as the course and duration of the affection, are such as belong to the
pulmonary diseases favoring its production, especially chronic
bronchitis and fibroid phthisis. The cough and dyspnoea of these
diseases are aggravated by bronchial dilatation; but these symptoms,
together with the impairment of nutrition, are due rather to the
underlying affections than to the mere fact of dilatation. Increased
and fetid expectoration, which often occurs in bronchial dilatation
from retained and altered secretion, is by no means characteristic of
this condition, since it may occur where no sign of dilatation exists.
There is generally some degree of dulness on percussion over a dilated
{229} bronchial tube, due to the condensation of the lung-tissue
surrounding it, and varying in extent and degree with the amount of
that condensation, and also with the amount of secretion retained
within the tube. Sometimes, however, increased resonance of a
tympanitic character is observed, especially if the dilatation be of
the saccular form and near the surface of the lung. Such differences in
the percussion sound are analogous to what occurs over a pulmonary
vomica, which will generally give a dull sound, though, if the cavity
be superficial and thin-walled, it may yield a tympanitic resonance. On
auscultation bronchial respiration may be heard along the course of
tubes affected with cylindrical dilatation when they are free from
secretion; and this is more intense in proportion as the tube is more
dilated and the lung-tissue around it more condensed. Bronchophony and
increased vocal resonance also occur, and if mucus be present in the
dilated tubes coarse moist râles will be heard. In a saccular
dilatation there may be true amphoric breathing, with the gurgling
sounds heard in a vomica. In some cases there is an alteration in the
appearance of the chest-wall, which is retracted by the shrinking of
the condensed lung beneath.
Now, of the auscultatory signs that have been mentioned, the
bronchophony and increased vocal resonance, together with the
percussion dulness, belong also to pneumonia, which, however, at least
in its acute form, can be distinguished from bronchial dilatation by
the previous history, the febrile movement, and the general phenomena
of the case, and by the fact that the tubal breathing of pneumonia,
besides being less persistent, is most frequently met with in the lower
part of the lung, and that of bronchial dilatation in the upper part.
But the diagnosis between a dilated bronchus and pulmonary phthisis is
in some cases a very difficult problem, the signs of the cylindrical
form closely simulating those of the stage of deposit in phthisis,
because involving the same physical condition, and those of the
saccular variety corresponding often with the auscultatory signs of a
cavity. In the former case there may be the same localized dulness on
percussion, the same bronchial or broncho-vesicular breathing, and the
same sinking or contraction of the chest-wall apparent on inspection.
In the latter case there may be equally in saccular dilatation and in a
vomica amphoric breathing, gurgling, and pectoriloquy. In the
establishment of the diagnosis between these two conditions Austin
Flint, Sr.,[1] justly attaches importance to the circumstance that
there is in general a greater degree of percussion dulness over a
cavity than over a dilated bronchus, so that a relatively greater
prominence of the auscultatory signs as compared with the degree of
dulness makes the diagnosis of dilatation more probable. But the most
important evidence on the point is to be gotten from the history of the
case. If in a case where the auscultatory signs would leave the
examiner in doubt there were found loss of flesh, fever, night-sweats,
quickened pulse, and the other general phenomena belonging to phthisis,
the existence of this affection would be rendered probable in the
highest degree, and the auscultatory signs should be taken as
corroborating an opinion founded on the general symptoms.
[Footnote 1: _Dis. of Resp. Organs_, p. 353.]
Positive evidence, again, may be furnished by a microscopic examination
of the sputa; the discovery of particles of lung-tissue or the
so-called bacillus tuberculosis pointing clearly to phthisis.
Conversely, the absence of the general symptoms of phthisis would, in a
case presenting the above auscultatory signs, render it probable that
they are due to bronchial dilatation. Long-continued cough and abundant
expectoration are the chief symptoms common in both forms of disease.
