ABSTRACT

Hyaline membrane disease (HMD) has been recognized for more than 80 years, and it was Hochheim 1 who first described the condition in 1903. Gruenwald, 2 in 1947, first proposed that extensive pulmonary atelectasis played an important role in the pathogenesis of HMD, but it was not until 1959 that Avery and Mead 3 demonstrated that pulmonary extracts of newborns who died of HMD could not decrease surface tension below 20 dyn/cm, thus explaining pulmonary atelectasis. Adams et al., studying premature animals in 1963, 4 then premature human newborns with HMD in 1970, showed that in these neonates the loss of normal properties of pulmonary extracts was correlated with a deficiency of tensioactive phospholipids in the pulmonary surfactant. Since these findings, and despite great progress in the management of premature births, the incidence of HMD in infants with a low gestational age (GA) remains elevated (80% at less than 28 weeks, 60% between 28 and 30 weeks, 20% between 31 and 32 weeks, and 5% after 32 weeks). In addition, and despite constant progress in techniques for management of such newborns, HMD remains an important factor in neonatal mortality — about 1 neonatal death per 1000 live births in the U.S. — and an especially important factor in respiratory and nonrespiratory morbidity for infants who survive.