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Polyhydramnios

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This is defined as an abnormally large volume of amniotic fluid. It is sometimes known by the shorter form, hydramnios.

Physiologically, the volume of fluid increases with gestation to a maximum of 800-1000 mL at 36-37 weeks.1 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. Fetal swallowing causes a reduction in the volume of fluid and absence of swallowing or a blockage of the fetal gastrointestinal tract may lead to polyhydramnios. Polyhydramnios is therefore strongly linked to fetal abnormality.

Epidemiology

A retrospective study of the ultrasound scans of patients attending a routine antenatal clinic in the UK showed a prevalence of 0.15%.2 The authors noted this was lower than previous studies and postulated that this was a reflection of improved screening and antenatal care.

Risk factors

One study found an association with maternal age, diabetes in pregnancy, and fetal macrosomia (excessive birth weight). The incidence of anaemia during pregnancy, Caesarean delivery rate and congenital anomalies were also found to be higher in the study group.3

Presentation

The condition is suspected when antenatal examination reveals a uterus that is large for dates.

Fetal parts may be difficult to palpate.

Occasionally the uterus enlarges rapidly. This is known as acute polyhydramnios and is commonest 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).4 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.5

Differential diagnosis
  • Abruptio placenta may cause rapidly expanding uterine size due to the development of intrauterine haematoma.6 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.7
Investigations

Ultrasound

Experienced operators can detect polyhydramnios subjectively.

A quantitative approach can be taken by dividing the uterine cavity into four quadrants or pockets. The largest vertical pocket is measured in centimetres and the total volume is calculated by multiplying this level by 4. This is known as the amniotic fluid index (AFI). Polyhydramnios is defined as an AFI of more than 24 cm or a single pocket of fluid of at least 8 cm deep that results in a total fluid volume of more than 2000 mL.1

AFI is one of the five component scores of a biophysical profile (a noninvasive test that detects the presence of absence of fetal asphyxia). The other components are fetal breathing movements, gross body movements, fetal tone and fetal heart monitoring.8

Enhanced modalities with the inclusion of colour Doppler techniques may be required if differentiation is needed from chorioangioma.

Laboratory tests

The following may be helpful in excluding associated diseases:

  • Blood glucose
  • Urea and electrolytes and urine osmolality if diabetes insipidus is suspected
  • If hydrops fetalis (excessive fluid in one or more fetal compartment - e.g. the pleural or abdominal space,9 common in rhesus haemolytic disease) is present the following may also be appropriate:
    • Screening for maternal antibodies against fetal red blood cells
    • Screening for cytomegalovirus, syphilis, rubella, toxoplasmosis, parvovirus 19
    • Genotyping
Associated diseases

Diseases associated with polyhydramnios5

Diabetes mellitus Hydrops fetalis Oesophageal atresia
Duodenal atresia/stenosis, Gastroschisis Diaphragmatic hernia
Thoracic and mediastinal masses Anencephaly Muscular dystrophy
Myotonic dystrophy Chromosomal anomalies (eg, trisomy 21), Cardiovascular diseases
Skeletal dysplasias (including achondroplasia), Neuromuscular anomalies Severe fetal anaemia
Sacrococcygeal teratoma Placental chorioangioma Placental arteriovenous fistula
Congenital syphilis Viral hepatitis Diabetes insipidus
Twin-twin transfusion syndrome Maternal substance abuse Beckwith-Wiedemann syndrome**
Pena-Shokeir syndrome* Maternal hypercalcaemia (causing fetal polyuria)10 Idiopathic

*Pena-Shokeir syndrome - contractures of the joints (arthrogryposis), growth problems, underdeveloped lungs, facial deformities.11

