the term asthma was employed by the older writers to designate a
variety of affections of which embarrassed respiration was the most
prominent symptom, thus including a great number of diseases which a
more extended knowledge of pathology has since distributed among other
nosological groups. By the earlier authors simple embarrassment of
breathing was designated as dyspnoea; if attended with wheezing it was
called asthma; while those forms in which the difficulty in respiration
was so great as to prevent the patient from lying down were
appropriately styled orthopnoea (Celsus). Ignorant to a great extent of
pathological anatomy and unprovided with the improved methods of
physical diagnosis which we now possess, they described as asthma not
only the dyspnoea due to cardiac and pulmonary diseases, but also that
occasioned by affections of the pleura and greater vessels. Covering
such an extensive range of territory, it was found necessary to
subdivide the disease into a number of varieties, each author
classifying them according to his conception of the cause, seat, and
nature of the trouble. Some of these--_e.g._ a. dyspepticum--still find
a place in medical literature, but the vast majority of them, having
ceased to be of any practical significance, have been discarded, and
are now only interesting as examples of the crude and fanciful notions
which prevailed in an age during which science rather retrograded than
advanced.[1] Of the writers of this period, Willis in the seventeenth
century is especially worthy of notice as being the first to describe
the nervous character of asthma. Without discarding the accepted forms
of the disease, he mentions another variety, characterized by spasmodic
action of the muscles of the chest, to which he gave the name asthma
convulsivum.
[Footnote 1: "Van Helmont, discarding the ancient doctrine of the four
humors, attributed asthma to an error of the Archeus, which he
conceived to be enthroned in the stomach and to constitute the source
of all diseased as well as of all healthy phenomena. This principle, he
supposed, sent forth from the stomach a peculiar fluid, which, when it
became diseased, gives rise to a morbid state of the parts to which it
was conveyed. He moreover imagined that this fluid sometimes mixed
itself with the male semen, and thus formed a compound which, as one of
its constituents is the means provided by nature for the propagation of
the species, possesses the power of generating a disease of hereditary
character. Thus, when this compound was conveyed to the articulations,
he affirmed it produced gout, and when it took its direction to the
lungs it then occasioned asthma" (_Baltimore Med. and Surg. Journ. and
Review_, Baltimore, 1833, p. 300).]
The improvement in physical diagnosis resulting from the brilliant
discoveries of Auenbrugger and Laennec greatly curtailed the domain of
asthma. {185} With the aid of auscultation and percussion it was
discovered that most of the cases hitherto regarded as asthma were only
symptoms of some organic disease. Many distinguished authorities,
particularly of the French school, went so far as to declare that there
existed no such disease as asthma, and that in every case the dyspnoea
and other phenomena described under that name were merely symptoms of
some organic affection.
Although very generally received at first, it was not long before this
too-sweeping reform encountered opposition from various quarters. Cases
were observed with marked asthmatic symptoms in which, after death, the
most careful examination failed to reveal the slightest trace of
textural lesion. The discovery by Reisseisen of muscular fibres even in
the minutest bronchi, and the demonstration of their electric
contractility by Longet and Williams, afforded a ready explanation of
these cases, and led to the opinion--which has since been generally
received--that asthma in the modern acceptation of the term is simply a
neurosis. The more recent theories in regard to the nature of asthma
will be more fully discussed in the portion of our article devoted to
the pathology of the disease.
SYMPTOMS AND COURSE.--The following description of an attack of asthma
by Trousseau, who was himself an asthmatic, is perhaps the best that
has ever been written: "An individual in perfect health goes to bed
feeling as well as usual, and drops off quietly to sleep, but after an
hour or two he is suddenly awakened by a most distressing attack of
dyspnoea. He feels as though his chest were constricted or compressed,
and has a sense of considerable distress; he breathes with difficulty,
and his breathing is accompanied by a laryngo-tracheal whistling sound.
The dyspnoea and sense of anxiety increasing, he sits up, rests on his
hands, with his arms put back, while his face is turgid, occasionally
livid, red, or bluish, his eyes prominent, and his skin bedewed with
perspiration. He is soon obliged to jump from his bed, and if the room
in which he sleeps be not very lofty he hastens to throw his window
open in search of air. Fresh air, playing freely about, relieves him.
