Sir: We have read with interest the article by Hoekstra and Boer [1] and would like to present a similar case with a different cause of oligohydramnios. A 23-yearold, gravida 2, para 1 woman was seen at a hospital because of threatened abortion at 7 weeks gestation. At 10 weeks gestation, ultrasonography revealed a high-echo mass in the placenta. Follow up ultrasonography at 14 weeks gestation revealed that the mass had enlarged to equal the fetal size and was accompanied by oligohydramnios. Fetal movements were reported to be decreased, though fetal breathing movements were not reported. When the woman was admitted to hospital because of massive genital bleeding at 28 weeks gestation, ultrasonography failed to demonstrate the placental mass or the amniotic fluid space. She underwent caesarean section at 29 weeks gestation for suspected amniotic infection 4 days after rupture of the membranes. A female baby weighing 1125g was delivered with Apgar scores of 1 and 5 at 1 and 5 min, respectively. Examination of the placenta (150g) revealed abscence of amniotic membranes, as well as a 100g haematoma, the histological examination of which suggested a subchorionic haematoma. Amnion nodosum or inflammatory change was not seen. The infant was intubated and transfered to NICU of Kanagawa Children's Medical Center. On admission, deformities with Potter facies, right equinovarus, left valgus, and bell-shaped thorax were noted. Chest X-ray films showed clear lung fields without signs of pulmonary hypoplasia. Initial respiratory settings were very severe, FiOa of 1.0 and mean airway pressure of 20 cmH20 which improved to 0.5 and 10, respectively, 2h later. She was exubated at 69h after birth. Urination started 3 h after birth, renal ultrasonography was normal. At age 2.5 years she was mentally and physically normal and the deformities of the feet had been successfully corrected. McInthosh [2] reported four cases of "dry lung syndrome" after oligohydramnios due to prolonged rupture of the membranes. In three of them onset of membranes' rupture was as late as 31, 24, or 21 weeks gestation. In all cases including our own clinical course was benign and quite similar to that reported by Hoekstra and Boer; i.e., initial asphyxia and severe cyanosis which rapidly improved. Right-to-left shunt via the ductus arteriosus was suspected in Hoekstra and Boer 's case. We think that a small number of infants delevered after prolonged oligohydroamnios do not have lethal pulmonary hypoplasia, although changes in their external features follow those of the Potter sequence. Initial severe cyanosis seems to be due to persistent pulmonary hypertension, as all of the infants had ashyxia and cardiorespiratory failure which rapidly improved. Neonatologists should not relinquish resuscitating these babies, because their prognosis is good if they are skillfully treated for asphyxia and for subsequent transient pulmonary hypertension.