Polyhydramnios and oligohydramnios

• Amniotic fluid surrounds and protects the fetus. Too little is oligohydramnios; too much is polyhydramnios (also called hydramnios). Both are findings, not diseases in themselves. ^[12]
• Most mild polyhydramnios is idiopathic (no cause found); most moderate or severe polyhydramnios has a maternal or fetal cause, especially maternal diabetes and fetal structural anomalies.
• Oligohydramnios is most often an error of fetal production (renal or placental) or loss (membranes), and is most worrying when it is severe and early.
• The two conditions are diagnosed with ultrasound using the deepest vertical pocket (DVP) and the amniotic fluid index (AFI), with different cut-offs for each.
• Management is by cause: identify why the volume is wrong (workup imaging, maternal glucose, infection, fetal anaemia), then treat that. Routine induction for isolated mild abnormalities is not supported by current evidence.

By the end of this page you should be able to:

1. Define normal, oligohydramnios and polyhydramnios amniotic fluid volumes and state the cut-offs used.
2. List the principal maternal, fetal and placental causes of each, ordered by frequency.
3. Explain why a fetus makes more or less urine and why that changes the volume.
4. Plan the ultrasound and laboratory workup of a woman found to have abnormal liquor.
5. Apply the current guideline positions on surveillance, amnioreduction, induction and intrapartum monitoring from ACOG, NICE, RCOG and WHO.
6. Explain how Rhesus sensitisation causes polyhydramnios and fetal anaemia, and how it is screened for and managed. ^[1]
7. Counsel a woman realistically about risks and about what is not shown to help.

The fluid is produced and removed in a cycle. Early on it is a transudate through fetal skin. From about 22 to 25 weeks, when the skin keratinises, the main inflows become fetal urine and lung liquid secretion and the main outflows become fetal swallowing and intramembranous absorption into the fetal blood. ^[1] Because production and swallowing are the controllable steps, nearly every disorder of volume maps to one of them.

Normal volume is commonly defined as an AFI between 5 and 25 cm or a single deepest vertical pocket (SDVP) between 2 and 8 cm. ^[1] The systematic mid-trimester scan guideline recommends that an AFI may be preferable for assessing polyhydramnios and DVP preferable for assessing oligohydramnios. ^[2]

Classification by severity matters because it drives management. The cut-offs in the table below are those used by the widely cited review of prenatal and neonatal outcomes; be aware that guideline panels use slightly different numbers.

The mild band is the place the guideline panels disagree: the Huri review used here classes mild polyhydramnios as an AFI of 25 to 29.9 cm, while ACOG Committee Opinion 828 (2021) classes it as 24.0 to 29.9 cm. Moderate and severe bands (30.0 to 34.9 cm and 35 cm or more) are stated the same way by both. ^{[1] [13]}

The 2 cm DVP threshold is based on randomised trials of biophysical profile testing: using the deepest vertical pocket produces fewer unnecessary interventions than using the AFI, with no increase in adverse outcomes. ^[1] ACOG Practice Bulletin 229 and Committee Opinion 828 suggest weekly to twice-weekly antenatal testing from 32 to 34 weeks for moderate to severe polyhydramnios and from diagnosis for isolated oligohydramnios. ^[7]

NICE lists anhydramnios and polyhydramnios as fetal indications for continuous cardiotocography in labour. ^[3]

Oligohydramnios complicates roughly 0.5 to 5% of singleton pregnancies depending on the population and cut-off used; polyhydramnios 1 to 2%. ^[1]

Maternal risk factors for polyhydramnios are dominated by diabetes (gestational and pregestational). ^[1] Other maternal associations include hypertensive disorders, and medications (including ACE inhibitors, angiotensin receptor blockers and indomethacin, which are also implicated in oligohydramnios). ^[1]

Fetal risk factors usually explain most severe early cases: structural anomalies of the central nervous system and face, congenital high airway obstruction, diaphragmatic hernia, gastrointestinal obstruction (oesophageal or duodenal atresia), neuromuscular disorders, chromosomal or genetic syndromes, fetal anaemia, hydrops, and infections of the TORCH group (association questioned). ^[1] In monochorionic twin pregnancies polyhydramnios in the recipient is the hallmark of twin-to-twin transfusion syndrome.