There are, however, some cases in which even with the most careful
examination and weighing of evidence the physician will be left in
doubt, inasmuch as in some cases of otherwise {230} well-marked
phthisis the usual constitutional symptoms are absent or imperfectly
declared. In such exceptional cases the estimate of probabilities is to
be based on the fact that while bronchial dilatation is comparatively
rare, pulmonary phthisis is extremely common.
PATHOLOGY AND MORBID ANATOMY.--Enlargement of the bronchi may be met
with throughout almost the entire extent of a lung; when limited to a
part of the organ the change most frequently occurs, according to
Laennec, Rokitansky, and other observers, in the superior lobe and
toward the anterior border. The tubes of the third or fourth order in
respect to size are most frequently affected, the primary bronchi being
never involved except in association with tracheal dilatation.
In the different forms of dilatation the bronchial walls are found in
various states. In the cylindrical variety they are for the most part
thickened and hypertrophied, both as to the mucous and the fibrous
coats; the mucous membrane being in a catarrhal state, covered often
with muco-purulent discharge, and easily broken down and detached,
while underneath the white fibrous coat is sensibly thickened.
In the sacculated form, on the other hand, the bronchial wall generally
presents a thin and atrophied appearance, the mucous membrane
undergoing but little change, except that the stretching to which it
has been subjected gives it a smooth and shining look. This difference
in the degree of thickening of the bronchial walls in the two forms of
dilatation is in part due to the fact that in the saccular variety the
enlargement in calibre is far greater than it is in the cylindrical
form for a corresponding extent of a tube, so that its wall is much
more stretched and attenuated, and thus the tendency to hypertrophy
which has play in the cylindrical form is more than overcome in the
saccular. But the chief reason of the difference in the state of the
walls in the two forms of dilatation is found in the different modes in
which they are respectively brought about, as already described.
DIAGNOSIS.--It has been shown that the determination of the existence
of bronchial dilatation is at times one of the most difficult problems
in diagnosis, from the fact that the auscultatory signs belonging to it
may be equally met with in other affections, especially in pulmonary
phthisis. The diagnosis is to be established, when this is possible,
only by a careful consideration of the physical signs in connection
with the general symptoms, so that the sources of doubt arising from
the one set of phenomena may be as far as possible corrected by the
other. These signs and symptoms, and the various affections to be
discriminated by them, have been sufficiently set forth under the head
of Symptomatology. While in this way a clear conclusion may be reached
in many cases, yet there are others in which, notwithstanding the
utmost care, there may still be a doubt as to whether the symptoms and
signs indicate a dilated tube or a pulmonary cavity.
PROGNOSIS.--The prognosis of bronchial dilatation is directly connected
with that of the affections which chiefly give rise to it--viz. chronic
bronchitis and fibroid phthisis. When chronic bronchitis has lasted
long enough to cause dilatation, it is seldom if ever cured, and,
though improvement may take place from time to time in its symptoms,
yet the dilated bronchi can hardly undergo diminution in their size.
And in fibroid phthisis, while the progress of the disease is often
very slow, yet it is on a downward grade, and the connective-tissue
contraction giving rise to the dilatation increases with the advance of
the malady.
TREATMENT.--The treatment of cases of bronchial dilatation resolves
itself in great degree into that of the underlying and causal diseases
on which it depends. As regards methods specially directed to the areas
of dilatation, they consist of alterative, astringent, stimulant, and
antiseptic remedies, either administered by the stomach or used by the
process of inhalation. Cough {231} may be allayed with the syrup of
lettuce containing in each dose from one-eighth to one-fourth of a
grain of sulphate of codeia or 10 or 12 drops of the spirit of
chloroform. If expectoration is very profuse, sulphate of atropia, in
the dose of one-hundredth to one-eightieth of a grain, or the extract
or tincture of belladonna, may be used. Turpentine and eucalyptol have
a controlling influence over this symptom, and are specially beneficial
if the bronchial secretion is fetid. They may be given by the mouth in
the dose of minim v-xx in emulsion, and applied also by inhalation of
their vapor or by spray. Inhalations of solutions of carbolic acid,
minim j-x to an ounce of water, are more effective than anything else
in checking fetor of the expectoration and the breath. This agent may
also be administered by the mouth in the dose of fluidrachm j-iv of a 1
per cent. solution.
