Section 1: Epidemiology and aetiology
In pregnancy, the amniotic sac contains the fetus surrounded by amniotic fluid.
Initially amniotic fluid is maternal body water partitioned in the fetoplacental extracellular space. As fetal membranes actively transport sodium and chloride ions, water passively enters the sac.
At 20 weeks' gestation the fetal skin starts to keratinise. Some fluid transfer occurs across the placenta but the initial mechanism of amniotic fluid synthesis is replaced by contributions from the fetal renal and respiratory systems.
The fetus swallows amniotic fluid and excretes it as urine.
The fetal lungs and oronasal cavities also secrete large volumes of fluid. This continues until delivery.
Function of amniotic fluid
The function of amniotic fluid is to protect the fetus in a low resistance space, cushion from trauma and extremes of temperature and allow development of muscular and skeletal systems.
Continuous fluid movement through fetal lungs, gut and urinary tract is essential for normal development.
The volume of amniotic fluid increases through the pregnancy, peaking at 34 weeks' gestation (see box).
Measuring fluid volume
Clinical assessment of amniotic fluid volume is unreliable. Ultrasound is the most commonly used method of assessment. It has the advantage of being a non-invasive, sensitive test.
Either the amniotic fluid index (AFI) can be measured, or the deepest vertical pool of fluid.2 The AFI is the sum of the deepest vertical pools measured in each of the four quadrants of the maternal abdomen. Tables of the normal limits for AFI based on the gestational age have been published.
Polyhydramnios is defined as a deepest vertical pool exceeding 8cm or an AFI above the 95th centile for gestational age.2 It complicates 2 per cent of pregnancies. It is an independent risk factor for perinatal mortality.
In two thirds of cases, the cause is unknown but in general it is caused by increased production of urine by the fetus or reduced swallowing and digestion of amniotic fluid.
Associated fetal disorders are seen in 20 per cent and include intestinal obstruction (tracheo-oesophageal fistula, duodenal atresia, impaired swallowing), anencephaly, muscular dystrophy, cardiac failure and fetal infections. Maternal diabetes mellitus can cause polyhydramnios by osmotic diuresis in the fetus as a result of hyperglycaemia.
Too little amniotic fluid (less than 2cm) is termed oligohydramnios. It complicates 4 per cent of pregnancies. Oligohydramnios is found with growth retardation of the fetus, due to insufficiency of the placenta.
As adequate amniotic fluid circulation is needed for development of fetal lungs and kidneys, low fluid levels can lead to pulmonary hypoplasia or abnormal renal function. With prolonged low levels of fluid, mortality rates approach 90 per cent. Management is usually by expediting delivery.
|Amniotic fluid volume|
|Amniotic fluid volume and gestational age1
10 weeks: 30 ml
20 weeks: 250 ml
30 weeks: 750 ml
34 weeks: 900 ml
40 weeks (term): 600 ml
Section 2: Making the diagnosis
Clinical features of polyhydramnios relate to distension of the uterus. The initial finding may simply be that on palpation the uterus feels larger than expected for the gestation.
The uterus may be tense and fetal parts may be difficult to feel. There may be abdominal discomfort, dyspnoea and dependent oedema. Any woman who is suspected to have polyhydramnios should be referred to her local antenatal clinic for assessment within the week of presentation.
At the antenatal clinic, each case will be evaluated in a systematic manner.
First, an ultrasound will be performed to confirm the suspected diagnosis.
Ultrasound will be used to confirm the diagnosis (Photograph: SPL)
After assessing amniotic fluid volume the fetus will be carefully examined for any structural abnormality. The thorax, abdomen, urinary tract and brain should be examined. Signs of fetal infection such as hydrops - gross universal oedema - should be sought.
Karyotype should be checked by amniocentesis if there are structural anomalies present.
Maternal history may indicate diabetes or viral infection.
Blood samples should be taken for glucose tolerance testing, rubella, toxoplasmosis, parvovirus and syphilis serology.
Maternal blood group and antibody status should be checked, as red cell alloimmunisation is a possible cause of polyhydramnios through fetal anaemia causing cardiac failure.
In a monochorionic (identical) twin pregnancy, polyhydramnios may arise following twin-twin transfusion syndrome.
The polyhydramnios can occur extremely quickly and usually affects one twin, causing oligohydramnios in the second twin.
This can be detected using ultrasound and is a complicated condition managed only by specialised fetal medicine units.
