In the prosecution of the scientific study of any disease, the great
temptation is to differentiate its various manifestations with the
intention of elaborating a classification. While there may be more or
less distinct types of pulmonary involvement in influenza, so many
intermediary forms appear in an extensive series of cases, that any
classification must necessarily be arbitrary. Here, such an attempt at
classification is beset with unusual difficulty, because, in the vast
majority of cases which come to anatomical observation, the disease is
fulminating. The lesions are more uniform in character than in an
experimental study where the material is arranged so as to include
intermediary and chronic stages, which in man are only encountered when
accident causes death. These gaps in the study cannot be supplemented
with experimental observations, because attempts to reproduce this
disease have failed, even in human subjects. From the literature it
appears also that variations in the extent, and perhaps in the
maturation, of the anatomical involvement may be represented in
different proportions for different localities (1, 2, 17, 55, 92, 162).
Therefore, no sharp differentiation may be drawn between the more or
less definite stages which are seen at the post-mortem table; still, for
convenience of description, certain of the lesions which occur more
frequently and are more widely differentiated may be considered
separately.
The disease, as has been indicated, may be confined to the bronchial
tree. In these circumstances, it is almost necessary to suppose that the
larger bronchi alone are involved. When the delicate bronchioles are
affected, there is always a more or less extensive involvement of the
pulmonary parenchyma (124), for the bronchioles have a more direct
communication with the alveoli, and their walls present a less
formidable barrier to the extension of the inflammation to the
surrounding air sacs.
[Illustration:
FIG. XI. AUTOPSY NO. 140. ILLUSTRATES A LATE CHANGE IN THE BRONCHIOLE;
THE EXUDATE IS BEING ORGANIZED AND THE EPITHELIAL LINING IS
PROLIFERATING AND HAS INVADED THE SURROUNDING LUNG TISSUE. COMPARE
FIGURES XLVIII AND XLIX.
]
[Illustration:
FIG. XII. AUTOPSY NO. 209. A SMALL BRONCHIECTATIC CAVITY FILLED WITH
PUS. THE GROSS APPEARANCE IS ILLUSTRATED IN FIGURE L.
]
[Illustration:
FIG. XIII. AUTOPSY NO. 96. RIGHT LUNG. A WATER COLOR DRAWING OF A
GROSS LUNG IN THE ACUTE STAGE. NOTE THE SIZE OF THE LUNG, THE
HEMORRHAGES ON THE PLEURAL SURFACE, AND THE BLUE AREAS OF
CONSOLIDATION.
]
Clinically, there is reason to believe that the disease may begin with a
period of general malaise, during which the respiratory symptoms may be
more or less severe. In the fulminating cases, the malaise may be
associated from the beginning, not only with a tracheobronchitis, but
also with pulmonary involvement. In less severe types the malaise may be
accompanied only by tracheobronchitis, and may present no symptoms
referable to the pulmonary parenchyma; there may follow or not, a
definite period of clinical improvement, after which pneumonic
involvement becomes evident. However, even where a fulminating type of
the disease is not associated with clinical evidence of pulmonary
involvement, the post-mortem examination may show extensive change in
the lung parenchyma (110).
Whether this grouping of the disease is correct or is based upon a
fallacious deduction from more or less satisfactory clinical histories,
is open to question; and a decision may be reached from comparison of
the opinions based upon carefully observed cases treated in different
institutions. From the report of the epidemic at the Johns Hopkins
Hospital (Bloomfield and Harrop (14)), where two hundred sixty-eight
cases were studied in which the complication of pneumonia was uncommon
as compared with cases in other hospitals—the New Haven Hospital, for
instance—and where the percentage of the deaths was low, the conclusion
was reached that the disease is primarily a general one and that the
pulmonary involvement is secondary, just as in an exanthem, like
measles. By way of comparison, at the New Haven Hospital, where more
than eleven hundred patients with influenza were observed, the type of
disease described by Bloomfield and Harrop was relatively rare. Of
course, there were cases of that type where general malaise, with or
without respiratory symptoms, was followed by a period—usually of from
two to three days—of definite improvement in the symptoms; and later
extensive and serious pulmonary complications ensued. However, in
another group, largely composed of individuals who entered the hospital
seriously ill, the histories indicate an acute onset resembling that of
lobar pneumonia and with early manifestations of pulmonary involvement
(2, 17, 52, 145). This discrepancy, probably, may be explained in part
by variations in the sensitivity to minor indisposition on the part of
the different individuals.
