Respiratory Distress Syndrome

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Respiratory Distress Syndrome

Respiratory distress syndrome (RDS) is the most common cause of respiratory failure in the preterm infant. Over the past several decades, a number of names have been used to identify infants with RDS (Box 34-1). A common thread running through most of the names is the term “respiratory distress,” which characterizes an immature lung disorder in a preterm infant caused by inadequate pulmonary surfactant. RDS is a major cause of morbidity and mortality in the premature infant born after less than 37 weeks’ gestation. The introduction of exogenous surfactant therapy has greatly improved the clinical course of this disorder and reduced the morbidity and mortality rates.

Anatomic Alterations of the Lungs

On gross examination, the lungs of an infant with RDS are dark red and liver-like. Under the microscope the lungs appear solid because of countless areas of alveolar collapse. The pulmonary capillaries are congested, and the lymphatic vessels are distended. Extensive interstitial and intraalveolar edema and hemorrhage are evident.

In what appears to be an effort to offset alveolar collapse, the respiratory bronchioles, alveolar ducts, and some alveoli dilate. As the disease intensifies, the alveolar walls become lined with a dense, rippled hyaline membrane identical to the hyaline membrane that develops in acute respiratory distress syndrome (ARDS) of the adult patient (see Chapter 27). The membrane contains fibrin and cellular debris.

During the later stages of the disease, leukocytes are present, and the hyaline membrane is often fragmented and partially ingested by macrophages. Type II cells begin to proliferate, and secretions begin to accumulate in the tracheobronchial tree. The anatomic alterations in RDS produce a restrictive type of lung disorder (see Figure 34-1).

As a consequence of the anatomic alterations associated with RDS, babies with this disorder often develop hypoxia-induced pulmonary arterial vasoconstriction and vasospasm, causing a state of transient pulmonary hypertension. This results in blood shunting from right to left through the ductus arteriosus and foramen ovale. Occasionally, intrapulmonary shunting may also occur. As a consequence, the blood flow is diverted away from the lungs (pulmonary hypoperfusion), which worsens the hypoxemia. It should be noted that if this condition does not resolve within 24 hours or so, shunting will begin to flow from left to right through the patent ductus arteriosus. This condition can lead to excessive lung fluid, pulmonary hyperperfusion, and pulmonary edema.

The major pathologic or structural changes associated with RDS are as follows:

Etiology and Epidemiology

Although the exact cause of RDS is controversial, the most popular theory suggests that the early stages of RDS develop as a result of (1) a pulmonary surfactant abnormality or deficiency, and (2) pulmonary hypoperfusion evoked by hypoxia. The pulmonary hypoperfusion evoked by hypoxia is probably a secondary response to the surfactant abnormality. The probable sequence of steps in the development of RDS is as follows:

1. Because of the pulmonary surfactant abnormality, alveolar compliance decreases, resulting in alveolar collapse.

2. The pulmonary atelectasis causes the infant’s work of breathing to increase.

3. Alveolar ventilation decreases in response to the decreased lung compliance and infant fatigue, causing the alveolar oxygen tension (Pao2) to decrease.

4. The decreased Pao2 (alveolar hypoxia) stimulates a reflex pulmonary vasoconstriction.

5. Because of the pulmonary vasoconstriction, blood bypasses the infant’s lungs through fetal pathways—the patent ductus and the foramen ovale.

6. The lung hypoperfusion in turn causes lung ischemia and decreased lung metabolism.

7. Because of the decreased lung metabolism, the production of pulmonary surfactant is reduced even further, and a vicious cycle develops (Figure 34-2).

It is estimated that approximately 30,000 cases of RDS occur annually in the United States. RDS is the leading cause of death in preterm infants. About 50% of the neonates born at 26 to 28 weeks’ gestation develop RDS. About 25% of the babies born at 30 to 31 weeks’ gestation develop RDS. RDS occurs more often in male babies and is usually more severe than in female babies. The higher incidence and severity of RDS in male infants is explained by the increased circulating androgens in males—which, in turn, slows the maturation of the infant’s lung. The delayed lung maturation results in immature alveolar type II cells (granular pneumocytes) and a decreased pulmonary surfactant production.

RDS is also more commonly seen in infants of diabetic mothers (the high fetal insulin levels decrease lung surfactant and structural maturation), white preterm babies compared with black preterm infants, and infants delivered by cesarean. RDS is also associated with low birth weight (1000 to 1500 g), multiple births, prenatal asphyxia, prolonged labor, maternal bleeding, and second-born twins.

Diagnosis

There are three primary tests that can be performed to determine the lung maturity of the fetus: the lecithin/sphingomyelin ratio, the presence of phosphatidylglycerol (PG), and, more recently, the surfactant/albumin ratio.

The lecithin/sphingomyelin ratio (L : S ratio) is commonly used to test lung maturity. Lecithin, also called dipalmitoyl phosphatidylcholine, is the most abundant phospholipid found in surfactant. When the concentration of lecithin is two times greater than that of sphingomyelin—an L : S ratio of 2 : 1—the infant’s lung maturity is likely great enough that the lungs will produce adequate pulmonary surfactant at birth. Most infants with an L : S ratio less than 1 : 1 develop RDS. The L : S ratio is not reliable in pregnancies associated with diabetes and Rh isoimmunization.

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