Part 27

The pathological changes found in the nose, pharynx and larynx were of relatively slight importance and most variable in their severity and incidence. The majority of individuals had few clinical manifestations of disease in these parts. Some, however, complained of dryness of the pharynx with slight feeling of fullness. An examination of these parts revealed some congestion, varying from a red injected mucosa to a bluish cyanosis. In the nose the reaction was rarely as acute as is seen in infectious coryza, but even where relatively little change was to be seen in the tissues hemorrhage from the erectile tissue was not uncommon during the acute stages. No particular lesion was to be found associated with nose bleed. There was an unusual absence of excessive secretion from nose and pharynx in the majority of cases. One was also struck with the infrequency with which the larynx was involved. A certain number of individuals complained of hoarseness, and in them injection of the vocal cords with some swelling was found. In many others, however, even where an intense infectious process was present in the lower respiratory tract the larynx was almost without change. It was from the level below the larynx that the acute reaction in the respiratory system was found.

In all of our cases the trachea showed definite inflammatory reaction. Of the 32 cases there were 26 having an acute tracheitis, 5 with an acute mucopurulent inflammation and 1 with a reaction in the subacute stage. In the majority of the cases with acute tracheitis there was a thin layer of exudate lying upon the mucosal surface. At times the trachea was filled with a frothy serous fluid, the greater part of which had its origin in the lung. Nevertheless, as we shall point out later, we did obtain microscopical evidence indicating that during the early acute stage of the tracheitis a considerable serous exudate escapes from its mucosa. This serous inflammatory reaction is an important one for all of the mucosal structures upon which the virus of influenza obtains a footing. This we have found true for the trachea, bronchi and alveoli of the lungs. In some cases the exudate was grey and lay in close contact with the injected tissues. At first sight this grey exudate suggested necrosis, but it was readily wiped from the underlying structure. Some leucocytes and cell debris with many bacteria made up the content of this grey exudate.

The macroscopic appearance of the trachea was that of an intensely injected structure which had largely lost its normal lustre. The naked eye could distinguish that anatomical change had occurred in the surface tissue of the trachea and that there was unusual evidence of intensely injected vessels lying in the submucosa. In only one instance was there an appearance of a true necrotic membrane lying upon the surface of this intensely inflamed layer. This apparent membrane was found to consist of a wide patch of desquamated epithelial cells which was lying as a delicate necrotic plate upon the surface. This thin layer was devoid of a meshwork of fibrin threads as usually accompanies a true false membrane of other sources.

The early intense inflammatory reaction of the surface membrane of the trachea was characteristic, and in our experience was never exceeded in intensity by other infections. A desquamation of the lining membrane was also a common finding. Naturally this intense reaction so commonly found in the trachea extended without interruption into the main bronchi and their divisions. The finding of this continuous surface inflammation is good evidence of the mode of spread of the infectious process along these membranes, beginning in the upper portions and by direct continuity involving more and more of the respiratory tubes toward the lung.

The varying grades in the intensity of the inflammatory reaction upon the inner surface of the trachea was well illustrated in the microscopic sections. Even with the different degrees of the reaction there was a fairly constant character to the inflammation. In this way the response was found to differ from that commonly observed in ordinary infections of the respiratory tract. The first striking feature is the marked response of the vascular channels, both blood and lymphatic. The vessels lying in the submucosa were found intensely engorged so that their walls were stretched to the point of bursting. In fact, not a few vessels were seen whose walls, probably under the stress of intoxication and dilatation, had given way leading to a flooding of the neighboring tissue with their contents. Where such vessels lay close underneath the surface the hemorrhage escaped into the lumen of the trachea. Accompanying this early vascular response there was found a marked serous exudate leading to a stretching of the submucosal tissues by distention of the interstitial spaces. This reaction resembled an acute inflammatory œdema and occupied the area between the mucosa and the inner border of the cartilage rings. Beyond this region no response was found. Thus in the earliest stages, and where the mucosa was still intact, the main reaction was of the nature of an intense serous inflammation with congestion of the blood vessels and frequent interstitial hemorrhages.

