19.2 Amniotic Fluid Assessment & Growth Disorders

Amniotic Fluid Production and Circulation

In early pregnancy amniotic fluid is largely a dialysate of maternal serum across the membranes. After approximately 16 weeks, fetal urine becomes the dominant source — near term the fetus produces several hundred milliliters to over a liter of hypotonic urine daily, supplemented by fetal lung fluid. Fluid is removed mainly by fetal swallowing (absorbed through the fetal gut) and by intramembranous transfer across the amnion into the maternal circulation. Volume peaks near 33-34 weeks at roughly 800-1000 mL. This production-removal loop explains the classic cause patterns: anything blocking swallowing raises volume, and anything reducing urine output lowers it.

Measuring Amniotic Fluid

Amniotic Fluid Index (AFI)

The uterus is divided into four quadrants by the linea nigra and umbilicus. In each quadrant, the deepest vertical pocket free of cord and fetal limbs is measured, and the four values are summed. Normal AFI is approximately 5-25 cm.

Single Deepest Pocket (SDP)

The single largest vertical pocket is measured; 2-8 cm is normal.

Polyhydramnios

Polyhydramnios complicates roughly 1-2% of pregnancies. It may be graded by deepest pocket (mild 8-11 cm, moderate 12-15 cm, severe 16 cm or more). Causes include:

• Maternal diabetes — fetal hyperglycemia causes osmotic diuresis and increased urine output
• Gastrointestinal atresia — esophageal or duodenal atresia prevents swallowing and absorption (look for an absent or small stomach bubble; "double bubble" with duodenal atresia)
• CNS anomalies — anencephaly impairs swallowing
• Twin-to-twin transfusion syndrome — the recipient twin becomes volume overloaded and polyuric
• Hydrops and chromosomal abnormalities
• Idiopathic — the largest single category, roughly half to two-thirds of cases

Maternal complications include preterm labor, malpresentation, and cord prolapse when membranes rupture.

Oligohydramnios

Oligohydramnios is ominous in the second trimester and carries risk of pulmonary hypoplasia and limb contractures. Causes include:

• Ruptured membranes — the most common cause overall
• Uteroplacental insufficiency / IUGR — chronic hypoxia shunts fetal blood away from the kidneys, reducing urine output
• Renal anomalies — bilateral renal agenesis, posterior urethral valves, multicystic dysplastic kidney (decreased or absent urine production)
• Post-term pregnancy — fluid normally declines after 40 weeks

Premature rupture of membranes (PROM) is membrane rupture before the onset of labor; preterm PROM (PPROM) occurs before 37 weeks. Sonography shows oligohydramnios, and the major risks are chorioamnionitis, preterm delivery, and cord prolapse.

Intrauterine Growth Restriction (IUGR)

IUGR is defined as estimated fetal weight (EFW) below the 10th percentile for gestational age. The two patterns differ in timing, cause, and biometric behavior:

In asymmetric IUGR the abdominal circumference is small (depleted hepatic glycogen and subcutaneous fat) while the head circumference is preserved, so the head circumference to abdominal circumference (HC/AC) ratio rises above the normal range. Doppler of the umbilical artery shows increased resistance — elevated systolic/diastolic ratio — reflecting placental vascular disease.

Macrosomia

Macrosomia is EFW above the 90th percentile, or a birth weight exceeding 4000-4500 g. The dominant association is maternal (especially diabetic) macrosomia, where fetal hyperinsulinemia drives fat deposition: the abdominal circumference is disproportionately large, while the head is normal — the mirror image of asymmetric IUGR. Macrosomia raises risk of shoulder dystocia and cesarean delivery, and sonographic weight estimates late in pregnancy carry an error margin of roughly ±15%.

Several exam-favorite refinements complete this topic. Anhydramnios — the complete absence of measurable fluid — most often reflects bilateral renal agenesis or prolonged ruptured membranes; severe early oligohydramnios produces the Potter sequence of pulmonary hypoplasia, flattened facies, and limb contractures. Polyhydramnios can also be graded by AFI (mild 25-30 cm, moderate 30.1-35 cm, severe above 35 cm), and a rapid acute onset before 24 weeks is more concerning than the common chronic form. When membranes rupture, sonography cannot distinguish PROM from PPROM directly — the finding is unexplained oligohydramnios correlated with clinical pooling or nitrazine testing. For growth disorders, the term IUGR describes a fetus that fails to reach its growth potential, while small for gestational age (SGA) is a neonatal birth-weight designation; not every SGA infant was pathologically restricted. In asymmetric IUGR, worsening placental resistance progresses from an elevated umbilical artery systolic/diastolic ratio to absent and then reversed end-diastolic flow, findings that mark severe compromise. Symmetric IUGR carries the poorer prognosis because the insult affected all cell lines from early development. For macrosomia, remember that the diabetic fetus specifically enlarges the abdomen and shoulders — the abdominal circumference grows disproportionately relative to head circumference — and that 4000 g is the threshold most often applied in diabetic pregnancies while 4500 g is the general cutoff in many references.