Amniotic Fluid — Physiology, AFI and SDP, Oligohydramnios, Polyhydramnios and Amniotic Fluid Embolism

Amniotic fluid is the fluid inside the amniotic sac. It cushions the fetus against blows to the maternal abdomen, protects the umbilical cord from compression between the fetus and the uterine wall, has natural antibacterial properties, and gives the fetus room to move — movement that the musculoskeletal system, gut and especially the lungs need in order to develop normally.

It is about 98% water and electrolytes; peptides, carbohydrates, lipids, hormones and signalling molecules make up the rest. Because the volume reflects fetal kidney function and placental perfusion, measuring it on ultrasound is one of the simplest windows on fetal wellbeing — it is a component of the biophysical profile.

Early pregnancy: the fluid is essentially a transudate of maternal serum across the membranes and the still non-keratinised fetal skin, under hydrostatic and osmotic forces, so its composition resembles fetal and maternal plasma. The extra-embryonic coelomic cavity shrinks as the amniotic cavity grows and has disappeared by about 12 weeks.

Fetal urine starts late in the first trimester — StatPearls chapters put the start of urine production at about 8–10 weeks — and from roughly 14–16 weeks it becomes the main source of amniotic fluid for the rest of pregnancy. Fetal skin becomes fully keratinised by about 25 weeks, after which fluid no longer moves freely across it.

Volume rises roughly linearly in the first half of pregnancy and keeps rising until about 34–38 weeks. StatPearls gives an average maximum of about 800 mL; after that it falls by about 8% per week, to as little as about 400 mL near 42 weeks. That late decline is why post-term pregnancy is a classic cause of reduced fluid.

• Peak: around 34–38 weeks; average maximum about 800 mL.
• Term: mean volume about 800 mL in large reference series.
• Post-term: falls by about 8% per week — down to about 400 mL near 42 weeks.
• Gold standard for true volume is the dye-dilution technique; AFI and SDP correlate only loosely with it but still predict outcome, so ultrasound is used in practice.

Single deepest pocket (SDP) — also called the deepest vertical pocket (DVP) or maximum vertical pocket (MVP) — is the vertical depth of the largest clear pocket of fluid. Amniotic fluid index (AFI) is the sum of the deepest pockets in the four quadrants of the uterus. By the 2014 NICHD workshop definition, a measured pocket must be at least 1 cm wide and free of umbilical cord and fetal parts; the probe is held perpendicular to the floor in the sagittal plane.

• Anhydramnios = no measurable fluid at all.
• Twins and other multiples: use the SDP for each sac — four quadrants cannot be assigned to each fetus. StatPearls also advises the SDP before 24 weeks.
• SDP preferred for diagnosing oligohydramnios: randomised trials show the SDP leads to fewer interventions (inductions, caesareans) with the same perinatal outcome, so SMFM, ACOG and AIUM recommend it over the AFI.
• Polyhydramnios threshold changed: the AFI cut-off was historically 25 cm; SMFM now uses 24 cm, because 24 cm exceeds the 97.5th percentile at every gestation after 20 weeks.
• Colour Doppler helps exclude cord from a pocket but reduces measurements by about 20%, which can over-diagnose oligohydramnios.

Low fluid means too little urine is reaching the sac or fluid is leaking out. Congenital anomalies are found in about half of second-trimester cases; in the third trimester about half are idiopathic and have a much better outlook.

• Work-up: confirm membrane status (speculum, ferning, nitrazine pH or amniotic protein tests), then a targeted scan — both kidneys, bladder (a never-seen bladder suggests renal agenesis; a large thick-walled bladder suggests outlet obstruction), fetal growth and markers of aneuploidy.
• Genetic testing (chromosomal microarray first) when anomalies are seen.

Severe oligohydramnios early in pregnancy compresses the fetus. The resulting Potter sequence comprises pulmonary hypoplasia, limb contractures and deformities, and flattened (compressed) facies. Bilateral renal agenesis is the classic cause — 'Potter syndrome' in the strict sense — but 'Potter sequence' describes the same chain of events from low fluid of any cause, including obstructive uropathy, polycystic kidneys and early membrane rupture.

Pulmonary hypoplasia is the main cause of death: the lungs need chest expansion and fluid to grow, and the damage is worst when oligohydramnios starts before 26 weeks, while the terminal sacs are forming. Babies with bilateral renal agenesis develop respiratory distress within an hour of birth; the condition is incompatible with life.

