circumstance that the bulk of the affected lungs has undergone
diminution from waste or atrophy of their tissue. Absolutely, the lungs
may contain no more air than they should in health--they may even
contain less--but, relatively, there is an increased amount of air in
them in consequence of the diminished amount of the lung-tissue. Such
relative increase of air in a given area of the lung may be very
considerable from the atrophy and destruction of the cell-walls, the
alveoli coalescing so as to form cavities, while the individual
air-cells are not dilated. The entire lung, however, is shrunken, the
chest-wall correspondingly depressed and contracted, and the thoracic
muscles atrophied. The function of the affected lungs is impaired in
consequence of their loss of size and the diminution of the respiratory
movements. This is of course especially noticeable when exertion is
made, while under other circumstances there may be little or no
embarrassment of breathing unless the disease is far advanced and has
involved a large amount of both lungs. But, in general, this form of
disease causes less distress and is a less formidable affection than
hypertrophic emphysema. In some cases a mingling of the two forms is
found, as when a person the subject of general atrophic emphysema has a
local vesicular dilatation developed at the top and margins of the
lungs.
The shrunken state of the lungs in atrophic emphysema prevents the
heart from being overlapped, so that the area of cardiac dulness is not
lessened, as it is in the hypertrophic form; and as the general waste
of the system is attended with a diminution of the amount of blood,
dilatation of the right ventricle, and consequent dropsy, are not apt
to occur, as they are in hypertrophic emphysema.
ETIOLOGY.--Atrophic emphysema is always due to constitutional causes.
It is found chiefly in old persons or in those in whom impaired
nutrition has produced the degenerative changes of old age. Hence it is
described by some writers as senile emphysema or senile atrophy of the
lungs.
SYMPTOMS.--Of the general symptoms of atrophic emphysema, apart from
those which belong also to the hypertrophic form, the most marked
are--first, the lessened size of the thorax; and, second, the character
of the dyspnoea, which is not urgent, and is not apt to occur except on
making exertion. The blood is lessened in amount from the general
impairment of nutrition, and is therefore adapted, so to speak, in
quantity to the diminished aërating space. Percussion in general gives
exaggerated resonance, from the relative increase of air in the lung
and the thinness of the thoracic wall, which thus vibrates more
perfectly. In some cases, however, from loss of elasticity in the
cartilages of the ribs, the resonance is even diminished. On
auscultation there are found somewhat prolonged expiration and, in
general, feeble inspiratory murmur--signs which belong also, but in
greater degree, to true hypertrophic emphysema, from which, however,
the atrophic form is to be distinguished by the contraction of the
chest that is seen throughout its entire contour.
In some cases of hypertrophic emphysema there may be, it is true, an
appearance of partial contraction of the chest-wall, since where the
{249} emphysema has produced a marked bulging of the upper portion of
the thorax the part below may seem by contrast to be contracted. But in
the atrophic form of the disease no distension is seen at any part of
the chest-wall, the whole surface being more or less sunken and
contracted. Even in hypertrophic emphysema with distension of the
thorax, when the disease has lasted a long time there may be some
degree of wasting of the lung-tissue; but this condition does not
constitute true atrophic emphysema, which is such from the beginning
without any preceding stage of hypertrophy.
DIAGNOSIS.--The diagnosis of atrophic emphysema is to be made by the
physical signs studied in connection with the conformation of the
chest.
PROGNOSIS.--The prognosis of this affection is hopeless as regards a
cure, since the organic change is due to the degeneration of age; yet
the disease may continue for years without materially or at all
affecting the duration of life.
TREATMENT.--The atrophied lungs can never be restored to their
integrity; treatment is therefore limited to the use of tonics and
nutriment in order to hold in check the process of waste; and to the
relief of bronchial catarrh, which is apt to be attended with profuse
purulent secretion. The agents best suited to these two purposes have
already been considered.
