The Preterm Newborn 637
Chapter 32 (p. 606). Suicient surfactant, synthesized by type II pneumocytes, is essential to stabilize the air-expanded alveoli. It expiration (Chap. 7, p. 133). If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, and RDS develops. Although respiratory distress syndrome is generally a disease of preterm neonates, it does develop in term newborns, especially with sepsis or meconium aspiration. In these cases, of meconium (Chap. 33, p. 619).
With inadequate surfactant, alveoli are unstable, and low pressures cause collapse at end expiration. Pneumocyte nutrition is compromised by hypoxia and systemic hypotension. Partial persistence of the fetal circulation may lead to pulmonary hypertension and a relative right-to-Ieft shunt. Eventually, alveolar cells undergo ischemic necrosis. When oxygen therapy is initiated, the pulmonary vascular bed dilates, and the shunt reverses. Protein-filled fluid leaks into the alveolar ducts, and the cells lining the ducts slough. Hyaline membranes composed of ibrin-rich protein and cellular debris line the dilated alveoli and terminal bronchioles. he epithelium underlying the membrane becomes necrotic. At autopsy, with hematoxylin-eosin staining of lung tissue, these membranes appear amorphous and eosinophilic, like hyaline cartilage. Because of this, respiratory distress syndrome is also termed hyaline membrane disease.
In typical RDS, tachypnea develops, the chest wall retracts, and expiration is accompanied by nostril flaring and by gruntingin an attempt to provide a positive end-expiratory pressure to prevent lung collapse. Shunting of blood through nonventilated lung contributes to hypoxemia and to metabolic and respiratory acidosis. Poor peripheral circulation and systemic hypotension may be evident. The chest radiograph shows a difuse reticulogranular infiltrate and an air-illed tracheobronchial tree-air bronchogram.
As discussed further in Chapter 33 (p. 619), respiratory insuiciency can also be caused by sepsis, pneumonia, meconium aspiration, pneumothorax, persistent fetal circulation, heart failure, and malformations involving thoracic structures, such as diaphragmatic hernia. Common mutations in surfactant protein production and the phospholipid transporter (ABCA3) contribute to RDS (Beers, 2017; Tredano, 2003; Wert, 2009).
An important factor inluencing survival is neonatal intensive care. Although hypoxemia prompts supplemental oxygen, excess oxygen can damage the pulmonary epithelium, retina, and other immature tissues. Despite this, advances in mechanical ventilation technology have improved neonatal survival rates. For example, continuous positive airway pressure (CPAP) prevents the collapse of unstable alveoli. This allows high inspired-oxygen concentrations to be reduced, thereby minimizing its toxicity. In an attempt to minimize the need for tracheal intubation and intermittent positive-pressure ventilation, CPAP has been studied in well-designed multicenter trials (Morley, 2008; SUPPORT Study Group, 2010b). An initial
CPAP strategy with subsequent selective surfactant use is a beneficial alternative to immediate intubation and surfactant for many neonates of extremely early gestational age (American
Academy of Pediatrics, 2014).