In two-thirds of cases no cause is found. The pregnancy is still defined as having polyhydramnios while the AFI exceeds the 95th centile.
Section 3: Managing the condition
Management depends on the underlying cause. Treatment of maternal diabetes through glycaemic control may prevent a continued rise in AFI.
If polyhydramnios is associated with fetal hydrops and anaemia due to infection or alloimmunisation, a fetal medicine unit should manage the pregnancy. Intensive surveillance with serial in utero transfusions may be used to correct the anaemia and hence reduce the polyhydramnios.
In cases where the fetus is abnormal, karyotype can establish whether there is an underlying chromosomal abnormality. In some cases, for example anencephaly, the parents may decide to terminate the pregnancy.
Identification of fetal abnormalities, such as congenital heart disease or neural tube defects, allows planning for the management of the neonate after delivery.
If no reversible underlying cause is found, management aims to reduce maternal discomfort and prolong the pregnancy.
As any intervention carries risk, interventions are usually only indicated when the AFI exceeds 40cm, or the deepest vertical pool exceeds 12cm.3,4
Severe pressure symptoms can be relieved by amniocentesis but the benefit is short term before fluid re-accumulates and there are risks of introducing infection and precipitating pre-term labour.
Severe pressure symptoms can be relieved by amniocentesis (Photograph: SPL)
Treating with indometacin or sulindac (cyclo-oxygenase inhibitors)4 reduces fetal urine production and consequently amniotic fluid volume.
Through their mechanism of action, these drugs can lead to renal failure and premature closure of the ductus arteriosus.
As this results in perinatal mortality, cyclo-oxygenase inhibitors are only used to prolong the pregnancy past extremely premature gestations.
Twin-twin transfusion syndrome
Polyhydramnios associated with twin-twin transfusion syndrome is usually treated with serial amniocentesis or disruption of the communicating placental vessels with a laser.
This corrects the haemodynamic inequality that is causing polyuria from one twin and resolves the polyhydramnios.
Severe polyhydramnios can lead to pre-term labour.4,5 Increased fluid volume makes it easier for the fetus to change position, hence an unstable lie.
When the waters break, placental abruption may occur due to sudden decompression inside the uterus and if the fetus is not engaged cord prolapse is possible. This scenario carries a fetal mortality of up to 60 per cent.
For this reason, if an unstable lie is detected the patient will be hospitalised to await delivery.
Section 4: Prognosis
Polyhydramnios is associated with increased perinatal morbidity and mortality.5 The exact prognosis for each case depends on the underlying cause.
If the cause is maternal, the impact on the fetus usually depends on gestation at delivery.
If the cause of the polyhydramnios is fetal, the prognosis depends on the severity of the underlying problem.
Regardless of cause, the main risk to the mother is of postpartum haemorrhage. Over-distension of the uterus through pregnancy leads to a lack of tone following birth.
Polyhydramnios can cause placental abruption and unstable lie of the fetus and so causes increased requirement for caesarean section with all its attendant risks.
As there are significant risks to mother and baby, delivery should occur in a hospital unit with immediate access to theatre and oxytocic drugs if needed.
Follow up of the patient with polyhydramnios includes serial ultrasound and a detailed plan for delivery.
Depending on the cause of the polyhydramnios, the patient may need to be managed by a fetal medicine unit in a tertiary referral centre. Even if no cause is found antenatally, it is vital for the neonate to be examined by a paediatrician to exclude any undetected underlying condition. Tracheo-oesophageal fistula must be excluded prior to feeding.6
Section 5: Case study
Debbie is a 27-year-old woman in her first pregnancy. She attends her 20-week anomaly ultrasound, which shows a normal fetus, normal liquor volume and normally sited placenta.
As she has no health problems, Debbie is 'low risk' and attends her midwife and GP for shared antenatal care.
At 30 weeks' gestation, Debbie presents to her GP feeling bloated and uncomfortable. On examination she is normotensive, apyrexial and not unwell. Her urine shows no abnormality. On palpation, Debbie's uterus measures 33cm from pubic symphysis to fundus. As this is within the allowed discrepancy from gestation (in weeks) this is noted and the fetal heart is heard.
A fortnight later, Debbie attends feeling breathless on minimal exertion. On examination her urine shows a trace of protein. Her BP and other observations are normal. Her ankles show mild oedema bilaterally.
Debbie's symphysiofundal height measures 40cm. This is significantly greater than expected (32 weeks = 32cm +/3cm). It is also noted that the fetus is difficult to palpate and seems very mobile inside the uterus. The fetal heart is heard but sounds slightly muffled.