{232}
EMPHYSEMA.
BY SAMUEL C. CHEW, M.D.
DEFINITION.--The term emphysema is derived from [Greek: emphysaô], to
inflate, and signifies an increased amount of air in a part or the
whole of one or both lungs. Accordingly as the situation of this excess
of air is _(a)_ in the air-vesicles or _(b)_ in the connective tissue
between the lobules, emphysema is divided into Vesicular emphysema and
Interlobular or extra-vesicular emphysema.
HISTORY.--These two affections are different pathologically and
anatomically, vesicular emphysema being a much more common and
important affection than the interlobular form. The distinction between
the two forms was first drawn by Laennec. Previously to his time the
essential difference between them was unknown; and, as the accurate
diagnosis of the disease can be made only by auscultation, its
existence was no doubt very often entirely overlooked. It has been
remarked by Rokitansky[1] that "had Laennec done nothing else for
medical science, his discovery of this diseased condition, and of the
causes giving rise to it, would have sufficed to render his name
immortal."
[Footnote 1: _Path. Anat._, vol. iv. p. 53, Am. ed.]
VESICULAR EMPHYSEMA.
Vesicular emphysema may be defined as an absolute or relative increase
in the amount of air contained in the vesicles of a part or the whole
of one or both lungs. As a substantive disease it occurs in two
principal forms--hypertrophic and atrophic; but besides these it is met
with as a secondary affection due to other diseases and limited to
certain areas of the lungs, sometimes acute and sometimes chronic in
its production and duration. It will therefore be best to consider the
disease under the following different forms:
1st. Acute lobular emphysema;
2d. Chronic lobular emphysema;
3d. Hypertrophic lobar emphysema;
4th. Atrophic lobar emphysema.
1. Acute Lobular Emphysema.
This form of the disease is the result of the rapid distension beyond
their natural size of air-vesicles which had previously been healthy.
It is most frequently met with in children and as the consequence of
bronchitis or {233} whooping cough. The paroxysms of cough occurring in
these affections, especially in the latter, are attended by deep
inspirations, by which the vesicles are directly distended, and by
violent expiratory efforts, with closure of the glottis, so that the
air is forced into those portions of the lungs where there is least
resistance, particularly at the apex and along the margins. In a large
proportion of cases of acute lobular emphysema, when the distending
cause is removed by the cessation of the cough, the vesicles return to
their normal size through their natural elasticity, which has not been
destroyed. But in some cases, when the cough has been of unusual
violence or of very long duration, the change may be permanent through
loss of this elasticity, and thus a form of chronic lobular emphysema
is produced.
SYMPTOMS AND SIGNS.--Unless emphysema of this form is extensive and
extreme in degree, it is not attended with symptoms additional to those
of the affections giving rise to it. When very great it may occasion
increased percussion resonance.
TREATMENT.--The treatment is only what is required by the causal
affections.
2. Chronic Lobular Emphysema.
In many cases emphysema is confined to a limited number of lobules,
especially at the apices, the anterior borders, or about the base of
the lung; and being gradual in development and permanent in duration,
it is then termed chronic lobular emphysema. This is the form
frequently met with in the different varieties of pulmonary phthisis,
in which its development seems supplementary to the incapacitation of
other portions of the lung. The lobules nearest to the surface of the
lung or immediately beneath the pleura are found to be most distended,
so that they often project beyond the adjacent surface.
Chronic lobular emphysema is chiefly of interest in connection with the
other pulmonary diseases which give rise to it. The mechanism of its
production is like that of acute lobular emphysema, but the diseases
occasioning it being chronic the emphysema to which they give rise is
equally permanent. At the apex of the lung, its most common situation,
it is very often associated with tubercle in a calcareous state. The
changes accompanying this deposit of tubercle favor the loss of
elasticity in the vesicles of the apex, and the violent expiratory
efforts, with closure of the glottis, occurring in the attacks of cough
to which phthisical patients are subject, force the air into this part
especially, and also into other regions of less resistance, and thus
occasion permanent distension of the vesicles.
