Chapter IV: Introduction (2)

Sections from those areas of the lung where the involvement is more marked may show a histological picture not unlike that described for the aplastic stage, but, in addition, there are groups of lobules where the exudate is typically purulent and pus cells not only form the greater part of the exudate in the lumen, but are prominent in the distended vessels of the alveolar wall (Fig. XXIX). Often these leucocytes are multilobed and frequently their protoplasm is granulated with phagocytized bacteria. The bacteria are also encountered free in the alveolus along with other elements; namely, red blood cells, strands of fibrin, or precipitated albumin (Fig. XXI). The bacteria, however, are not particularly conspicuous, for generally they are either single, in pairs, or in chains; and it is only when they become clumped to form large masses, often larger than any normal tissue cell, that they attract attention. When this appearance is encountered, the alveolar wall is no longer distinct and well preserved. Although the wall may still be made out, it often stains rather homogeneously and much of the finer architecture is lost in the thrombo-necrotizing process that has been instituted (Fig. XVII).

From this intermediary stage the picture of actual abscess with mortification of bronchiolar and alveolar tissue, as well as of the exudate itself, is readily approached (25, 48, 110, 140) (Fig. XXXI). In the necrotic mass that forms the center of such a focus, the most prominent feature is the bacteria. With hematoxylin they stain intensely as black, irregular masses, and their prominence is accentuated by the homogeneous staining qualities (with eosin) of the dead tissue, whether lung or exudate (Fig. XXXII). These abscesses may have central cavities which represent a discharge of their contents and may indicate the position of a bronchiole (Fig. XXXI). The necrosis of the alveolar walls, focal in its distribution as previously described, suggests itself as a forerunner of the more extensive necrosis encountered at this stage.

The most extreme form of mortification is seen in the wall of a gangrenous cavity, and several layers can be distinguished there. Beginning with that portion of the lung the least involved, the lesion may be limited to congestion of the alveolar wall with a serofibrinous exudate in the lumen, but this stage passes rather rapidly into another where cellular exudate, chiefly of polymorphonuclear leucocytes, predominates. Moreover, the leucocytes form not only the bulk of the alveolar content, but also distend the vessels and accumulate in the interstitial tissue around blood vessels and lymphatics. Passing toward the center of the gangrenous cavity, the lung rapidly changes in appearance. The blue zone of leucocytic infiltration makes more conspicuous the inner area of necrosis—where nuclei no longer stain and the alveolar wall is a homogeneous pink.

Gradually this phantom architecture, spotted only here and there with disintegrating polymorphonuclear leucocytes, ends in a ragged compressed border of a shaggy pink material which has no identifying qualities (Fig. XXXV). In the inner zone of pink an occasional vessel or, at times, a bronchiole more resistant to the process remains; frequently it is accentuated by the presence of partially destroyed polymorphonuclear leucocytes at its periphery. Probably these cells invade the necrotic areas along the sheath of the bronchus or vessel and not across the dead area. The thrombotic process described in the previous stage (Fig. LII) associated with an acute arteriolitis, may be associated with these gangrenous areas as well as with infarcts (82), but more likely gangrene is preceded by the acute diffuse necrosis of the alveolar wall which occurs in the fulminating cases. Furthermore, this is suggested where a typical grey hepatization is associated with marked thinning, but not actual disappearance, of the alveolar wall. Before concluding the description of this stage of the disease, mention should be made of the granular nodules of fibrin superimposed upon the swollen pleural cells and also of the older pleural exudate, either typically fibrinopurulent or more homogeneous with broken nuclear fragments (Fig. XXXVIII).

_Summary._

In this stage of the disease the respiratory change is characterized by a localization of the inflammatory process with cellular invasion of the exudate. Pneumonia results, varying in extent from peribronchial to lobar, a pneumonia in which one of the most frequent complications is necrosis of the lung. Consequently, abscesses, even gangrene, are found.

(3) ORGANIZATION OF BRONCHIOLAR AND PNEUMONIC PROCESSES.

The processes described for the preceding group which involve not only the alveoli, but also the bronchi and the bronchioles, were predicted from the extensive hyalinization of these structures—a characteristic change in the more fulminating and acute phases of the disease. Likewise, it can be predicted that where death does not terminate the process such lesions will be followed by organization, which, by converting the exudate into scar, will produce deformities and offer serious mechanical interference with the ingress and egress of alveolar air and similar interference with the flow of blood through the pulmonary circulation (82).

