any other condition occurring at birth, and is sufficiently denoted by
the signs already described.
Imperfect expansion of the lungs continuing for some days after birth
might suggest patency of the foramen ovale from the purplish hue of the
surface common to both conditions. The expansion of the chest and the
resonance that it yields on percussion in the cardiac affection will be
sufficient to discriminate them except in those cases in which they
exist together.
Acquired atelectasis or collapse of the lung may require to be
distinguished from bronchitis, from pleural effusion, and from
catarrhal pneumonia.
Even uncomplicated bronchitis is in children sometimes accompanied with
so much dyspnoea as to cause apprehension that collapse of lobules has
taken place, but the absence of percussion dulness, either diffused or
in patches, will exclude the supposition.
From pleural effusion collapse of the lung may be distinguished by the
fact that the dulness due to pleurisy is generally on one side only,
that it is more intense and diffused than that of collapse, and that
its line of demarcation may often be made to shift with the position of
the patient.
Catarrhal pneumonia is in general distinguishable from collapse by the
history, course, and symptoms of the disease, especially the sudden
rise of temperature that belongs to pneumonia; as also by the
auscultatory signs. The percussion dulness of pneumonia is more
extensive than that of collapse, and is accompanied with bronchial
breathing; whereas in collapse the respiratory sounds are feeble and
mingled with moist râles.
{255} PROGNOSIS.--In congenital atelectasis, if there be no expansion
of the lungs within the first few minutes after birth, the prognosis is
generally bad. In some apparently hopeless cases, however, the
persistent employment of means tending to arouse the respiratory
function, and especially of those acting through a reflex influence, is
crowned with success. The prognosis varies according to the amount of
unexpanded lung; for even when some respiratory efforts have been made,
if the air enter only a limited extent of the lungs, the infant will
drag on a feeble existence for perhaps a few days, and then perish from
apnoea and exhaustion. When the lungs are once fully inflated the
danger from congenital atelectasis is past.
In acquired collapse of the lung the prognosis is dependent both upon
the number of lobules involved and upon the amount of strength
possessed by the patient. A larger amount of disease may be recovered
from if the nutrition and nervous system be not much depressed, while a
smaller amount may prove fatal in less favorable conditions of the
general system. Much also depends upon the extent and duration of the
coexisting bronchitis, and the degree to which it has affected the
constitutional powers.
TREATMENT.--In the treatment of congenital atelectasis the main
endeavor must be directed to arousing the respiratory function; and
this is best accomplished by means acting reflexively through the
centres of respiration. Sprinkling the chest and back with cold water,
the application of cold water to the spine by a sponge or by affusion,
or the alternate use of cold and hot water in the same way, will often
induce a deep inspiration by which the lungs will be unfolded and
respiration perfectly established. If this be not fully accomplished,
it is of the utmost importance that the child should be carefully
watched as long as the atelectasis continues in any degree, and that
the same means should be again resorted to when the failure of
respiration is threatened. The temperature of the surface should be
maintained by artificial heat and woollen wrappings, as a depression
below the normal standard easily takes place, and serves to lower all
the vital processes and increase the difficulty of keeping up
respiration.
In acquired atelectasis treatment must to a great degree be directed to
the superinducing bronchial catarrh. Counter-irritation of the chest
may be practised with Stokes's liniment, which consists of equal parts
of oil of turpentine, acetic acid, and camphor liniment, or with
mustard poultices prepared with special reference to the sensitiveness
of a child's skin by mixing the mustard with a double portion of flour
or Indian-corn meal. With the same view, dry cups may sometimes be
advantageously used.
Expectorants are serviceable by relieving the bronchitis, the best
being the syrup or wine of ipecacuanha in the dose of 5 to 10 drops, or
the muriate of ammonia in the dose of 1 to 3 grains in simple syrup or
syrup of liquorice, every two or three hours.[5] These agents may
modify the inflammatory state of the bronchial mucous membrane, and
thus prevent the extension of the collapse. If bronchial secretion be
profuse, the question of the use of emetics becomes very important.
