Pathophysiology of Respiratory Distress Syndrome

In infants with Respiratory Distress Syndrome, where an inability to inflate the lungs and alvoeli open. Respiratory Distress Syndrome in infants who are not mature cause respiratory failure due to an immature chest wall, lung parenchyma, and an immature capillary endothelium that cause lung collapse at end expiration.

In infants with respiratory distress syndrome caused by a decrease in the amount of surfactant or surfactant qualitative change, thus risking the inability to expand the alveoli. Ekstrathoracic change in pressure and decrease in air exchange.

Naturally improvement started after 24-48 hours. Cells that are defective will be replaced. Hyaline membrane of the cell that contains necrotic debris caught in proteinaceous serum filtrate (filter serum proteins), in phagocytes by macrophages. Cuboidal cells put on the damaged alveolar epithelium and airway, then there is a development of new capillary cells in the alveoli. Synthetic surfactants start again and then help repair the alveoli for development.

Factors that facilitate the occurrence of RDS in infants caused by alveoli pematur still small so difficult to grow, the development is less than perfect because of the wall of the thorax is still weak, the production of surfactant is less than perfect. Deficiency of surfactant resulted in the collapse of the alveoli so the lungs become stiff. This causes physiological changes in the lungs so that the power development of the lung (compliance ) decreased 25 % from normal, breathing becomes heavy, intrapulmonary shunting increased and became severe hypoxemia, hypoventilation which causes respiratory acidosis. It is known that the surfactant contains 90 % phospholipids and 10 % proteins, lipoproteins, this function lowers the surface tension and keep the alveoli remain inflated. Macroscopically, lungs filled with air and does not seem like a reddish colored hearts. Therefore lungs requires high opening pressure to inflate. Histologically, the presence of extensive atelectasis of the distal part of the air cavity causing interstitial edema and congestion of the alveoli walls causing desquamation of alveolar epithelial type II cells, alveolar duct dilatation, but the alveoli become interested because of the presence of this surfactant deficiency.

With the progressive atelectasis with barotrauma, or volutrauma and oxygen toxicity, causing damage to endothelial and epithelial cells of the distal part of the respiratory path, thus causing exudate fibrin matrix derived from the blood. Hyaline membrane covering the alveoli formed in one half hour after birth. This healing process is complex ; immature infants and suffered severe pain and infants born to mothers with chorioamnionitis often continues into reticulogranular as atelectasis and air bronchogram.

Progressive clinical symptoms of RDS is : 60x/menit above tachypnea, expiratory grunting, subcostal and intercostal retractions, cyanosis, nasal pharynx in extremely premature infants ( LBW ) may apat continue apnea, and or hypothermia. In the RDS without complications then will return in lung surfactant at the age of 36-48 hours. Symptoms can worsen gradually in 24-36 hours. Furthermore, if the situation is stable within 24 hours then it will get better in 60-72 hours and cured at the end of the first week.