constitutional weakness, bad habits, etc., which lay a foundation for
unhealthy inflammatory processes, and for the pathogenetic elements
that bring about the gangrenous and septic and exhausting conditions;
second, to the special symptoms, such as severe pain in the side,
harassing cough, dyspnoea, etc. Remedies of the first class are quinia,
turpentine, early alcoholic stimulation, carbonate of ammonium,
antiseptics, as carbolic acid, etc. An anticipation from the beginning
of any irregular form of acute pulmonary disease of its termination in
gangrene is impossible, and hence early treatment is necessarily
general. It would be properly confined to the use of quinia, which
would be useful, either before or after the gangrenous element had
developed, in small doses frequently given, unless high temperature or
the septic process indicate the use of large ones. Turpentine
internally is desirable in proportion to the infectious or typhoidal
character of the attack. Its use by inhalation is beneficial when
gangrenous destruction has already taken place. Brandy or whiskey in
moderate and frequent quantities, one-half to one tablespoonful every
three hours, and carbonate of ammonium, meet the requirements which the
tendencies to debility indicate. Milk, milk-punch, beef and chicken
extracts should be given in the intervals between the administration of
medicines. This general plan is applicable throughout the pre- and
post-gangrenous stages. In the symptomatic treatment pain and a general
respiratory distress often demand attention. Opium is then useful, both
in relieving pain and moderating dyspnoea and cough. As these symptoms
are often urgent in the later stages of gangrene of the lung, the
treatment of the disease harmonizes both in its constitutional and
symptomatic aspects. Prescriptions can also be readily prepared which
contain remedies that have a decided effect in correcting the fetor of
the breath and expectoration, and thus evincing an influence on the
putrefactive process or ferment, which has become the prominent feature
of the disease. The author recommends that carbolic acid, in the dose
of one grain every four hours, be given for that purpose, and also its
use by inhalation. Assistance can sometimes be given by putting the
patient in such a position on the side as to promote the emptying of
the cavity.
Tapping a gangrenous cavity and the introduction of drainage-tubes may
be successfully resorted to. The cases suitable for such surgical
treatment have {306} been described by Fenger and Hollister[18] as
those where, "the presence of a gangrenous or ichorous cavity having
been ascertained, it is found that notwithstanding an outlet through
the bronchi for a portion of the contents of the cavity, it steadily
fills up again; the partial evacuation does not relieve the patient;
the infection of the healthy portions of the lung from the decomposed
contents of the cavity has commenced or is evidently about to take
place; the breath and expectoration continue fetid; absence of
appetite; increasing weakness, with or without fever, etc." For the
steps of the operative procedure reference may be made to the complete
directions given by the same authors or to works on surgery. The double
opening advised by the above authors would be the most efficient plan.
[Footnote 18: _Amer. Journ. Med. Sci._, Oct., 1881, p. 385.]
{307}
CROUPOUS PNEUMONIA.
BY ALFRED L. LOOMIS, M.D.
SYNONYMS.--English and American: Acute sthenic exudative pneumonia;
Primary lobar pneumonia; Vera peripneumonia; and Pneumonitis. _Fr._
Fluxion du poitine and Fièvre pneumonique; _Ger._ Pneumonia lobaris and
Lobäre Lungenentzündung.
DEFINITION.--Croupous pneumonia is an acute general disease with a
characteristic local pulmonary lesion. Anatomically considered, it is
an acute inflammation of the vesicular structure of the lungs,
resulting in infiltration of the alveoli, with inflammatory products,
which renders them impervious to air. This condition is known as
hepatization.
HISTORY.--Until the time of Laennec, pneumonia and pleurisy were
described as one disease. Hippocrates said that pleurisy was "a disease
quickly fatal, and characterized by sputa of various colors." Although
these two diseases were undifferentiated, accurate descriptions of the
lesions and objective signs of pneumonia have come to us from the
earliest medical writers.[1]
[Footnote 1: Thucydides, _The Plague at Athens_, B.C. 430.]
Much of the early history of this disease is interwoven with the
detailed accounts of a great variety of pulmonary symptoms which
occurred in the epidemics and plagues which prevailed in Eastern Europe
in the centuries just preceding the Christian era, and in Western and
Southern Europe during the sixteenth and seventeenth centuries. The
black death has been regarded by some as an epidemic of pneumonia.