When employed judiciously with reference to the real needs of the case,
they may be eminently beneficial, acting partly by removing the
accumulation in the bronchi which may have occasioned the {256}
collapse and may favor its further extension, and partly perhaps by the
deep inspiration which precedes emesis serving to expand the collapsed
lobules. It must be remembered, however, that there is always a
tendency to failure of the vital powers in acquired atelectasis, and
that this may be dangerously increased by emetics of a depressing
character. The best for the purpose are alum, sulphate of zinc, and
ipecacuanha. The repetition of the emetic must be determined by its
effect on the breathing and on the patient's strength.
[Footnote 5: One of the following formula may be used:
Rx. Syr. ipecac. drachm i-ij;
Syr. prun. virginian. drachm vj;
Ammon. muriat. drachm ss;
Aquæ, ounce j. M.
Dose, teaspoonful for a child of three to six months.
Or,
Rx. Ammon. muriat. drachm ss-drachm j;
Syr. glycyrrhiz.
Aquæ, _aa_ ounce j. M.
Dose, as above.]
Tonics and supporting measures are always called for in the treatment
of atelectasis, in view of the fact that the condition is essentially
dependent on failure of constitutional strength. Milk, wine-whey, and
animal broths are appropriate articles of food; alcoholic stimulants
are generally required; and in emergencies, if sudden increase of
prostration occur, the carbonate of ammonia in the dose of 1 or 2
grains may be given.
During the whole course of the malady such tonics as quinia or the
compound tincture of cinchona or one of the soluble salts of iron may
be administered.
Brown Induration of the Lungs.
DEFINITION.--Increased density of certain portions of the lungs, which
are of a reddish color, with brown or yellowish-brown spots scattered
throughout the indurated tissue.
SYNONYMS.--Pigment induration; Congestive carnification.
HISTORY.--This affection is a form of passive congestion of the lungs,
in regard to which it is somewhat uncertain whether the morbid process
is simply one of congestion or whether along with this an inflammatory
element is likewise present. It is beyond question, however, that the
changed condition of the lung is primarily and chiefly congestive, and
that it originates from causes which produce congestion.
ETIOLOGY AND MORBID ANATOMY.--The etiology and morbid anatomy of this
affection are so closely related that they are best considered
together. The most important fact both in the etiology and pathology of
brown induration of the lungs is that it is gradually brought about as
the consequence of obstruction to the pulmonary circulation from
disease of the mitral valve, either constrictive or regurgitant in
character. Interference with the return of the blood to the left side
of the heart is in this way produced, with consequent stasis in greater
or less degree within the pulmonary capillaries.
The most marked changes observed in lungs which have undergone this
form of congestion are that they do not collapse when the chest is
opened, and that they are more compact and less elastic and crepitant
than healthy lungs. On section they present a reddish color
interspersed with spots of yellowish- or reddish-brown, which sometimes
are of a very dark hue.
Microscopic examination shows an increased size of the capillaries of
the lung, which seem to encroach upon the air-cells and thus lessen
their capacity. Whether the walls of the alveoli have themselves
undergone thickening is a question about which different opinions have
been entertained. Rokitansky states that "when stasis has continued for
a longer period the walls of the air-cells and the interstitial tissue
become swollen, so that the former may become perfectly impermeable to
air;"[6] and although, in the passage quoted, he is writing of
pulmonary congestion in general, and not of this form in particular,
yet, as he is describing a stasis which has continued for some time,
the observation would seem applicable to the affection under
consideration.
[Footnote 6: _Path. Anat._, vol. iv. p. 59.]
Wilson Fox affirms that he has found alveolar thickening in
considerable tracts in this affection, with a distinct increase of
fibrous tissue in the walls {257} of the alveoli; but this change, he
goes on to say, is not uniformly present, and in some places the
alveoli are found filled with epithelial products like those of
catarrhal pneumonia.
