Potter's sequence includes which findings?

Potter's sequence includes which findings?

• A. Renal agenesis, oligohydramnios, limb defects, facial defects, and pulmonary hypoplasia
• B. Esophageal atresia and TE fistula
• C. Polyhydramnios and hydrops
• D. Fetal macrosomia

Answer: (A)

Potter sequence starts with severe oligohydramnios caused by absent or nonfunctional fetal kidneys (most classically bilateral renal agenesis). Fetal urine is a major contributor to amniotic fluid, so when urine production drops, the fluid volume falls and the fetus is chronically compressed in the uterus. This compression leads to the distinctive pattern of findings: facial anomalies such as a flattened facies and low-set ears, limb deformities like clubbing or other positional abnormalities, and a failure of the lungs to develop properly, resulting in pulmonary hypoplasia. The combination of renal failure with oligohydramnios and the downstream effects on facial structures, limbs, and lungs is what defines Potter sequence. The other scenarios don’t fit because they involve different amniotic fluid dynamics or unrelated outcomes. Esophageal atresia or TE fistula often causes polyhydramnios because the fetus can’t swallow amniotic fluid, not the reduced fluid seen in Potter. Polyhydramnios with hydrops indicates fluid excess, again not the oligohydramnios-chronic compression pattern of Potter. Fetal macrosomia has nothing to do with amniotic fluid deficiency.

Potter sequence starts with severe oligohydramnios caused by absent or nonfunctional fetal kidneys (most classically bilateral renal agenesis). Fetal urine is a major contributor to amniotic fluid, so when urine production drops, the fluid volume falls and the fetus is chronically compressed in the uterus. This compression leads to the distinctive pattern of findings: facial anomalies such as a flattened facies and low-set ears, limb deformities like clubbing or other positional abnormalities, and a failure of the lungs to develop properly, resulting in pulmonary hypoplasia. The combination of renal failure with oligohydramnios and the downstream effects on facial structures, limbs, and lungs is what defines Potter sequence.

The other scenarios don’t fit because they involve different amniotic fluid dynamics or unrelated outcomes. Esophageal atresia or TE fistula often causes polyhydramnios because the fetus can’t swallow amniotic fluid, not the reduced fluid seen in Potter. Polyhydramnios with hydrops indicates fluid excess, again not the oligohydramnios-chronic compression pattern of Potter. Fetal macrosomia has nothing to do with amniotic fluid deficiency.