Bronchiectasis
Acute dilatation of the bronchi is a common result of the bronchitis of influenza, and its frequent occurrence is an index of the severity of the changes in the bronchial wall. In some instances the smaller bronchi in well-localized areas are uniformly dilated; in other instances, large cavities, several centimeters in diameter, are formed and all transitions between the two extremes occur.
The occurrence of bronchiectasis following influenza is mentioned by Leichtenstern[[86]]. He states that evidence of bronchiectasis can persist for weeks or months and nevertheless end with complete restitution of the lungs to normal. Lord[[87]] has described instances of bronchiectasis occurring in association with infection by B. influenzæ and Boggs[[88]] has recorded similar observations.
We have had abundant opportunity to observe early stages in the production of bronchiectasis and to study the much discussed pathogenesis of the condition.
The following figures show the predilection of bronchiectasis for the left lung and for the lower lobes: Bronchiectasis occurred 30 times in the left lung alone, 9 times in the right lung alone and 13 times in both lungs, the total being 52. Among 30 instances in which the lesion occurred only in the left lung, in 24 it was limited to the lower lobe, and in 15 of these 24 instances to the base of the lower lobe. Among 9 instances in which dilatation of bronchi occurred only in the right lung, it was limited to the lower lobe in 4 instances and to the base of the lower lobe in 2 of these 4 instances.
When the lesion is limited to the base of the lower lobes small bronchi with no recognizable cartilage in their wall are dilated to a diameter of from 3 to 6 cm. and are distended with thick mucopurulent fluid. The tenacious character of the bronchial contents and the action of gravity doubtless have a part in the production of the dilatation. In several instances dilatation of the bronchi was limited to the basal parts of both upper and lower lobes.
When bronchiectasis occurs throughout a whole lung, usually the left, or in both lungs, the lesion is more advanced and conspicuous (Fig. 26). There is diffuse dilatation of small and medium-sized bronchi. Dilated bronchi with deeply injected mucosa and filled with yellow mucopurulent fluid, are seen throughout the sectioned lung. A bronchus cut longitudinally may have a nearly uniform diameter of from 5 to 9 mm. for a distance of 5 or 6 cm., maintaining this diameter to within 1 cm. of the pleural surface, where normally only small bronchi occur.
More advanced bronchiectasis is represented by the occurrence of spherical bronchiectatic cavities, having a diameter from 1 to 2.5 cm. In some instances there have been two or three of these cavities but occasionally there may be many. Cylindrical dilatation of the bronchi usually occurs widely distributed in the lungs. In Autopsy 440 a small bronchus, cut longitudinally, was dilated to a diameter of 5 mm. for a distance of 5 cm. and terminated in a spherical cavity 2 cm. in diameter; there was another smaller spherical cavity nearby and dilated bronchi occurred elsewhere. In Autopsy 467, in the upper part of the lower lobe, two spherical cavities 1 and 1.5 cm. in diameter communicated with a bronchus of medium size.
Autopsies with bronchiectasis are listed in the order of the duration of illness to show the parallel increase in the severity of the lesion (Table LI). In 2 instances (Autopsies 244 and 314) bronchiectatic cavities surrounded by firm fibrous tissue have evidently existed before the onset of the fatal illness, which has lasted in one instance approximately four and in the other six days; these autopsies have been omitted from the table.
The table shows that bronchiectasis observed within twelve days after onset of illness with symptoms of influenza is moderately advanced and almost invariably limited to the left lower lobe and usually to the base of the lobe. Advanced dilatation, indicated by the formation of spherical or cylindrical cavities, occurs with increasing frequency as the duration of the respiratory disease increases.