Idiopathic polyhydramnios is usually mild and transient. ^[1]

Oligohydramnios more often has a clear cause: fetal genitourinary anomalies (renal agenesis or dysplasia, autosomal recessive polycystic kidney disease, lower urinary tract obstruction), congenital infections, fetal growth restriction from placental insufficiency, pre-eclampsia, post-term pregnancy, premature rupture of membranes, and medications. ^[1] A history of oligohydramnios or polyhydramnios as a risk factor for fetal structural problems in other contexts (for example congenital malformations such as oesophageal atresia) is well recognised; in those disorders the abnormal liquor is a clue rather than the disease.

A practical grouping is by where the problem lies. ^[1]

• Mother (production/ environment): diabetes (polyhydramnios), hypertension and placental insufficiency (oligohydramnios), drugs, smoking, posture, hydration status.
• Fetus (swallowing/ urine): impaired swallowing and gastrointestinal obstruction (polyhydramnios); renal or urinary tract disease (oligohydramnios); hydrops and fetal anaemia including Rhesus isoimmunisation (polyhydramnios).
• Placenta/ membranes: chorioangioma, twin-to-twin transfusion syndrome, rupture of membranes, chronic abruption.
• Gestation: polyhydramnios often worsens in the third trimester; oligohydramnios is the normal trend at 41 weeks and beyond.

Medications deserve emphasis because they are reversible: ACE inhibitors, angiotensin receptor blockers and indomethacin can all reduce fetal urine output and cause oligohydramnios; NSAIDs given to the mother can affect the fetal ductus and renal perfusion. ^[1]

Polyhydramnios accumulates through three mechanisms. ^[1]

1. Impaired fetal swallowing from an anatomical or neuromuscular problem (oesophageal or duodenal atresia, facial clefting, micrognathia, anencephaly, cystic lung masses, congenital high airway obstruction, diaphragmatic hernia, fetal akinesia).
2. High cardiac output (severe fetal anaemia from maternal Rhesus alloimmunisation or parvovirus infection, sacrococcygeal teratoma, chorioangioma, large arteriovenous shunts, cardiac arrhythmia or failure), which raises renal perfusion and urine output.
3. Excess fetal urine production, seen with some renal or urinary tract anomalies and with maternal diabetes (fetal hyperglycaemia drives an osmotic diuresis).

Plus the placental mass effect of a chorioangioma or twin-to-twin transfusion in the recipient. The mother's side contributes through maternal diabetes via fetal hyperglycaemia.

The overdistended uterus then produces its own problems: maternal dyspnoea and discomfort, unstable fetal lie, and, after membrane rupture, sudden uterine decompression with placental abruption or umbilical cord prolapse. ^[1]

Oligohydramnios follows the opposite logic. ^[1]

• In the second trimester, before fetal skin keratinisation is complete is irrelevant: the serious issue is that without fluid the fetus cannot move. Prolonged early oligohydramnios produces the oligohydramnios deformation sequence (Potter sequence): contracted limbs, pulmonary hypoplasia, a compressed facies and often perinatal death. The mechanism is that low intra-amniotic pressure increases the alveolar-to-amniotic gradient and drains lung fluid, the main stimulus for lung development.
• In the third trimester, reduced fluid limits fetal lung fluid volume and cushioning; umbilical cord compression produces fetal heart rate decelerations and operative deliveries. Severe oligohydramnios is an independent predictor of neonatal respiratory morbidity when membranes have ruptured preterm.
• In fetal growth restriction, chronic hypoxaemia from placental insufficiency shunts blood away from the kidneys; fetal urine output falls, and this is an early and useful marker of placental trouble.

In isolated oligohydramnios (no growth restriction, no anomalies, no rupture) the cause is uncertain: possible altered aquaporin-mediated absorption rather than reduced fetal urine, because measured hourly fetal urine production has not differed. ^[1] Some placental studies suggest it sits within the "placental insufficiency" spectrum in milder form.

Most mild cases are discovered incidentally on scan and produce few symptoms. With moderate or severe disease the mother notices a rapid increase in abdominal girth, tightness, dyspnoea, orthopnoea, ankle swelling, abdominal pain and heartburn from stomach compression. ^[1] On examination the uterus is large for dates, tense and tympanitic, fetal parts are hard to palpate, fetal lie is often unstable, and the fetal heartbeat may be muffled by the excess fluid. ^[1]

A clinical vignette: a woman in the third trimester with gestational diabetes and a sudden rise in symphysis-fundal height; scan shows an AFI of 32 cm and a macrosomic fetus. The most likely driver is fetal hyperglycaemia from poorly controlled maternal glucose. The mother is breathless on lying flat and the fetus is in an unstable transverse lie, so counselling includes the risk of cord prolapse if membranes rupture.

Oligohydramnios is usually asymptomatic and is an ultrasound finding. The mother may notice reduced fetal movements if fluid is very low. Examination may show a small-for-dates uterus with easily palpable fetal parts and limbs; fetal movements may be restricted. ^[1]

Where it is compensatory to rupture of membranes, the woman instead gives a history of a gush or persistent trickle of clear fluid.

The differential is of the underlying cause, because the fluid is only the marker.

For polyhydramnios, distinguish maternal diabetes (glucose tolerance testing), fetal anomalies (detailed anomaly scan, especially stomach, duodenum, face, neck, chest, spine, kidneys, heart), fetal anaemia and hydrops (maternal blood group and antibody screen; parvovirus serology; middle cerebral artery peak systolic velocity), infection (maternal serology if suspected), and placental causes (detailed scan for chorioangioma; monochorionicity in twins). ^{[1] [11]}

For oligohydramnios, distinguish PPROM, fetal growth restriction/placental insufficiency, fetal renal or urinary tract disease, post-term pregnancy, and drug exposure.

The table below compares the two principal amniotic fluid disorders directly.

Ultrasound is the diagnostic test. Assess the liquor by DVP (single deepest vertical pocket) and AFI, together and not one alone, because the two measures handle high and low extremes differently; the mid-trimester scan guideline recommends AFI for polyhydramnios and DVP for oligohydramnios. ^[2]

Every woman with an abnormal volume should have:

• A detailed anomaly scan: fetal stomach, bowel (double bubble, dilated loops), face and palate, neck and chest, heart, spine, kidneys, bladder, limbs and umbilical cord insertion. ^[1]
• Fetal biometry and umbilical artery Doppler to look for growth restriction. ^[1]
• Maternal glucose testing: oral glucose tolerance test when polyhydramnios is discovered. ^[1]
• Blood group and antibody screen to exclude Rhesus and other red cell alloimmunisation, because alloimmunisation is a treatable cause of severe polyhydramnios. ^{[9] [11]}
• Serology (TORCH) only if there are signs of congenital infection such as hydrops, intracranial calcification or hepatosplenomegaly, or relevant maternal history; polyhydramnios alone is not an indication. ^[1]
• Fetal middle cerebral artery peak systolic velocity if anaemia is suspected (see below).
• Amniocentesis when structural anomalies or suspected congenital infection are found, or for karyotype/microarray in an anomalous fetus.
• Tests of membrane integrity (speculum examination, nitrazine, insulin-like growth factor binding protein-1 or placental alpha-microglobulin-1) whenever rupture is possible.

An SDVP below 2 cm with a normal AFI should still be taken seriously; a discrepancy between the two measures is common at the high end, where the AFI is the more reliable measure of polyhydramnios. ^{[1] [2]}

Oligohydramnios in the second trimester needs detailed renal and urinary tract imaging and, if early and severe, counselling about pulmonary hypoplasia and the limits of intervention.

The severity classes above (mild, moderate, severe) are those derived from the AFI or SDVP value. Persistence matters as much as severity: transient polyhydramnios that resolves through gestation carries a better outlook than persistent disease, and a severe but resolving reduction is reassuring. ^[1]

Hydrops is a separate staging concept: polyhydramnios with hydrops mandates an urgent search for anaemia or cardiac failure.

The principle is treat the cause, not the volume. ^{[1] [7] [9]} The options are observation, treatment of the underlying condition, reduction of the fluid, and delivery.

• Maternal diabetes: tight glycaemic control; the polyhydramnios usually resolves with control. ^[1]
• Fetal anomalies: refer to a fetal medicine unit; plan delivery in a centre with neonatal support; pass a nasogastric tube before the first feed to exclude oesophageal atresia.
• Fetal anaemia (including alloimmunisation, parvovirus): treat the anaemia; polyhydramnios then improves. See the Rhesus section.
• Infection: treat where a specific antimicrobial exists.
• Maternal symptoms: bedside measures first (left lateral rest, hydration, propped posture). Amnioreduction (therapeutic drainage of liquor) is recommended only for severe maternal discomfort or dyspnoea in severe polyhydramnios, and only in a fetal medicine centre with the expertise to manage sudden decompression. ^[7] It is not a cure because fluid re-accumulates.
• Amnioinfusion is a specialist procedure for selected severe oligohydramnios with a structurally normal fetus and should only be carried out in a specialist centre; NICE records that its benefit and safety are still uncertain. ^[5]