The preceding review should aid in the correlation of the clinical types
of the disease with the respiratory lesions. All pulmonary lesions, from
the least to the most localized, may be explained either by a subsidence
of a less acute initial and diffuse involvement of the parenchyma, or by
a less rapid and progressive spread of the necrotizing and inflammatory
process from the upper respiratory tract through the bronchioles to the
alveoli. This conception does not take into account the significance of
the period of malaise, interpreted by the clinician as the period of
invasion, but attempts to correlate the respiratory symptoms with the
pulmonary lesions and their etiology.
Our own experience, like that of other observers (26, 104, 162), is that
all fatal cases of this disease show pulmonary involvement in the form
of pneumonia. The lesion varies greatly in intensity and in the amount
of pulmonary tissue affected. In the descriptions which follow, the more
diffuse and intense processes will be discussed first, and later those
in which the inflammation localized and terminated in pseudolobar,
lobar, lobular, or peribronchial pneumonia.
(1) ACUTE DIFFUSE FULMINATING TYPE OF PNEUMONIA
The majority of influenzal deaths have been examples of this acute type.
Out of ninety-five cases, the total number studied, forty-four belong to
this group in which the average duration of illness was nine days. They
form the basis of the description which follows.
_Gross Picture._
A striking feature of the external examination of the body is the
intense rigor which involves all the muscles and is broken only with
difficulty (78). This is associated with a rapid settling of the
unclotted blood in the dependent parts which gives them an intense blue
or bluish-purple color. The erythema of the skin which has been
described clinically is not recognizable at the post-mortem table. There
is, however, cyanosis of the face which reaches an intensity explained
by the fact that this disease so often affects healthy, well nourished,
muscular individuals. In a few instances the cyanosis is more extensive
and gives a plum color to the entire body. All the mucous membranes
share in the intense congestion and discoloration of the face. Slight
jaundice is common, but marked variations in intensity occur. The
external nares and the lips are almost invariably covered with
blood-stained crusts. Even in the decubitus position, a thin, sanguinous
fluid tends to escape in large quantities from the nose and mouth. The
large veins of the neck are usually prominent, and the chest voluminous.
Distinct splanchnic engorgement is evident as soon as the peritoneal
cavity is opened. The liver extends below the costal margin and is dark
in color, but otherwise the abdominal cavity presents nothing
characteristic of the disease. The diaphragm does not extend as high as
usual, and the pleural cavity almost invariably contains an excess of
fluid. Usually the quantity is small, but, on the other hand, it may be
considerable, and in twenty-one of the forty-four cases the fluid
exceeded one hundred cubic centimeters. The turgidity of the mediastinal
tissues varies somewhat in degree (27). Generally the pericardial sac is
smooth and glistening on both visceral and parietal surfaces; the
pericardial fluid is not materially changed. Frequently (seventy per
cent) there is dilatation of the right side of the heart (138, 141,
157), but aside from an occasional small endocardial or subepicardial
hemorrhage (90, 108, 156), there are no lesions of consequence in the
heart attributable to this disease[5] (162).
[Illustration:
FIG. XIV. AUTOPSY NO. 96. LEFT LUNG. NOTE ITS SIZE AND THE PATCHY
CONSOLIDATION.
]
[Illustration:
FIG. XV. AUTOPSY NO. 149. ILLUSTRATES ONE OF THE MOST STRIKING EARLY
PULMONARY LESIONS; THE DILATATION OF THE TERMINAL BRONCHIOLES AND
THE HYALINIZATION OF THEIR EPITHELIUM. COMPARE FIGURE XVI.
]
[Illustration:
FIG. XVII. AUTOPSY NO. 133. HYALINE THROMBI AND NECROSIS OF THE
ALVEOLAR WALL. COMPARE FIGURES V, XV, XVIII, XIX, XXXI AND XXXII.
]
The lungs are extremely voluminous (12, 17) due in part to an
accumulation of liquid within them. This finds its way into the trachea
and completely fills the latter structure with blood-stained, syrupy
fluid, with purulent material, or with a mixture of these (2, 90, 107,
157, 162). At first the pleural surface is smooth and often quite even,
but on closer inspection, a minute granulation is suggested. In many
cases even close examination does not allow the conclusion that an
exudation of anything but serum has occurred through this membrane,
except in localized foci. These foci more frequently involve the
interlobar pleura and that of the lower lobes (112, 143). The volume of
the lungs, often great enough to obliterate the pericardial area, is one
of the two most characteristic features of the external examination. The
other feature is their color. Small, bright red hemorrhages may occur
anywhere. The larger patches are the most striking. Violet, purple, or
dark brown areas, irregular in shape and distribution, are more
frequently found on that portion of the pleura over the lower two-thirds
of the lung. Between the deeply colored zones, there are pale pink areas
which involve the lowermost edge to the least degree, the anterior
margin somewhat more, and the apex of the lung most of all. The darker
portions just referred to may project above the surface and may be
circumscribed, resembling huge, fresh hemorrhagic infarcts (41, 108).