The true explanation of the condition is probably this: that, beginning
as a passive congestion, such as might be expected to result from the
mitral disease with which it is almost constantly associated, the
affection afterward assumes an inflammatory condition of a low type
with epithelial proliferation, and in some cases with thickening of the
alveolar walls and the interlobular connective tissue. Passive
hyperæmia is, however, always the basis of the disease. The brownish
spots visible in a section are caused by the leakage of blood from the
congested capillaries into the alveoli or interstitial tissue without
the occurrence of any large extravasation. The blood thus exuded
undergoes pigmentary change, with the production of hæmatoidin, the
shades of color varying accordingly as the exudation has been recent or
of longer duration.
The failure of the lungs to collapse is due to the encroachment of the
dilated capillaries on the air-cells, and perhaps to the thickening of
the cell-walls and the partial occupation of the cells themselves by
epithelial products.
SYMPTOMS.--The general symptoms and the physical signs of this
affection are of the same character as those that occur in other forms
of pulmonary congestion. Dyspnoea is felt, especially on making
exertion; and this may be attributable in part to the associated
cardiac disease as well as to the condition of the lungs. Loss of
resonance on percussion and feebleness of respiratory murmur are
observable; and when the condensation is great bronchial breathing may
be heard.
DIAGNOSIS.--It is evident that there is nothing in these signs
distinctive of this particular form of congestion, which is, in fact,
not diagnosticable with absolute certainty during life. The probability
of its existence may, however, be inferred if along with the above
symptoms and signs a presystolic or regurgitant mitral murmur is heard,
showing constriction or incompetency of the mitral valve.
PROGNOSIS.--The prognosis of this affection is of course always
unfavorable, because the condition depends upon mechanical disease of
the heart of an incurable nature. Temporary improvement may, however,
sometimes take place under proper treatment.
TREATMENT.--Such treatment must be used as serves to support the
weakened heart and hold in check the tendency to dilatation. With this
view digitalis or convallaria may be employed, with tonics and
alcoholic or ammoniacal stimulants as occasion may require.
Counter-irritation over the lungs may be used and expectorants may be
given. If dyspnoea be urgent, the preparations of ether, such as
Hoffman's anodyne, or the carbonate of ammonia, may be administered.
{258}
CONGESTION AND OEDEMA OF THE LUNGS (HYPOSTATIC PNEUMONIA).
BY SAMUEL C. CHEW, M.D.
Congestion and oedema of the lungs are often found together, but they
are different morbid conditions, and each may occur independently of
the other. It is best, however, to consider them in connection with
each other.
DEFINITION.--By congestion of the lungs is meant an active or passive
hyperæmia of the pulmonary vessels, which are surcharged with blood.
Oedema of the lungs signifies an effusion of fluid consisting mainly of
the serum of the blood into the air-vesicles and, to some extent, into
the pulmonary connective tissue. Congestion is at times the determining
cause of oedema, but the latter condition may arise from causes not
tending to produce the former.
HISTORY AND ETIOLOGY.--As pulmonary congestion and oedema are almost
always secondary and dependent affections, their etiology is an
essential part of their history, so that these subjects will be best
considered together.
Active congestion of the lungs may result from any cause producing an
increased afflux of blood to these organs, such as hypertrophy or
functional over-action of the heart, or the sudden recession of the
blood from the surface and perhaps from other internal organs, such as
may take place under the influence of cold. Violent exercise, rapid
walking up hill, or even mental excitement, may in some impressible
subjects suffice to produce it.
Why vascular congestion should occur in a greater degree and more
readily in the lungs than elsewhere from the effect of cold is
sufficiently evident when it is considered that the pulmonary
capillaries are not supported by surrounding tissue, as those of other
parts are. And for the same reason the direct action upon them of cold
air or of certain irritant gases, such as ammonia or chlorine, may
suffice to cause an undue afflux of blood to them.
How far a neurotic influence exercised reflexively through the
vaso-motor system may serve to produce active congestion has not yet
been fully determined; but it is probable that the sudden pulmonary
congestions which have been known to follow the drinking of a large
quantity of cold water when the body is heated may be attributed to
such an action.
Passive congestion may be occasioned by a retardation of the blood-flow
from the lungs; as, for example, by a hindrance to its onward passage
through the left chambers of the heart in consequence of obstructive
valvular disease, especially a great degree of mitral or aortic
stenosis. So also mitral or aortic incompetency, by allowing the blood
to be crowded backward in the pulmonary veins, may interfere with its
passage through the lungs, and in this way set up passive hyperæmia.
By some writers mere weakness of the heart is spoken of as a cause of
{259} passive congestion of the lungs; but it can hardly be regarded as
such apart from influences affecting the blood itself or the tonicity
of the pulmonary vessels; for it is to be considered that while
weakness of the left chambers of the heart might impede the onward
course of the blood received from the lungs, yet at the same time the
right chambers, if weakened in a corresponding degree, would send less
blood into those organs, and then the conditions of passive hyperæmia
would not exist. It is well known, moreover, that cardiac weakness
coming on suddenly as in syncope, or gradually as in various asthenic
diseases, may be present without the occurrence of any signs of
pulmonary congestion. Yet it is not impossible that there may be a
disturbance of the balance between the actions of the right and left
sides of the heart, and that thus passive congestion of the lungs may
result from a relatively greater weakness on the left than on the right
side of the heart, so that the left auricle and the pulmonary veins may
be obstructed, and backward pressure produced while the right ventricle
is still sending blood into the lungs.
It is probable, however, that, in addition to the propulsive power
exercised on the blood by the contraction of the heart, another agency
affecting its passage through the lungs is the interchange of gases in
respiration; and therefore any interference with the reception of
oxygen and the elimination of carbonic dioxide may tend to retard the
blood-flow, and thus favor stasis or passive congestion. In this way
the inhalation of impure air, especially air containing an undue amount
of carbonic dioxide, may occasion passive hyperæmia.
Pulmonary oedema is never a primary affection, but is always due to
some preceding disease. In the first place, it may, as already stated,
take its origin directly from congestion of the lungs, the walls of the
obstructed vessels allowing the transudation of serum, which will
collect in the air-cells and connective tissue and also in the mucous
membrane of the terminal bronchi. In an early stage it may be present
in the walls only of the alveoli without being effused into their
cavities.
Another cause of pulmonary oedema is obstruction of the circulation of
a part of a lung, such as may take place in pneumonia or miliary
tuberculosis, the vessels of other parts becoming distended by backward
pressure, so that the serum of the blood will exude into the air-cells
or interstitial tissue. When this occurs in pneumonia it may be a most
alarming and dangerous complication.
Still another and very frequent cause of pulmonary oedema is Bright's
disease in its different forms, in which the oedema occurs as a part of
the general dropsy incident to these affections. In acute congestive
nephritis it may come on very rapidly, constituting acute pulmonary
oedema. Hertz remarks that an acute oedema may take place in the course
of an acute nephritis, as has been reported by Lebert, but that such an
occurrence is not frequent.[1] The writer of this article has himself
seen several cases of acute pulmonary oedema occurring as a part of the
dropsy of scarlet fever.
[Footnote 1: _Ziemssen's Cyclop._, v. p. 279.]
More frequently it is met with in chronic albuminuria, and varies in
amount from time to time, as dropsical effusions elsewhere do in this
condition.
Attacks of asthmatic dyspnoea are not uncommon in the course of
Bright's disease, especially in cases of chronic contracted kidney.
They are described as uræmic asthma, and are referred by some writers
to the action of the depraved blood on the centres of respiration. This
explanation may be correct in some cases, but it seems likely that they
are due in part to dropsical oedema of the bronchial mucous membrane,
the connective tissue, or the air-cells. A weakened condition of the
heart, such as is apt to occur {260} in advanced periods of Bright's
disease, has probably some share in determining the oedema.