While it is probable that in most of these epidemics the lung was early
involved, and that its implication hastened death, yet no proof exists
to sustain the belief that they were other than epidemics of typhus
fever, dysentery, and those (as yet unknown) fevers which collectively
were named plagues. That many of these plagues were complicated by
pneumonia there is scarcely room for doubt.
French investigators were the first to separate the pneumonic process
from all other morbid processes which occur in the thoracic organs.
Valsalva, Morgagni, and Boerhaave gave accurate descriptions of
pneumonia, but they did not sharply distinguish it from pleurisy.
Bichat and Pinel separated collapse of the lung attending pleuritic
effusion from inflammation of the lung-substance.[2] Laennec was the
first to draw the line sharply between pneumonia and pleurisy, and to
him, more than to any other observer, is due the credit of describing
pneumonia as a distinct disease. With his labors begins a new era in
the history of pulmonary inflammations.
[Footnote 2: _Nos. phil._, ii., Pinel.]
Grisolle's work[3] is especially valuable in statistics relating to the
climatic element in the development of pneumonia and its comparative
frequency among different races. The elaborate treatise on the
geographical distribution of pneumonia by Ziemssen has furnished data
for a more accurate knowledge of its geographical boundaries. Following
in the footsteps of Laennec, {308} Chomel, Stokes, Addison, and many
laborers of our own day have furnished the material from which the
clinical and pathological history of pneumonia is now being
constructed.
[Footnote 3: _Traité de la Pneumonie_.]
Recently, Jürgensen has strongly advocated the infection theory of
pneumonia, and has presented strong arguments in support of his
opinions. Sturges of London and Cohnheim[4] advocate the use of the
term pneumonic fever, and the former gives a most interesting general
comparison between it and the affections which he regards analogous to
it. Careful pathological experiments have recently been made by
Heidenhain, Sommerbrodt, Schuppel, and Klebs[5] with a view to
establish the germ-theory of pneumonia.
[Footnote 4: _Leçons de Chir. méd._, 1877, p. 17.]
[Footnote 5: _Arch. für experiment. Pathol._, p. 420.]
The literature of the past ten years is richer in the development of
facts and experimental investigations than all the centuries that have
preceded; and these recent experiments, combined with modern statistics
and the results of the microscope in pathological histology, have given
to croupous pneumonia a separate and distinct place in the list of
pulmonary diseases.
MORBID ANATOMY.--Anatomically as well as clinically, there are three
recognized stages in croupous pneumonia: 1, Stage of engorgement or
congestion; 2, Stage of red hepatization; 3, Stage of gray
hepatization, resolution, or purulent infiltration (suppuration).
It has been claimed that the stage of engorgement is preceded by a dry
stage, or "stage of arterial injection," in which the lung-tissue is
dry and of a bright-red color. It is evident that congestion of the
minute branches of the pulmonary artery would not give to the
lung-tissue a bright-red color, and if such a condition exists it must
be due to injection of the bronchial vessels. It is by no means proven
that such injection ever precedes pneumonic engorgement. In the stage
of engorgement that portion of the lung which is involved in the
pneumonic process does not collapse when the thoracic cavity is opened.
The affected portion of lung is distended and firmer than normal
lung-tissue, and when pressed upon crepitates less, often remaining
indented after the pressure is removed. The lung is not entirely
airless, for by pressure the air can be forced from one portion of it
to another. Its color is darker than normal, usually being of a
brownish-red or purple. There is an increase not only in its actual
weight, but in its specific gravity. On section a thin, frothy,
blood-stained serum exudes, and sometimes on pressure flows freely from
the cut surface; occasionally this exudation is tenacious. When alcohol
is added to this fluid, it coagulates into a granular, amorphous mass.
The capillaries around the air-cells are distended, and dark blood
oozes from their divided ends. Occasionally, upon close examination,
there may be seen beneath the pleura and between the air-sacs small
points of blood-extravasation. A portion of lung in this stage, when
placed in water, does not float as near the surface as healthy
lung-tissue.
When examined with the microscope, the lumen of the alveoli are seen to
be diminished by the encroachment of the varicosed and tortuous
capillary vessels. As a rule, the air-sacs are uniformly dilated; some,
however, may be collapsed--a condition probably due to pressure during
the early period of the pneumonic process. The epithelia of the alveoli
are swollen, and contain a granular protoplasm with free nuclei. The
air-vesicles also contain exfoliated epithelial cells and white and red
blood-corpuscles. The serum which escapes into the alveoli from the
distended capillary vessels is the fluid in which these cell-elements
float. Since the enlarged epithelia often suffer a division of their
protoplasm, embryonic mono-nucleated cells are intermingled with the
other elements. It is still a disputed question whether the bronchial
or the pulmonary capillaries are the chief source of the pneumonic
exudation.
Physiology teaches that lung-tissue is nourished by the blood in the
{309} ramifications of the bronchial arteries, and that the pulmonary
capillaries are the passive media for the interchange of gases. Hence
it is claimed that the bronchial capillaries only are implicated in the
inflammatory process. Virchow has shown that the pneumonic process can
be completely established in places where pulmonic capillaries cannot
be traced on account of the plugging of a large branch of the pulmonary
artery;[6] yet even he admits that secondarily the pulmonary vessels
have much to do in the inflammatory process.
[Footnote 6: _Ges. Abhang._, p. 369, Virchow.]
On the other hand, it is claimed that in the early stages of the
pneumonic process the parts that are supplied by the bronchial
capillaries are not reddened or injected, as they would be were these
vessels primarily concerned in the inflammatory process. Reasoning from
the above, it would seem that both sets of vessels are involved, but
that usually one set is implicated at the very commencement to a
greater extent than the other.
It is often difficult, and sometimes impossible, to differentiate
between the anatomical appearances produced by pulmonary congestion and
oedema and the first stage of pneumonia. In pulmonary congestion and
oedema the fluid in the alveoli is serum, and contains none of the
pathological cell-elements found in the first stage of pneumonia. The
alveolar capillaries are turgid, and in this respect resemble the
capillaries in pneumonic congestion, but when a stream of water flows
over a portion of lung in the first stage of pneumonia its dark color
remains, while in hyperæmia of a non-inflammatory character this is not
the case.
On account of its color and its resemblance to liver-tissue the name
red hepatization has been given to the second stage of croupous
pneumonia. The lung in this stage has a dark liver or mahogany color,
and is slightly mottled, the mottling becoming more marked the farther
advanced is the hepatization. The color is of a brighter red when the
lung is first removed from the body than after it has been exposed to
the air.
The volume of the lung is increased--at times so as to bear the impress
of the ribs. It is solid and firmer than normal; pressure does not
indent but tears it; it is very friable, and its torn surface presents
a granular appearance. Its specific gravity is increased. It is
airless, and there is an entire loss of crepitation.
Upon section it is seen that the granular appearance of the cut surface
is due to the pneumonic exudation which fills the alveoli. This
granular appearance is not so well shown on the cut as on the torn
surface. The granules can be readily removed from the air-cells by
means of a fine needle. A dirty, red, viscid fluid slowly oozes from
its cut surface, which is more apparent after the lung has been exposed
to the air for twelve or twenty-four hours and has undergone
post-mortem changes. At any time this viscid, rusty-looking material
may be scraped from the cut surface, or it exudes when a portion of the
lung is firmly compressed. A portion of the inflamed lung quickly sinks
in water, and small spots of blood-extravasations may be seen scattered
here and there throughout its substance. When a stream of water is
poured over the cut surface of the implicated lung the color changes
from a maroon to a gray or yellow-gray, the usual color of fibrillated
fibrin.
Not infrequently the material in the infundibula and air-cells extends
into the minute bronchi, but these tubes are rarely completely filled
with the pneumonic exudation. When examined under the microscope the
alveoli are found filled with a solid material composed of a network of
fibrillated fibrin, in whose meshes are leucocytes, red blood-globules,
and changed epithelia. These latter are in various forms, usually round
or oval. They may, however, become quadrangular, triangular, or
irregular. They are granular, and may contain a single nucleus, a
nucleolus, or multiple nuclei. These cells finally become granular, and
fat-globules accumulate in them. {310} They also become discolored from
imbibition of blood-coloring matter, so that in the latter part of the
process there is quite an accumulation of pigment-granules, not only in
the free cells, but in the fixed epithelia. The larger cells discharge
their nuclei into the accumulation of corpuscular elements, and the
whole contents of an alveolus present a more or less round shape. The
alveolar walls remain unchanged, or are slightly thickened by the
capillary turgescence. All of these different cell-elements have been
regarded by different observers as characteristic of pneumonia. The red
globules give the color to the consolidated lung. The pus-cells are
always numerous.
