26 引起新生兒持續性肺動脈高壓之原因，以下何者為非？

敗血症 橫膈膜疝氣

波特（Potter）症候群 開放性動脈導管（patent ductus arteriosus）

Persistent pulmonary hypertension of the newborn is defined as the failure of the normal circulatory transition that occurs after birth. It is a syndrome characterized by marked pulmonary hypertension that causes hypoxemia and right-to-left extrapulmonary shunting of blood. Because a patent foramen ovale and patent ductus arteriosus are normally present early in life, elevated pulmonary vascular resistance in the newborn produces extrapulmonary shunting of blood, leading to severe and potentially unresponsive hypoxemia. With inadequate pulmonary perfusion, neonates are at risk for developing refractory hypoxemia, respiratory distress, and acidosis.

PDA: left to right

POTTER syndrome:

Potter syndrome refers to the typical physical appearance and associated pulmonary hypoplasia of a neonate as a direct result of oligohydramnios and compression while in utero. The term was coined after the pathologist Edith Potter, who in 1946 described the facial characteristics of infants with bilateral renal agenesis.¹ From her research, she was able to deduce the sequence of events that lead to these features. Other conditions resulting in oligohydramnios, such as obstructive uropathy, cystic kidney diseases, renal hypoplasia, and premature rupture of membranes lead to the same clinical findings. Hence, the terms Potter sequence or oligohydramnios sequence emerged. However, regardless of the root cause for oligohydramnios, the terms Potter syndrome, Potter sequence, and oligohydramnios sequence are used interchangeably in the published literature.

Pathophysiology

Prior to 16 weeks' gestations, the amount of amniotic fluid is dependent on the transmembrane flow. After that, fetal urine production is the predominant mechanism that determines the amniotic fluid volume. The fetus continuously swallows amniotic fluid, which is reabsorbed by the GI tract and then reintroduced into the amniotic cavity by the kidneys. Oligohydramnios occurs if the volume of amniotic fluid is less than normal for the corresponding period of gestation. This may be due to decreased urine production secondary to bilateral renal agenesis, obstruction of the urinary tract, or, occasionally, prolonged rupture of membranes. The resulting oligohydramnios is the cause of the deformities observed in Potter syndrome. The mechanism of lung hypoplasia in this condition is not clear. It is believed that adequate space in the fetal thorax and the movement of amniotic fluid into the fetal lungs is required for the normal development of lungs.

renal agenesis = oligohydramnios = pulmonary hypoplasia