During the acute phase of RDS, hypoxia, hypercapnia, and acidosis lead to pulmonary arterial vasoconstriction. The pulmonary and systemic pressures may be equal, and flow through the ductus may be small or bidirectional. When RDS improves and pulmonary vascular resistance declines, flow through the ductus arteriosus increases in a left-to-right direction. Significant systemic-to-pulmonary shunting may lead to heart failure and pulmonary edema. Excessive intravenous fluid administration may increase the incidence of symptomatic PDA. The infant’s respiratory status deteriorates because of increased lung fluid, hypercapnia, and hypoxemia.
Clinical manifestations of a PDA usually become apparent on day 2 to 4 of life. Because the left-to-right shunt directs flow to a low-pressure circulation from one of high pressure, the pulse pressure widens; a previously inactive precordium shows an extremely active precordial impulse, and peripheral pulses become easily palpable and bounding. The murmur of a PDA may be continuous in systole and diastole, but usually only the systolic component is auscultated. Heart failure and pulmonary edema result in rales and hepatomegaly. A chest radiograph shows cardiomegaly and pulmonary edema; a two-dimensional echocardiogram shows ductal patency; and Doppler studies show markedly increased left-to-right flow through the ductus.
Treatment of a PDA during RDS involves initial fluid restriction and diuretic administration. If there is no improvement after 24 to 48 hours, a prostaglandin synthetase inhibitor, indomethacin or ibuprofen, is administered. Contraindications to using indomethacin include thrombocytopenia (platelets <50,000/mm3), bleeding, serum creatinine measuring more than 1.8 mg/dL, and oliguria. Because 20% to 30% of infants do not respond initially to indomethacin and because the PDA reopens in 10% to 20% of infants, a repeat course of indomethacin or surgical ligation is required in some patients.
Assisted ventilation with high peak inspiratory pressures and positive end-expiratory pressures may cause overdistention of alveoli in localized areas of the lung. Rupture of the alveolar epithelial lining may produce pulmonary interstitial emphysema as gas dissects along the interstitial space and the peribronchial lymphatics. Extravasation of gas into the parenchyma reduces lung compliance and worsens respiratory failure. Gas dissection into the mediastinal space produces a pneumomediastinum, occasionally dissecting into the subcutaneous tissues around the neck, causing subcutaneous emphysema.
Alveolar rupture adjacent to the pleural space produces a pneumothorax (Fig. 61-3). If the gas is under tension, the pneumothorax shifts the mediastinum to the opposite side of the chest, producing hypotension, hypoxia, and hypercapnia.
Figure 61-3 Pneumothorax. Right-sided hyperlucent pleural air is obvious. The findings of linear interstitial air and the resultant non-compliant but collapsed lung are noted. (From Heller RM, Kirchner SG: Advanced exercises in diagnostic radiology: the newborn, Philadel-phia, WB Saunders, 1979.)
The diagnosis of a pneumothorax may be based on unequal transillumination of the chest and may be confirmed by chest radiograph. Treatment of a symptomatic pneumothorax requires insertion of a pleural chest tube connected to negative pressure or to an underwater drain. Prophylactic or therapeutic use of exogenous surfactant has reduced the incidence of pulmonary air leaks.