Mendelsohn G, Hutchins G M
Am J Dis Child. 1977 Nov;131(11):1220-3. doi: 10.1001/archpedi.1977.02120240038008.
We describe a case of extreme primary pulmonary hypoplasia. No other congenital anomalies and none of the conditions known to be associated with pulmonary hypoplasia were present. Pregnancy had been complicated by substantial polyhydramnios. The hypoplasia was due to a marked deficiency of the respiratory parenchyma in the presence of normal upper airways and bronchi. Virtually no parenchymal development had occurred and there were very few bronchioles, alveolar ducts, and alveoli. The changes differ from those seen in pulmonary hypoplasia secondary to congenital diaphragmatic hernia, bilateral renal agenesis, anomalies of the urinary outflow tracts, and malformations of the thoracic cavity, in which the pulmonary hypoplasia appears to be compressive in nature. While neither the etiology or pathogenesis of the pulmonary hypoplasia are apparent in this case, the presence of substantial polyhydramnios during pregnancy suggests the possibility that the developing lungs may offer an important surface area for reabsorption and recycling of constituents of amniotic fluid.
我们描述了一例极严重的原发性肺发育不全病例。未发现其他先天性异常,也不存在已知与肺发育不全相关的任何情况。孕期并发大量羊水过多。肺发育不全是由于上呼吸道和支气管正常的情况下呼吸实质显著缺乏所致。实际上几乎没有实质发育,细支气管、肺泡管和肺泡极少。这些改变与先天性膈疝、双侧肾缺如、尿路异常及胸腔畸形继发的肺发育不全不同,后者的肺发育不全本质上似乎是受压所致。虽然该病例中肺发育不全的病因和发病机制均不明确,但孕期大量羊水过多提示,发育中的肺可能为羊水成分的重吸收和再循环提供了重要的表面积。