The alveolar walls are not seen through the pleural surfaces in these
darker zones. The pale pink areas, usually at the level of the more
intensely colored zones, may be elevated and the dilated air sacs are
distinctly made out through the pleura (Fig. XIII). At the hilum, the
lymph glands are large and soft. When cut, fluid escapes and is often
blood-stained. The cross section may present a distinct, diffuse,
hemorrhagic appearance (162). At the hilus, too, the lymphatics,
distended here and there over the surface of the pleura, are most
affected. The congested bronchial mucous membrane and the exudate in
these structures has been described.
After removal, the lung retains its shape, but is more flaccid than the
consolidated lung of lobar pneumonia. It cuts with very little
resistance and immediately a large amount of a syrupy, pink fluid
escapes and obscures the entire area. With the fluid scraped away, the
variations in the consistency of the lung become visible. The pale areas
around the borders and chiefly at the apex in which the air sacs are
discernible with the naked eye, sink slightly below the remainder of the
surface, and the pleural edge inverts. The individual lobules of the
lung in these areas are more conspicuous than normal, because the
interstitial tissue bearing the lymphatics and vessels, as well as that
around the bronchi and larger blood vessels, does not lose its edematous
appearance as quickly as the alveoli (40, 92, 110, 164), and,
consequently, these grey lines and points stand up somewhat more
prominently.[6] In contrast with the paler areas which are prone to
slight collapse, the remainder of the cross section retains its more
smooth and even surface. The alveolar walls are not distinctly made out,
but the terminal bronchioles often make themselves evident by the nature
of the material which is within and by their distinct dilatation (1, 67,
110, 149, 162). The more firm areas stand out, too, on account of their
difference in color. The scheme is not unlike that seen on the pleural
surface, and while dark, almost black, infarct-like areas occur on the
cut surface, the solid areas are more likely to be translucent, dull,
light red, brown or even grey. They have a surface similar to a very
fresh, tuberculous, gelatinous pneumonia, but the color differs from the
cloudy grey of the latter on account of the admixture of blood in the
exudate and the great congestion of the vessels (Fig. XIV).
_Summary._
The well developed post-mortem muscular rigidity, the lividity of the
dependent parts, of the face with its mucous membranes, and often of the
trunk, the jaundice variable in extent, the crusts of blood on the nares
and mouth, and the splanchnic dilatation are features which prepare for
the gross picture presented by the thoracic organs. The increased
moisture within the pleural cavities associated with the even,
translucent pleural surface, whose dilated lymphatics become more and
more prominent towards the hilum, the large succulent lymph glands, and
the exudate in the bronchial tree, are all striking, but more
characteristic of the gross picture, is the great increase in volume of
the lung itself, mottled with brilliant colors. The lung, too, is very
wet and on section, after the syrupy, blood-stained fluid escapes from
the less definitely consolidated zones, the latter appear, not as the
usual granular, firm areas of hepatization, but have more the
consistency of a gel, and also its translucence. Characteristic of this
disease as these changes may be, the specificity of the fundamental
lesion in the respiratory tract, becomes more emphatic after study of
its histology (92, 162).
_Histological Picture._
No matter what the portion of the lung from which the sections are
derived, the fundamental changes found are the same. The subpleural
sheets are spread wide apart, now by empty spaces, now by coagulated
fluid. The process extends from the surface through the interlobular
septa (Fig. XX), and is accentuated where the connective tissue is more
prominent around vessels and bronchi. The nature of the infiltrate in
the subpleural and interstitial tissues becomes more evident in the
alveoli, which likewise are filled. The material varies somewhat in
appearance, probably dependent upon its proteid content. Not
infrequently the alveoli contain a homogeneous, pink-staining mass,
which resembles the colloid of the thyroid gland. Again, it may be
simply a coarse granular precipitate (Fig. XXIII), and in still other
instances, small sticks and strands form the bulk of the alveolar
content (47, 92, 140, 156). This subpleural, interstitial, perivascular,
peribronchial, and alveolar edema, which is a term applicable to this
collection of fluid, is very prominent, and although its intensity
varies in different portions of the lung; and although it may be
replaced in some areas by other types of exudate, unquestionably, this
is the dominating expression of the inflammatory process in the early
stage of the disease.