Shortly following the development of the serous exudate in the submucosal tissues, the epithelial lining is found to suffer from the reaction. The serous exudate does not remain confined to the interstitial tissues, but is poured out through the mucosa into the trachea. It would appear that the amount of this clear exudate may become greater than can be dealt with by the mucosa, with the result that an accumulation of this serous fluid takes place between this epithelial layer and its basement membrane. We have repeatedly seen considerable stretches of the mucosa lifted from the basement membrane and shed in large plaques into the lumen. These mucosal cells at the time of their desquamation retain fairly well their morphological characters, and do not show evidence of necrosis prior to their removal. Disintegration of these cells naturally occurs while lying in the secretion of the trachea, and a variable cellular mass in stages of disintegration may often be found both in smears and sections. When the epithelial cells are lifted in wide plates, a type of bleb develops which is easily broken and then disintegrates.

The desquamation of the lining membrane is a fairly constant occurrence in the cases coming to autopsy. In the majority of those which we have examined the greater portion of the trachea was completely denuded, save for small islands lying in the recesses near the mouths of the mucous ducts. In one case this lesion was accompanied by a process of ulceration, due in all probability to the invasion by other micro-organisms. The denuded tracheal surface usually shows a further inflammatory reaction in which a cellular exudate then makes its appearance. This reaction is mainly one in which lymphocytes and plasma cells infiltrate the spaces previously occupied by the serous fluid. The reaction is limited to the submucosa and does not extend into the tissues beyond the cartilages. We have found only occasional polymorphonuclear leucocytes lying close below the surface. During this period, however, varying grades of degeneration may occupy the upper layers. The basement membrane particularly seems to suffer by losing its characteristic outline and staining qualities. This membrane becomes swollen, softened and indefinite. At times a homogeneous precipitate occurs along its free surface giving rise to an appearance resembling a false membrane. This deposit is, however, distinctively different from the diphtheritic membrane of other infections. It is interesting, however, that where such deposits and degeneration occur in the basement membrane more or less degeneration and necrosis also occur in the connective tissues immediately neighboring to it. These tissues show a peculiar granular destruction and alter their staining qualities. Moreover, and what is more important, under these conditions the dilated blood vessels are found to suffer from the injuries taking place in their neighborhood. We have repeatedly found partially or completely thrombosed capillaries, arterioles and venules in these surface layers. These thromboses took place while the vessel was in its distended state and thus produced a mold of the dilated vessel. This observation is of importance in indicating the severity of the effect of the virus and toxin upon the tissues of the trachea, and it is also of importance to appreciate that this damaging influence is very different from that which we encounter in pneumococcus infections, and we shall point out in our discussion on lung a reaction very similar to that which takes place very superficially in the trachea may also occur in the alveolar walls of the lung.

Having referred to the intensity of the responses of the blood vascular system, we must also indicate the part played by the lymphatics. Simultaneously with the reactions taking place about the blood vessels of the trachea we observed similar responses in the lymphatic channels. At first these dilated structures contained only fluid. Later the migration of the lymphocytes took place along these routes, and rarely micro-organisms could be demonstrated either free or within an occasional leucocyte. The sharp response of the lymphatics during the serous inflammation is noteworthy, inasmuch as we have found that the lymph glands lying about the respiratory tubes and lungs were early in their response to the irritating virus.

Bacteria were demonstrated in the secretions lying upon the surface of the trachea. In those specimens in which the mucous membrane was still intact we attempted to demonstrate the clustering of the micro-organisms about the ciliated cells as was described by Mallory in whooping cough. Although the organisms, and particularly small Gram negative bacilli, could be demonstrated lying about these cells no characteristic arrangement was found. Furthermore where the mucosa was still attached to its basement membrane we were never able to demonstrate organisms below the surface of the epithelial layer. In several cases where the mucosa was lifted in bleb-like structures a number of organisms were detected below the epithelial layer and in contact with the basement membrane of the submucosa. We have rarely demonstrated bacteria in the interstitial spaces of the submucosa, even where large numbers of organisms were lying upon the inner denuded surface.

The distinction which was made by the gross examination of the trachea between the acute tracheitis with serous exudate, subacute tracheitis and mucopurulent tracheitis was not so readily distinguished in the microscopic sections. In the gross the character of the exudate lying upon the surface was the main guide suggesting the nature and intensity of the inflammatory reaction. In the microscopic sections this exudate was largely wanting, or was not sufficiently characteristic to confirm the gross findings. On the other hand, differences in the nature of the injury were to be found mainly in the reaction of the submucosa. As we have indicated above, the early inflammatory reaction of the trachea is mainly evident in an intense congestion accompanied by an inflammatory œdema of the submucosal tissues, hemorrhage sometimes accompanying this response. In the later stages of the reaction a cellular deposit takes the place of the inflammatory œdema and usually consists of lymphocytes and plasma cells. It is only in those cases where the intensity of the irritant continues to act over a longer period of time that a superficial necrosis with leucocytic infiltration makes its appearance. The epithelial layer of the trachea is desquamated early in the acute reaction, and hence a denudation of the surface is to be found in all stages of the acute lesion. The mucous glands have not been found to show any particular involvement in the inflammatory process, and in the majority of instances they were found to have escaped entirely the damaging effect of the virus. Their response in an over-secretion of mucus may be the outcome of a stimulation by toxins or soluble irritants; but on the other hand, may also probably be a reflex response to the injury of the mucosal surface, which being bared of its covering is highly sensitive. The increased discharge of mucus from the deep glands may well be a protective response to such injury.

Bronchi

The lesions in the bronchi were in every way comparable to those in the trachea. The main bronchial tubes differ in no material way from the structure of the trachea, and the extension of the inflammatory process from above downwards leads to a reaction in their walls similar to what has been above described. As we follow the subdivisions of the bronchi we gradually lose some of the characteristics contained in the larger tubes. The mucous glands gradually become fewer and eventually disappear. The cartilage rings become smaller and no longer completely encircle the bronchus, and with the further diminution in the size of these structures disappear entirely. A relatively greater amount of muscle tissues takes the place of the cartilage rings. This change in the anatomy of these structures has a certain influence in modifying the character and distribution of the inflammation.

TABLE V

BRONCHITIS AND TRACHEITIS

═════════════════════════════════════ Acute bronchitis and tracheitis 26 Subacute bronchitis and tracheitis 1 Acute mucopurulent tracheitis 5 Acute purulent bronchitis 2 Acute mucopurulent bronchitis 7 Ulcers of trachea 1 Acute bronchiectasis 1 ─────────────────────────────────────

Thus whereas we have indicated that the inflammation of the trachea and of the large bronchi is of a peculiar kind and remains confined to the tissue lying inwardly from the cartilage rings, we found that where these structures give place to a loose muscle tissue with a more extensive lymphatic drainage the zone of inflammation is not so limited, but proceeds outwardly into the neighboring tissues. We often use the terms bronchus and bronchioles very freely without clearly distinguishing any real difference. In a study of the inflammatory reactions of the respiratory tubes in epidemic influenza (as well as in other infections) it is best to accept the anatomical definition that the bronchioles not only represent the minute tubules passing to the alveoli, but also those small air passages which devoid of cartilage, mucous glands and heavy connective tissue stroma are in close relation to the parenchymatous tissues of the lung. These soft muscular tubes possess blood and lymphatic vessels which freely communicate with the blood vessels of the lung alveoli. It is in association with these distant tubes that concomitant inflammatory reactions are found in the alveoli and in the bronchial tubes.

Desquamation of the epithelial lining is to be found in every size of bronchial tube where the infection has caused an acute inflammatory reaction. Throughout the pulmonary tissues where the lung is found in some stage of influenzal pneumonia the bronchial tubes, both large and small, are either entirely denuded of the mucosa or show only remnants attached to irregular areas. In the smaller passages dense clusters of desquamated cells are sometimes found within the lumen and indicate the accumulation of a desquamated epithelium obtained from portions of the tubular system in deeper portions of the lung. In the early stages, this desquamation is accompanied by a serous exudate and a certain amount of hemorrhage. Later we find masses of leucocytes which fill up the tube, and though appearing to arise from these structures have in fact largely come from the lung alveoli. Like the larger bronchial tubes the distant ramifications show relatively little cellular reaction in their walls in the early period. It is only when the neighboring lung tissues are extensively implicated in a purulent inflammation that we find a similar exudate occupying the tissues of the bronchioles. Polymorphonuclear leucocytes are equally distributed through the region of the basement membrane, submucosa, muscular coat and outer connective tissue layer. Some grades of degeneration may occupy the inner surface wherein the basement membrane first shows a homogeneous swelling and later a granular degeneration. In a few instances where the small bronchioles have communicated with regions with abscess formation an ulcerating surface occupied the inner boundary.

The evidence in the smaller bronchial tubes, both those with cartilage and those without, that an inflammatory reaction of some degree may occupy the muscular coat is of importance. We have found reactions of inflammation in the muscular coat varying from a mild œdema and cellular exudate to an intense polymorphonuclear leucocyte involvement. In the latter the muscle fibers showed evidence of degenerative change and suggested an acute weakening of this layer. We lay particular importance upon this finding as indicating a causative factor in the development of acute bronchiectasis as was met with in one of our cases. In this particular instance the bronchi passing to the lower lobes of each lung were unusually dilated and could be followed, in the gross, to their distant extremities. The dilatation was more or less uniform and no large pouches or cavities had developed. A mucopurulent exudate was found occupying these dilated tubes. Others have likewise observed the development of acute bronchiectasis under these conditions. Goodpasture and Burnett found that as early as the second to the fourth day one of the striking appearances was the gaping dilated condition of the infundibula, and the tendency to dilatation of the air passages was manifested in a bronchiectasis in 4 out of 30 cases. Boggs as well as Lord have reported upon chronic bronchiectasis associated with the B. influenzæ and there appeared to be evidence that a certain percentage of cases recovering from influenza permanently develop irregular dilatations of the bronchial tubes.

The recognition of inflamed bronchi or bronchioles was never difficult. In the gross the presence of the abnormal exudate and the intense injection of the mucosal surfaces always attracted attention to the inflammatory state. Furthermore where the mucosa had been desquamated the surface of these tubes was found to be quite granular if closely observed. With moderate magnification by means of a hand lens the granular appearance was shown to be due to the engorged vessels. Much easier, of course, was the recognition of the inflammatory reaction by the microscope. The importance, however, of the bronchitis and bronchiolitis lay in the amount of involvement which had occurred in the neighboring tissues. As we, however, indicated elsewhere, we do not doubt that many of the cases of three-day fever have a state of tracheitis and bronchitis equal to that which we have observed in many of our cases. Whether the inflammatory reaction progressed beyond the firmer bronchial tubes to the softer and more vascular structures would be difficult to say where our evidence rests upon the clinical findings alone. It is, however, probable that a certain number of the severe and sharp attacks of influenza not only cause a tracheitis and bronchitis of the larger tubes, but also extend more deeply into the smaller ramifications tending to simulate the reactions which we have above described. When we ask ourselves, however, how distantly must the infection invade the smaller bronchial tubes before involving the parenchymatous tissues of the lung we are at a loss to enunciate a general rule. It is more than probable that there are modifying influences which determine whether the bronchitis with a certain amount of its bronchiolitis will progress to a true pneumonia or will remain localized to these tubular systems. I can well appreciate that in the event that a bronchitis has an inflammatory reaction accompanied by much serous exudate there is great danger of flooding the neighboring alveoli with this inflammatory fluid and of carrying the large numbers of the micro-organisms within the tubes to the air sacs of the lung. Under these conditions the virus has an unusual ability to develop the disease from one localized in the air passages to that of a true pneumonia. It is probable that the peculiar early acute reaction which is present in the air passages in epidemic influenza is responsible for the extensive involvement of the lung in the severe and dangerous form of inflammation.

TABLE VI.

EXTENT AND DISTRIBUTION OF PNEUMONIA.

═══════╤════╤════════════════════════════╤════════════╤══════════════════════ AUTOPSY│AGE.│ RIGHT LUNG. │ TYPE OF │ LEFT LUNG. NUMBER.│ │ │ LESION. │ ───────┼────┼──────┬─────────────────────┼────────────┼────────┬───────────── │ │WEIGHT│INVOLVEMENT OF LOBES.│ │ WEIGHT │ INVOLVEMENT │ │ OF │ │ │OF LUNG.│ OF LOBES. │ │LUNG. │ │ │ │ ───────┼────┼──────┼──────┬───────┬──────┼────────────┼────────┼──────┬────── │ │ │UPPER.│MIDDLE.│LOWER.│ │ │UPPER.│LOWER. ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 741│ 18│720 G.│ + │ + │ ++ │Lobar S. & │ 850 G.│ + │ ++ │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 743│ 20│825 G.│ + │ + │ + │Lobular S. &│ 1375 G.│ +++ │ +++ │ │ │ │ │ │ H. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 744│ 30│900 G.│ + │ – │ ++ │Lobar and │ 900 G.│ ++ │ ++ │ │ │ │ │ │ Lobular S.│ │ │ │ │ │ │ │ │ & H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 745│ 18│575 G.│ + │ – │ ++ │Lobular S. &│ 480 G.│ – │ ++ │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 746│ 21│900 G.│ + │ ++ │ +++ │Lobar S. & │ 650 G.│ + │ +++ │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 747│ 27│ 1510│ +++ │ ++ │ +++ │Lobar S. & │ 1000 G.│ +++ │ +++ │ │ G.│ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 748│ 22│900 G.│ + │ + │ +++ │Lobar and │ 1250 G.│ + │ +++ │ │ │ │ │ │ Lobular S.│ │ │ │ │ │ │ │ │ & H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 749│ 23│ 1480│ ++ │ ++ │ +++ │Lobar S. & │ 1250 G.│ ++ │ +++ │ │ G.│ │ │ │ H. Slight │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 750│ 24│ 1200│ +++ │ + │ +++ │Lobar and │ 825 G.│ + │ +++ │ │ G.│ │ │ │ Lobular. │ │ │ │ │ │ │ │ │ Early │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 751│ 22│ 1250│ – │ – │ +++ │Lobar │ 610 G.│ ± │ ± │ │ G.│ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 752│ 27│ 1125│ +++ │ + │ +++ │Lobar S. & │ 775 G.│ ± │ +++ │ │ G.│ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 756│ 22│ 1000│ ++ │ ++ │ ++ │Lobar S. & │ 820 G.│ +++ │ ++ │ │ G.│ │ │ │ H. Slight │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 757│ 21│815 G.│ ++ │ – │ ++ │Lobular S. &│ 1075 G.│ +++ │ +++ │ │ │ │ │ │ H. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 758│ 22│ 1150│ +++ │ + │ + │Lobar │ 1400 G.│ +++ │ +++ │ │ G.│ │ │ │ Purulent │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 761│ 21│ 1250│ +++ │ ++ │ +++ │Lobar S. & │ 550 G.│ + │ + │ │ G.│ │ │ │ H. and │ │ │ │ │ │ │ │ │ Lobular │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 762│ 21│680 G.│ + │ + │ + │Lobular S. &│ 750 G.│ + │ +++ │ │ │ │ │ │ H. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 763│ 22│920 G.│ + │ – │ + │B. P. and │ 540 G.│ – │ + │ │ │ │ │ │ Lobar S. &│ │ │ │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 764│ 23│725 G.│ – │ + │ + │Lobular S. &│ 550 G.│ + │ + │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 765│ 25│ 1100│ ++ │ – │ ++ │Lobar S. & │ 1400 G.│ – │ +++ │ │ G.│ │ │ │ H. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 767│ 25│ 1075│ + │ +++ │ +++ │Lobar and │ 850 G.│ – │ ++ │ │ G.│ │ │ │ Lobular S.│ │ │ │ │ │ │ │ │ & H. and │ │ │ │ │ │ │ │ │ Lobular │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 770│ 21│900 G.│ ++ │ ++ │ ++ │Lobar S. & │ 750 G.│ ++ │ ++ │ │ │ │ │ │ H. and │ │ │ │ │ │ │ │ │ Lobular │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 773│ 22│ 2050│ +++ │ ++ │ +++ │Lobar S. & │ 780 G.│ – │ +++ │ │ G.│ │ │ │ H. and │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 778│ 22│ 1100│ ++ │ + │ ++ │Interstitial│ 975 G.│ ++ │ ++ │ │ G.│ │ │ │ Pneumonia.│ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 781│ 21│ 1000│ +++ │ ++ │ +++ │Lobar S. & │ 540 G.│ + │ +++ │ │ G.│ │ │ │ H. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 782│ 18│650 G.│ + │ – │ ++ │Lobular S. &│ 875 G.│ ++ │ +++ │ │ │ │ │ │ H. Slight │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 783│ 21│ 1250│ +++ │ +++ │ +++ │Lobar S. & │ 580 G.│ + │ ++ │ │ G.│ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 784│ 21│ 1590│ +++ │ +++ │ +++ │Lobar │ 1400 G.│ +++ │ +++ │ │ G.│ │ │ │ Purulent. │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 786│ 20│ 1100│ ++ │ +++ │ +++ │Lobar S. & │ 700 G.│ – │ ++ │ │ G.│ │ │ │ H. Slight │ │ │ │ │ │ │ │ │ Lobular │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 787│ 21│750 G.│ ++ │ – │ ++ │Lobular S. &│ 1125 G.│ +++ │ +++ │ │ │ │ │ │ H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 791│ 21│775 G.│ + │ ++ │ ++ │Lobular S. &│ 1050 G.│ ++ │ +++ │ │ │ │ │ │ H. and │ │ │ │ │ │ │ │ │ Purulent. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 792│ 21│ 1050│ + │ + │ +++ │Lobar and │ 950 G.│ + │ ++ │ │ G.│ │ │ │ Lobular S.│ │ │ │ │ │ │ │ │ & H. │ │ │ ───────┼────┼──────┼──────┼───────┼──────┼────────────┼────────┼──────┼────── 793│ 18│500 G.│ – │ – │ + │Slight │ 435 G.│ - │ + │ │ │ │ │ │ Lobular S.│ │ │ │ │ │ │ │ │ & H. │ │ │ ───────┴────┴──────┴──────┴───────┴──────┴────────────┴────────┴──────┴──────

