Polyhydramnios and Oligohydramnios

Introduction

Amniotic fluid volume is one of the few directly measurable indicators of fetal wellbeing, and abnormalities of it are markers rather than diseases. The clinical task in both polyhydramnios and oligohydramnios is the same: work out what the fluid volume is telling you about the fetus, the placenta or the mother, and act on that rather than on the number itself.

Polyhydramnios complicates around 1-2% of pregnancies and oligohydramnios a similar proportion, although the true incidence of the latter depends heavily on which measurement threshold is used. Both are usually detected either because the symphysis-fundal height is discrepant from the gestation, or incidentally at a scan performed for another reason.

Physiology of amniotic fluid

In the first trimester amniotic fluid is essentially a transudate across the fetal skin and the amnion. From around 16 weeks the fetal skin keratinises and this route closes, and the fluid becomes almost entirely fetal urine, supplemented by fluid secreted from the fetal lungs. Clearance is by fetal swallowing, which accounts for the majority, and by intramembranous absorption across the fetal surface of the placenta into the fetal circulation.

A term fetus produces roughly 800-1200 mL of urine and swallows a similar volume every 24 hours, so the entire pool turns over daily. Amniotic fluid volume is therefore a real-time report on fetal renal perfusion and on the patency of the fetal gastrointestinal tract, and it changes far faster than fetal growth does. Volume rises to a peak of around 800-1000 mL at 32-34 weeks, falls to around 500 mL by 40 weeks, and declines steeply thereafter, which is one reason post-term pregnancy is monitored.

Measuring the volume

The single deepest pocket is now generally preferred. Using the amniotic fluid index diagnoses substantially more cases of oligohydramnios and leads to more inductions and more caesarean sections, without any improvement in perinatal outcome. In twin pregnancies the deepest pocket is used in each sac, since an index cannot meaningfully be constructed.²

Polyhydramnios

Polyhydramnios is an excess of amniotic fluid. Severity is graded by the deepest pocket: mild 8-11 cm, moderate 12-15 cm, and severe 16 cm or more. Severity matters because the likelihood of an underlying fetal abnormality rises steeply with the volume: idiopathic polyhydramnios accounts for most mild cases but a much smaller proportion of severe ones.

Causes

Clinical features

The uterus is large for dates, tense, and difficult to palpate through, so fetal parts are hard to feel and the fetal heart may be difficult to auscultate. The woman may report rapid abdominal enlargement, breathlessness, heartburn and abdominal discomfort, and may have peripheral oedema, vulval oedema or varicose veins from inferior vena cava compression by the distended uterus.

Investigations

• Detailed ultrasound - quantify the fluid, survey fetal anatomy with particular attention to the stomach bubble (absent or small in oesophageal atresia) and the duodenum (the double bubble of duodenal atresia), assess growth and look for hydrops
• Middle cerebral artery peak systolic velocity Doppler - raised in fetal anaemia and the non-invasive way to detect it
• Oral glucose tolerance test - polyhydramnios is an indication for testing regardless of other risk factors
• Maternal red cell antibody screen - to detect alloimmunisation
• Serology for parvovirus B19, cytomegalovirus, toxoplasmosis and syphilis
• Fetal karyotype or microarray where a structural anomaly is identified
• Consider maternal testing for myotonic dystrophy where there is polyhydramnios with reduced fetal movements, since the mother may be undiagnosed and demonstrate delayed hand grip release

Management

• Treat the underlying cause where one is found: optimise glycaemic control, intrauterine transfusion for fetal anaemia, laser ablation for twin-to-twin transfusion syndrome
• Serial ultrasound to monitor fluid volume, growth and fetal wellbeing
• Amnioreduction for severe maternal symptoms; it relieves breathlessness but recurs, and carries risks of infection, preterm labour and abruption
• Indometacin reduces fetal urine output and can be used before 32 weeks, but not beyond, because prostaglandin inhibition causes premature closure of the ductus arteriosus and oligohydramnios
• Antenatal corticosteroids if preterm birth is likely
• Advise birth in an obstetric unit, and involve the neonatal team antenatally where a structural anomaly is suspected
• Pass a nasogastric tube after birth if oesophageal atresia is suspected

Oligohydramnios

Oligohydramnios is a reduced volume of amniotic fluid, and anhydramnios is its complete absence. The causes fall into three logical groups: fluid is leaking out, it is not being produced, or the pregnancy has simply gone past the point at which production declines.

Clinical features and assessment

The uterus is small for dates and the fetus is unusually easy to palpate, sometimes described as being moulded around by the uterine wall. The woman may report a gush of fluid or persistent dampness, and may have reduced fetal movements because there is no room to move.

• Sterile speculum examination to look for pooling of liquor in the posterior fornix; avoid a digital examination if the membranes have ruptured and the woman is not in labour, because it introduces infection
• IGFBP-1 or PAMG-1 testing of vaginal fluid where the diagnosis of ruptured membranes is uncertain on speculum
• Ultrasound - quantify the fluid, identify the fetal bladder and both kidneys, assess growth and umbilical artery Doppler
• Review the drug history for NSAIDs and renin-angiotensin blockers
• Maternal observations, FBC and CRP where infection is a possibility

Management

Management is entirely determined by the cause and the gestation. Where preterm prelabour rupture of membranes is confirmed, management is with erythromycin for 10 days, antenatal corticosteroids, surveillance for chorioamnionitis, and planned birth from 37 weeks or earlier if infection develops. Where oligohydramnios reflects placental insufficiency, the fetus is monitored with growth scans, umbilical artery Doppler and cardiotocography, and delivered when the risks of remaining in utero exceed those of birth. Post-term oligohydramnios is an indication for induction of labour.

Amnioinfusion, the instillation of warmed saline into the uterine cavity, is used in some units for repeated variable decelerations in labour attributed to cord compression, but the evidence base for antenatal amnioinfusion is weak and it is not routine UK practice. Maternal oral or intravenous hydration produces a transient rise in amniotic fluid volume but does not alter outcomes.²

Complications

Red flags

Prognosis

Idiopathic mild polyhydramnios that is stable and not associated with any structural or biochemical abnormality carries a good prognosis, and the pregnancy is managed with surveillance and a plan for controlled amniotomy rather than intervention. Where a cause is found, the prognosis is that of the cause, and this is worth saying explicitly to parents: the fluid itself is rarely the problem.

Oligohydramnios carries a worse outlook overall, because its commonest causes, ruptured membranes and placental insufficiency, are themselves associated with preterm birth and with fetal compromise. The prognosis in early severe oligohydramnios is dominated by pulmonary hypoplasia, which is determined by how early and how complete the fluid loss was rather than by anything done subsequently. Later-onset oligohydramnios in an otherwise well-grown fetus at term is a reason to deliver, not a reason for alarm.^1,2