As might be expected from the gross appearance, the alveoli vary in
size. At times slightly collapsed and at other times overdistended,
their lumina are still the seat of the inflammatory exudate, although
the mechanical change may allow of some variation in the appearance of
their walls. As a rule, however, the alveolar wall is prominent and owes
its conspicuousness to the tortuous, engorged vessels within. These
vessels contain red blood cells almost exclusively, and on account of
the partial, occasionally complete, loss of the lining epithelium, the
alveolar wall appears as a huge, dilated arteriole (101) separating the
lakes of coagulated material in the spaces (Fig. XXIII). There are
areas, as indicated above, where the alveolar content may be more
definitely arranged in the form of beaded or homogeneous strands of
different caliber; the smallest resemble delicate threads. They tend to
converge toward the alveolar wall like wheat in a sheaf, and often pass
through this wall by way of the so-called pores of Cohn; as soon as the
body of the neighboring alveolus is reached, they again present a
fan-like expansion into innumerable, fine strands (Fig. XXII). Where the
exudate is more fibrinous, the alveolar wall is less likely to be
distended, its vessels are not so prominent, and their content of red
blood cells is definitely decreased. Still this is not the most extreme
type of alveolar exudate met with at this stage. Perhaps, the most
striking, although not the most frequent, exudate has a superficial
resemblance to a huge, red blood clot, and it may be difficult to make
out the alveolar walls separating the masses of well preserved red blood
cells that fill the alveolar spaces. These areas are indistinguishable
from infarcts and may be associated with thrombotic arteritis in near-by
pulmonary vessels (47) (Figs. XXIV and XXV). Among the red blood cells
an occasional strand of fibrin, a desquamated alveolar epithelial cell,
and rarely a polymorphonuclear leucocyte may be encountered. The
alveolar wall itself varies in the definition of its outline. When its
vessels are greatly distended, when its alveolar epithelium is gone, and
when its content consists largely of red blood cells, it is difficult to
distinguish from the exudate which it encloses. However, when it is more
compressed or when its epithelial lining cells are still more or less
intact, it may be seen as a blue-staining strand under the low power of
the microscope, for the well preserved nuclei lend it prominence.
[Illustration:
FIG. XVI. AUTOPSY NO. 112. BACTERIA DEVELOP IN THE HYALINE NECROTIC
EPITHELIUM OF THE TERMINAL BRONCHIOLES. HERE THEY FORM CIRCUMSCRIBED
MASSES THAT SIMULATE NUCLEI. COMPARE FIGURES V, VIII, XV, AND XVII.
HELIOTYPE CO. BOSTON
]
[Illustration:
FIG. XVIII. AUTOPSY NO. 155. ILLUSTRATES A MILD FORM OF PULMONARY
INTERSTITIAL EMPHYSEMA.
]
[Illustration:
FIG. XXII. AUTOPSY NO. 175. AN ALMOST PURE FIBRINOUS EXUDATE. THE
ALVEOLAR WALLS ARE SLIGHTLY HYALINIZED AND THEIR EPITHELIUM IS
ALMOST ENTIRELY LACKING.
]
There are, of course, variations in the extent of the serum, the fibrin,
and the hemorrhage in the exudate of the alveoli, and while these
different types may occur as pure forms, often they are associated. In
still other areas and varying in prominence, one finds as characteristic
an exudate, not only of serum, strands of fibrin, and red blood cells,
but also a diffuse dotting of the exudate with bacteria, singly, in
pairs, clumps, and chains (92, 164) (Fig. XXI). This type of reaction is
uncommon in pulmonary disease. It resembles more closely a streptococcus
cellulitis such as is encountered frequently in the subcutaneous
tissues, for example, a woody phlegmon, or a sero-hemorrhagic exudate
like the avirile response to a rapidly fatal hemolytic streptococcus
serositis. A similar reaction has been reproduced experimentally in
animals which have been rendered aplastic with benzol previous to
pulmonary insufflation, and it is conceivable that the lack of
polymorphonuclear response in the inflammatory exudate may be associated
with some such general destruction or temporary suspension of leucocytic
formation (160).
A more striking picture, however, even than this aplastic alveolar
exudate appears in the terminal bronchioles. In many instances, these
are conspicuous on account of their size, for they are dilated to form
prominent, often irregular, sacs (Fig. XV). The distention of these
terminal bronchioles may be so great that the surrounding alveoli are
compressed. What makes them even more conspicuous is their lining, once
epithelium, but now a swollen, thick, homogeneously staining material,
with complete loss of architecture; the material forms (with hematoxylin
and eosin) a red band limiting the lung tissue and sharply demarcating
it from the exudate within the bronchioles (48, 92). However, this
ribbon of red, often thickened by fibrin deposition, is not always pure,
for bacteria thrive in the dead tissue. They occur singly, paired, in
chains, and also as circumscribed, dense masses which in size and
position, simulate nuclei (162) (Fig. XVI). This same hyalinization of
the epithelium, it will be recalled, occurs in the larger bronchi (Fig.
