Middleton P, et al; Repeat doses of prenatal corticosteroids for women at risk of preterm birth for improving neonatal health outcomes. Cochrane Database Syst Rev. 2015 Jul 57:CD003935. doi: 10.1002/14651858.CD003935.pub4.

  9. Dickinson JE, Tjioe YY, Jude E, et al; Amnioreduction in the management of polyhydramnios complicating singleton pregnancies. Am J Obstet Gynecol. 2014 Oct211(4):434.e1-7. doi: 10.1016/j.ajog.2014.05.036. Epub 2014 May 29.

  10. Erez O, Shoham-Vardi I, Sheiner E, et al; Hydramnios and small for gestational age are independent risk factors for neonatal mortality and maternal morbidity. Arch Gynecol Obstet. 2005 Apr271(4):296-301. Epub 2004 Jul 9.

  11. Chen KC, Liou JD, Hung TH, et al; Perinatal outcomes of polyhydramnios without associated congenital fetal anomalies after the gestational age of 20 weeks. Chang Gung Med J. 2005 Apr28(4):222-8.

Hi - my son had this condition and was operated on at 4 weeks. We were told at the time it is usually noticed at 3 months plus and he was very young and the muscle was very thick. He is now nearly 2...

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