To a certain degree we were able to analyze the types of the lesions as they occurred in the different stages and progress of the pulmonary inflammation. Briefly, these were as follows: the earliest stage of congestion following rapidly upon the infection from the bronchi was followed by (1) inflammatory œdema, (2) hemorrhage, (3) cellular exudate (a. mononuclear cells, b. leucocytes, c. interstitial infiltration) and (4) resolution or organization, abscess, infarct and gangrene. The majority of our cases died during the stages of congestion, hemorrhage or early purulent infiltration. In the early stages the amount of fibrin was small or entirely absent, later, with the appearance of leucocytes, some fibrin was present.
For the estimation of the time elapsing between the onset of the pneumonia and death we are dependent upon the clinician. This is often quite difficult to do, in as much as with a primary respiratory disease, such as epidemic influenza represents, it is very difficult to determine the time when there is a transition from the inflammatory process of the upper respiratory tubes to that of the pulmonary tissue. In many of the cases where from the onset there was intense prostration and every evidence of marked intoxication the clinical manifestations of localized processes taking place in the respiratory system were very much in the background and often of insidious progress. In four of our cases it appeared as if the pulmonary manifestations had made their appearance with the first sudden and severe onset of the influenza. On the other hand, also, the clinical signs and symptoms of lung involvement were different from those of frank lobar pneumonia. We would, from our experience at the autopsy table, say that where in the cases of epidemic pneumonia there are present the signs of pulmonary consolidation like those of true lobar pneumonia, that there has been an antecedent period of a pulmonary lesion which passed unrecognized by the clinician. To more clearly state the case, whereas in lobar pneumonia the stage of congestion preceding the stage of red hepatization gives rise to no signs whereby the clinician can indicate the time of its onset or determine the time when it has passed into the succeeding stage, and moreover, the stage of congestion is of short duration to be measured in a period of a few hours, this stage in epidemic influenza though equally indefinite in its clinical manifestations is much prolonged, lasting not only a period of hours but even a period of several days. It is this pulmonary state which is difficult or even impossible to recognize in the living. All gradations of it occur and the clinician can only broadly suggest from all the evidence at hand, the period when inflammation with definite exudate began in the lung. In as much as the total length of illness of a number of cases was only three, four and five days, whereas there was nothing at the onset to suggest pulmonary involvement, we can estimate approximately, at least, the duration of the lung condition. This makes it possible to give a relative estimate of the character of the lesions present at different periods of time. The outstanding finding, as we will discuss again, was that a distinct and peculiar pulmonary reaction was primarily imposed upon the lung, which made its appearance at periods different from those of frank lobar pneumonia.
We were repeatedly surprised at finding death to have occurred during the stage of acute congestion with some hemorrhage and inflammatory œdema of lung and in the absence of any sign of grey hepatization or purulent infiltration. In many of these cases the involved areas of lung though heavy and œdematous, were still partly air-containing and the amount of lung involvement was insufficient, on the basis of mechanical interference, in accounting for the severity of the clinical symptoms and the fatal outcome. This must have impressed everyone dealing with the autopsies during the acute epidemic. It immediately suggests that in some cases at least the pulmonary lesion, in as far as incapacitating the external respiratory system, was not the sole or even the important cause of death, but that a condition of intoxication, borne out by the evidence of damage in muscles, blood and kidney is a large factor of danger in this disease.
We shall briefly describe the important pulmonary findings as we have met with them in the successive stages of influenza-pneumonia. This, we hope, will make clear the interpretation of the pathology of the lung lesion of the epidemic as it came under our observation.
The earliest pulmonary lesion which we encountered was one of congestion, inflammatory œdema and hemorrhage. These three conditions were usually present at the same time and were found in the height of intensity in all of the cases dying within the first four days of illness. During this early period these manifestations of inflammation were not accompanied by definite red or grey hepatization as might ordinarily be expected. The lesions varied greatly in their intensity, the œdema always being very prominent, while the hemorrhage varied from a diffuse infiltration of the involved lobe or added to this, was localized in massive collections four or five cm. in diameter and commonly occupying the central portions of the lobes. We have seen several hemorrhages lying in close proximity to each other with their borders coalescing and leading to a larger central involvement. In the regions where the hemorrhage and inflammatory œdema were diffuse, air was still present within the lung tissue, sometimes to an extent permitting the lung tissue to float on water but more often in quantity sufficient only to suspend the tissue at various depths. On pressure the fine air bubbles were recognized amidst the blood-stained fluid. Acute compensatory emphysema often occupied the anterior borders of the lobes or formed interstitial blebs beneath the pleura. The quantity of fluid, inflammatory œdema and hemorrhage, contained within these bulky lobes was often very surprising. A lobe when compressed would leak fluid with the ease that it could be obtained from a sponge. Out of the lower lobe on one occasion we pressed 700 c.c. of limpid blood-stained exudate. The acute emphysema which may make its appearance suddenly, is
TABLE VIII
Distribution of Pneumonic Lesions and Grades of Severity
| Degree of Involvement | + | ++ | +++ | Total |
|---|---|---|---|---|
| Left upper lobe | 10 | 6 | 7 | 23 |
| Left lower lobe | 4 | 10 | 17 | 31 |
| Right upper lobe | 12 | 8 | 9 | 29 |
| Right middle lobe | 10 | 9 | 4 | 23 |
| Right lower lobe | 5 | 9 | 18 | 3 |
| All lobes were simultaneously involved in some grade of pneumonia in 18 cases—56 per cent. | ||||
at times quite remarkable. It may appear very early in disease. We have not met with a single case where the emphysema of the lung led to a rupture of the air sacs and an interstitial infiltration of air through lung, mediastinum, neck and subcutaneous tissues. Some very remarkable cases are reported by different authors where this emphysema was of astounding grade leading to a crepitating infiltration throughout the mediastinum, neck and the subcutaneous tissues over the thorax and abdomen as low as the pubis. The milder grade of emphysema consisted mainly of an abnormal expansion of the air sacs which were not infiltrated by exudate and which probably had some effect in preventing the diffusion of the inflammatory fluid from entering certain regions. These emphysematous areas could be readily recognized by the naked eye along the anterior borders of the lung as well as between the involved pneumonic patches within the lung.
These lungs, involved in this early serous and hemorrhagic exudate varied considerably in their appearance according to the regional and quantitative involvement. As is seen from Table viii, the lower lobes were more commonly occupied by massive exudate than the upper, and the involvement of multiple lobes was the usual. Still more remarkable is the fact that all lobes were simultaneously involved in some grade of reaction (pneumonia) in 56 per cent. of cases. In complicated influenza-pneumonia Goodpasture and Burnett found the inflammatory reaction in both lungs and involving to a greater or less degree the lobes on each side. Most commonly this involvement consisted of a lobar distribution in one or two lobes with a lobular or patchy disposition of exudate in one or more of the remaining lobes. Where the distribution was lobar the involved lobe was distended to its fullest and the pleura tightly stretched over the lung tissue which, heavy with fluid, was not solid but flabby. The lung could be moulded under the finger and could be compressed into various shapes. At first sight this flabby, heavy lung tissue suggested the appearance of the waterlogged lung which one encounters in renal disease or failing circulation. A closer analysis, and particularly when the lung was sliced, showed an entirely different character.