Guideline positions on delivery and surveillance:

• ACOG and SMFM recommend that mild idiopathic polyhydramnios should not itself be an indication for induction of labour, so labour may be allowed to occur spontaneously at term with the mode of delivery decided on usual obstetric grounds; timing for moderate or severe disease should be individualised; severe polyhydramnios should be delivered in a tertiary centre because of the substantial chance of an underlying fetal anomaly; antenatal fetal surveillance is not required for mild idiopathic polyhydramnios. ^[1]
• NICE recommends continuous cardiotocography in labour when polyhydramnios or anhydramnios is present. ^[3]
• RCOG / local practice (notably the RCOG Green-top on umbilical cord prolapse and regional guidelines) emphasises confirming cephalic presentation before amniotomy, controlled artificial rupture of membranes with theatre readiness, continuous fetal monitoring, and anticipating shoulder dystocia and postpartum haemorrhage where macrosomia coexists. ^[10]
• WHO antenatal care guidance prioritises cause-finding, screening for diabetes where feasible, and evidence-based maternity care rather than routine intervention; WHO specifically lists antenatal anti-D prophylaxis for non-sensitised Rhesus-negative women as a research-context recommendation rather than universal practice. ^[6]

For mild idiopathic polyhydramnios, no change in management is often needed; delivery can occur spontaneously at term with usual obstetric indications, although the risk of emergency caesarean section is increased. ^{[3] [1]}

• Rupture of membranes: confirm, then follow the PPROM/preterm labour pathway (corticosteroids if before 36 weeks, antibiotics, delivery timing by gestation).
• Growth restriction or hypertension: manage under the fetal growth restriction pathway, with umbilical artery Doppler and adjusted delivery timing.
• Renal/urinary tract disease: refer for a detailed fetal medicine assessment; consider fetal therapy where appropriate; counsel about prognosis.
• Post-term: induction of labour is standard practice beyond term; oligohydramnios adds to the indication.
• Isolated oligohydramnios at term: the evidence is conflicting. ACOG suggests induction between 36 and 37+6 weeks of gestation (or at diagnosis if diagnosed later); Italian guidance states there is insufficient evidence to support intervention. ^[1] Most meta-analyses do not show a clear neonatal benefit from induction, and the number of stillbirths in available studies is too small to settle the question. ^[1] The safe practical position is close fetal surveillance, daily fetal movement awareness, and individualised timing decided by the senior obstetrician with the woman.
• Maternal hydration (oral and intravenous) can raise the amniotic fluid volume in some studies, but clinical benefit has not been established; it is reasonable alongside the main plan but not a treatment in itself. ^[5]
• Second trimester severe oligohydramnios: consider amnioinfusion in a specialist centre, with realistic counselling; the outcome depends on the underlying cause and whether pulmonary hypoplasia is already established. ^[5]

Because both disorders increase labour risk (fluid buffering, lie stability, cord compression), NICE recommends continuous cardiotocography when polyhydramnios or anhydramnios is present. ^[3] The first hour of monitoring and a personal risk assessment matter most. For oligohydramnios with a reassuring fetal heart rate, intermittent auscultation may be acceptable in spontaneous term labour without other risk factors, in consultation with the obstetrician. ^[1] In polyhydramnios, anticipate shoulder dystocia and postpartum haemorrhage when macrosomia coexists, and keep the woman on a delivery suite with continuous monitoring. ^[10]

This is the polyhydramnios cause that is both dangerous and preventable, and it is included on the original book page.

How it works. A Rhesus-negative (D-negative) mother carrying a Rhesus-positive fetus can be sensitised when fetal red cells cross into her circulation (fetomaternal haemorrhage), particularly in the third trimester and during delivery. She produces anti-D antibodies that cross the placenta in a later pregnancy and destroy fetal red cells, causing haemolytic disease of the fetus and newborn. Anti-D (IgG) haemolyses fetal erythrocytes; severe anaemia leads to high cardiac output, then polyhydramnios, hydrops and stillbirth. ^{[8] [9] [11]}

