The fetus and newborn infant are susceptible to a large number of diseases. Because many disorders have a different presentation and course in term as compared with preterm infants, they are considered separately (see Chap. 36, Mortality Rates of Preterm Infants). Disorders that are the direct consequence of maternal disease are discussed in chapters pertinent to specific maternal conditions. Because most perinatal infections arise as a result of maternal infection or colonization, they are considered in Chapters 58 and 59.
Respiratory Distress Syndrome
To provide blood gas exchange immediately following delivery, the lungs must rapidly fill with air while being cleared of fluid. Concurrently, pulmonary arterial blood flow must increase remarkably. Some of the fluid is expressed as the chest is compressed during vaginal delivery, and the remainder is absorbed through the pulmonary lymphatics. Sufficient surfactant, synthesized by type II pneumocytes, is essential to stabilize the air-expanded alveoli. It lowers surface tension and thereby prevents lung collapse during expiration (see Chap. 4, Lungs). If surfactant is inadequate, hyaline membranes form in the distal bronchioles and alveoli, and respiratory distress develops.
Although respiratory distress syndrome (RDS) is generally a disease of preterm neonates, it does develop in term newborns, especially in the setting of sepsis or meconium aspiration. In recent years, mortality rates from RDS have decreased because of antenatal corticosteroid and newborn surfactant therapy (Jobe, 2004; Martin, 2004). Male infants are more likely to develop RDS than females, and white infants are more frequently and severely affected than black infants.
In typical RDS, tachypnea develops, the chest wall retracts, and expiration is accompanied by grunting and nostril flaring. Shunting of blood through nonventilated lung contributes to hypoxemia and metabolic and respiratory acidosis. Poor peripheral circulation and systemic hypotension may be evident. The chest radiograph shows a diffuse reticulogranular infiltrate and an air-filled tracheobronchial tree—air bronchogram.
Respiratory insufficiency also can be caused by sepsis, pneumonia, meconium aspiration, pneumothorax, persistent fetal circulation, heart failure, and malformations involving thoracic structures, such as diaphragmatic hernia. Evidence is also accruing that there may be common mutations in surfactant protein production that cause RDS (Garmany and colleagues, 2008; Shulenin and associates, 2004).
With inadequate surfactant, alveoli are unstable, and low pressures cause collapse at end expiration. Pneumocyte nutrition is compromised by hypoxia and systemic hypotension. There may be partial persistence of the fetal circulation that leads to pulmonary hypertension and a relative right-to-left shunt. Eventually, there is ischemic necrosis of alveolar cells. 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 fibrin-rich protein and cellular debris line the dilated alveoli and terminal bronchioles. The epithelium underlying the membrane becomes necrotic. ...