Bronchiectasis has been almost invariably associated with purulent bronchitis. The dilated bronchi contain mucopurulent material and throughout the lungs the same condition is usually widespread. Among 137 instances of purulent bronchitis bronchiectasis consequent upon influenza has been present in 50.
| Table LI | |||||
|---|---|---|---|---|---|
| NO. OF AUTOPSY | DURATION OF ILLNESS IN DAYS | TYPE OF PNEUMONIA | LOCATION OF BRONCHIECTASIS | CHARACTER OF BRONCHIECTASIS | BACTERIA IN BRONCHUS |
| 394 | 5 ? | Broncho | Rt. base | Dilatation | |
| 359 | 7 + | Lobar and broncho | Lt. lower lobe | Dilatation | |
| 322 | 8 | Abscess (staph.) | Lt. base | Dilatation | |
| 325 | 8 | Interst. suppuration | Lt. base | Dilatation | S. hem., B. inf., staph. |
| 352 | 8 | Lobar and broncho | Lt. lower lobe | Advanced dilatation | |
| 429 | 8 ? | Broncho | Rt. base | Dilatation | |
| 288 | 10 | Abscess | Lt. base | Dilatation | S. hem., B. inf. |
| 374 | 10 | Lobar and broncho | Rt. and lt. lungs | Advanced dilatation | |
| 376 | 10 | Abscess | Lt. base | Dilatation | S. hem. |
| 437 | 11 | Lobar | Rt. lower lobe | Advanced dilatation | |
| 482 | 11 | Broncho | Lt. base | Dilatation | B. inf., Pneum. IV, S. hem. |
| 489 | 11 | Lobar and broncho | Lt. lung | Dilatation | B. inf., Pneum. IV. |
| 287 | 12 | Lobar and broncho | Lt. lower lobe | Advanced dilatation | Pneum. IV., B. inf., staph. |
| 289 | 12 | Broncho | Lt. lower lobe | Advanced | Pneum. IV., B. inf. staph. |
| 295 | 12 | Interst. sup. and abscess | Rt. lung | Advanced dilatation | S. hem., B. inf. |
| 336 | 12 | Broncho | Lt. base | Dilatation | |
| 375 | 12 | Broncho | Rt. and lt. bases | Dilatation | |
| 422 | 12 ? | Lobar and broncho | Lt. base | Dilatation | |
| 381 | 13 | Abscess | Lt. base | Spherical | |
| 391 | 13 | Lobar and broncho | Lt. lung | Dilatation | |
| 401 | 14 ? | Lobar and broncho | Rt. and lt. lungs | Spherical | |
| 402 | 14 | Chronic broncho | Rt. lower lobe | Dilatation | |
| 410 | 14 ? | Abscess | Rt. upper lobe | Dilatation | |
| 333 | 15 | Abscess (staph.) | Lt. upper lobe | Dilatation | S aur., B. inf. S. hem. |
| 389 | 15 | Interst. suppuration | Lt. lung | Advanced dilation | |
| 412 | 15 | Lobar and broncho | Lt. lower lobe | Cylindrical | |
| 398 | 16 | Broncho | Rt. and lt. lungs | Advanced dilatation | |
| 423 | 16 | Broncho | Lt. base | Dilation | |
| 488 | 16 | Abscess | Lt. lower lobe | Dilatation | S. hem., Pneum. atyp. II. |
| 312 | 17 | Broncho | Rt. and lt. lungs | Dilatation | S. hem., B. inf. staph. |
| 372 | 17 | Broncho | Rt. lung | Dilatation | |
| 385 C | 17 | Interst. suppuration | Lt. base | Dilatation | |
| 448 | 17 | Broncho | Lt. lung | Dilatation | |
| 460 | 17 | Abscess | Lt. lower lobe | Spherical | S. hem., B. inf., staph. |
| 291 | 18 | Broncho | Lt. base | Advanced dilatation | B. inf., staph. |
| 296 | 18 | Abscess | Lt. base | Dilatation | S. hem., B. inf., |
| 387 | 19 | Abscess | Rt. and lt. lungs | Advanced dilatation | S. hem., B. inf., S. aur. Pneum. II. |
| 421 | 19 | Chronic broncho | Rt. lung | Advanced dilatation | |
| 440 | 19 | Chronic broncho | Rt. and lt. lungs | Spherical | B. inf., S. aur. |
| 419 | 20 | Broncho | Rt. lung | Dilatation | Pneum. II, B. inf. |