• Treat the cause — PPROM, growth restriction, pre-eclampsia, abruption or an anomaly each has its own delivery plan.
• Isolated oligohydramnios: fetal surveillance once or twice a week (non-stress test plus fluid measurement, a modified biophysical profile), growth scans every 3–4 weeks, and — per ACOG — delivery at 36⁺⁰ to 37⁺⁶ weeks, or at diagnosis if found at 38 weeks or later.
• Maternal hydration: about 2 L of oral fluid raises the AFI by roughly 4–5 cm; oral hydration works slightly better than IV, and the effect fades within about a day unless continued daily.
• Vesicoamniotic shunt: considered between 16 and 28 weeks for suspected lower urinary tract obstruction without life-limiting anomalies, at referral centres.
• Transabdominal (antepartum) amnioinfusion for severe mid-trimester oligohydramnios or early PPROM has not improved perinatal mortality in trials; for lower urinary tract obstruction it is offered only in research settings.
• Intrapartum (transcervical) amnioinfusion: older studies showed that prophylactic amnioinfusion in labour with oligohydramnios reduced fetal heart rate abnormalities, caesarean deliveries, acidaemia at birth and low 5-minute Apgar scores — it relieves cord compression (variable decelerations).

Polyhydramnios affects 1–2% of pregnancies. About 50–60% are idiopathic — a diagnosis of exclusion. Of the pathological causes, gestational (maternal) diabetes is among the commonest: glucose crosses the placenta, fetal hyperglycaemia causes an osmotic diuresis, and fetal urine output rises.

• Anomalies are uncommon in mild disease but present in about 30–40% of severe polyhydramnios.
• Work-up: repeat diabetes screening, antibody screen (alloimmunisation), infection serology if suspected, and a targeted scan of the face, neck, stomach, heart, spine and placenta; MCA peak systolic velocity if hydrops (fetal anaemia).

• Mild idiopathic: often resolves; no extra surveillance needed. Let labour start spontaneously at term — no induction before 39 weeks without another indication. Confirm presentation on admission and use continuous fetal monitoring in labour.
• Moderate to severe: antenatal fetal surveillance from 32–34 weeks; deliver at a tertiary centre.
• Amnioreduction for symptomatic severe disease: ultrasound-guided needle drainage of about 1.5–3 L; fluid re-accumulates, and 42–46% need more than one procedure.
• Indomethacin reduces fetal urine output, but SMFM advises against using it only to reduce fluid; it is contraindicated from 32 weeks (after 32 weeks it is linked to periventricular leukomalacia, severe intraventricular haemorrhage and necrotising enterocolitis). A short course is reasonable as a tocolytic before 32 weeks.
• Twin-twin transfusion syndrome: fetoscopic laser photocoagulation of the connecting vessels (SMFM: stages II–IV before 26 weeks) has replaced serial amnioreduction as first-line treatment.

Amniotic fluid embolism (AFE) is a sudden cardiorespiratory collapse with disseminated intravascular coagulation around delivery. It is now called the anaphylactoid syndrome of pregnancy: amniotic fluid and fetal material entering the maternal circulation trigger an abnormal inflammatory and coagulation response, not a simple mechanical blockage. Estimated incidence is about 2–6 per 100,000 births.

• Classic triad: hypoxia, hypotension and coagulopathy, without fever. Premonitory agitation, a sense of impending doom, then seizures, cardiac arrest and massive bleeding.
• Timing: about 70% during labour, 19% during caesarean section and 11% after vaginal delivery; it can occur up to 48 hours after delivery, and rarely after abortion or amniocentesis.
• Pathophysiology: intense pulmonary vasoconstriction → acute right-ventricular failure (septum bowing into the left ventricle — a 'D-shaped' ventricle on echo) → left-sided failure; tissue factor activates clotting and fibrinolysis → DIC in most patients, worsened by uterine atony.
• Risk factors: maternal age over 35, induction of labour, polyhydramnios, multiple pregnancy, placenta praevia and placenta accreta spectrum (about ten-fold, the strongest association), abruption, eclampsia, operative delivery and amnioinfusion.
• Diagnosis is clinical, by exclusion. Fetal squamous cells in the maternal pulmonary circulation are not diagnostic — they are found in labouring women without AFE. The 2016 SMFM research criteria: sudden collapse or hypotension (systolic below 90 mmHg) with hypoxia (SpO₂ below 90%), overt DIC, onset in labour or within 30 minutes of placental delivery, and no fever.
• Management is supportive: high-quality CPR with left uterine displacement; delivery of the fetus (perimortem caesarean / resuscitative hysterotomy) if there is no return of circulation within about 4 minutes; vasopressors (norepinephrine), inotropes (dobutamine, milrinone) and pulmonary vasodilators for right-heart failure; avoid large fluid volumes; 1:1:1 blood products, tranexamic acid; ECMO in refractory cases.

• Amniocentesis is done after 15 weeks, mainly to obtain fetal cells for chromosomal diagnosis; the procedure-related miscarriage risk quoted in StatPearls is 0.5–1%.
• Meconium-stained fluid: green staining from bile pigments in meconium suggests fetal stress; it raises the risk of meconium aspiration, especially with oligohydramnios.
• Rupture of membranes: vaginal fluid shows ferning on microscopy, its pH can be checked with nitrazine paper, and point-of-care tests detect amniotic fluid proteins.