Abstract
IT has been demonstrated that pulmonary hyaline membranes in newborn infants have a basic fibrin composition that resembles a plasma clot.1 , 2 The presence of fibrin in the lungs of these infants is considered by some investigators to be the end result of failure of the left side of the heart and pulmonary edema.3 4 5 6 7 8 9 Others believe that a more important factor is the inability of certain fetuses to dissolve intra-alveolar fibrin deposits,10 11 12 13 and it has been postulated that this fibrin may be precipitated from a capillary transudate during the formation of a portion of amniotic fluid by the lungs.12 In earlier . . .