Retinopathy of prematurity (ROP) is caused by the acute and chronic effects of oxygen toxicity on the developing blood vessels of the premature infant’s retina. The completely vascularized retina of the term infant is not susceptible to ROP. ROP is a leading cause of blindness in very low birth weight infants (<1500 g). Excessive arterial oxygen tensions produce vasoconstriction of immature retinal vasculature in the first stage of this disease. Vaso-obliteration follows if the duration and extent of hyperoxia are prolonged beyond the time when vasoconstriction is reversible. Hypercarbia and hypoxia may contribute to ROP. The subsequent proliferative stages are characterized by extraretinal fibrovascular proliferation, forming a ridge between the vascular and avascular portions of the retina, and by the development of neovascular tufts. In mild cases, vasoproliferation is noted at the periphery of the retina. Severe cases may have neovascularization involving the entire retina, retinal detachment resulting from traction on vessels as they leave the optic disc, fibrous proliferation behind the lens producing leukokoria, and synechiae displacing the lens forward, leading to glaucoma. Both eyes usually are involved, but severity may be asymmetrical.
The incidence of ROP may be reduced by careful monitoring of arterial blood gas levels in all patients receiving oxygen. Although there is no absolutely safe Pao2 level, it is wise to keep the arterial oxygen level between 50 and 70 mm Hg in premature infants. Infants who weigh less than 1500 g or who are born before 28 weeks’ gestational age (some authors say 32 weeks) should be screened when they are 4 weeks of age or more than 34 weeks’ corrected gestational age, whichever comes first. Laser therapy or (less often) cryotherapy may be used for vitreous hemorrhage or for severe, progressive vasoproliferation. Surgery is indicated for retinal detachment. Less severe stages of ROP resolve spontaneously and without visual impairment in most patients.
Transient tachypnea of the newborn is a self-limited condition characterized by tachypnea, mild retractions, hypoxia, and occasional grunting, usually without signs of severe respiratory distress. Cyanosis, when present, usually requires treatment with supplemental oxygen in the range of 30% to 40%. Transient tachypnea of the newborn usually is noted in larger premature infants and in term infants born by precipitous delivery or cesarean section without prior labor. Infants of diabetic mothers and infants with poor respiratory drive as a result of placental passage of analgesic drugs are at risk. Transient tachypnea of the newborn may be caused by retained lung fluid or slow resorption of lung fluid. Chest radiographs show prominent central vascular markings, fluid in the lung fissures, overaeration, and occasionally a small pleural effusion. Air bronchograms and a reticulogranular pattern are not seen; their presence suggests another pulmonary process, such as RDS or pneumonia.
Meconium-stained amniotic fluid is seen in 15% of predominantly term and post-term deliveries. Although the passage of meconium into amniotic fluid is common in infants born in the breech presentation, meconium-stained fluid should be considered clinically as a sign of fetal distress in all infants. The presence of meconium in the amniotic fluid suggests in utero distress with asphyxia, hypoxia, and acidosis.
Aspiration of amniotic fluid contaminated with particulate meconium may occur in utero in a distressed, gasping fetus; more often, meconium is aspirated into the lung immediately after delivery. Affected infants have abnormal chest radio-graphs, showing a high incidence of pneumonia and pneumothoraces.