3A-S4-4

FUNCTIONAL SURFACTANT DEFICIENCY IN THE NEWBORN

Ogawa Y, Shimizu H, Takasaki J, Arakawa H, Nakamura T, Obata M

Department of Pediatrics, and Center for Maternal, Fetal and Neonatal Medicine, Saitama Medical Center, Saitama Medical School, Kawagoe 350-8550, Japan

Functional surfactant deficiency can be detected in major neonatal diseases such as meconium aspiration syndrome (MAS), hemorrhagic lung edema, acute (or adult) respiratory distress syndrome (ARDS), pneumonia, chronic lung disease (CLD), and congenital alveolar proteinosis (CAP). In some of these conditions, surfactant production may also be inhibited, but major pathology resides in the functional deficiency.

There are 3 major mechanisms for surface activity by inhibitors, such as plasma proteins, meconium, cytokines, chemical mediators, proteolytic enzymes, oxygen radicals, nitric oxide. The second mechanism is the acceleration of surfactant subtype conversion from surface activity large vesicle to less surface activity small vesicle along with the cyclic expansion and contraction of alveoli. This subtype conversion is accelerated by excessive alveolar expansion (volutrauma), meconium and proteolytic enzyme. The third one is the abnormal composition of pulmonary surfactant due to genetic anomaly such as surfactant protein mice have also shown the important roles of surfactant specific proteins not only on the surface activity but also on the innate defense mechanism of the lung.

Different approaches rather than surfactant replacement with multiple doses should be pursued for surfactant dysfunction. For instance, tracheobronchial lavage for MAS with surfactant-TA solution, 60mg/10ml/Kg, in 5 divided doses by changing body position, resulted in the dramatic improvements of a/APO and compliance.

For the protection from the infection, the surfactant preparation containing SP-A and SP-D is preferable. And in the near future, tailor-made surfactant preparation will be adopted for the different purposes and different disease states.