Polyhydramnios and Oligohydramnios — AFI/SDP Cut-offs, Causes, Complications and Management

Amniotic fluid volume is judged on ultrasound by two methods. The single deepest vertical pocket (SDP, also called MVP) is the deepest clear fluid pocket, free of cord and fetal parts and at least 1 cm wide. The amniotic fluid index (AFI) is the sum of the deepest vertical pockets in the four abdominal quadrants. The probe is held perpendicular to the floor, in the sagittal plane parallel to the fetal spine.

Which method? AFI can be used only in singleton pregnancy, because four quadrants cannot be assigned to each of two fetuses. The SDP works in singletons and multiples. SMFM, ACOG and AIUM prefer SDP for diagnosing oligohydramnios, as it leads to fewer obstetric interventions without worse perinatal outcomes. SDP tends to overestimate volume, so SDP alone can over-diagnose polyhydramnios. Both measures correlate poorly with true volume (dye dilution is the gold standard) but abnormal values still predict adverse outcomes.

• Colour Doppler helps to exclude cord and fetal parts from a pocket but lowers AFI and SDP by about 20%, and may overcall oligohydramnios without changing outcomes.
• Frequency: polyhydramnios occurs in 1–2% of pregnancies; about 65–70% is mild, 20% moderate and under 15% severe.

Fluid volume is a balance of production versus removal. In the first trimester it comes from fetal lung secretions and transport of maternal plasma across the membranes. From 14–16 weeks, fetal urine becomes the main source. Estimated fetal urine output is about 4.2 mL/h at 20 weeks, 22.7 mL/h at 30 weeks and 52.2 mL/h at 40 weeks (roughly 100, 545 and 1,250 mL/day). Larger fetuses make more urine; growth-restricted fetuses make less.

Removal is mainly by fetal swallowing (about 500–1,000 mL/day near term) and absorption through the gut. A second route is intramembranous absorption across the fetal surface of the placenta (about 200–500 mL/day), driven by the fact that amniotic fluid is hypotonic to fetal plasma. Swallowing rises as volume rises, which helps self-regulation.

In 50–60% of patients no cause is found (idiopathic), and that label is a diagnosis of exclusion made only after a work-up. Among pathological causes, gestational diabetes is among the commonest, and chromosomal abnormalities are also relatively common. Rarely, transplacental infection is responsible.

Most patients are asymptomatic and the finding is incidental, or arises from a symphysis–fundal height more than expected (3 cm above gestational age in weeks, or rapid uterine enlargement). Moderate-to-severe cases cause dyspnoea (the diaphragm is pushed up), lower-limb oedema and a grossly distended abdomen with shallow breathing.

• Look for the cause: glucose screening (rescreen if more than 1 month since the first test), anomaly scan, alloimmunisation and syphilis screening, serology for congenital infection if risk factors are present.
• Targeted ultrasound: growth (macrosomia or restriction), hydrops, face and palate, neck masses, heart, stomach bubble (absent or small in oesophageal atresia), hands and feet (arthrogryposis), kidneys, spine and pelvis (sacrococcygeal teratoma), placenta (chorioangioma), movements. MCA peak systolic velocity is used to screen for fetal anaemia, especially in hydrops.
• Genetics: offer amniocentesis with karyotype; microarray or whole-genome sequencing if severe polyhydramnios or an anomaly is found. About 5.5% of moderate or severe polyhydramnios carry a clinically significant genetic anomaly.
• Monochorionic twins: screen for twin-twin transfusion syndrome every 2 weeks from 16 weeks to delivery.

The differential diagnosis for a uterus large for dates includes macrosomia, multiple gestation, maternal fluid overload (cirrhosis, heart failure, end-stage renal disease, pre-eclampsia), placental tumour and concealed abruption. Breathlessness in these women also needs pulmonary embolism, pre-eclampsia and cardiac disease excluded.