SYMPTOMS AND SIGNS.--The signs of this form of emphysema are so often
masked by those proper to phthisis that the detection of the former is
difficult or impossible. This, however, is of no practical importance
in respect to treatment. At times the distension of the vesicles at the
apex is so great as to produce bulging in the supra-clavicular region
and to overcome the dulness due to deposit by the resonance it
occasions.
TREATMENT.--No special treatment beyond that of the causative
affections is required.
3. Hypertrophic Lobar Emphysema.
This is a substantive affection, and is much the most important form of
the disease, both in its origin and development and in the consequences
to which it leads. Though sometimes limited to one lung, or even to a
single lobe of {234} one lung, yet it more commonly involves the
greater part of both lungs, which are increased in size, as shown by
the alteration of the contour of the chest during life and by the
appearance of the organs after death. This enlargement of a lobe or of
a whole lung is of course the aggregate of the increase in size of the
individual vesicles, the changes in which form the pathological units
of the disease.
ETIOLOGY.--In no disease is the study of etiology as throwing light on
treatment, both medicinal and hygienic, of more value than in
emphysema, the important question being as to whether it takes its
origin from some immediate mechanical cause acting upon the healthy
cell-walls, and thus distending them, or whether they suffer such
distension only when they have been previously weakened by some
degenerative process in their tissue. The importance of determining
this point correctly with reference to treatment is obvious.
In partial and lobular emphysema the change may have been wrought by
causes mechanical in their nature and directed specially to the
affected parts, such as have been already referred to; but in the
general diffused or lobar form of the disease, in which by degrees the
greater part or the whole of a lung is involved, we are almost
compelled to assume the existence of some degenerative process or
tendency coextensive with the malady and determining its existence.
That any one form of degeneration is present in all cases has never
been proved; indeed, it may be said to have been disproved. Rainey's
view, that the change in the air-cells is essentially dependent on
fatty degeneration of their walls, was based mainly on observations
made upon a single case, and, although favored by the eminent authority
of C. J. B. Williams, it has not been substantiated. The same thing
must be said of Sir William Jenner's teaching, that fibroid
degeneration is the essential lesion. Though both fibroid and fatty
changes are found in not a few cases, yet in others a careful
examination has failed to detect either the one or the other of them,
so that neither can be regarded as the essential condition explaining
all cases. Nevertheless, it is probable in the highest degree that a
degenerative change of some kind, due to imperfect or perverted
nutrition of the cell-walls, always exists in general lobar emphysema,
though its nature may sometimes elude observation.
In cases of well-marked emphysema there may be no discoverable
morphological changes in the walls of the alveoli, though, as remarked
by Hertz,[2] "a tissue-relaxation may be present in the lung without
our being able to recognize any corresponding microscopic abnormality."
[Footnote 2: _Ziemssen's Cyclop._, vol. v. p. 373.]
It may be said, then, that while in partial or local emphysema the
alteration in the air-vesicles may be effected by extraordinary efforts
brought to bear upon healthy cell-walls, in general or lobar emphysema,
on the other hand, it may be produced by ordinary efforts acting upon
weakened and diseased cell-walls. The morbid change is probably not in
all cases alike, being sometimes fatty, sometimes fibroid,
degeneration, and in other cases of a kind not ascertained.