| 463 | 20 | Chronic broncho | Rt. and lt. lungs | Spherical | B. inf., staph., Pneum. IV |
| 431 | 23 | Chronic broncho | Lt. base | Dilatation | |
| 468 | 23 ? | Lobar and broncho | Lt. lung | Dilatation | S. aur., B. inf., S. vir. |
| 465 | 25 ? | Broncho | Lt. base | Dilatation | S. hem., B. inf., staph., S. vir. |
| 445 | 27 | Broncho | Lt. lower lobe | Spherical | S. aur. |
| 449 | 27 | Abscess | Rt. and lt. lungs | Spherical | S. hem., B. coli. |
| 378 | 28 | Abscess | Lt. base | Cylindrical | S. hem., B. inf., Pneum. atyp. II. |
| 473 | 28 | Chronic broncho | Lt. lung | Advanced dilatation | B. inf., S. vir., staph., M. catarr. |
| 425 | 29 | Abscess (staph.) | Rt. and lt. lungs | Cylindrical | |
| 467 | 30 | Abscess | Rt. lower lobe | Spherical | S. hem., B. inf. |
| 472 | 37 | Chronic broncho | Rt. and lt. lungs | Advanced dilatation | B. coli |
| 487 | 55 | Abscess | Rt. and lt. lungs | Cylindrical | B. inf. S. hem. |
The bacteriology of autopsies with bronchiectasis is shown in Table LII.
| Table LII | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| NO. EXAMINED | PNEUMOCOCCUS | S. HEMOLYTICUS | STAPHYLOCOCCUS | B. INFLUENZÆ | |||||
| NO. POSITIVE | PER CENT POSITIVE | NO. POSITIVE | PER CENT POSITIVE | NO. POSITIVE | PER CENT POSITIVE | NO. POSITIVE | PER CENT POSITIVE | ||
| Bronchus | 29 | 9 | 31.0 | 15 | 51.7 | 16 | 55.2 | 23 | 79.3 |
| Lung | 37 | 16 | 43.2 | 18 | 48.6 | 10 | 27.0 | 19 | 51.4 |
| Blood | 50 | 12 | 24.0 | 22 | 44.0 | ||||
Comparison of the percentage incidence of the organisms which have to be found associated with bronchiectasis and with purulent bronchitis unaccompanied by bronchiectasis shows that there is no noteworthy difference in the occurrence of pneumococci, hemolytic streptococci or B. influenzæ within the bronchi. When allowance is made for the difficulty of demonstrating B. influenzæ in the presence of a large number of other microorganisms, it is not improbable that this organism has been constantly present in the purulent contents of the bronchi with purulent bronchitis, with and without bronchiectasis. Pneumococci, streptococci and staphylococci are each present in the bronchi in about one-half of the instances of bronchiectasis and mixed infections are very common, S. viridans, B. coli and M. catarrhalis being occasionally found in the bronchi. The table shows that pneumococci, streptococci and staphylococci show no greater tendency to enter the lungs and blood when bronchiectasis and purulent bronchitis coexist than with purulent bronchitis alone.
Moderate dilatation of the small bronchi at the base of the left lung was found in several instances eight days after onset of symptoms referable to the respiratory passages. Advanced, diffuse dilatation of the bronchi was seldom seen before the lapse of two weeks, and bronchiectasis with formation of spherical or cylindrical cavities was found with few exceptions three weeks after onset of the fatal illness. Long continued, purulent bronchitis does not necessarily produce dilatation of the bronchi. It is noteworthy that the average duration of the fatal illness in 137 instances of pneumonia and purulent bronchitis with no bronchiectasis was 12.5 days, whereas the average duration of 49 instances of pneumonia with purulent bronchitis and bronchiectasis was only 16.5 days.