II. INTERLOBULAR OR EXTRA-VESICULAR EMPHYSEMA.
Interlobular or extra-vesicular emphysema is, as has been previously
stated, an affection differing anatomically and pathologically from the
form of disease already described. In the vesicular form air is present
where it normally belongs, but in undue amount; in the interlobular
form it is present where it ought not to be--that is, in the meshes of
the connective tissue between the lobules, beneath the pleura, and
around the bronchial tubes and pulmonary vessels. These situations may
be reached by the air through a rupture of the vesicles, and thus in
some cases vesicular may be associated with interlobular emphysema, the
rupture having occurred from violent cough; or the emphysematous
infiltration may be gaseous, as the result of gangrene occurring during
life or of decomposition after death.
DIAGNOSIS.--The presence of air in the connective tissue of the lungs
cannot be determined by any signs or symptoms; if, however, it should
be discovered in the subcutaneous tissue of the neck, face, or chest,
giving rise to puffiness and crackling of the integument, its presence
in the areolar tissue of the lungs may be suspected, especially if
there be coexisting vesicular emphysema, the air having passed into the
mediastinum and thence into the tissue beneath the skin.
The existence of interlobular emphysema is not, in general, of serious
significance, as the air commonly disappears from the subcutaneous
tissue in a few days; whence it may be inferred that it likewise
disappears from the connective tissue of the lung, the opening which
had admitted it there having become closed. If present in large amount
in the lung-substance, it may, however, increase the difficult
breathing of an emphysematous subject by compressing a number of the
air-vesicles. Or, again, if the interstitial emphysema be subpleural,
the bulla may burst, and the air, escaping into the cavity of the
chest, may occasion pneumothorax, or even hydro-pneumothorax, from the
resulting inflammation. Such an occurrence is, however, very uncommon.
Even when the diagnosis of interlobular emphysema is established, no
treatment is needed or practicable.
{250}
COLLAPSE OF THE LUNG (ATELECTASIS).
BY SAMUEL C. CHEW, M.D.
DEFINITION.--The term atelectasis is derived from [Greek: atelês],
incomplete, and [Greek: echtasis], expansion, and designates a
condition in which the lung has failed to expand or has returned in
part or throughout its whole extent to the state of non-expansion which
is normal in foetal life. In the former case the state is one of
congenital atelectasis, and is of course met with only in the new-born;
in the latter it is acquired atelectasis, or collapse of the lung, a
portion or portions of the organ which have once been expanded having
the air excluded from their alveoli, so that these collapse and return
to the pre-natal state. To this condition of acquired atelectasis the
term apneumatosis, from [Greek: a] negative, and [Greek: pneumatôsis],
filling with air, was applied by Fuchs in 1849, and it has since been
adopted by Graily Hewitt.
HISTORY.--For a long time this affection was regarded as a peculiar
form of pneumonia, for the reason that at post-mortem examinations
patches of collapsed lung-tissue were found which appeared to have
undergone solidification. Inasmuch as the condition was most frequently
met with in young children, and the supposed solidification was often
limited to certain lobules of the lung with intervening healthier
spaces, it was described as the lobular pneumonia of children.
The secondary nature of the affection, and the fact that it is very
generally preceded by bronchitis, and sometimes by catarrhal pneumonia,
were pointed out by Barthez and Rilliet in 1838. Some other important
distinctions between this affection and general or lobar pneumonia had
been referred to by various writers, but it was not until 1844 that its
true nature was satisfactorily elucidated by Bailly and Legendre, who
showed, by blowing air into the lungs after death, that the lobules
supposed to be hepatized were not really solidified by exudation, but
had simply collapsed for want of air.
ETIOLOGY.--The congenital atelectasis of new-born children may be due
to original feebleness, to protraction of labor interfering with the
blood-supply through the cord, or to obstruction of the air-passages by
mucus or other substances. In any case, it is the result of
non-expansion of the chest, so that the lungs are not unfolded. This
constitutes atelectasis in the strict sense.
Acquired atelectasis, apneumatosis or collapse of the lung, is an
affection most frequent in early infancy, though not limited to that
period of life, since bronchitis with defective innervation and great
impairment of strength, the essential factors in the production of the
disease, may occur at any period of life.