In addition to other considerations, the markedly hereditary nature of
emphysema in not a few instances would of itself render the existence
of some constitutional predisposing cause highly probable. On this
point A. T. H. Waters[3] quotes the observations of Greenhow and
Jackson. Out of 42 cases collected by Greenhow, 23 showed an hereditary
tendency, and in 28 reported by Jackson, 18 were of emphysematous
parentage. In stating his belief that substantive or general emphysema
is the result of some degenerative process, Waters bases it on the
following considerations: 1st. The high degree of development which the
disease often reaches, without any {235} previous history of violent or
long-standing cough, in connection with either bronchitis, whooping
cough, or any similar affection. 2d. The frequency with which the
disease attacks the whole of both lungs, and the uniform character of
the morbid changes often observed throughout all parts of the lungs.
3d. The hereditary nature of the disease, as shown by observations.
4th. The manner in which the disease is influenced by certain remedial
measures which are known to act beneficially on other diseases attended
with degeneration of tissue.
[Footnote 3: _Diseases of the Chest_, pp. 122, 123.]
As to the nature of the immediate exciting cause of emphysema, whether
in the general or local form, different views have been maintained. The
most important of these are the inspiratory and expiratory theories.
The former of these theories, that in accordance with which the disease
is referred to inspiratory action, was maintained by Laennec, and under
the influence of his authority was at one time generally accepted. In
accordance with this view, the existence of bronchitis is an important
factor in the production of emphysema, as undoubtedly it often is in
the lobular form. The dilatation of the air-vesicles was attributed to
their over-distension by inspiratory efforts allowing the free entrance
of air, the escape of which was impeded by bronchial mucus. Inspiration
was thus regarded as a more powerful act than expiration, which was
considered too feeble to drive the air beyond the accumulated mucus. In
this way the air was supposed to accumulate in gradually increasing
amount within the cells, which thus became distended.
But in opposition to this view it has been shown by Hutchinson's
researches that Laennec was wrong in supposing inspiratory power to be
greater than that of expiration; and it is further opposed by the
researches of Mendelssohn and Traube, and those of Gairdner, which have
shown conclusively that the presence of a pledget of mucus in a
bronchial tube, so far from causing distension of the air-vesicles to
which it leads, must ultimately ensure their collapse. The collapse
thus occasioned, which is most common in the lower parts of the lungs,
may lead, partly perhaps through inspiratory pressure, to vicarious
emphysema in the upper portions, which receive a relatively larger
quantity of air, in accordance with Williams' theory of negative
inspiratory pressure.
It is true, then, as maintained by Laennec, that bronchitis may
occasion emphysema, but the emphysema does not occur in the vesicles to
which the affected tubes directly lead, nor from the force of
inspiration applied to these vesicles, as Laennec taught, but in other
portions of the lungs.
The expiratory theory affords a more satisfactory explanation of
emphysema than does the inspiratory theory, and one more completely in
accordance with the physiology of respiration and the anatomy of the
thorax.
In ordinary expiration, in which the lungs are uniformly and equably
compressed by the chest-walls, there is nothing tending to force air
into one part of these organs more than into another, and thus produce
emphysematous dilatation. But in forced expiration, such as occurs in
the act of coughing, it may be plainly seen, if the chest be uncovered,
that the air is driven upward to the top of the lungs, so as to produce
a perceptible bulging in the supra-clavicular region. This bulging is
notably increased in the coughing-spells of emphysematous subjects; and
this fact is urged by Sir William Jenner both as throwing light upon
the expiratory act as a principal factor in the disease, and as
accounting for the special frequency of emphysema in the upper parts of
the lungs. The explanation of this phenomenon is found in the
circumstance that in the strong expiratory efforts of coughing the
abdominal muscles force the diaphragm upward, and thus compress the
lungs from below; at the same time the strong lateral anterior and
posterior thoracic walls resist pressure, while the superior part of
the thorax, covered over {236} with fascia, but not completely
protected by a bony structure, offers least resistance. To this
unprotected part of the lungs and to the free margins and borders,
which contain normally the smallest amount of air, will the strong
currents produced by violent expiratory efforts be driven, so as to
cause distension of their vesicles. Thus, the frequent coughing-spells
of bronchial catarrh, so commonly associated with emphysema, give rise
to the expiratory efforts which are the immediate cause of the
emphysema.