Perinatal and maternal morbidity rise with severity. Perinatal mortality in one series of 7,562 high-risk pregnancies was 1.97 per 1,000 with normal fluid and 4.12 per 1,000 with polyhydramnios. The overdistended uterus explains most obstetric complications.

Management depends on severity and the underlying cause (for example laser for TTTS). Mild idiopathic polyhydramnios rarely needs treatment, and about 37% of patients in one study resolved spontaneously, all mild.

Causes fall into four groups: maternal (uteroplacental insufficiency, drugs), fetal (urinary tract anomalies, growth restriction, chromosomal), placental/membrane (PROM, abruption, TTTS) and idiopathic. Rupture of membranes is the commonest obstetric cause; preterm PROM alone accounts for over 37% of oligohydramnios diagnosed in the second and third trimesters. In the third trimester about half of cases are idiopathic, and these carry better outcomes.

Severe oligohydramnios or anhydramnios in the second trimester can cause intrauterine death or previable and periviable birth. Without fluid the fetal chest and limbs are compressed: lungs cannot expand and limbs cannot move. Pulmonary hypoplasia is the most important predictor of fetal mortality in second-trimester oligohydramnios, and is worst when oligohydramnios begins before 26 weeks, when the terminal lung sacs are developing.

• Potter sequence: pulmonary hypoplasia, limb contractures and flattened facies from fetal compression (classically with bilateral renal agenesis).
• Late oligohydramnios (third trimester, isolated): cord compression, abnormal fetal heart rate patterns, caesarean birth, meconium aspiration syndrome and NICU admission.
• Prognosis: worse with underlying genitourinary malformation, chromosomal anomaly or growth restriction. In one series of 131 fetuses with renal-cause oligohydramnios, 35% chose termination, 8% had intrauterine death, 27% died after birth and 30% survived.

First establish the cause: confirm membrane status, then do a targeted scan for fetal growth and kidneys and bladder; genetic testing if anomalies are present (chromosomal microarray preferred over karyotype); infection serology only if clinically suspected. Anyone with fundal height at least 3 cm smaller than expected, known renal or gut anomaly, aneuploidy markers or risk of uteroplacental insufficiency needs an amniotic fluid scan.

TTTS affects 8–10% of monochorionic twin pregnancies. Vascular anastomoses within the shared placenta shunt blood from the donor to the recipient. The donor becomes hypovolaemic, with little urine and oligohydramnios (the 'stuck twin'); the recipient becomes overloaded, with polyuria, polyhydramnios, hydrops and high-output cardiac failure. Fluid discordance, not just growth discordance, is the hallmark. The Quintero staging system defines stage I as the oligo-poly sequence (donor pocket under 2 cm, recipient pocket over 8 cm) with a visible donor bladder and normal Dopplers; stage II adds a donor bladder not seen over 60 minutes; stage III abnormal Dopplers; stage IV ascites or hydrops; stage V demise of one or both twins.

Screen monochorionic twins by ultrasound every 2 weeks from 16 weeks to delivery. Selective fetoscopic laser photocoagulation of the anastomoses treats the cause and is recommended for stage II–IV disease, typically performed at 16–26 weeks. Asymptomatic stage I is usually managed expectantly with at least weekly surveillance, since about 75% remain stable or regress. See twin pregnancy and chorionicity for why only monochorionic twins are at risk.

• High fluid = high output or low swallow; low fluid = low output or leak. Gut atresia, CNS and neuromuscular disease raise fluid; renal agenesis and PROM lower it.
• Renal agenesis gives oligohydramnios, not polyhydramnios. Oesophageal and duodenal atresia give polyhydramnios.
• ACE inhibitors, ARBs and NSAIDs are drug causes of oligohydramnios; indomethacin (an NSAID) is used to treat polyhydramnios but only below 32 weeks.
• AFI cannot be used in twins; use the single deepest pocket.
• Amnioreduction is for symptomatic severe polyhydramnios only; fluid usually returns.
• Oligohydramnios before 26 weeks gives pulmonary hypoplasia; PROM is the commonest obstetric cause.