═══════╤════════════╤════════════╤════════════╤══════════ AUTOPSY│ TYPE OF │ PLEURA. │ ABSCESS OF │ DAY OF NUMBER.│ LESION. │ │ LUNG. │ DISEASE. ───────┼────────────┼──────┬─────┼────────────┼────────── │ │ │ │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── │ │RIGHT.│LEFT.│ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 741│Lobar S. & │S.F. │S.F. │ │ 3d. │ H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 743│Lobar S. & │F. │S.F. │ │ 5th │ H. Early │ │ │ │ │ P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 744│Lobar S. & │S.F. │S.F. │ │ 7th │ H. │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 745│B.P. with │S.F. │– │ + │ 10th │ Necrosis. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 746│Lobar S. & │– │– │ │ 5th │ H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 747│Lobar S. & │S.F. │– │ │ 6th │ H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 748│Lobar S. & │– │– │ │ 4th │ H. and │ │ │ │ │ B.P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 749│Lobar S. & │F. │– │ │ 4th │ H. Slight │ │ │ │ │ P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 750│Lobar and │F. │F. │ │ 9th │ Lobular. │ │ │ │ │ Early P. │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 751│B.P. slight.│S.F. │– │ │ 7th │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 752│B.P. and │F. │S.F. │ │ 13th │ Lobar P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 756│Lobar and │F. │S.F. │ │ 8th │ Lobular S.│ │ │ │ │ & H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 757│Lobar S. & │F. │F. │ │ 6th │ H. and │ │ │ │ │ Purulent. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 758│Lobar │F. │F. │ │ 14th │ Purulent. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 761│Lobular S. &│– │– │ │ 7th │ H. │ │ │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 762│Lobar S. & │S.F. │S.F. │ │ 10th │ H. and │ │ │ │ │ Lobular P.│ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 763│B.P. │F.P. │– │ │ 11th │ │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 764│B.P. │– │– │ │ 9th │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 765│Lobar S. & │– │– │ │ 9th │ H. and │ │ │ │ │ Early P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 767│Lobar S. & │– │F. │ │ 10th │ H. Lobular│ │ │ │ │ P. │ │ │ │ │ │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 770│Lobar S. & │S.F. │F. │ + │ 11th │ H. Lobular│ │ │ │ │ P. │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 773│Lobar S. & │F. │F. │ │ 20th │ H. Lobular│ │ │ │recurrence │ P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 778│Interstitial│S.F. │S.F. │ │ 23d │ Pneumonia.│ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 781│Lobar S. & │S.F. │S.F. │ + │ 5th │ H. │ │ │ │ │ Purulent. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 782│Lobar S. & │F. │F. │ │ 8th │ H. and │ │ │ │ │ Early P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 783│Lobar S. & │S.F. │S.F. │ │ 8th │ H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 784│Lobar S. & │S.F. │S.F. │ │ 8th │ H. and │ │ │ │ │ Purulent. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 786│Lobar S. & │S.F. │– │ │ 4th │ H. and │ │ │ │ │ Early P. │ │ │ │ │ │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 787│Lobar S. & │S.F. │S.F. │ │ 8th │ H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 791│Lobar S. & │F. │S.F. │ │ 6th │ H. and │ │ │ │ │ Slight P. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 792│Lobar and │S.F. │S.F. │ │ 6th │ Lobular S.│ │ │ │ │ & H. │ │ │ │ ───────┼────────────┼──────┼─────┼────────────┼────────── 793│Slight │– │F. │ Strep. │ 10th │ Lobular │ │ │Bacteriemia.│ │ Purulent. │ │ │ │ ───────┴────────────┴──────┴─────┴────────────┴──────────