It is probably in almost every case secondary to bronchitis, and due to
the occlusion of the smaller bronchi by the presence of mucus allowing
the egress, but impeding the ingress, of air, so that the lobules to
which they lead are gradually evacuated of air, and thus finally
collapse.
Obstruction of a bronchial tube by a foreign body or by the pressure of
a {251} morbid growth within the lung may produce collapse of the
lobules to which such tube leads, a smaller or larger part of the lung
being involved in proportion to the size of the obstructed bronchus.
Such cases are, however, very rare, and they more closely resemble the
condition brought about by the pressure of a pleural effusion giving
rise to the state of carnification, which is, in effect, an atelectasis
involving the greater part or the whole of a lung, and not limited to
certain lobules nor taking place lobule by lobule.
The principal cause of lobular collapse is no doubt bronchial catarrh,
the action of which is aided by impairment of the general strength and
of muscular respiratory power; for the natural elasticity of the
lung-tissue would favor the exit and oppose the entrance of air unless
it were counterbalanced by muscular action in inspiration. If, then,
this inspiratory action is lessened, the requisite amount of air will
not enter the alveoli, and that which they already contain will be in
part driven out, and perhaps in part absorbed into the blood, by the
pressure to which it is subjected. Deficient innervation and lower
vital power are thus important elements in determining collapse, which
is most common in very young infants or in those who, though somewhat
older, have had their nutrition impaired by malhygienic influences or
by other diseases.
The mechanism of the production of lobular collapse by the presence of
mucus in the bronchial tubes has been well explained by the classical
observations and experiments of Gairdner and of Hutchinson. They showed
that the physical result of collapse is in part due to the force of
expiration being greater than that of inspiration, and in part to the
anatomical formation of the bronchial tree. As to the former of these
causes, it was shown by the experiments of Hutchinson, already alluded
to in the article on EMPHYSEMA, that the force of expiration capable of
being applied for the overcoming of obstruction in the bronchial tubes
is greater than that of inspiration--in opposition to the teaching of
Laennec, who regarded the inspiratory as the greater force. Repeated
efforts to clear the bronchial tubes of accumulated secretion by the
forced expiration of coughing must therefore remove air from the
alveoli in greater amount than it can be returned to them by
inspiration, and so they must ultimately be evacuated of their contents
and consequently collapse.
The second mechanical cause to which Gairdner refers is found in the
shape of the bronchial tubes, which taper in size as they advance
toward the air-cells. The mucus contained within a tube may in
consequence of this shape act as a ball-valve, being displaced forward
in the direction of the greater diameter by the expiratory efforts,
thus allowing the exit of air, the entrance of which will be impeded
because inspiratory action will at once close the valve. This
valve-action of a plug of mucus is well illustrated and proved by the
experiments of Mendelssohn and Traube. In one of these a shot was
introduced into the left bronchus of a dog, and in two days the left
lung was found collapsed and the right one in a state of supplementary
emphysema. The collapsed lung was afterward distended by inflation. In
a like manner pledgets of mucus may establish an air-pump action that
will empty the cells to which the obstructed tubes lead and cause them
to collapse. It is, moreover, not improbable that a portion of the
contained air is absorbed by the blood-vessels, as is maintained by
Fuchs.
As a predisposing cause age has a remarkable influence in producing
atelectasis, the condition being much more frequent under five or six
years of age than after that time. This is explained by two
considerations: The first is the greater prevalence of catarrhal
affections of the air-passages in young children than in other
subjects; the second is the fact that the chest-walls in a child are
more pliable and less firm and resistant than those of an adult, so
that when the diaphragm descends in inspiration a portion of the
chest-wall {252} may sink in, and the lung immediately beneath such
portion will not expand to meet the costal wall as it does in older
persons. According to Graily Hewitt, the part at which the chest-wall
is most depressed is "at the junction of the cartilages with the ribs,
and the ribs which more especially exhibit this want of power to resist
the atmospheric pressure are those just above and below the nipple, the
fourth to the seventh inclusive."[1]
[Footnote 1: _Reynolds's Syst. Med._, vol. iii. p. 872.]