V), and there, too, bacteria frequently develop in the dead tissue (Fig.
VIII). In the smallest bronchiolar ramifications, acute epithelial
necrosis is not infrequently encountered, even when the surrounding lung
tissue is relatively normal (Fig. XVI). That the process does not stop
with the epithelium, but, as in the larger bronchi, may extend through
the entire structure of the bronchioles, is manifest. Even the alveolar
walls may be involved and frequently homogeneous pink or red bands, now
the phantom of the former viable lung tissue, mark the presence of the
old wall of the alveolus (Fig. XVII). Occasionally, some architecture
remains in this pink ribbon and then the involvement seems to be
primarily in the vessels of the wall. Not all the vessels are involved,
and next to a hyaline thrombus in one, there may be fresh blood, usually
red blood, in its neighbor. The alveolar epithelium is usually denuded
and thus accentuates the intensity of the change.
The acute death which involves the tracheal, bronchial, and bronchiolar
epithelium and which may extend beyond the epithelium into the walls of
these structures and kill en masse the walls of the alveoli, is a lesion
which does not occur in other types of acute pulmonary infection.
However, in influenza, as after exposure to pulmonary irritating gases,
it is the lesion of characterization (158,159). The effects of this
change, of course, where it involves the alveolar wall, will vary with
the extent of the process; but given an absolutely necrotic wall, as yet
unstrengthened by inflammatory reaction, an expected result would be its
rupture with respiratory movement. The point of rupture is important,
but where so many alveoli are involved, disturbance of continuity will
occur, occasionally in such position that the result will be the escape
of air into the interstitial tissues.[7] There is ample evidence that
this happens. Indeed, among the clinical manifestations of the disease,
interstitial emphysema of the lung spreading through the fascial planes
to the subcutaneous tissues of neck and thorax is well known; the
phenomenon is more frequent and extensive in influenza than in any other
disease (8, 17, 52, 143).
Interstitial emphysema is very striking at the post-mortem table. The
escaped air appears as beads along the interlobular septa, but on
account of their size they are always most conspicuous between the lobes
and along the vessels toward the hilum (162) (Fig. XVIII).
Histologically, a small bubble of escaped air confined to the
interlobular septum compresses the surrounding tissue with almost
complete atelectasis of many neighboring alveoli (Fig. XIX).
_Summary._
The diffuse involvement of all the lung tissue, chiefly with a serous
exudate in the subpleural, interstitial, perivascular, and peribronchial
tissues, as well as in the alveoli, is associated with other elements
which occur in aplastic reactions; red blood cells, fibrin, and
bacteria. Added to the aplastic exudate is an acute necrosis of
bronchial and alveolar epithelium involving at times the walls of these
structures; consequently, the histology of this disease is almost as
specific as that of any biological reaction.
(2) LOCALIZATION AND NECROTIZATION OF THE PNEUMONIC PROCESS
In the preceding description, the gross and microscopic anatomical
changes in the lung have been discussed minutely. The picture presented
persists, even though it becomes less intense, and forms a background
upon which later variations may be superimposed. There is no
justification for the opinion that the changes described are necessarily
the most acute, but it is presumably correct to suppose that an
aplastic, inflammatory reaction will terminate fatally more quickly than
a cellular reaction (160), and upon this basis the sequential
description in this narrative is arranged.
In the group of fatal cases of influenza, now to be discussed, the
lesions of the pulmonary parenchyma are characterized by more definite
lung consolidation. Thirty-nine examples presenting an average illness
of ten days are included in the following description.
_Gross Picture._
The external examination of the body includes nothing not described in
the previous group.
[Illustration:
FIG. XIX. AUTOPSY NO. 123. A SMALL AIR BUBBLE IN THE INTERSTITIAL
TISSUE. COMPARE FIGURE XVIII.
HELIOTYPE CO. BOSTON
]
[Illustration:
FIG. XX. AUTOPSY NO. 90. THE ACUTE SEROFIBRINOUS EXUDATE INVOLVES NOT
ONLY ALVEOLI, BUT ALSO SUBPLEURAL AND INTERLOBULAR BANDS OF
CONNECTIVE TISSUE. COMPARE FIGURES XXI, XXII, AND XXIII.