**Beckwith-Wiedemann syndrome - congenital overgrowth syndrome.12

Management
  • The first step is to identify any underlying cause.
  • Mild polyhydramnios can be simply monitored and treated conservatively.
  • Pre-term 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 and bed rest towards the latter stages.1
  • Intramuscular steroids should be given to the mother antenatally if preterm deliver is considered.13 This helps to improve lung maturity.
  • Serial ultrasound scans should be carried out to monitor the AFI and monitor foetal growth.
  • Fetal hydrops anaemia should be treated with erythrocyte transfusion, either intravascularly or via the foetal abdomen. This reduces the likelihood of fetal congestive failure, thereby allowing prolongation of the pregnancy and improving survival.14
  • If gestational diabetes is diagnosed, tight glycaemic control should be maintained. This is usually done with dietary manipulation and insulin is rarely needed.15
  • Indometacin is the drug of choice for the medical treatment of polyhydramnios. It is very effective,16 particularly in cases where the condition is related to increasing fetal urine production.5 The mechanism of action appears to be an effect on urine production by the fetal kidney, possibly by enhancing the effect of vasopressin. It is not effective in cases where the underlying cause is neuromuscular disease affecting fetal swallowing, or hydrocephalus.1 It is contraindicated in twin to twin syndrome or after 35 weeks, as adverse effects outweigh benefits in these cases.
  • Amniocentesis is recommended in cases where indometacin is contraindicated, in severe polyhydramnios, or in patients who are symptomatic.5 It is contraindicated in premature rupture or detachment of the placenta, or chorioamnioitis (inflammation of the chorioamniotic membranes and fluid, usually infective).
  • Induction of labour should be considered if fetal distress develops.1 Beyond 35 weeks it may be safer to deliver anyway. 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.
  • Polyhydramnios associated with twin to twin syndrome may benefit from laser ablation of the connecting placental vessels.1
Complications

There is a higher incidence of preterm labour and delivery. Other maternal complications include premature rupture of the membranes, abruptio placenta, malpresentation, post-partum haemorrhage and cord prolapse.1 There is a higher incidence of Caesarean section.

A study of pregnancies associated with polyhydramnios but not congenital malformation showed that polyhydramnios was an independent risk factor for low birth weight, low Apgar scores and fetal death.17

Prognosis
  • The prognosis of mild polyhydramnios is usually good. Only 16.5% of such pregnancies have a significant associated problem.1
  • A poor prognosis is associated with fetal or placental malformation. The perinatal mortality rate in such cases is 61%.18
  • 20% of infants in polyhydramniotic pregnancies have an abnormality. The severity of the prognosis is dependent on the severity of the abnormality.
  • The more severe the polyhydramnios, the more likely the chance of finding an underlying cause.1

Document references
  1. Boyd R, Carter B; Polyhydramnios and Oligohydramnios. eMedicine, February 2008.
  2. Thompson O, Brown R, Gunnarson G, et al; Prevalence of polyhydramnios in the third trimester in a population screened by first and second trimester ultrasonography. J Perinat Med. 1998;26(5):371-7. [abstract]
  3. Mathew M, Saquib S, Rizvi SG; Polyhydramnios. Risk factors and outcome. Saudi Med J. 2008 Feb;29(2):256-60. [abstract]
  4. Twin2Twin; The UK Twin 2 Twin Transfusion Syndrome Association
  5. Rajiah P; Polyhydramnios. eMedicine, July 2006.
  6. Deering S; Abruptio Placentae. eMedicine, January 2007.
  7. Chatterjee M; Chorioangioma. TheFetus.net 1993.
  8. Gearhart P, Sedhev H, Ritchie W; Biophysical Profile: Ultrasound. eMedicine, October 2008.
  9. Hamdan A; Hydrops Fetalis. eMedicine, August 2008.
  10. 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 Oct;199(4):410.e1-5. [abstract]
  11. Pena-Shokeir syndrome; Madisons Foundation
  12. Beckwith-Wiedemann Syndrome Support Group
  13. Crowther CA, Haslam RR, Hiller JE, et al; Neonatal respiratory distress syndrome after repeat exposure to antenatal corticosteroids: a randomised controlled trial.; Lancet. 2006 Jun 10;367(9526):1913-9. [abstract]
  14. Remacha AF, Badell I, Pujol-Moix N, et al; Hydrops fetalis-associated congenital dyserythropoietic anemia treated with intrauterine transfusions and bone marrow transplantation.; Blood. 2002 Jul 1;100(1):356-8. [abstract]
  15. Management of Diabetes in Pregnancy; Management of Diabetes SIGN Guidance 2005
  16. Cabrol D, Jannet D, Pannier E; Treatment of symptomatic polyhydramnios with indomethacin. Eur J Obstet Gynecol Reprod Biol. 1996 May;66(1):11-5. [abstract]
  17. 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 Apr;28(4):222-8. [abstract]
  18. Desmedt EJ, Henry OA, Beischer NA; Polyhydramnios and associated maternal and fetal complications in singleton pregnancies. Br J Obstet Gynaecol. 1990 Dec;97(12):1115-22. [abstract]
Acknowledgements EMIS is grateful to Dr Laurence Knott for writing this article and to Dr Huw Thomas for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
DocID: 1611
Document Version: 22
DocRef: bgp24695
Last Updated: 2 Dec 2008
Review Date: 2 Dec 2010

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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