HYALINE MEMBRANE DISEASE
Saturday, August 16, 2008
Essentials of Diagnosis & Typical Features
The most common cause of respiratory distress in the preterm infant is hyaline membrane disease. The incidence increases from 5% of infants born at 35–36 weeks’ gestation to more than 50% of infants born at 26–28 weeks’ gestation. This condition is caused by a deficiency of surfactant. Surfactant decreases surface tension in the alveolus during expiration, allowing the alveolus to remain partly expanded and in that way maintaining a functional residual capacity. The absence of surfactant results in poor lung compliance and atelectasis. The infant must expend a great deal of effort to expand the lungs with each breath, and respiratory failure ensues (Figure 1–6).
Clinical Findings
Infants with hyaline membrane disease demonstrate all the clinical signs of respiratory distress. On auscultation, air movement is diminished despite vigorous respiratory effort. Chest x-ray demonstrates diffuse bilateral atelectasis, causing a ground-glass appearance. Major airways are highlighted by the atelectatic air sacs, creating air bronchograms. In the unintubated child, doming of the diaphragm and underexpansion occur.
Treatment
Supplemental oxygen, early intubation and ventilation, and placement of umbilical artery and vein lines are the initial interventions required. A ventilator that can deliver breaths synchronized with the infant’s respiratory efforts (synchronized intermittent mandatory ventilation) should be used if available. High-frequency ventilators are also available for rescue of infants doing poorly on conventional ventilation or who have air leak problems.
Three exogenous surfactants (colfosceril palmitate [Exosurf Neonatal], beractant [Survanta], and calf lung surfactant extract [Infasurf]) are approved in the United States by the Food and Drug Administration for use in infants with hyaline membrane disease. Surfactant replacement therapy, used both in the delivery room as prophylaxis and with established hyaline membrane disease as rescue, decreases the mortality rate in preterm infants and decreases air leak complications of the disease. During the acute course, ventilator settings and oxygen requirements are significantly less in surfactant-treated infants than in control subjects. The dose of the artificial surfactant Exosurf is 5 mL/kg intratracheally, the bovine-derived Survanta is 4 mL/kg, and the calf-derived Infasurf is 3 mL/kg. When the first dose is given in the delivery room to prevent hyaline membrane disease the usual dosing schedule is a total of two or three doses given 8–12 hours apart as long as the infant remains ventilated on over 30–40% inspired oxygen concentration. Rescue surfactant is given as two to four doses 8–12 hours apart. The first dose is administered as soon as possible after birth, preferably before 2–4 hours of age. As the disease process evolves, proteins that inhibit surfactant function leak into the air spaces, making surfactant replacement less effective. The second dose should be administered to infants who continue to require ventilation and more than 30% inspired oxygen concentration. A prophylactic strategy may offer some advantage in those infants born at 26 weeks’ gestation or less. For infants over 26 weeks’ gestation, early rescue therapy (as soon as a diagnosis of surfactant deficiency can be made) is the strategy of choice. The availability of surfactant replacement therapy has encouraged earlier intubation of infants with hyaline membrane disease. Surfactant replacement has also been used with some success in term infants with secondary surfactant deficiency resulting from pneumonia or meconium aspiration.
Antenatal administration of corticosteroids to the mother is an important strategy used by obstetricians to accelerate lung maturation. Infants whose mothers were given corticosteroids more than 24 hours prior to preterm birth have less respiratory distress syndrome and a lower mortality rate. Antenatal corticosteroids and exogenous surfactant administration after birth appear to have a synergistic effect on outcome.
- Tachypnea, cyanosis, and expiratory grunting.
- Poor air movement despite increased work of breathing.
- Chest x-ray showing hypoexpansion and air bronchograms.
The most common cause of respiratory distress in the preterm infant is hyaline membrane disease. The incidence increases from 5% of infants born at 35–36 weeks’ gestation to more than 50% of infants born at 26–28 weeks’ gestation. This condition is caused by a deficiency of surfactant. Surfactant decreases surface tension in the alveolus during expiration, allowing the alveolus to remain partly expanded and in that way maintaining a functional residual capacity. The absence of surfactant results in poor lung compliance and atelectasis. The infant must expend a great deal of effort to expand the lungs with each breath, and respiratory failure ensues (Figure 1–6).
Clinical Findings
Infants with hyaline membrane disease demonstrate all the clinical signs of respiratory distress. On auscultation, air movement is diminished despite vigorous respiratory effort. Chest x-ray demonstrates diffuse bilateral atelectasis, causing a ground-glass appearance. Major airways are highlighted by the atelectatic air sacs, creating air bronchograms. In the unintubated child, doming of the diaphragm and underexpansion occur.
Treatment
Supplemental oxygen, early intubation and ventilation, and placement of umbilical artery and vein lines are the initial interventions required. A ventilator that can deliver breaths synchronized with the infant’s respiratory efforts (synchronized intermittent mandatory ventilation) should be used if available. High-frequency ventilators are also available for rescue of infants doing poorly on conventional ventilation or who have air leak problems.
Three exogenous surfactants (colfosceril palmitate [Exosurf Neonatal], beractant [Survanta], and calf lung surfactant extract [Infasurf]) are approved in the United States by the Food and Drug Administration for use in infants with hyaline membrane disease. Surfactant replacement therapy, used both in the delivery room as prophylaxis and with established hyaline membrane disease as rescue, decreases the mortality rate in preterm infants and decreases air leak complications of the disease. During the acute course, ventilator settings and oxygen requirements are significantly less in surfactant-treated infants than in control subjects. The dose of the artificial surfactant Exosurf is 5 mL/kg intratracheally, the bovine-derived Survanta is 4 mL/kg, and the calf-derived Infasurf is 3 mL/kg. When the first dose is given in the delivery room to prevent hyaline membrane disease the usual dosing schedule is a total of two or three doses given 8–12 hours apart as long as the infant remains ventilated on over 30–40% inspired oxygen concentration. Rescue surfactant is given as two to four doses 8–12 hours apart. The first dose is administered as soon as possible after birth, preferably before 2–4 hours of age. As the disease process evolves, proteins that inhibit surfactant function leak into the air spaces, making surfactant replacement less effective. The second dose should be administered to infants who continue to require ventilation and more than 30% inspired oxygen concentration. A prophylactic strategy may offer some advantage in those infants born at 26 weeks’ gestation or less. For infants over 26 weeks’ gestation, early rescue therapy (as soon as a diagnosis of surfactant deficiency can be made) is the strategy of choice. The availability of surfactant replacement therapy has encouraged earlier intubation of infants with hyaline membrane disease. Surfactant replacement has also been used with some success in term infants with secondary surfactant deficiency resulting from pneumonia or meconium aspiration.
Antenatal administration of corticosteroids to the mother is an important strategy used by obstetricians to accelerate lung maturation. Infants whose mothers were given corticosteroids more than 24 hours prior to preterm birth have less respiratory distress syndrome and a lower mortality rate. Antenatal corticosteroids and exogenous surfactant administration after birth appear to have a synergistic effect on outcome.
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