Scale. Without prophylaxis, 13 to 16% of at-risk pregnancies sensitise; postpartum RhD immune globulin alone reduces this to 0.5 to 1.8%; adding routine antenatal administration reduces it further to 0.14 to 0.2%. ^[8] In settings without prophylaxis programmes, 14% of affected fetuses are stillborn and half of liveborn affected infants die neonatally or suffer brain injury. ^[8]

Screening. ^{[9] [11]}

• ABO and D (Rhesus) type and antibody screen early in pregnancy, with a repeat test in the third trimester, for every woman (NICE CG62, White et al.). ^[9]
• Rhesus-negative women: give anti-D immunoglobulin for any potentially sensitising event (bleeding, invasive procedure, trauma, external cephalic version, miscarriage, termination).
• Routine antenatal anti-D prophylaxis (RAADP): one of several regimens - two doses of 500 IU at 28 and 34 weeks; two doses of 1000 to 1650 IU at 28 and 34 weeks; or a single 1500 IU dose at 28 weeks (or 28 to 30 weeks). ^[4]
• A maternal antibody sample should be taken before the first dose of anti-D prophylaxis, because passive anti-D can be mistaken for immune anti-D. ^[11]
• Non-sensitised D-negative women are not offered routine antenatal prophylaxis as universal WHO policy in resource-limited settings: WHO 2016 recommends antenatal anti-D at 28 and 34 weeks only in the context of rigorous research, with postnatal anti-D still given when indicated. ^{[6] [9]}

Managing the sensitised woman. ^[9]

• Test the antibody at least monthly to 28 weeks and fortnightly thereafter; monitor the concentration (NIBSC reference).
• Critical anti-D concentrations guide management: lower values make haemolytic disease unlikely (continue monitoring), intermediate values carry moderate risk (refer to fetal medicine), and higher values indicate high risk (urgent referral). ^[9]
• Determine the Rhesus D status of the fetus from cell-free fetal DNA in maternal blood (false negative rate below 1%), so that an RhD-negative fetus needs no further intervention. ^[9]
• Fetal middle cerebral artery (MCA) peak systolic velocity Doppler is the non-invasive test of choice for fetal anaemia; current guidance starts weekly MCA-PSV surveillance by 16 weeks' gestation, and a value above 1.5 multiples of the median strongly correlates with moderate to severe fetal anaemia. ^{[13] [9]}
• An intrauterine transfusion is indicated when MCA-PSV is consistently above 1.5 MoM (confirmed by fetal blood sampling), performed in a tertiary centre; most clinicians do not perform IUT beyond 34 weeks. ^[9] The 2025 JAMA Network Open clinical practice guideline, by contrast, recommends continuing intrauterine transfusion to the end of the 35th week unless technical limitations prevent it. ^[13]
• Deliver at not later than 37 to 38 weeks unless earlier delivery is indicated. ^[9]
• At delivery, send cord blood for direct antiglobulin (Coombs) test, haemoglobin and bilirubin; monitor the neonate for jaundice, with phototherapy, exchange or top-up transfusion as needed. ^[9]

Side (difference) note: WHO, BSH and ACOG all agree on postnatal RhD immune globulin; they differ on universal antenatal prophylaxis scheduling, and low-resource settings may not have anti-D available for all events.

• Polyhydramnios: unstable fetal lie; placental abruption from sudden decompression; umbilical cord prolapse at membrane rupture; preterm labour; postpartum haemorrhage from uterine atony; maternal respiratory compromise; and, in the rare infected or anomalous case, perinatal death.
• Oligohydramnios: early severe disease causes Potter (oligohydramnios) sequence with pulmonary hypoplasia and a high mortality; late disease causes cord compression, fetal distress, operative delivery, and admission to neonatal care.
• Rhesus disease: fetal anaemia, hydrops, stillbirth, neonatal anaemia and late (up to 12 weeks) anaemia requiring top-up transfusion.

Idiopathic mild polyhydramnios resolves in many pregnancies and, on its own, mainly raises the caesarean rate rather than perinatal mortality; severe and persistent disease carries the risks above. ^[1] Oligohydramnios secondary to an identified cause carries the prognosis of that cause; isolated term oligohydramnios has conflicting outcome data and is probably a spectrum of placental insufficiency. ^[1] Rhesus haemolytic disease is now rare where prophylaxis exists, but it is fatal or brain-injuring where it does not. ^[8]

• Screening for structural anomalies at the mid-trimester scan and again in the third trimester is the best prevention of severe avoidable polyhydramnios: the anomaly scan detects the fetal causes before they become emergencies.
• Diabetes screening in pregnancy reduces the commonest maternal cause.
• Blood group and antibody screening in early pregnancy prevents Rhesus disease; anti-D prophylaxis after potentially sensitising events and RAADP where resources allow do the rest. ^[11]
• Drug history before prescribing an NSAID or ACE inhibitor/ARB in pregnancy prevents drug-induced oligohydramnios.
• Maternal hydration is a sensible general measure but is not evidence-proven prevention.
• Termination/early delivery decisions in severe early oligohydramnios are made case by case and are outside the scope of this page.