FIG. XXIV. AUTOPSY NO. 92. AN ALMOST PURE HEMORRHAGIC ALVEOLAR
EXUDATE. COMPARE FIGURES VI, XXV, AND XXVI.
]

FIG. XXVI. AUTOPSY NO. 103. THE LARGER ILLUSTRATION OF AN HEMORRHAGIC
ALVEOLAR EXUDATE IS ELABORATED BY TWO HIGHER POWER DRAWINGS. THESE
SHOW (1) AN ANEURSYMAL DILATATION OF A CAPILLARY IN THE ALVEOLAR
WALL AND (2a) A RUPTURE OF THE CAPILLARY WALL WITH THE ESCAPE OF RED
BLOOD CELLS INTO THE ALVEOLUS; (2b) NECROSIS WITH EARLY THROMBOSIS
OF THE CAPILLARY IN THE ALVEOLAR WALL.
]

It is probable that chronic processes, not sufficiently severe to terminate fatally in a few weeks or months, may occur, but few examples of that kind have been observed. A total of twelve cases of our series in which organization of the bronchiolar (47), or alveolar exudate (156) was found, include three of the lobar, three of the pseudolobar, two of the lobular, and four of the peribronchial types. Such a differentiation, it will be understood, is purely arbitrary. The majority of the cases show, not only a reparative process, but also a continuance of the acute change, and, indeed, both gross and microscopic pictures of the lung may be complicated. It will be impossible to give an inclusive description of these changes, and therefore a few of the most diverse and characteristic will be presented in the form of case abstracts.

_Autopsy No. 140._

A white female, aged 19 years, entered the New Haven Hospital after
five days of fever, prostration, and cough. She was moderately
cyanotic and dyspnœic, but examination of the lungs was negative
except for a few râles at the right base. She was delivered of a
six-months’ fœtus two days later. On the eleventh day of her
illness, definite signs of consolidation had developed in the
midback on both sides and spread gradually to include the left base
and all of the right back to the level of the 4th dorsal spine. The
temperature varied irregularly between 100°F. and 105°F. The pulse
followed the temperature, but averaged 102 per minute, while the
respirations remained about 40 per minute.

The white blood count on admission was 5,800, but rose gradually to
28,320 cells per cubic millimeter, with 90% of polymorphonuclear
leucocytes. The patient died on the twenty-second day of the
disease.

Post-mortem examination showed little of interest aside from the
thorax. The left pleural cavity contained 75 cubic centimeters of
slightly cloudy fluid. The right was almost completely obliterated
by an organizing fibrinopurulent exudate which bound together the
visceral and parietal layers. The left lung was partially collapsed
and covered by a thickened pleura, bluish purple in color, which at
the base and in the interlobar area was finely granular. Crepitation
was present at the apex, the anterior surface, and the borders of
the lung; elsewhere the consistency was increased. On section there
was a frothy exudate from the apex and extreme base. These were deep
red in color, while the intervening surface of the lung was paler,
but broken by many small, white, elevated nodules which at first
glance resembled tubercles (Fig. XXXIX). On close examination each
of these was seen to have a small, depressed center from which pus
could be expressed, and on dissection this was seen to be the wall
of a bronchiole. The right lung was more voluminous and covered by a
thick, grey, fibrinopurulent exudate except on the upper anterior
border where there were a few small areas of interstitial emphysema.
On section the pleural exudate was seen to be sharply demarcated
from the lung parenchyma by a fine red line. The pseudotubercles of
the other lung were here even more marked and from each exuded a
yellow pus which partially obscured the pinkish-grey translucence of
the surface (Fig. XL). The lumina of the larger bronchi were
distended. The hilic and bronchial glands were enlarged and grey.

Microscopic examination of sections from the lung showed an
extensive bronchopneumonia. The alveoli of an occasional group of
lobules were filled with serum or red blood cells, while still other
areas showed foci of necrotizing pneumonia, actual miliary abscesses
in which there were large clumps of bacteria (Fig. XLI). Throughout
the sections, however, the striking change was an organization of
the exudate, which varied from a few fibroblasts to a well defined
connective tissue almost obliterating the normal architecture (Figs.
XLI and XLIV). The alveolar walls in some areas showed edema only,
in others they were almost replaced by a thin line of fibrous
tissue, and in still others, by a hyperplasia of the epithelium
which almost filled their lumina. The bronchi exhibited similar
changes, their lumina were filled with an exudate of desquamated
epithelium and leucocytes, which in some places was organizing (Fig.
XI), and there was a regeneration of epithelium evidenced by a
piling up of the cells and the presence of mitotic figures in them.
The interstitial tissue showed some edema. The tracheal epithelium
was intact, but a few leucocytes and lymphocytes were scattered
through the submucosa.

Pneumococcus Type II was recovered from the blood, pleural fluid,
and lung. B. influenzæ was also demonstrated in the lung by smears
and cultures.

In contrast to this example of a very diffuse, organizing pneumonia, associated with a marked peribronchial organization where the illness lasted for three weeks with hardly a remission throughout its course, the following example of necrotizing and organizing lobar pneumonia may be considered.

_Autopsy No. 183._

A white male, aged 46 years, was admitted to the New Haven Hospital
on January 9, 1919, complaining of “pneumonia.” The family history
was unimportant. He stated that he was in the hospital twelve years
ago with typhoid fever and again five years ago with acute
cholecystitis.

His present illness began two weeks previous to admission with
chills, fever, anorexia, nausea, vomiting, and a slightly productive
cough. He was prostrated and drowsy, but could not sleep. On
admission his temperature was 101.5°F., the pulse 124, and the
respirations 34 per minute. He was cyanotic and dyspnœic. The right
chest showed signs of consolidation, and fluid below the 3rd
interspace. The white blood count was 8,200 cells per cubic
millimeter, 89% being polymorphonuclear leucocytes. The patient died
eighteen hours after admission.

The autopsy was held four hours after death and the essential
findings were as follows:—

Twelve hundred cubic centimeters of fibrinopurulent fluid were found
in the right pleural cavity and the visceral and parietal pleura had
a thick, yellow coat of fibrin. The right lung was voluminous,
retained its shape on removal, and weighed 1,800 grams. The lower
two lobes were consolidated and the upper lobe was atelectatic. On
section the latter was slightly congested, but not consolidated. The
lower two lobes were fairly smooth and grey, mixed with red areas,
and exuded thick, sanguinous pus. They also showed several necrotic
areas in the central portion and, in some instances, cavities 1
centimeter in diameter filled with sanguinous pus had formed. The
bronchi contained the same material, and on its removal a deep red
mucosa was exposed. The left lung showed some fibrous pleurisy over
its lateral, posterior, and diaphragmatic surfaces. There was a
firm, puckered scar at the apex. The lung crepitated throughout, and
on section was essentially normal except for moderately intense
injection of the bronchi. The hilic nodes were enlarged, soft,
succulent, moderately injected, and pigmented. The trachea was pale,
but was covered by a mucopurulent exudate. The right side of the
heart was moderately dilated. The spleen was not enlarged, but was
softened and congested. The liver was pale, slightly decreased in
consistency, and congested. The kidneys and adrenals showed cloudy
swelling. The gall-bladder contained several stones, had a thickened
wall, and was bound to the pylorus by firm, fibrous adhesions.

Microscopic examination of the lung showed the alveoli filled with
an acute inflammatory exudate in many stages of degeneration and
hyalinization (Fig. XLII). Abscesses were frequent, but were for the
most part small. A similar necrotic mass was contained in the
bronchi. There were, however, features of the microscopic picture
that outweighed those already described. The alveolar and
bronchiolar exudates were everywhere being invaded by a young
granulation tissue, rich in fibroblasts and capillaries. Mononuclear
cells abounded in the new tissue. Even more striking than the
mesodermal new growth was the epithelial proliferation which could
be seen in many areas. It not only attempted to cover the denuded
bronchial surfaces, but stretched over masses of exudate and
granulation in the lumina and extended in tongue-like projections
for a considerable distance into the surrounding lung tissue (Fig.
XLVIII).