Debbie's GP arranges a next-day appointment for her in the hospital day assessment unit.
The ultrasound scan shows a live fetus in transverse lie, with an AFI exceeding the 95th centile for 32 weeks. The deepest vertical pool of liquor measures 11cm. The fetus appears to be structurally normal. A glucose tolerance test and bloods taken for viral serology are normal. Debbie is discharged with a follow-up ultrasound arranged.
The day before her follow-up scan, at 33 + 5 gestation, Debbie starts having painful contractions. She attends the delivery suite where she is found to have a soft, effacing cervix. The fetus is still in transverse lie.
Debbie is now contracting two to three times in a 10-minute period. As the pregnancy is less than 34 weeks' gestation, her obstetrician prescribes steroids (to enhance fetal lung maturity) and a tocolytic to relax the uterus for long enough that the steroids can take effect. Debbie is admitted to the ward.
Two days later, Debbie's waters break. The attending midwife immediately places her in the knee-chest position. This is adopted when membranes rupture with a transverse or unstable lie. There is a risk of cord prolapse in this situation and knee-chest aims to take any pressure of gravity off the possibly prolapsed cord.
Debbie is transferred for caesarean section.
A live male infant is born in good condition and examination confirms him to be normal. Tracheo-oesophageal fistula is excluded by passing an nasogastric tube.
No cause is found for the polyhydramnios so Debbie is advised that the risk of recurrence is extremely low.
Section 6: Evidence base
As patients with polyhydramnios are generally managed in antenatal clinics and fetal medicine units there are few guidelines published for use by GPs.
Articles listed below are mainly reviews or observational studies. There are few recent publications, but thinking has not changed since these were published.
- Carlson DE, Platt LD, Medearis AL. Quantifiable polyhydramnios; diagnosis and management. Obstet Gynaecol 1990; 75 (6); 989-93.
- Mazor M, Ghezzi F, Maymon E. Polyhydramnios is an independent risk factor for perinatal mortality and intrapartum morbidity in preterm delivery. Eur J Obstet Gynaecol Reprod Biol 1996; 70 (1): 41-7.
- Yeast J. Polyhydramnios: etiology, diagnosis and management. Neoreviews 2006; 7; 6 e300.
- NICE. Intrapartum care. CG55. NICE, London, 2007. www.nice.org.uk/nicemedia/live/11837/36280/36280.pdf
- Contributed by Dr Polly Weston, senior registrar and Mr David Walker, consultant obstetrician and gynaecologist, at the Royal United Hospital, Bath, Somerset.
- Luesley D, Baker P, Drife J. Chapter 16 Aberrant Liquor Volume. In: Obstetrics and Gynaecology; an evidence based text for MRCOG. Hodder Arnold, 2004.
- The RCGP covers this topic in statement 10.1 Women's Health
- Polyhydramnios: www.patient.co.uk/doctor/Polyhydramnios.htm A patient plus article.
- Oligohydramnios: emedicine.medscape.com/article/405914-overview An article looking at aberrations in liquor volume.
- Polyhydramnios and oligohydramnios: emedicine.medscape.com/article/975821-overview
- Dealing with polyhydramnios.
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Contributed by Dr Polly Weston, senior registrar and Mr David Walker, consultant obstetrician and gynaecologist, at the Royal United Hospital, Bath, Somerset
1. Luesley D, Baker P, Drife J. Aberrant Liquor Volume. In: Obstetrics and Gynaecology; an evidence based text for MRCOG Hodder Arnold 2004.
2. Carlson DE, Platt LD, Medearis AL. Quantifiable polyhydramnios; diagnosis and management. Obstet Gynaecol 1990; 75 (6): 989-93.
3. Hill LM, Breckle R, Thomas ML et al. Polyhydramnios; ultrasonically detected prevalence and neonatal outcome. Obstet Gynaecol 1987; 69 (1): 21-5.
4. Yeast J. Polyhydramnios: etiology, diagnosis and management. Neoreviews 2006; 7: 6 e300.
5. Mazor M, Ghezzi F, Maymon E. Polyhydramnios is an independent risk factor for perinatal mortality and intrapartum morbidity in preterm delivery. Eur J Obstet Gynaecol Reprod Biol 1996; 70 (1): 41-7.
6. Cardwell MS. Polyhydramnios. Obstet Gynaecol Surv 1987; 42 (10): 612-7.