| Table XLII | |||
|---|---|---|---|
| AUTOPSY | BLOOD | LUNG | BRONCHUS |
| 253 | Pneum. II | Pneum. II, B. inf. | Staph., B. inf. |
| 374 | Pneum. IV | ||
| 387 | Pneum. II, S. hem. | Pneum. II, staph., B. inf. | Pneum. II, S. hem., staph., B. inf. |
| 392 | Pneum. II | ||
| 402 | Pneum. IV, S. hem. | ||
| 424 | ? | Pneum. IV | |
Pneumococcus has been found in every instance either in the lungs or blood. Pneumococcus II, which has been uncommon with the pneumonia following influenza at Camp Pike and has occurred only ten times in more than 200 autopsies, has been present in one-half of these cases. The constant association of the lesion with pneumococcus is particularly significant when a comparison is made between the incidence of pneumococcus with peribronchial hemorrhage, on the one hand, and peribronchial pneumonia on the other; pneumococcus has been present in less than a third of the instances of hemorrhage but in all instances of pneumonia.
In addition to the instances in which gross peribronchial consolidation has been noted at autopsy, microscopic examination has demonstrated the presence of fibrinous pneumonia surrounding bronchi in a considerable number of autopsies. In a zone encircling small bronchi (with no cartilage) alveoli are filled by plugs of dense fibrin (Fig. 20) containing in variable number polynuclear leucocytes and mononuclear cells. The width of the zone is often equal or greater than the diameter of the bronchus. Alveoli outside the zone of fibrinous inflammation may contain red blood corpuscles or serum, and desquamated epithelial cells are often abundant.
Of 21 instances of peribronchial fibrinous pneumonia 20 were associated with purulent bronchitis. Further evidence of the relation of the lesion to profound injury to the bronchi is its association with bronchiectasis in 17 instances.
Peribronchial fibrinous pneumonia, like other lesions encircling the small bronchi, bears a direct relation to the severity of microscopic changes in the bronchus. The epithelium of the bronchus is either partially or completely lost. Occasionally epithelium is raised by hemorrhage or leucocytes from the underlying tissue but more frequently it is wholly lost and the surface is covered by a layer of fibrin. In the early stages of the lesion, polynuclear leucocytes may be numerous throughout the bronchial wall, indicating that the inflammatory irritant within the lumen is affecting the entire wall and extending its influence to the surrounding pulmonary tissue. Later lymphoid and plasma cells are more abundant than polynuclear leucocytes. Coagulative necrosis and disintegration of the bronchial wall, proceeding from the inner surface outward, may extend more or less deeply, and fibrinous inflammation of adjacent alveoli is often more extensive about that segment of the bronchus which shows the greatest change. In some instances segments of the bronchial wall or even the entire wall has disappeared, so that alveoli containing fibrin form part of the wall of the cavity thus formed. When bronchiectasis has occurred, there are often fissures from the lumen through the entire wall extending into the surrounding lung tissue: here fibrinous pneumonia is particularly conspicuous, occurring in a zone about the edges of the defect. This deposition of fibrin within the alveoli adjacent to the injury doubtless has a part in limiting the distribution of bacterial infection. Nevertheless breaks in the continuity of the bronchial wall are not essential to the production of the lesion and the irritant, which is responsible for the lesion, may penetrate through the bronchial wall to surrounding alveoli and from alveoli to other alveoli immediately adjacent.
With this peribronchial pneumonia the smallest bronchi are distended with pus and their walls are infiltrated with polynuclear leucocytes, lymphoid and plasma cells. In a broad zone encircling the bronchus the alveoli are filled with plugs of fibrin. Bronchioles are similarly distended with polynuclear leucocytes; the alveoli which occur upon the wall of the bronchiole are often limited to one side of the wall and are filled with fibrin. This fibrin occasionally projects into the lumen of the bronchiole and forms a continuous layer in contact with the wall on the same side. The alveolar duct and infundibulum are distended with polynuclear leucocytes. The alveoli upon the wall of the alveolar duct and upon the proximal part of the infundibulum are filled with fibrin. The bronchus, bronchiole, alveolar duct and part of the infundibulum are thus surrounded by a continuous zone of alveoli containing fibrin. The alveoli about the distal part of the infundibulum may be filled with polynuclear leucocytes. Lung tissue between adjacent zones of fibrinous pneumonia may contain serum and desquamated epithelial cells.
Organization of peribronchial fibrin was found in 10 of the 22 autopsies in which peribronchial fibrinous pneumonia had been found. Fibroblasts have invaded the fibrin and newly formed capillaries have penetrated into it. In some instances the interalveolar septa are thickened and infiltrated with lymphoid and plasma cells, and in 7 instances there was chronic pneumonia with thickening and mononuclear infiltration of the interstitial tissue about the bronchi and blood vessels, and elsewhere. The duration of the fatal illness in 12 instances with no organization was usually from ten days to two weeks, though in 3 instances there was no organization although the respiratory disease had lasted from seventeen to nineteen days (average duration with no organization, 13.5 days). The duration of illness in 10 instances with organization of fibrin was slightly less than three weeks (average 18.9 days). These figures do not accurately represent the duration of pneumonia which usually develops after a period of several days following onset of influenza.
This group of instances of peribronchial fibrinous pneumonia has offered an opportunity to study the bacteriology of pneumonia with organization and to determine if it presents any unusual characters. The bacteriology of autopsies with peribronchial fibrinous pneumonia with no organization is shown in Table XLIII:
| Table XLIII | |||
|---|---|---|---|
| AUTOPSY | BLOOD | LUNG | BRONCHUS |
| 289 | Pneum. IV | Pneum. IV | Pneum. IV, B. inf., staph. |
| 372 | |||
| 376 | S. hem. | S. hem. | S. hem., B. inf., S. aur. |
| 409 | 0 | ||
| 410 | S. hem., B. inf. S. aur. | ||
| 412 | Pneum. II | Pneum. II, B. inf. | |
| 420 | S. hem. | S. hem., B. inf. S. aur. | |
| 423 | S. hem. | S. hem., B. inf. | |
| 440 | 0 | B. inf., S. aur. | B. inf., S. aur. |
| 448 | 0 | 0 | 0 |
| 482 | 0 | B. inf., Pneum. IV | B. inf., Pneum. IV, S. hem. |
| 489 | 0 | Pneum. IV, B. inf. | Pneum. IV, B. inf. |
The bacteriology of instances of peribronchial fibrinous pneumonia with organization of the intraalveolar fibrin is shown in Table XLIV: