The lungs of<unk> s with<unk><unk><unk>  are developmentally deficient in a material called surfactant, which helps prevent the collapse of the terminal air spaces (the future site of alveolar development) throughout the normal cycle of inhalation and exhalation. This deficiency of surfactant is related to inhibition from the insulin that is produced in the newborn, especially those of diabetic mothers. Pulmonary surfactant is a complex system of lipids, proteins and glycoproteins that is produced in specialized lung cells called Type II cells or Type II pneumocytes. The surfactant is packaged by the cell in structures called lamellar bodies, and extruded into the air spaces. The lamellar bodies then unfold into a complex lining of the air space. This layer reduces the surface tension of the fluid that lines the alveolar air space. Surface tension is responsible for approximately 2/3 of the inward elastic recoil forces. In the same way that a bubble will contract to give the smallest surface area for a given volume, so the air/water interface means that the liquid surface will tend toward being as small as possible, thereby causing the air space to contract. By reducing surface tension, surfactant prevents the air spaces from completely collapsing on exhalation. In addition, the decreased surface tension allows reopening of the air space with a lower amount of force. Therefore, without adequate amounts of surfactant, the air spaces collapse and are very difficult to expand. Microscopically, a pulmonary surfactant-deficient lung is characterized by collapsed air spaces alternating with hyperexpanded areas, vascular congestion, and, in time, hyaline membranes. Hyaline membranes are composed of fibrin, cellular debris, red blood cells, rare neutrophils and macrophages. They appear as an eosinophilic, amorphous material, lining or filling the air spaces and blocking gas exchange. As a result, blood passing through the lungs is unable to pick up oxygen and unload carbon dioxide. Blood oxygen levels fall and carbon dioxide rises, resulting in rising blood acid levels and hypoxia. Structural immaturity, as manifested by a decreased number of gas exchange units and thicker walls, also contributes to the disease process. Therapeutic oxygen and positive-pressure ventilation, while potentially life-saving, can damage the lung.
Infant respiratory distress syndrome
Alveolar capillary dysplasia
Neonatal sepsis
Neonatal meningitis
Shaken baby syndrome
Apnea of prematurity
Transient tachypnea of the newborn
Omphalitis of newborn