In any case of oedema, according to its situation, whether it is in the
connective tissue, the bronchial mucous membrane, or the air-cells, and
according also to the amount in which it is effused, it will interfere
more or less with breathing. If there be interstitial infiltration with
swelling of the bronchial mucous membrane, lessening the calibre of the
tubes, there may be merely some embarrassment of respiration; but if
the effusion invade any considerable number of the air-cells, urgent
dyspnoea will be produced. Oedema is generally most abundant at the
lower part of the lungs, and is not uncommonly associated with pleural
effusion, the two conditions being due to the same cause; and then the
interference with respiration is greater and more perilous.
SYMPTOMS.--It is possible that a slight degree of pulmonary congestion
may exist when the circulation is hurried without the occurrence of any
other symptoms except moderate acceleration of the breathing. Under
such circumstances, however, the existence of congestion cannot be
proved. When it is brought about in greater degree, either by
over-action of the heart or sudden recession of blood from other parts,
the earliest and most prominent symptoms are a sense of oppression in
the chest and quickened, laborious respiration, which may rapidly
increase until the dyspnoea becomes most urgent and distressing. The
heart's action grows more hurried, the pulsations in the carotid and
temporal arteries are strongly felt, and the face is deeply flushed.
Cough is always present, at first dry in character and afterward
accompanied with expectoration of frothy mucus, which may be tinged
with blood or may be even mingled with a considerable amount of
bright-red blood.
The different appearances of the expectoration are probably due to the
fact that in some cases the distended pulmonary capillaries allow the
transudation of blood-corpuscles, and in others they are actually
ruptured by the strain, so that pure blood escapes from them.
If the congestion is due to weakened action of the heart, with remora
of the venous circulation, and is passive in character, the symptoms
may be less acutely developed and less urgent than they are in the
active form; indeed, in some cases in which very considerable portions
of the lung are involved there may be no excessive dyspnoea while the
patient is quiet, in consequence of the organism having become
gradually accustomed to the imperfect respiration.
As the congestion increases, however, and the lungs become more
affected, the signs of malaëration are more conspicuous. Dyspnoea is
more oppressive, the face and surface generally, especially the lips
and extremities, become cyanotic and cold, and the patient perishes
from apnoea and from coma occasioned by oedema of the brain or medulla
or stasis of blood in the cerebral veins, the respiratory centres being
paralyzed. With the occurrence of somnolence the efforts to free the
air-passages from fluid by coughing and expectoration grow less and
less as the sensibility is obtunded.
When the congestion is not very extensive the amount of air in the
lungs is not lessened sufficiently to materially affect the percussion
note, which may remain resonant, though it may have a somewhat
tympanitic quality. The vesicular murmur is still heard, but it is
rather rough in character. When the general symptoms indicate a graver
degree of congestion there will be corresponding changes in the
physical signs; resonance will be lessened, or even replaced by
dulness, in consequence of the filling of the alveoli with serum or
blood; and the respiratory murmur will be completely masked by coarse
and fine mucous râles. If the dulness is very marked, bronchial
breathing and bronchophony may be observed. Elsewhere in parts not
{261} involved in the congestion exaggerated or puerile breathing may
be heard from the supplementary action that takes place there.
The physical signs may vary as to their situation with the patient's
position as the blood in the congested vessels and the serum in the
alveoli and connective tissue gravitate from side to side. But when the
change described as hypostatic pneumonia has taken place, and the
affected portion of the lung has become condensed in texture, position
has little or no influence on the physical signs, which will still
remain even when the affected side is kept uppermost.
When oedema of the lungs is produced by serous effusion invading the
air-cells, there is some degree of dulness on percussion, especially at
the lower part of the chest. Respiratory murmur is feeble or
suppressed, and fine moist râles are heard, with an intermixture at
times of the true crepitant râle. These signs are generally heard on
both sides, but when an area of oedema is due to pneumonia the signs
may be present only on the affected side.