Bronchiectasis is almost invariably associated with purulent bronchitis in which tenacious mucopurulent fluid accumulates in the bronchi. It begins at the bases of the lower lobes and is usually more advanced here than elsewhere. Mechanical distention of the small bronchi by viscid fluid, expelled with difficulty, brings about their dilatation and gravity appears to have a part in accentuating the process. Histologic examination of the changes accompanying bronchitis show that lesions which penetrate into the muscular layer and presumably weaken the bronchial wall are not uncommon and partial or complete destruction of the wall may result. To what extent infiltration of the muscular wall by polynuclear leucocytes or by lymphoid and plasma cells is accompanied by changes which weaken the wall may be questioned. When the epithelial lining of the bronchus is destroyed coagulative necrosis of the underlying tissue occurs and may extend a variable distance into the bronchial wall, not infrequently penetrating into or entirely through the muscular layer. These changes furnish an explanation of the occurrence of bronchiectasis following influenza.
Fig. 17.—Acute bronchiectasis showing fissures penetrating into bronchial wall and at one place entering surrounding alveolar tissue; the surrounding alveoli are filled with fibrin. Autopsy 425.
Acute bronchiectasis may be found following influenza after the illness has lasted eight or ten days. There is no increase of fibrous tissue. Small bronchi with no cartilage, which in normal lungs have a diameter approximating 1 mm., are dilated to 3 mm. or more. The surface epithelium is wholly or partially lost. Necrosis occurs in places and extends deep into the tissue, destroying muscle and often penetrating the entire thickness of the wall which in these small bronchi consists in large part of fibrous tissue containing greatly engorged blood vessels. In this necrotic material nuclei are absent and the tissue containing fibrin stains deeply with eosin. In it occur fissures or tears which extend from the lumen a variable distance, very frequently penetrating the entire thickness of the wall and entering adjacent alveoli (Figs. 17 and 19). Alveoli thus exposed almost invariably contain plugs of dense fibrin. Where these rents have occurred, adjacent edges of the bronchial wall, held together by underlying lung tissue, have separated from one another, so that the circumference of the bronchus has been increased (Fig. 18). These breaks in the continuity of the wall may occur in several places, so that a fourth or a third of the circumference may be formed by exposed alveolar tissue which has become the site of fibrinous pneumonia (Fig. 20). During life, though the inflamed bronchus is filled by mucopurulent exudate, distention of loose alveolar tissue, uniting the interrupted bronchial wall, is doubtless greater than it appears in the lung fixed by hardening fluids.
Fig. 18.—Acute bronchiectasis showing fissures in the bronchial wall extending into neighboring alveoli which in zone about are filled with fibrin; one fissure has separated widely; peribronchial fibrinous pneumonia (fibrin is black). Autopsy 425.
Recently dilated bronchi have an irregularly stellate lumen as the result of clefts penetrating at intervals into or through the bronchial wall (Fig. 26). Longitudinal fissures mark the lining of these dilated bronchial tubes.
When the fatal illness has lasted more than two weeks, abundant new formation of fibrous tissue occurs in a zone surrounding the dilated bronchus. Adjacent alveolar walls are thickened by young fibrous tissue. Alveoli, much diminished in size, are filled by hyaline fibrin into which fibroblasts and newly formed blood vessels have penetrated. These changes are limited to a wide zone in immediate contact with the dilated bronchus, whereas at a greater distance alveolar walls have undergone no thickening and alveoli contain no fibrin.
Fig. 19.—Acute bronchiectasis; the bronchial wall indicated by engorged mucosa shows a varying degree of destruction, fissures extending into and through the bronchial wall. Autopsy 352.
