We have previously intimated that the œdema present in the early stages of the reaction is to be looked upon as an inflammatory œdema or better as a true serous exudate, and must not be confused with the transudation of fluids in non-inflammatory conditions. We have on several occasions collected the fluid expressed from the soggy lungs and have made some determinations of their chemical qualities. The difficulty immediately arises in separating the materials arising from cellular degeneration from the natural constituents of the serous exudate. We were unable to obtain specimens in which laked blood was not present, so that even though the cellular constituents and fibrin were removed, decomposition products could not be separated. The analyses, however, gave a differentiation from the transudate seen in renal and cardiac conditions.
During the period of the accumulation of this inflammatory fluid the clinician could often recognize a profuse watery exudate within the lung or even observed an abundant serous discharge arising in bronchi and trachea. At times the quantity of expectoration was great. Frothy serous fluid accumulated in the air passages and would periodically be expectorated. At other times the hemorrhage was of quite serious extent and the patient would suddenly bring up several mouthfuls or more of bright blood. This pulmonary hemorrhage was without manifestations different from the acute illness with cyanosis of other individuals. The two most acute cases, which we have referred to above, were of this kind, both of them having marked hæmoptysis with the loss of upwards of a pint of blood at a time.
The early pulmonary lesion which we have described, we have called acute serous pneumonia and acute hemorrhagic pneumonia (or we might speak of it as an acute sero-hemorrhagic pneumonia) and is one which is distinctive for epidemic influenza. The cut surface of a lobe involved in this reaction is wet, glassy, meaty and oozes much blood-stained fluid. It contains no visible fibrin and presents no characters of a “cellular consolidation.” As a serous inflammation of the lung it is unique. The further remarkable character to the pulmonary lesion is that in advancing through the other stages, it never passes through a stage of “red hepatization.” Here again we have a distinctive difference from the pneumococcus-pneumonia. From what we have previously said about the nature of this early acute inflammation of the lung in this disease it is apparent that red hepatization has no place in its process. The stage of red hepatization is attained only when the inflammatory reaction is accompanied by certain constituents in the exudate, which upon coagulation (separation out of the fibrin) renders the lobe dry and solid, while there is a sufficient abundance of red blood cells and congestion to maintain a dark red color. The hepatized lung on section is dry, more or less granular, containing fibrin, red cells and leucocytes within the alveoli. Extensive œdema is unusual except in the cases of hypostatic pneumonia, which in well marked cases bears some resemblance to the gross appearance of the early influenza pneumonia. We have not encountered a single case of the red meaty lung of influenza which showed evidence of true red hepatization in the gross.