HELIOTYPE CO. BOSTON
]
The fluid of the pleural cavities varies volumetrically as described in
the preceding section. It is, however, usually not a clear fluid, but
varies from a slightly turbid, blood-stained material to a typical
purulent exudate. The cloudiness may be associated with minute flecks of
suspended material, but in no instance has this fluid been of the thick
inspissated type which formerly would have been designated as
empyema.[8] (This is mentioned with the knowledge that the term empyema
is being applied now to less viscid, purulent, pleural exudates). The
turgidity of the mediastinal tissue also persists, but it is very rare
indeed to find anything more than a small amount of clear fluid in the
pericardial sac. Only once was there a typical, fibrinous pericarditis
with effusion, and this occurred where a most extensive pleural exudate
was also present.[9] Where such complications have been described in
serous membranes, the bronchial lymph glands, particularly at the hilum
of the lung, are more involved and show, not only an increase in size
and a red color on cross section, but frequently also focal areas of
necrosis at the periphery, which appear as yellow patches and
subsequently undergo suppurative disintegration (2, 47).
The lung remains increased in volume and its surface is mottled with
vivid colors. Often these are an indication of deeper parenchymatous
change. The pale pink zones, through the pleural surface of which
distended alveoli are discernible, are still prominent in the upper
lobe, around the margins, and on the anterior surface of the lung. The
darker purple, slightly elevated, often circumscribed, infarct-like
areas (25, 34, 108) may occur anywhere, but are more frequent in the
lower lobes. Small, maroon, slightly depressed areas of atelectasis may
also involve the borders of the lung, usually the posterior borders; or
they may occur between larger and more elevated areas on either lobe.
Besides the purple, firm, projecting foci, paler pink or grey nodules of
similar consistence may be present and show no structure when viewed
through the pleura. The distribution of the different types of change is
variable, and, aside from the fact that they involve the middle and
lower lobes more frequently than the upper, no general statement is
possible. In a few instances, one lobe, almost always the lower, may be
more voluminous than the others, and although its pleura often suggests
lobular involvement, the masses tend to be confluent and suggest a
pseudolobar change. Sometimes, though rarely, this approaches a true
lobar type of consolidation. (Compare Figs. XIII and XXVII.)
Occasionally, the changes in the lung, except its increase in size, are
obscured by pleural exudate which may form a thick, buttery, rather
sticky mass on the surface (12, 19, 157) (Fig. XXXVII). Such pleural
exudates are rare, and likewise it is uncommon to find so little pleural
granulation as in the previous group. The roughening, as a rule, is not
uniform, but is more prominent over the lower lobes and in the
interlobar spaces than elsewhere. It may occur when there is no definite
increase in the fluid content of the pleural sac.
The lung, now sectioned, presents a surface in accord with the changes
suggested from the description of its external appearance. As compared
with the first stage the amount of syrupy, blood-stained exudate may be
definitely decreased, especially in the upper lobe or in those portions
of the lung where the solidification is less marked. Its character, too,
may be more cloudy, and more ropy, or viscid; it bathes the surface and
is scraped off in abundance with the blade of a knife from the
underlying consolidated foci (108, 156). The bronchi and bronchioles,
however, may be prominent, irrespective of the change in the parenchyma
itself. From their lumina, thick, yellow pus wells forth and their
mucous membrane is intensely congested. Where such involvement occurs in
unconsolidated portions of the lung, the bronchioles are even more
striking than in the hepatized areas in which the more widespread
changes obscure the process. The dilatation of the bronchioles,
especially in their smaller ramifications, is still conspicuous.
The consolidated areas vary greatly in size and number;[10] often they
are small and involve only single lobules, which now stand out as
granular, generally elevated patches on the surrounding congested plane.
Their color, as on the pleura, varies. They may be dark, almost
hemorrhagic, fading through the reds, pinks, and greys. They may be
firm, or, at the other extreme, honeycombed by small, often narrow,
cavities, from which a material similar to that described on the surface
wells forth. The latter change is more frequent if the consolidated area
is large. It has occurred most often in the pseudolobar and in the lobar
types of the process. The pseudolobar change is differentiated, not only
by the confluence of more or less definite lobular patches and by its
involvement of portions of contiguous lobes rather than a single lobe,
but also by variations in the color and consistence of the different
lobular foci. This is in contrast with lobar involvement where the
entire lobe is affected by a uniform process usually at the same stage
of development. Although the consistence may vary in different portions,
usually the same color is present throughout. (Compare Figs. XIV and
XXVIII.) In one instance where a solid, yellow lobe was found, its
center contained an irregular, fresh blood clot (Fig. XVIII), which
would be sufficient to differentiate this type of consolidation from
that of respiratory disease in which the initial lesion is less
destructive. Sometimes the softening in a hepatized lobule or group of
lobules is much more evident, and the zone becomes divided by irregular
channels filled with viscid, grey or brown material (108, 149, 162).
