An increase in the quantity of fluid in the pleural sacs was the most common indication of pleural irritation. The quantity varied from 50 to 500 c.c. of a clear or slightly turbid fluid. Not uncommonly this fluid was blood stained and evidence of superficial extravasation of blood could be recognized directly beneath the pleural membrane. These serous reactions accompanied the early acute stage, while hemorrhage was the accompaniment of the early period of the influenzal pneumonia when similar hemorrhages were found in the lung substance. The pleural reactions were almost entirely confined to the visceral pleura, and only in the very severe responses did we obtain a marked inflammatory reaction with hemorrhage upon the chest wall. Goodpasture and Burnett state that “there is commonly a moderate serous effusion in one or both pleural cavities amounting to 50 or 250 cubic centimeters. The fluid is clear and has the color of blood-stained serum. The pleural surfaces are smooth, shiny and wet, though occasionally a thin, granular fibrinous exudate may be seen by reflected light over limited areas. Often numerous small, red, discrete, or confluent pleural hemorrhages are present over consolidated portions, especially posteriorly on the surface of the lower lobes.” Where organisms other than the influenza bacillus had invaded the pleural sac and had been present for a sufficient time to obtain a reaction, the serous type of exudate observed in the early lesions changed to the turbid type of fluid accompanied by more or less fibrin deposit. There was one case where the intense reaction with fibrin and leucocytes gave rise to a new character to the pleural exudate, a fibrino-purulent pleurisy or empyema.
As we have subsequently learned the pleurisies developing late in the course of the influenza and those which persist after the pulmonary inflammation has passed are prone to be of a purulent kind. There have been a fair number of cases of empyema brought to our attention by the surgical department in the bacteriological laboratory of the hospital, subsequent to the wave of epidemic influenza. If one were to base his finding alone upon observations obtained in the operating room, he would be impressed by the fact that the pleurisy accompanying the epidemic of influenza is of a purulent type. On the other hand, if one were alone to consider the findings at the autopsy table during the five weeks of the epidemic, one would be of the opinion that the pleurisy is of very minor consequence and of a serous type. It is this changing picture which is particularly to be kept in mind. And our experience indicates that during the height of the influenzal lesions of the lung when the pulmonary lesions develop so rapidly that we obtain a pleural reaction closely resembling the inflammatory conditions in the lung and also containing bacteria not unlike the pulmonary flora. Dr. Holman has obtained the influenza bacillus and other varieties from the pleura during these early periods of the pulmonary inflammation. It is more than probable that just as in the infection of the lung tissue where there is a change in the type of the bacteria present, so, too, the flora of the pleura alters in the succeeding stages of the pulmonary reaction. In the late event of empyema we have not observed the influenza bacillus. The majority of the empyemas possess hemolytic streptococci and occasionally pneumococci.