Pulmonary Pathology Online
Pathology of Neonatal Respiratory Distress Syndrome
Infant Respiratory Distress Syndrome; Hyaline membrane disease.
The respiratory distress syndrome is one of the major clinical problems affecting premature babies.
Incidence - RDS occurs primarily in the immature lung.
(1) 60% of cases occur in infants born at less than 28 weeks’ gestation
(2) 5% of cases occur in infants born at less than 37 weeks’ gestation.
Causes of Neonatal Respiratory Distress syndrome:
Aspiration during birth of blood and amniotic fluid ; Brain injury with failure of central respiratory centers ; Asphyxiating coils of umbilical cord around the neck of the infant; Excessive maternal sedation.
Idiopathic respiratory distress syndrome is also known as hyaline membrane disease.
Although the exact pathogenesis of the syndrome is not clear, the evidence indicates that it is related to or caused by immaturity of the lung and inadequate release or storage of surfactant by type II pneumocytes.
At term the fetal lungs are anatomically mature and functionally prepared to adapt for the transition from an intrauterine to extrauterine environment.
The alveoli are fully formed by the 25th week, and by the 31st week the type II pneumocytes already produce adequate amounts of surfactant, which still differs from that of the term newborn.
The bronchial and pulmonary circulations are characterized in utero by high pressure and low flow.
This situation leads to a high pulmonary resistance, which exceeds the systemic resistance.
Most of the blood circulates through the placenta, and only 5% to 10% perfuses the lungs.
Neuromuscular control of respiration is effectively established long before birth.
External compression of the thorax during passage through the vaginal canal ejects some of the amniotic fluid from the lungs and also leads to subsequent recoil of the chest wall.
These actions facilitate the first active inspiratory movement and the entry of air into the lungs, which inflates the alveoli.
The amniotic fluid is exhaled and resorbed, leaving the alveoli coated with surfactant.
The sequence of events decreases the external compression of the capillaries in the alveolar walls, and the pulmonary blood flow suddenly rises.
Increased alveolar oxygen tension further expands the precapillary vascular space through dilatation of arteries and arterioles.
Decreased vascular pressure in the entire pulmonary circulation, accompanied by an enormous influx of blood from the right ventricle, further facilitates the absorption of alveolar fluid and results in increased lymph flow and increased flow of oxygenated blood into the left atrium.
These events, followed in early infancy by the closure of the ductus arteriosus, lead to the transformation of the fetal high-resistance, low-flow pulmonary circulation into the adult low-resistance, high-flow circulation.
Disturbances in lung maturation and in the various transitions from fetal to adult pulmonary circulation, mechanical factors, and disturbances in the neural control of respiration all cause respiratory distress in newborn.
Among the identifiable causes are incidents affecting the respiratory center in the central nervous system.
For example, oversedation of the mother during the delivery may affect the fetal brain.
Traumatic brain injury of the fetus at birth, with bleeding into or ischemic necrosis of the respiratory centers, prevents normal respiration.
Asphyxia may be due to mechanical factors, birth trauma, or umbilical cord strangulation.
Metabolic disorders in the mother- for instance, diabetes mellitus-may impair respiration.
Blockage of the air passages due to particulate matter, blood clots, or aspirated meconium from the amniotic fluid can also cause respiratory distress.
However, more common than all other forms of respiratory distress is the idiopathic syndrome, p