FIG. XXVII. AUTOPSY NO. 115. HERE THE HEMORRHAGIC CONSOLIDATION
INVOLVES THE DEPENDENT PORTION OF THE LUNG; CONTRAST THIS WITH THE
EDEMATOUS AND EMPHYSEMATOUS UPPER LOBE.
]

FIG. XXVIII. AUTOPSY NO. 118. THE CONSOLIDATION IS GREY IN COLOR AND
LOBAR IN TYPE. IN THE CENTER OF THE HEPATIZED LOBE THERE IS A
LARGE HEMORRHAGE. THE UPPER LOBE IS CONGESTED AND EDEMATOUS.
]

Cultures of the blood, lung, and pleural fluid showed gram-positive,
bile insoluble diplococci which formed chains, and morphologically
and culturally were Streptococcus mucosus capsulatus.

These two examples differ widely in the distribution of the pulmonary involvement. They show the acute inflammatory process persisting and complicating the attempt at repair, which manifests itself, not only by the formation of granulation tissue, but also by extensive epithelial proliferation.

Still a third type of chronic lesion is manifested in Autopsy No. 209, where the necrotizing and organizing process in the pulmonary parenchyma is associated with typical saccular bronchiectatic cavities.

_Autopsy No. 209._

A white woman, aged 55 years, was admitted to the New Haven Hospital
complaining of weakness and ill health following pleurisy. For the
past seventeen years she had suffered from a gradually progressing
arthritis, which had resulted in marked deformity and disability.
Five weeks before admission she became ill with chills, fever,
cough, and pain on both sides of the chest. Thereafter, her general
condition had gradually grown worse.

Physical examination showed a markedly emaciated white woman with a
high degree of arthritis deformans. Dullness and fine râles were
present at the left apex. The temperature was but slightly elevated
until three days before death, when it rose to 101°F. and slight
dullness developed at the right base with bronchial breathing and
fine râles. The white blood count, which on admission had been 9,200
cells per cubic millimeter, rose to 15,000 per cubic millimeter. She
died after a seven-weeks’ illness.

At necropsy, with the exception of the joints, little of interest
was found outside the thoracic cavity. On the posterior and
diaphragmatic surfaces of both lungs fibrous adhesions were present
binding the visceral to the parietal pleura. The right lung was
moderately voluminous and grey in color over the upper lobe, but had
darker red areas over the surface of the lower lobes. Patches of
increased consistency were found in the lower part of the upper
lobe, in the middle lobe, and at the base. On section there was a
slight, red, serous exudate. The surface over the more solid areas
was somewhat translucent, grey or light red, and was firm and not
friable. The bronchi of the lower lobes were conspicuous, and at the
extreme base so dilated as to give almost a honeycombed appearance.
From them yellow pus exuded. The left lung was less voluminous and
showed some increase in consistency throughout. In the lower lobe
this was more uniform, but the upper had a shotty feeling. On
section the upper lobe showed many hard or caseous nodules, with
occasional patches of grey, gelatinous pneumonia. One small cavity
was present about 3 centimeters from the apex. The lower lobe showed
no gross evidence of any tuberculous process. Many pseudotubercles
projected from the red surface, but from each pus could be expressed
exposing the slightly congested wall of a bronchiole. At the extreme
base two small cavities filled with yellow pus were present (Fig.
L).

Sections from the left upper lobe showed, microscopically, both a
chronic and acute tuberculous process. Tubercles with a definite
wall were present, but there were also large areas of caseation. The
tissue between showed interstitial organization with mononuclear
infiltration and occasional groups of leucocytes. The bronchial
epithelium exhibited no marked change, but the bronchi were filled
with pus cells.

Sections from the left lower lobe and from the right lung showed
both necrotization and organization. The alveoli contained an
exudate, fibrinous, serous, and hemorrhagic, but predominantly
leucocytic. There was slight necrotization of alveolar walls in some
areas with infiltration of leucocytes in them and in the
interstitial tissue. Several sections showed a marked degree of
interstitial organization (Fig. XLVI). The bronchi were filled with
a purulent exudate which sometimes involved the walls to form a
peribronchial abscess. The walls of other bronchi showed great
thickening with infiltration of both mononuclear cells and
leucocytes, and many saccular dilatations were found (Fig. XII).