The principal cause of collapse involving an entire lobe or the whole
lung is the presence of liquid in the thorax in the form either of
inflammatory serous effusion, empyema, or hydrothorax. The admission of
air into the cavity of the chest by perforation of the lung or by a
penetrating wound of the thorax may also lead to the same result by
allowing atmospheric pressure on the lung. In such cases the lung may
again expand on the absorption or withdrawal of the liquid or air, but
it sometimes remains permanently compressed and carnified.
SYMPTOMS.--It is probable that atelectasis in very limited degree may
exist without being discovered or suspected, the amount of lung
involved being insufficient to interfere by its loss of function with
respiration or to give rise to appreciable symptoms.
In congenital atelectasis the symptoms are obvious from the moment of
birth, and all point to obstructed or imperfect respiration; but they
vary in degree. Should expansion of the chest not take place at all,
the heart, which at first may be felt feebly beating, will soon stop,
and death will occur. In other cases, in which the atelectasis is not
absolute, but yet expansion is not accomplished sufficiently for
respiration to be kept up, the infant is more or less cyanotic,
especially about the lips and face and at the extremities. The
movements of the thorax are slight in degree, and the cry is weak and
suppressed, and at last inaudible. In such cases death usually occurs
in a few hours, but sometimes life is protracted for several days. The
symptoms then are like those of acquired atelectasis or collapse of the
lung.
In this condition--which, as already stated, is generally the result of
bronchitis occurring in debilitated children--the symptoms show
malaëration of the blood. Sometimes they are gradually developed, and
sometimes they occur quite suddenly, according to the rapidity with
which the collapse spreads through the lung and the number of lobules
involved in it.
The signs of bronchitis are present before the occurrence of collapse,
and are more or less mingled with those pointing to the collapsed
state. The hurried respiration so often met with in bronchitis is
increased by the collapse of any considerable numbers of lobules in the
lung. The evidences of imperfect oxygenation of the blood, which in
children are often apparent in bronchitis, are greatly augmented on the
occurrence of collapse, the breathing becoming more rapid and
oppressed, the working of the alæ nasi increased, and the dusky hue of
the surface spreading and becoming deeper. The character of the
respiration is modified in a very remarkable way, as pointed out by
George A. Rees of London, in consequence of the pliable and yielding
condition of the chest-walls in early childhood. When the upper part of
the chest is elevated in inspiration and the diaphragm descends, the
space thus produced cannot be filled by the lungs in consequence of
their partially collapsed state; and for this reason the intercostal
spaces and the lower end of the sternum are sunken by the atmospheric
pressure at each inspiratory act. This character of breathing may also
be observed in older subjects of collapse as regards the depression of
the intercostal spaces, though in less degree than in children, in
consequence of the greater rigidity of the thorax after childhood.
As collapse of the lung in very limited degree may be unattended with
general symptoms, so likewise it may have no positive auscultatory
signs. A {253} moderately extensive tract of the lungs must be affected
in order to produce these to an appreciable extent. This amount cannot
be stated exactly, but, according to Gerhardt, it is from an eighth to
a sixth of one lung.[2]
[Footnote 2: _Ziemssen's Cyclop._, vol. v. p. 332.]
Dulness on percussion, varying in degree and extent with the number of
affected lobules and their nearness to each other, is a very constant
sign of collapse; but it must be kept in mind that if the collapsed
lobules are disseminated or central the dulness may be hardly
observable. Sometimes there is difficulty in detecting dulness, because
from the bilateral character of the bronchitis the collapse of lobules
may take place in about equal degree on both sides, so that one side
cannot be contrasted with the other. Ordinarily, however, there is a
difference in the degree of dulness between the two sides, because the
affection is more extensive in one than in the other; and in general
the loss of resonance over the collapsed lobules is determinable
without comparison of the two sides. Not uncommonly, patches of dulness
are found with intervals of comparatively clear resonance.
On auscultation the respiratory sounds are feeble or entirely absent in
an area in which a number of adjacent lobules are involved together in
collapse.