The transition from red to gray hepatization is never well defined. The
mottling gradually becomes more marked, so that the affected portion of
lung assumes a marbled or granite appearance. As the deep-red color of
the second stage fades the density of the pneumonic consolidation
becomes less and less, until it is a mere pulp, breaking down under
slight pressure. The decoloration is due to the pressure on the
blood-vessels, to decoloration of the blood-corpuscles that were
present in the second stage, and to fatty degeneration of the other
cell-elements which occupied the air-sacs.
The weight and density of the affected lung-tissue are diminished, and
toward the end of this stage the lung crepitates. On section a nearly
uniform dirty-gray, bloodless surface is exhibited, from which flows
spontaneously or upon slight pressure a dirty-white or reddish-gray
puruloid fluid. The granular red hepatized look has disappeared or is
very indistinct. The amount of oedema in the affected portion of the
lung varies in different cases. When it is excessive a large quantity
of serum exudes from the cut surface, which then exhibits a smooth,
non-granular, glistening appearance, and it does not so readily break
down when pressed upon as do other forms of gray hepatization. When
examined under the microscope, the alveoli are seen to be filled with
numerous round mono-nucleated cells, the intercellular fibrils that
bound the elements together having disappeared; in other words (the
fibrillated having become granular fibrin), the alveoli are filled with
a fluid or semi-fluid mass in which numbers of discrete oil-globules
and protein granules are freely mingled.
The granular and fatty elements are due to the rapid degenerative
changes that occur in the cell-elements. In this stage leucocytes still
emigrate from the blood-vessels. The masses that occupy the alveoli are
now shrunken, and between them and the alveolar wall is a layer of
fluid, so that in a thin section the contents of the air-sacs are
readily lifted out by a camel's-hair brush. All of the affected portion
of the lung is rarely in the same stage of the inflammatory process,
and to distinguish red from gray hepatization, or the latter from the
beginning of some of the conditions next to be mentioned, is often
impossible.
The changes which take place subsequent to the stage of gray
hepatization, and the modifications due to age, remain to be
considered.
Croupous pneumonia may terminate--1, in resolution [recovery]; 2, in
suppuration, purulent infiltration; 3, in abscess; 4, in gangrene; 5,
and very rarely, in chronic (fibroid) pneumonia.
1. During resolution the lung is moist, lighter than in the stage of
hepatization, has a yellow or yellowish-green color, and still shows a
marked loss in elasticity. On section, the lung appears to be
non-granular, and a tenacious, puruloid fluid escapes when the section
is pressed upon. Some oedema may still remain. When examined under the
microscope the alveolar capillary vessels are seen to have returned to
their normal calibre; the alveolar epithelium is restored; the cells in
the air-sacs are degenerated, broken down, and resolved into a
detritus. The degeneration of these cells is both fatty and mucoid, and
the coloring matter of the blood gives origin to the granular {311}
pigment which is scattered throughout the disintegrated and liquefied
mass. Some of the pigment is supposed to come from the connective
tissue between the alveoli. In this condition the alveolar contents are
either expelled by expectoration or undergo absorption, the lung being
finally restored to its normal condition.
2. When purulent infiltration or suppuration of the lung occurs, its
surface becomes yellow--more so than in any of the preceding
conditions; it is soft, moist, and friable, and gives somewhat the
sensation of an abscess. It is well described as miry.[7]
[Footnote 7: _Pneumonia_, Sturges, 1876, pp. 110, 113.]
On section, a diffluent, purulent fluid exudes from a surface whose
yellow color is due both to the large number of cells which are
undergoing fatty degeneration, and to the anæmia which results from
over-distension of the alveoli with these cell-elements.
When examined under the microscope, the cells are found not only
crowding the alveoli, but infiltrating the inter-alveolar tissue. This
corpuscular infiltration of the alveolar walls may so interfere with
their nutrition that they will undergo softening and degeneration.
Whether these cells (in all respects resembling pus-cells) have
emigrated from the blood-vessels or are the result of epithelial
changes is still unsettled. Reason and analogy seem to point to a dual
origin. Now and then these cells are pigmented. Occasionally the
alveolar walls become thinned, indistinct, and finally rupture.
There has been much discussion over the term suppuration of the lung,
but the appearances reported by those who uphold, as well as by those
who protest against, the term are identically the same, all agreeing
that the "lung is filled with pus."
