One of the difficulties in attempting to find an explanation of either the hemorrhage or the huge edema1 of the lungs in influenzal pneumonia is that many different stages are encountered, most of them well along or late in the disease.
Very early in this attempt, attention was directed to the presence of a layer of fibrin close to the lining of the alveoli and ducti alveolares, often a very thin layer and in some instances the only fibrin present. With lobar pneumonia (by this term I mean a disease which is lobar pneumonia not only anatomically but also clinically), such a limitation of the fibrin deposit to the alveolar lining is not common.
Another outstanding condition is the necrosis of the alveolar lining epithelium, which appears early as a hyaline layer in which the outline of the separate cells is entirely lost, thus becoming a layer of necrotic