Fig. 20.—Acute bronchiectasis; with destruction of bronchial wall exposing alveoli filled with fibrin; peribronchial fibrinous pneumonia is seen about several bronchi present in the section; Gram Weigert fibrin stain. Autopsy 425.
This stage is well represented by Autopsy 421 after an illness of nineteen days. Bronchiectatic cavities, from 3 to 6 mm. in diameter, are numerous in sections of the lung; their lumina are irregular in outline and often irregularly stellate. Microscopic examination shows the presence of clefts which interrupt the bronchial wall at intervals throughout its entire circumference. The original wall is well indicated by the very richly vascularized connective tissue containing scattered muscle bundles and is infiltrated with lymphoid and plasma cells in great number. Where fissures have occurred the adjacent edges of the interrupted wall have separated from one another, leaving a wide interval where underlying alveolar tissue is exposed. Two changes tend eventually to render the fissures inconspicuous, namely, regeneration of epithelium and new formation of fibrous tissue. Exposed alveoli filled with fibrin are in process of organization and epithelium which has assumed a squamous type has grown down over the exposed surfaces of the interrupted bronchial wall. It has begun to cover or in some instances has completely covered the surface of rents entering alveoli plugged with fibrin (Fig. 21). In the periphery of the bronchus alveolar walls are thickened and infiltrated with lymphoid and plasma cells. The same changes affect bronchi containing cartilage which is undergoing atrophy.
The reinforcement of the fissured bronchial wall by new formation of fibrous tissue, by thickening of the interalveolar walls and by organization of fibrin within the alveoli is well shown after four weeks (Autopsy 425; Fig. 28). There are spherical bronchiectatic cavities more than a centimeter in diameter surrounded by a dense fibrous wall in which are atrophied alveoli lined by epithelium of cubical form. Occasionally, the fibrous wall is interrupted and alveoli, plugged with organizing fibrin, are in immediate contact with the lumen. When these plugs of fibrin which are slowly absorbed disappear, evidence of preexisting rents in the bronchial wall are lost, and there are in this lung bronchiectatic cavities of which the wall is a continuous circle of dense fibrous tissue.
Fig. 21.—Bronchiectasis with fissures extending through the bronchial wall into alveolar tissue which is the site of fibrinous pneumonia; epithelium has grown down into these fissures and has covered the exposed surfaces. Autopsy 463.
Fig. 22.—Regeneration of epithelium over fissures which have been formed in the wall of a bronchus; the epithelium in the neighborhood of and within the fissure is squamous.
Epithelium lining the dilated bronchi is at times completely destroyed (Fig. 28), but more frequently it persists in part. That which remains has almost constantly the character of squamous epithelium (Figs. 22 and 23). The lowermost cells are cubical; those above them are polygonal, tending to become flatter as the surface is approached; upon the surface are cells often much flattened and occasionally they have lost their nuclei and stain deeply with eosin as the result of superficial necrosis. The change should not be regarded as metaplasia, for the epithelium assumes this squamous type when the superficial columnar cells have been lost. Actual necrosis of superficial ciliated columnar cells is occasionally seen (Autopsy 352); injured cells have separated from one another and desquamated into the lumen of the bronchus. The epithelium which remains after the superficial cells are lost consists of cells which become flatter from base to surface, but the intercellular bridges characteristic of the epithelium of the skin are not found. When epithelium is in process of regeneration, a layer gradually diminishing in thickness extends over the denuded surface, the advancing edge being formed by very flat cells in a single layer. The epithelium growing into fissures which have penetrated the bronchial wall may completely cover the exposed alveolar tissue. The newly formed epithelium may follow a fissure into an alveolus which has been opened and come into contact with the fibrin which fills the alveolus.
Fig. 23.—Squamous epithelium growing over the defect in the bronchial wall shown in Fig. 22 more highly magnified; squamous epithelium is present above and columnar epithelium below.