3. Abscess of the lung, as a termination of croupous pneumonia, is
exceedingly rare, and is always preceded by extensive cellular or
interstitial oedema; small abscesses are formed by the rupture of
several of the alveolar septa. It may follow purulent infiltration.
These abscesses vary in size from that of a pea to one which may occupy
the greater part of a lobe. They may have a thick, well-defined,
irregular wall, their interior being crossed by shaggy shreds of
broken-down lung-tissue, or they may form irregular excavations in
softened lung-tissue. They may be single or multiple. Several abscesses
are often found in the same lobe. They increase in size by peripheral
growth or by fusion of several small abscesses.
Abscesses are more common in the upper than in the lower lobes; their
frequency is variously estimated as 1 in 30 or 60 cases. These
pus-cavities, if of small size, may ultimately close by cicatrization,
in which case they may open into a bronchus of sufficient size to allow
of the discharge of their contents. Under such circumstances the
contents of the abscess are expectorated; interstitial inflammation is
set up around their site, which after a time encloses them in a firm
connective-tissue wall; contraction ensues, and finally only a line of
cicatricial tissue marks their former situation. Or if no such
bronchial opening occurs, the abscess becomes encapsulated in firm
cicatricial tissue, and the contents undergo cheesy and calcareous
transformation. Sometimes these abscesses perforate the pleura and
discharge their contents into the pleural cavity, causing
pyo-pneumothorax. External fistulous openings have occurred, but they
are a rare termination of pulmonary abscess.
4. Gangrene is said to be a termination of croupous pneumonia in about
2 per cent. of cases, but this estimate is based on too few statistics
to be wholly reliable. It is met with in bad constitutions where there
is very great vital depression, in chronic alcoholismus, and in cases
of intense septic poisoning. Interference with the blood-supply,
causing the formation of pulmonary or bronchial thrombi, leads to its
development.[8] While usually limited to a {312} small area of
lung-tissue, it may invade large tracts, and be either circumscribed or
diffuse.
[Footnote 8: Huss, _Pneumonia_; Carswell, _Ill. El. Forms of Disease_.]
The gangrenous portion of the lung is changed to a dark, dirty, pulpy
mass, sometimes wanting the fetor of gangrene. When the mass has become
diffluent, a sort of cavity is formed, in which are found fetid fluid
and shreds of gangrenous lung-tissue. Around the gangrenous mass there
is a zone of gray hepatized, friable tissue, which in turn is bounded
by a zone of red hepatized tissue. When the above-named zones are not
present in diffused gangrene, the cavities are large, and shreds of
tissue and vascular bands traverse the cavity, which swarms with
bacteria. Such a gangrenous mass may lead to sloughing of the pleuræ.
It has been denied that a croupous pneumonia can terminate in gangrene,
but modern pathologists all support the opposite view. It may be
mentioned that gangrene in croupous pneumonia of the horse is of
frequent occurrence.
5. Chronic (interstitial fibroid) pneumonia may result when the process
of resolution in croupous pneumonia is delayed and the inflammatory
process does not advance beyond the stage of gray hepatization. In such
cases the walls of the alveoli, and finally the inter-alveolar tissue,
become the site of new connective-tissue developments.
The peculiarly hard and oedematous condition that sometimes marks gray
hepatization is, by some observers, regarded as an intermediate stage
between croupous and interstitial pneumonia. An abundant
cell-production in the second or third stage of croupous pneumonia may
be followed by shrivelling of the alveolar contents, and subsequent
cheesy changes may bring about one form of phthisis. Whether this can
ever occur independent of tubercle is still a mooted question. This is
called (by those who believe in such an origin of phthisis) cheesy
infiltration, and is to be differentiated from tubercular infiltration.
In childhood croupous pneumonia is not of so frequent occurrence as
catarrhal. In its anatomical changes it does not differ from croupous
pneumonia in adults. In old age the pneumonic changes usually begin in
the upper lobes of the lung, and extend downward--the reverse of what
occurs in adult life. In the stage of engorgement crepitation is
usually wholly absent, and when the stage of red hepatization is
reached the color is found much darker than in adults, sometimes being
blue or black; the lung is much more strikingly marbled, and on section
the granules, in those cases where they are present, are much larger
than in adult life. Frequently in senile pneumonia the granular look is
absent. Gangrene is a far more frequent termination of croupous
pneumonia in old age than at any other period. The highly-rarefied
condition of the lungs at this period seems to favor the development of
small abscesses.