RESPIRATORY DISTRESS SYNDROME INFANTS

Respiratory distress syndrome
An early complication of extreme prematurity is respiratory distress syndrome (RDS), which is caused by surfactant deficiency. Clinical signs include tachypnea (>60 breaths/min), cyanosis, chest retractions, nasal flaring, and grunting. Untreated RDS results in increased difficulty in breathing and an increased oxygen requirement over the first 24-72 hours of life. Chest radiographs reveal a uniform reticulogranular pattern with air bronchograms. Since the incidence of RDS correlates with the degree of prematurity, most ELBW infants (Extremely Low Birth Weight Infants) are affected. As a result of surfactant deficiency, the alveoli collapse, causing a worsening of atelectasis, edema, and decreased total lung capacity. Surfactants decrease the surface tension of the smaller airways so that the alveoli or the terminal air sacs do not collapse, which results in less need for supplemental oxygen and ventilatory support.

Common complications include air leak syndromes, CLD, and retinopathy of prematurity (ROP). Surfactant agents may be administered as prevention or prophylactic treatment or as rescue intervention after hyaline membrane disease (HMD) is established. Synthetic surfactants lack the proteins found in animal-derived surfactants and may not be as effective as the latter.

Available evidence based on cost analysis and clinical outcome suggests that surfactants should be administered routinely as prophylaxis in infants younger than 30 weeks' gestation. When used as prophylactic treatment, surfactants should be administered as soon after birth as possible. When administered as rescue treatment, a reasonable guideline is to administer surfactants when the infant reaches an arterial-to-alveolar (a/A) oxygen ratio of 0.22 or less. Typically, this is seen in an infant who requires greater than 35% oxygen to maintain a PaO2 of 50-80 mm Hg.

A major morbidity of premature birth is CLD, which is defined as receiving supplemental oxygen at 36 weeks' postmenstrual age, which has become more frequently accepted than the former definition of oxygen dependence beyond age of 28 days. BPD is included in the spectrum of CLD and was originally described by Northway et al in 1967 as the clinical sequelae of prolonged ventilation associated with radiographic and pathologic findings.

Lemons et al looked at the outcomes of 4438 infants in the National Institutes of Child Health and Human Development Neonatal Research Network (NICHD) registry with birth weights between 501-1500 g born from 1995-1996. They found that 52% of the infants in the 501- to 750-g group had CLD and 34% of the infants in the 751- to 1000-g group also were affected. Hack et al, looking at 333 ELBW infants born from 1992-1995 also found that of the 241 infants who survived to 20 months' corrected age, 40% (89) had CLD. CLD is also a risk factor for poor neurodevelopmental outcome. The exact reason is not clear but appears to be related to poor growth and prolonged episodes of hypoxia, which may contribute to neuronal injury.

Apnea of prematurity (AOP) is common in ELBW infants and is defined as cessation of breathing, typically lasting 15-20 seconds, with or without bradycardia or cyanosis. The incidence is inversely correlated with gestational age and weight. As many as 90% of infants weighing less than 1000 g at birth have AOP. Apnea can be caused by decreased central respiratory drive, which causes what is termed central apnea. Apnea also can be caused by an obstruction in which no nasal airflow occurs despite initiation of respiration, by a combination of central and obstructive apnea, or by mixed apnea, in which a lack of central respiratory stimulation is followed by airway obstruction.

In addition, apnea can be caused by hypoxia, sepsis, hypoglycemia, neurologic lesions, seizures, and temperature irregularities. Apnea is diagnosed clinically and can be detected via use of cardiorespiratory monitors and pulse oximetry. A pneumogram can be used to illustrate the number and severity of the apneic episodes, with or without bradycardia, in conjunction with a continuous electrocardiogram reading. Treatment of AOP includes nasal continuous positive airway pressure (CPAP) and use of pharmacologic agents, such as theophylline and caffeine citrate. Caffeine appears to be more effective in stimulating the central nervous system and has a wider therapeutic range than theophylline, and caffeine causes less tachycardia than theophylline. Theophylline is more efficacious than caffeine as a bronchodilator and diuretic.

Premature infants who are believed to have AOP at the time of discharge may be sent home with an apnea monitor. In one study, as many as 40% of babies born weighing less than 750 g went home with a monitor; however, the use of home apnea monitors remains controversial. AOP often persists beyond 40 weeks' corrected age, which is longer than was previously believed. AOP does not appear to be related to an increased incidence of sudden infant death syndrome.