Bronchiectasis usually affects the small bronchi with no cartilage. It is not uncommon to find greatly dilated bronchi with no cartilage in close proximity to cartilage containing bronchi of smaller caliber. In one instance (Autopsy 421) a bronchus of medium size with cartilage measured 3 mm. in diameter, whereas two bronchi with no cartilage were dilated to 4 and 6 mm., respectively. Nevertheless, larger bronchi are occasionally the site of superficial loss of epithelium, necrosis extending into the bronchial wall, formation of fissures and stretching of the wall at the spot which is weakened. In association with these changes atrophy of the cartilage may occur (Autopsies 421, 425, 440, 463). Plates of cartilage in process of atrophy are readily recognized by their irregularly indented outline and often by their small size. The fibrous tissue surrounding the cartilage is the site of chronic inflammation and is densely infiltrated with lymphoid and plasma cells among which polynuclear leucocytes are scant. Nevertheless, polynuclear leucocytes are abundant in immediate contact with the cartilage and appear to have an important part in the solution of its matrix, for about them occur indentations of the edge. Leucocytes penetrate into the cartilage.
The necrosis and tears which occur in the wall of the bronchus are not always limited to the bronchus, but may extend deeply into the surrounding tissue. In Autopsies 312 (Fig. 21) and 423 wide areas of necrosis have penetrated deeply into the tissue about the bronchi.
Autopsy 312.—Illness began with influenza on September 26, seventeen days before death; a diagnosis of lobar pneumonia with consolidation of the right lower lobe was made ten days after onset and Pneumococcus IV, B. influenzæ and S. hemolyticus were found in the sputum. At autopsy there was bronchopneumonia with red and gray lobular and confluent lobular patches of consolidation and right and left serofibrinous pleurisy; there was purulent bronchitis; no abscesses were seen. Small bronchi throughout both lungs were dilated and often surrounded by a zone of hemorrhage.
Hemolytic streptococci were found in the heart’s blood, in the pleural exudate, consolidated lung and bronchus; B. influenzæ was found in the lung and in a small bronchus, and staphylococci in the contents of a small bronchus.
Fig. 24.—Acute bronchiectasis with fissures extending through bronchial wall which is marked by great engorgement of blood vessels; at one point a fissure has penetrated deep into the alveolar tissue and formed a small cavity containing purulent exudate and surrounded by fibrinous pneumonia. Autopsy 312.
Bronchi which are the site of acute inflammation have lost their epithelium wholly or in part, and deep fissures penetrate the entire thickness of the bronchial wall, extending into the surrounding lung tissue which is the site of fibrinous pneumonia. In some instances plugs of fibrin within the alveoli are bisected by these tears. There is some superficial necrosis along the edge of each fissure, in several places extending outward from defects in the walls of small bronchi dilated to approximately 1.5 mm. There are wide patches of necrosis affecting both alveolar walls and contents of alveoli and extending 2 mm. into the lung tissue. When a fissure has penetrated from the lumen of the bronchus into necrotic tissue (Fig. 21), polynuclear leucocytes have accumulated within the necrotic tissue, disintegration of tissue occurs, and a small cavity communicating with the bronchus is formed.
Autopsy 423.—C. H., white, aged twenty-five, resident of Oklahoma, had been in military service one month. Death occurred sixteen days after onset of influenza.
Anatomical Diagnosis.—Chronic bronchopneumonia with peribronchiolar consolidation throughout right lung and in left lower lobe; right purulent pleurisy; purulent bronchitis; bronchiectasis at base of left lung.
The right lung weighs 1,260 grams; in the upper lobe are yellowish gray nodules having the appearance of tubercles clustered about small bronchi; in places similar nodules occur upon a background of pinkish gray consolidation occupying the greater part of the lower lobe. Bronchi contain purulent fluid. The left lung weighs 760 grams; it is edematous and small, yellowish gray nodules of consolidation in the lower lobe are clustered about terminal bronchi. Bronchi at the base of the lower lobe are dilated.