When a considerable part of a lobe is affected, bronchial breathing may
sometimes be heard, but this is in general less marked than the degree
of dulness and the amount of condensation would lead the examiner to
expect, because the breathing is too feeble to give rise to the
vibrations necessary for the production of this sign.
An important indication of lobular collapse is the rapidity with which
the signs just described are developed; a part or parts of the lung
which had been clear on percussion and normal in respiratory character
becoming in a day, or sometimes in a few hours, dull and nearly silent
to the ear. This very suddenness with which the physical signs are
developed in a case of bronchitis or catarrhal pneumonia in a child
points very plainly to the occurrence of collapse of the lung.
PATHOLOGY.--The pathological appearances in collapse of the lung vary
according to the extent of tissue involved in the change, and also
according to the cause which has induced it. In the disseminated
lobular form which is due to bronchitis the collapsed portions are
chiefly seen on the surface and at the margins of the lung, and they
extend more deeply into the organ as it becomes more involved in the
atelectatic condition. On the surface or on a section the collapsed
patches are depressed somewhat below the surrounding parts and are of a
darker hue, so that they are readily seen as dark-red or purplish spots
surrounded by the lighter healthy tissue. The contrast is sometimes
enhanced by the fact that the non-collapsed parts are even paler than
natural from the vicarious emphysema that has been established in them.
The consistence of the affected part varies in different cases. If the
change has occurred without previous congestion, the texture may be
somewhat flaccid; but if there has been hyperæmia, the part will be
leathery, non-crepitant, and resisting pressure. If no crepitation can
be detected the part will sink in water from the complete expulsion of
air from the affected lobules. A cut surface is smooth and does not
present the granular appearance of a hepatized lung, nor can
exudation-matter be pressed or scraped from it.
The collapsed lobules may be made to swell up and resume their normal
appearance and rosy color by forcing air with a blowpipe into the
bronchus leading to them. This is so generally true, at least, that it
has been regarded as a certain test by which to discriminate between
atelectasis and pneumonic consolidation when there may be a doubt at a
post-mortem examination as to which condition exists. In general, the
attempt to inflate will succeed when the air is directed into a
collapsed lobule; but the test is of less value than it was once held
to be because it has been shown, on the one hand, that lobules {254}
which have been collapsed for some time will not always expand under
the inflating force, and, on the other, that in recent catarrhal
pneumonia the alveoli may for a time still be inflated with air.
Meigs and Pepper, while stating that in general the results of the
attempt to produce inflation are altogether different in the two
conditions, yet hold, in accordance with Gairdner's teaching, that
"partially pneumonic lung may be inflated when the affection is recent
and combined, as it frequently is, with bronchitic collapse; while in
the latter lesion--_i.e._ collapse of lobules--in its purest forms
complete inflation is often very difficult or impossible after the
collapsed state has been of some duration."[3]
[Footnote 3: _Diseases of Children_, p. 143, 4th ed.]
Nevertheless, the test is of value when applied along with others; for,
as stated by J. Lewis Smith, "the inflated pneumonic lung is more solid
and resisting when pressed between the thumb and fingers than is the
collapsed lung."[4]
[Footnote 4: _Diseases of Children_, p. 570, 5th ed.]
The chief differences between the two conditions are--1st, the color,
which in collapsed lobules is purplish or livid, and in pneumonia
reddish-brown; 2d, the microscopic appearance, showing the alveoli
filled with cell-proliferation in pneumonia and free from change in
collapse; and 3d, the state of the adjacent pleura, which is inflamed
and often covered with lymph in pneumonia, while it is entirely healthy
in non-complicated collapse.
The bronchial tubes present the appearances met with in bronchitis,
being more or less congested, showing a softened state of their lining
membrane, and containing liquid mucous secretion and sometimes firmer
pledgets which have caused the obstruction.
As regards changes in the heart, extensive atelectasis may prevent
closure both of the foramen ovale and of the ductus arteriosus. From
the obstruction to the flow of venous blood offered by the collapsed
portions of the lungs the right ventricle may become so distended that
a portion of its blood may still be forced through the ductus
arteriosus, and another portion backward into the auricle and through
the foramen ovale, so that both of these channels may be kept pervious.