The post-mortem blood culture showed a small, gram-negative,
hemoglobinophilic bacillus (B. influenzæ). Cultures from lungs and
bronchi yielded hemolytic streptococci, and Staphylococcus aureus
was also present in the lung.

_Summary._

Of the ninety-five cases included in this report, twelve showed the reparative process in a more or less marked degree. Furthermore, the twelve showing organization had an illness averaging twenty-seven days in duration, whereas for the eighty-three cases in which there was no organization, the period of illness averaged nine days. Thus, it appears that the early fatal termination of the disease in the latter group is responsible for the absence of organization.

With one exception, when organization was encountered, the disease had run a relatively acute course without marked remission until death. In this instance, the fatal outcome was the result of an accident at a time when all the clinical evidence pointed toward a subsidence of the acute disease. The history of this patient is abstracted below, for it may throw light upon possible relapse and upon late, chronic, respiratory changes.

_Autopsy No. 163._

A white male, aged 35 years, was admitted to the New Haven Hospital
on December 5, 1918, complaining of “cough, pain in the chest, and
headache.” For six days he had had fever, chills, and severe frontal
headache, and for three days pains in the chest. He had also had
“coryza” and epistaxis. The family and past histories were
unimportant.

The physical examination showed a well developed and well nourished
male, who was slightly jaundiced and markedly prostrated. The
conjunctivæ were injected. The heart, abdomen, extremities, and
right lung were negative. In a small area outside the left nipple
and extending into the axilla, tubular breathing and subcrepitant
râles were heard, but no definite signs of consolidation were made
out. The physical signs remained the same during the eight-day stay
in the hospital. At entrance his temperature was 102.8°F. In twelve
hours it fell to 100°F., then rose to 103°F., where it stayed for
twenty-four hours, falling by lysis and remaining normal for the
three last days. On his eighth day in the hospital, the patient
suddenly collapsed and died within fifteen minutes.

The autopsy was held one hour after death and the essential findings
were as follows:—

The peritoneal cavity contained 100 cubic centimeters of clear,
straw-colored fluid and the viscera, particularly the liver, were
acutely congested. The right side of the heart was greatly dilated;
and on opening the pulmonary artery _in situ_ considerable blood
gushed forth under pressure and a huge, tortuous embolus completely
filled the vessel and its branches (Fig. LIII). The veins of the
vesicoprostatic plexus on the right, and the right internal and
external iliac veins contained thrombi, and it was evidently from
this region that the embolus had been set free. The pleura of the
lower third of the left lung over an oval area about 13 × 5
centimeters was bound to the parietal pleura by pinkish-grey,
translucent adhesions which were evidently of comparatively recent
origin. Here the lung was firmly consolidated, but it was apparently
normal elsewhere. On section the consolidated area was silvery grey,
with a pink tinge, comparatively dry and smooth. In some areas,
especially about the bronchi, delicate, silvery grey, translucent
strands could be seen sweeping out into the surrounding lung, which
contained no air. The remainder of the lung was air-containing. The
trachea showed moderate congestion most marked near the bifurcation.
The hilic lymph nodes were enlarged, soft, congested, and succulent,
as well as anthracotic.

FIG. XXIX. THE VESSELS OF THE ALVEOLAR WALLS ARE CONGESTED AND
CONTAIN A LARGE NUMBER OF LEUCOCYTES. THE EXUDATE IS COMPOSED
ALMOST ENTIRELY OF WHITE BLOOD CELLS, IN THE BODIES OF WHICH
INNUMERABLE BACTERIA MAY BE SEEN. COMPARE FIGURES XXI, AND XXXII.
]

Microscopic examination of the viscera showed acute congestion and
some degree of cloudy swelling in the liver and kidneys. The
sections of the lung through the consolidated area showed the pleura
replaced by a thick layer composed of large and small mononuclear
cells, some red blood cells, a rare polymorphonuclear cell, and
great numbers of fibroblasts and budding capillaries. Some of the
alveoli contained many red blood cells, a few polymorphonuclear and
mononuclear cells, some fibrin, and in many areas fibroblasts were
organizing this exudate (Fig. XLV). Organization was also present
around the bronchi and these contained mucus, pus, and desquamated
epithelium. Frequently strands of fibroblasts were seen sweeping
through the bronchiolar exudates, and in a few instances they had
completely filled the lumina.