Bacteriologic examination shows the presence of hemolytic streptococci in the blood of the heart; hemolytic streptococci and B. influenzæ in the lung.
Microscopic examination shows that the walls of the bronchi are infiltrated with lymphoid and plasma cells; these cells are very numerous in peribronchiolar patches of consolidation. A small bronchus 1 mm. in diameter has squamous epithelium along one side; on the opposite side, the wall is completely absent and there is superficial necrosis of exposed alveoli filled with fibrin. A deep fissure passes from the bronchus into the consolidated tissue; its edges are necrotic and it is filled with polynuclear leucocytes. A small cavity in contact with the bronchus has been formed. In another part of the lung a distended bronchus has lost its epithelium on one side, and here alveoli filled with fibrin form the wall of the bronchus which is filled with leucocytes. Extending outward from the eroded wall is a focus of necrosis where both alveolar walls and contained exudate have lost their nuclei.
The necrosis which has had its origin in the bronchi is soon followed by accumulation of polynuclear leucocytes, softening and disintegration of tissue. Discharge of the disintegrated tissue through the bronchi results in the formation of a small cavity continuous with the bronchus. These changes are well illustrated by the bronchiogenic abscesses which have been described elsewhere (Autopsies 376, p. [206], and 387, p. [206]). When disintegrated tissue is discharged by way of the bronchi no accumulation of pus occurs, but cavities will be formed, in part by dilation of bronchi, in part by erosion of the adjacent lung tissue. Histologic examination shows that these changes have produced the advanced bronchiectasis found in Autopsy 445 (Fig. 25).
Autopsy 445.—W. F., white, aged twenty-three, from Mississippi, had been in military service one month. His illness began September 22, twenty-seven days before death, with severe coryza, weakness, nausea and vomiting; great pain in bones, cough and sore throat. He was admitted to the base hospital one week later with diagnosis of influenza and bronchitis. On October 3, sixteen days before death, signs of consolidation were found on the left side over the back and a diagnosis of lobar pneumonia was made. On October 18 there was severe headache, pupils were dilated, and there was rigidity of neck; lumbar puncture was made and pneumococci were found in the fluid obtained. Death occurred on the following day.
Anatomic Diagnosis.—Bronchiectasis with unresolved pneumonia limited to the left lower lobe; acute bronchopneumonia with peribronchiolar consolidation in right lung; purulent bronchitis, peribronchial hemorrhage and organizing bronchiolitis in right lung; adherent pleura on left side; purulent meningitis.
The left upper lobe is crepitant throughout. The outer and posterior two-thirds of the left lower lobe is riddled with cavities often rounded and varying in diameter from 0.5 to 3 cm. but not infrequently irregular in shape and in communication with adjacent cavities (Fig. 25). In places cavities pass in a tortuous course from pleura to the midpart of lung. The lining of these cavities is usually smooth, but in places is covered by gray necrotic material. Communication between the cavities and medium-sized bronchi is occasionally found. The lung tissue between the cavities is in part grayish red and consolidated, in part pink and air containing. The right lung is edematous throughout; the bronchi in the lower part of the right lung contain purulent fluid and are in places surrounded by zones of hemorrhage.
The spleen is very large (14 × 11 × 5 cm.) and firm.
The spinal fluid is cloudy and blood vessels over the lumbar enlargement and lower thoracic region are congested; in the upper thoracic region the cord is covered by purulent exudate.
Bacteriologic examination demonstrates the presence of hemolytic streptococci in the blood of the heart; plates from the left lung contain a few colonies of S. aureus and Pneumococcus IV; plates from the right main bronchus contain S. aureus and a large bacillus which does not stain by Gram’s method. Three plates from the spinal meninges contain Pneumococcus IV.