When such a condition lies just beneath the pleural surface, it may be
distinctly seen from without (Fig. XXXIII). The pleura bulges, the
normal topography of the local zone is lost, and it appears as a dull,
somewhat projecting, circumscribed patch, two or three or more
centimeters in diameter, the surface of which has a more or less
characteristic brown or brownish black opacity. As soon as this is
sectioned there pours from the cavity the liquefied exudate in which the
destroyed pulmonary parenchyma is mixed (Fig. XXXIV). Occasionally,
strands of tissue still traverse the cavity, but, as a rule, it empties
itself completely, and leaves a brownish black wall. The delicate, sweet
but persistent and penetrating odor is not so marked as with typical
gangrene.
_Histological Picture._
Sections from the least involved areas of the lung show a subsidence of
the alveolar exudate and the walls are no longer intensely engorged.
Perhaps the most prominent feature within the alveoli is the desquamated
cells, presumably alveolar cells with broken or pyknotic nuclei. Despite
the fact that so many cells of this type occupy the lumen of the
alveolus, its wall has a prominent lining of cubical epithelium. Often
mitotic figures abound in this new alveolar epithelial lining (Fig.
XLVII), an evidence of rapid regeneration in that portion of the lung
where the initial irritative process has subsided and where the
destruction has not been as deep as elsewhere (79). This picture may be
taken as positive evidence of an initial, diffuse, and general pulmonary
involvement, which, with the subsidence of the primary reaction, is
followed by localization resulting in the different types of
consolidation now encountered.
[Illustration:
FIG. XXI. AUTOPSY NO. 95. A TYPICAL APLASTIC ALVEOLAR EXUDATE COMPOSED
Of RED BLOOD CELLS, FIBRIN, AND BACTERIA. COMPARE FIGURES XX, XXII,
AND XXIII.
HELIOTYPE CO. BOSTON
]
[Illustration:
FIG. XXIII. AUTOPSY NO. 175. NOTE THE ABSENCE OF ALVEOLAR EPITHELIUM,
THE ENGORGEMENT OF THE VESSELS OF THE ALVEOLAR WALLS, AND THE SEROUS
EXUDATE.
]
[Illustration:
FIG. XXV. AUTOPSY NO. 92. THE EXUDATE CONSISTS ALMOST ENTIRELY OF A
MASS OF RED BLOOD CELLS. THE DESQUAMATED ALVEOLAR EPITHELIUM IS
SCATTERED THROUGH THE HEMORRHAGIC EXUDATE. COMPARE FIGURES XXIV AND
XXVI.
]
However, in such areas of slight change, the bronchi and bronchioles may
be distended and filled with polymorphonuclear leucocytes, exfoliated
epithelium, and bacteria (Fig. X). It is, of course, possible that
infection of the parenchyma may recur from these sources. Here the
extent of involvement of the bronchiolar wall is variable and analogous
to those described previously. Occasionally, too, where the alveolar
change has subsided, the interstitial tissue, particularly that which
divides groups of neighboring lobules, may retain its increased size
with fibrous tissue framework spread apart by exudate and punctuated
with an occasional circumscribed purulent mass (92, 95, 110, 156) (Fig.
XXXVI). Such a miliary abscess within the lymphatics of the interstitial
tissue may compress the neighboring air sacs, themselves entirely free
of inflammatory involvement. That these strands of interstitial tissue,
the conduits for the lymphatics, are important barriers against the
spread of an inflammatory process from lobule to lobule by direct
extension, is evidenced by the extreme variation in the amount and type
of involvement in neighboring lobules (Fig. XXX). This variation is
repeatedly encountered and the band of interstitial tissue, often
prominent on account of its edema, separates these lobules the more
clearly. In all probability, the sharp demarcation of the lobular
consolidation as described in the gross picture depends upon the change
in the interstitial tissue which tends to localize the infection (93).
This fact suggests that the process within the pulmonary parenchyma
spreads along the bronchial tree rather than from lobule to lobule.
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).
[Illustration:
FIG. XXIV. AUTOPSY NO. 92. AN ALMOST PURE HEMORRHAGIC ALVEOLAR
EXUDATE. COMPARE FIGURES VI, XXV, AND XXVI.
]
[Illustration:
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).
[Illustration:
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.
]
[Illustration:
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.
[Illustration:
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.
II. INFLUENCE OF THE RESPIRATORY COMPLICATION OF INFLUENZA UPON
TUBERCULOSIS OF THE LUNG
Thirteen of the ninety-five cases included in this report occurred at
the United States General Hospital No. 16, one of the large tuberculosis
camps. In five instances the patients had active pulmonary tuberculosis.
