Sawardekar (2005) conducted a study to establish the prevalence of major congenital malformations in children born during a 10-year period in an Omani hospital in Nizwa. Of the 21,988 total births in the hospital, three children were born with Lung Hypoplasia.

Rosenak et al. (1991) reported a term amelic female infant born to an apparently non-consanguineous Muslim couple. The parents had four other normal children. Afterwards, in 2 subsequent pregnancies, 2 amelic fetuses were diagnosed by transabdominal ultrasonography in the 18th and 12th week of gestation. Pregnancies were terminated and on autopsy both amelic fetuses had severe lung hypoplasia and aplasia of the peripheral pulmonary vessels. The first fetus also had apparently low-set ears and micrognathia, whereas the last had hydrocephaly and left cleft lip beside the lung hypoplasia and aberrant pulmonary artery.

Al-Hathal et al. (1998) conducted a retrospective analysis of all neonates with respiratory distress at birth due to congenital diaphragmatic hernia (CDH) who were treated with neither extracorporeal membrane oxygenation nor nitric oxide being used. Analysis included all neonates with CDH and respiratory distress at birth who were treated between August 1, 1992 through March 1, 1997. There were 21 patients, 11 male and 10 female. There were 17 full-term and 4 premature infants and surgery was performed in 18 infants. Al-Hathal et al. (1998) reported that one infant died during preoperative stabilization from severe pulmonary hypoplasia and pulmonary hypertension and one infant died postoperatively from the same conditions.

Al-Senan et al. (2003) reported a family with one proven case and two suspected cases of isolated congenital acinar dysplasia. The index case was a female infant born at 37 weeks gestation to healthy and unrelated parents. Antenatal ultrasound (US) examination in the 32nd week of gestation showed mild oligohydramnios with no congenital malformations. There was no history of premature rupture of membrane or intrapartum fetal distress. The mother had one abortion, one intrauterine fetal death, and 2 infantile deaths. The remaining siblings are alive and well. Of the 2 infantile deaths, the first infant was a female, product of a full-term normal delivery, which developed severe respiratory failure of unknown etiology shortly after birth, and died at 2 months of age. The 2nd infant, also a female, developed severe respiratory failure soon after birth and died at 75 days on mechanical ventilator. At 6 hours of age, the index infant developed progressively severe respiratory distress with hypoxemia and hypercapnia, which required intubation and mechanical ventilation. The chest x-ray showed reduced lung volume and increased pulmonary vascularity. Gradually, the condition of the infant worsened that requires higher ventilator settings. The infant did not tolerate trials of weaning from mechanical ventilation, and each time showed deterioration despite the administration of steroids to facilitate weaning. Microscopically, the lung biopsy showed pulmonary hypoplasia with arrest of lung growth at the acinar stage, and the electron microscopy showed plenty of lamellar bodies in type II peumocytes. Shortly thereafter, at the age of 3 months, the infant expired. Al-Senan et al. (2003) reviewed the world cases with primary pulmonary hypoplasia as a result of congenital acinar dysplasia and suggested that these observations may raise the possibility of X-linked dominant type of inheritance for this disease.