Placental and Amniotic Fluid Abnormalities
Core concepts
Know normal placental development, cord insertion variants, and the gross and microscopic correlates of placental insufficiency: villous hypoplasia, distal villous immaturity, infarction, and maternal vascular malperfusion. Understand amniotic fluid volume as a functional readout-oligohydramnios from renal agenesis or prolonged rupture, polyhydramnios from impaired swallowing (esophageal atresia, neurologic impairment) or diabetes. Recognize the oligohydramnios sequence (Potter sequence): pulmonary hypoplasia, limb deformities, and characteristic facies from compression.
Be able to identify molar pregnancy categories (complete vs partial) by genetics and histology, and understand the risk of persistent trophoblastic disease. Know placental inflammatory lesions (chorioamnionitis, villitis) and their clinical meaning.
Traps
Examiners conflate maternal vs fetal vascular malperfusion patterns. Another trap: attributing polyhydramnios to renal causes-renal agenesis causes oligohydramnios because fetal urine is the main fluid source. Complete mole (diploid, paternal) vs partial mole (triploid) genetics is frequently tested; do not reverse them. Remember that a single infarct may be incidental while extensive infarction signals insufficiency.
Worked example / rule of thumb
A newborn with pulmonary hypoplasia, flattened facies, and limb contractures plus maternal oligohydramnios: think Potter sequence from renal agenesis. Rule of thumb: "Urine makes fluid; swallowing removes it"-so renal failure → oligo, swallowing failure → poly.