The remaining eight were members of the detachment and may be added to
the eighty-two from the New Haven Hospital, making a total of ninety
cases in which there was no clinical evidence of active pulmonary
tuberculosis at the onset of the acute respiratory disease. When these
ninety cases are analyzed, it is found that only two of them show
definite activation of an old tuberculous focus (82). One has already
been referred to (Autopsy No. 209); the other, presenting a much more
acute exudative and ulcerative tuberculosis, deserves special
consideration.
_Autopsy No. 194._
A white female, aged 27 years, was admitted to the New Haven
Hospital on November 8, 1918, complaining of “cold on the chest,
fever, cough, and prostration.”
The past and family histories were unimportant. Her illness began
one week before admission with dizziness, headache, vomiting, cough,
pains in back and legs, chilly sensations, and fever. She went to
bed the day after. The acute onset became definitely worse and pains
developed in her chest. On admission she was very weak, had a
temperature of 101.4°F., a pulse of 120, and respirations of 40 per
minute. The physical examination showed a very well developed and
nourished woman who was cyanotic but not dyspnœic. The pharynx and
tonsils were definitely injected. There were signs of consolidation
at the base of the left lung. The pneumonic process gradually
increased in the left, spread to the right, and involved the greater
portion of both lungs. Otherwise the physical signs did not change
greatly during her stay of thirteen weeks in the hospital.
Thrombosis of the left femoral vein was diagnosed about two days
before her death. The temperature curve was of interest. During the
first two days in the hospital it remained at 104°F. For two weeks
it was septic in character, being 102°F. in the morning and 104°F.
in the afternoon. Then for thirty days it was practically constant
at 102°F., only to become septic again, 98.6°F. in the morning and
103.4°F. in the afternoon, and it remained so until death. The pulse
curve ran essentially parallel to the temperature curve, varying
from 100 to 140 per minute. The respirations varied between 46 and
64 per minute.
The sputum showed Type IV pneumococcus. The blood culture was
negative.
[Illustration:
FIG. XXX. AUTOPSY NO. 169 (LEFT) AND AUTOPSY NO. 97 (RIGHT). THIS
CONTRAST IN THE EXTENT OF INFLAMMATORY INVOLVEMENT BETWEEN
NEIGHBORING LOBULES IS FREQUENTLY ENCOUNTERED.
]
[Illustration:
FIG. XXXIII. GANGRENE OF THE LUNG.
]
The autopsy was held four hours after death. The body was markedly
emaciated. The peritoneal cavity and its contents appeared normal,
though the liver was low. The right pleural cavity contained 150
c.c. of slightly cloudy, yellow fluid. The left was free from fluid.
Both lungs were bound to the chest wall by silvery grey, translucent
adhesions which were broken with slight difficulty. The right lung
was heavy, voluminous, retained its shape on removal, and was
consolidated throughout. Thick, creamy pus exuded from the cut
trachea. For the most part, the lung was covered by a recently
organized exudate several millimeters thick in which delicate blood
vessels could sometimes be made out. Beneath the pleura of the lower
three-fourths of the lung, were numerous, irregularly rounded,
slightly elevated, opaque, greenish-yellow areas resembling
conglomerate tubercles. These gave the lung a shotty or nodular
feeling. In the lowest lobe several of these areas had fused and
softened to form semifluctuant areas several centimeters in
diameter. On section the lower two-thirds of the lung was studded
with areas corresponding to those seen on the surface, which in many
instances had broken down and formed irregular cavities filled by
thick, green pus (Fig. LI). Between the green areas delicate strands
of new-formed fibrous tissue could be made out in all parts of the
lung. The bronchial mucosa was injected, the walls were irregularly
thickened and dilated and they opened into the ragged cavities noted
above. New-formed fibrous tissue was prominent along the bronchi.
One chalky white, old, encapsulated, tuberculous focus was found
near the apex of the left lung.
Microscopically, there were two distinct processes found in the
sections taken from various parts of the lung: an early miliary and
exudative tuberculosis, and a necrotizing and organizing
bronchopneumonia. Often the two processes were side by side, but
sharply demarcated, in the same section. In others, they might be so
intermingled that they could not be differentiated. The bronchi were
filled with pus and often could be seen opening into large abscess
cavities. The proliferation of the bronchial epithelium, as noted
elsewhere, also was a striking feature in these sections. The
pleural exudate was undergoing organization.
Streptococcus hemolyticus was found in the cultures of the lung,
blood, pleural fluid, and bronchi. In addition, the bronchi and
abscess cavities also showed Type IV pneumococcus and Staphylococcus
albus.
_Summary._
In this series of ninety-five cases, two examples of activation of an
old tuberculous focus by the acute respiratory process were encountered.
In both the pulmonary tubercular process was acute and played an
important rôle in the fatal outcome.