S—Serous. H—Hemorrhagic. P—Purulent. B.P.—Broncho-pneumonia. S.F.—Serofibrinous. F.—Fibrinous. F.P.—Fibrinopurulent.

It was very evident that the smaller bronchi and bronchioles were much more readily involved in a severe inflammatory reaction than the larger tubes. A purulent inflammation was not uncommonly found in the bronchioles of the lung when a pneumonic state with leucocytic infiltration was present. Even where such purulent infiltration of the walls of the bronchioles was readily demonstrable the trachea and main bronchi were devoid of this intense reaction. These purulent inflammations were not uniformly distributed in the bronchioles of the lung, but only occurred in those regions where the parenchymatous tissues were in themselves involved in a purulent reaction. It was difficult to find the evidence whether the purulent bronchitis preceded or followed the presence of a purulent pneumonia. The intimacy of the lung tissues with those of the small bronchioles makes it impossible for one or other of these structures to escape when one of them is implicated in a purulent reaction. It is equally important to appreciate that to a considerable extent the lung tissue surrounding the small bronchioles becomes involved by a direct radial extension through the walls of the thin respiratory tubes. Such extension laterally is assisted by the free lymphatic communication lying about the bronchioles and stretching into the lung parenchyma. Purulent processes of the small air tubes always showed a similar reaction in the interstitial tissues of the neighboring air sacs.

Our material did not permit of following the bronchial reactions to their conclusion. In some instances we have found that where abscesses developed within the lung the contiguous bronchi and bronchioles either became eroded or suffered intense suppurative inflammatory lesions on their inner surface. The manner in which repair of the more common inflammatory processes of the bronchi is accomplished could not be demonstrated in the cases dying during the acute stage. In one case an organizing bronchitis was associated with an organizing lobular pneumonia. In this instance the connective tissues were proliferating freely from the inner wall of the bronchi, there being no evidence of a basement membrane at the point where the connective tissue was growing. The development of the connective tissue appeared to be spontaneous and was not taking place within an unresolved fibrinous exudate. In as much as the fibrosing process was largely scattered through all of the lobes, the numerical involvement of the respiratory tubes was quite great. In this instance the amount of obstruction which was imposed upon the respiratory tissues by the fibrosing pneumonia and bronchitis was sufficient to cause considerable distress and dyspnœa during the last few days of the patient’s life. The amount of dyspnœa was out of proportion to the clinical manifestations of pulmonary involvement, and from a clinical point of view it was difficult to arrive at a conclusion of the nature of the lung lesion.

Undoubtedly during the subsidence of the inflammatory process within the bronchi the gradual restitution of the tissues with little or no fibrosis is accompanied by a reproduction of the lining membrane arising from the epithelial remnants in the small mucous crypts. In a few cases lately coming to autopsy where the patients had suffered an influenza five or six weeks previously, the mucosa of the trachea and bronchi had assumed its normal appearance and was fully clothed by a normal epithelial covering.

Lung—Early Stage