Fig. 25.—Advanced bronchiectasis throughout lower left lobe. Autopsy 445.
Microscopic examination shows that the cavities which have been described are lined by very vascular connective tissue containing many cells; there is no epithelial lining and the surface is in places covered by fibrin. On the surface polynuclear leucocytes are numerous, but immediately below, large mononuclear cells occur and frequently contain one or several ingested polynuclear leucocytes. None of the structures peculiar to the bronchi can be identified in the wall of these cavities, and in many places it is evident that lung tissue has undergone destruction, for in places the lining of vascular connective tissue is interrupted and an extension of the cavity penetrating into the lung substance is surrounded by alveoli filled with fibrin; in contact with the cavity there is some necrosis.
The cavities communicate with the bronchi and are lined in part by vascular connective tissue which may in part represent preexisting bronchial walls, but no epithelium is present and the relation to the bronchi cannot be established with certainty. These cavities have extended by necrosis which has broken the vascular connective tissue of their wall and penetrated into adjacent lung tissue. Death has been the result of purulent meningitis caused by pneumococcus, and the histologic changes in the walls of the cavities suggest that the activity of the inflammatory reaction here is subsiding, for large mononuclear cells are numerous and are ingesting polynuclear leucocytes. The changes described would, if continued, result in the formation of cavities lined by fibrous tissue and resembling many of those formed as the result of dilatation of the bronchi.
A study of the progress of the changes which result in the formation of bronchiectatic cavities has shown how the inflammatory irritant within the bronchus destroys the epithelium of the bronchus, penetrates into the deeper tissues and produces fissures which extend through the entire thickness of the bronchial wall at one or usually several places. These longitudinal fissures, which at first often give a stellate outline in cross section to the cavity of the affected bronchus, permit the separation of the edges of the fissure, so that an increase in the circumference occurs. The base of the fissure is formed by surrounding alveolar tissue and its edges are the site of necrosis. Tears may extend into the surrounding alveolar tissue, thus permitting further stretching of the bronchial wall. The consequences of rupture of the small bronchi into the adjacent alveoli are to some extent overcome by the inflammatory reaction which plugs the adjacent alveoli with fibrin.
Compression of the lungs by forced expiration, even though the glottis were closed as in coughing, would not dilate the bronchi, because pressure outside and within the bronchi would be equally elevated (Thornton and Pratt[[89]]). The pressure within the bronchi does not differ greatly from atmospheric pressure, whereas the negative pressure within the pleural cavity may vary from approximately 6 mm. of mercury during quiet inspiration to 30 mm. with forced inspiration. Excess of pressure upon the inner surface of the bronchial walls will vary with coughing and other respiratory efforts, between these limits depending upon the readiness with which pressure is equalized within and without the bronchi by penetration of air into the alveoli. The presence of viscid mucopurulent fluid within bronchioles will obstruct these tubules and retard the entrance of air into alveoli.
Weakening of the bronchial wall by the changes which have been described will cause lasting dilatation of the bronchi. Whatever increases pressure within the bronchi will increase the tendency to dilatation; the bronchi being filled with mucopurulent exudate dilatation usually appears first at the bases of the lung, since gravity increases intrabronchial pressure here. New formation of fibrous tissue within the wall of the bronchus, thickening of adjacent alveolar walls, and organization of fibrin reinforce the weakened bronchial wall and limit the dilatation which follows injury to the wall. Regeneration of epithelium covering the dilated tube will further obscure the early changes which have made dilatation possible. The changes which weaken the bronchial wall permit dilatation at a time when there is no new formation of fibrous tissue. When the bronchial lesion has persisted several weeks, chronic pneumonia is associated with it. It has been suggested that the contraction of newly formed fibrous tissue within the substance of the lung might cause bronchi to be enlarged by traction upon their walls. Newly formed connective tissue is most abundant in the wall of the bronchiectatic cavity, and here contraction would tend to diminish the size of the cavity.