Pregnancy. The whole page is pregnancy.

Children. Polyhydramnios is not a childhood disorder. Survivors of severe early oligohydramnios may have pulmonary hypoplasia, chronic lung disease and renal impairment; neonatal care should be planned in a centre with appropriate expertise. Neonates born after polyhydramnios should have an early swallowing assessment and nasogastric-tube check when any gastrointestinal obstruction is suspected.

Older adults. Not applicable directly; grand-maternal age and chronic disease affect placental function and therefore oligohydramnios risk.

Low-resource settings. Ultrasound with DVP is usable almost everywhere; anhydramnios is unmistakable clinically. Amnioinfusion, intrauterine transfusion and tertiary delivery for severe cases may not be available, so early referral along the referral pathway, early glucose management and postnatal RhD immune globulin save lives. Where cell-free fetal DNA and MCA Doppler are unavailable, serial antibody titres and bilirubin on amniotic fluid are the fallback, and delivery timing is decided by an experienced clinician.

Volume abnormalities can be confused with:

• Preterm prelabour rupture of membranes (PPROM): a history of leaking and a speculum test distinguish it; a low volume with intact membranes is not PPROM.
• Fetal growth restriction without oligohydramnios: placental insufficiency often produces both, but growth restriction can occur with normal liquor and oligohydramnios can be isolated.
• Hydrops fetalis: presents with fluid in serous cavities and skin oedema; polyhydramnios is often the first sign, so hydrops should be excluded when polyhydramnios is found.
• Macrosomia without polyhydramnios: fetal diabetes may exist without excess liquor; the two are separate risks.
• Multifetal pregnancy with twin-to-twin transfusion syndrome: a recipient with polyhydramnios and a donor with oligohydramnios is diagnostic.
• Intrauterine growth restriction with compensatory liquor: sometimes liquor is normal even when the fetus is growth-restricted; do not reassure solely on the basis of liquor.

• Amniotic fluid is a dynamic balance of fetal urine inflow and swallowing; every volume disorder maps to production, swallowing, loss or absorption.
• Normal volume is AFI 5 to 25 cm or a deepest vertical pocket of 2 to 8 cm; oligohydramnios is a pocket below 2 cm and polyhydramnios a pocket of 8 cm or more or an AFI of 24 to 25 cm or more.
• Polyhydramnios severity is mild (AFI 25 to 29.9 cm on the Huri review, 24.0 to 29.9 cm on ACOG CO828; pocket 8 to 11 cm), moderate (30 to 34.9 cm; 12 to 15 cm) or severe (35 cm or more; 16 cm or more). ^{[1] [13]}
• Idiopathic polyhydramnios is common; maternal diabetes and fetal anomalies are the other frequent associations.
• Oligohydramnios is usually secondary to membrane loss, placental insufficiency, post-term gestation, maternal disease or fetal renal/urinary tract disease.
• Severity (cut-off) and persistence (transient vs persistent) both matter; transient severe reductions are reassuring.
• Ultrasound detail, glucose testing, blood group and antibodies, and clinically indicated serology form the workup.
• Management targets the cause; amnioreduction is symptom relief only, and indomethacin should not be used to reduce liquor.
• ACOG and SMFM hold that mild idiopathic polyhydramnios should not itself be an indication for induction, and that it needs no special antenatal surveillance; NICE wants continuous CTG in labour; RCOG-style practice addresses lie, amniotomy and haemorrhage.
• Isolated term oligohydramnios has conflicting evidence; ACOG suggests induction at 36 to 37 completed weeks, others ask for more evidence.
• Rhesus sensitisation causes polyhydramnios through fetal anaemia and hydrops; blood group and antibody screening, postnatal anti-D, and RAADP where available, are the prevention.
• Rhesus sensitised pregnancies are monitored with MCA-PSV above 1.5 MoM and delivered by 37 to 38 weeks at the latest. ^[9]

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