Yet the fit lasts one or two hours or more, and then terminates. The
face recovers its natural complexion and ceases to be turgid. The
urine, which was at first clear and was passed rather frequently, now
diminishes in quantity, becomes redder, and sometimes deposits a
sediment. At last the patient lies down and falls to sleep."
The next day the patient may feel well enough to pursue his accustomed
avocation, and may remain free from all symptoms of the disease until
another attack comes on; but more frequently he is confined to the
house, if not to bed, the slightest exertion being sufficient to cause
dyspnoea; and during the following night there is a repetition of the
paroxysm.
If unchecked by treatment, the disease may continue for days, weeks,
and in some instances even for months, the paroxysms often increasing
in severity until, as in other nervous affections, it ultimately wears
itself out.
There is no regularity in the occurrence of the attacks. In some cases
they recur every few days, while in others there may be an interval of
weeks or months between the seizures. Even in the same case, although
the individual paroxysms of the attack may come on at the same hour,
there is, except in rare instances, no regularity in the recurrence of
the attack itself; and when it does recur at a certain time it is
almost always due to some cause which, as in hay asthma, exerts its
influence only at that particular period.
In the great majority of cases asthma comes on without any warning
whatsoever, but occasionally it is preceded by certain sensations which
to the experienced asthmatic are a sure indication that an attack is
impending. With some it is only a feeling of ill-defined discomfort;
others complain of various disorders of the digestive system--a sense
of dryness of the mouth and pharynx, uncomfortable distension of the
epigastrium with eructation of {186} gases from the stomach, and more
or less obstinate constipation. A troublesome itching of the skin often
precedes the attack. Some experience a feeling of constriction around
the throat; a profuse secretion of clear urine is a symptom of this
stage. Frequent gaping, frontal and occipital headache, are mentioned;
but far more constant than all of these are certain symptoms indicative
of a mild grade of acute catarrh of the respiratory organs--coryza,
with swelling of the Schneiderian membrane and discharge from the
nostrils, sneezing, redness of the conjunctivæ with increased
lachrymation, and later, as the irritation extends downward, more or
less cough.
The attack almost always comes on after midnight, and, as a rule,
between the hours of two and six o'clock in the morning. Salter states
that nineteen out of twenty cases occur between two and four A.M. There
are, however, occasional exceptions to this rule; sometimes the patient
is attacked soon after retiring, and Trousseau cites the case of his
mother, who always had her attacks between eight and ten in the
forenoon, and also that of a tailor, whose paroxysms invariably came on
at three o'clock in the afternoon. Indeed, there is no hour of the
twenty-four during which the seizure may not take place. Various
attempts have been made to explain why it is that the paroxysms of
asthma almost invariably occur during the latter half of the night.
Many attribute it to a stasis of blood in the lungs caused by the
recumbent posture of the patient, while others claim that it is due to
a dulling of reflex impression, the patient during sleep failing to
perceive the necessity of breathing. Germain Sée, who discredits both
theories, inquires why, if the above explanations are correct, does the
attack not come on soon after retiring, as is the case with the
dyspnoea of cardiac diseases.
The paroxysm of asthma develops very rapidly, but not so suddenly as is
claimed by many authors, several minutes to half an hour or more
elapsing before it attains its full height.[2]
[Footnote 2: Germain Sée in _Nouveau Dictionnaire de Médecine et de
Chirurgie_, tome iii. p. 617, Paris, 1865.]
The patient, experiencing an urgent desire for breath, instinctively
places himself in the position most favorable for the ready admission
of air into the lungs. If in bed he sits up, and, resting on his hands
or grasping his knees with them, he so fixes the body that the muscles
of respiration may work to the greatest advantage. The shoulders are
drawn up and the head thrown back. The expression of the face is one of
great anxiety--pale at first, then red, and as the attack increases in
severity assumes a dusky, bluish tint; the mouth is partially opened,
the nostrils are dilated; the eyes, the conjunctivæ of which are much
injected, are prominent, with a wild, staring look; and the forehead is
moist with perspiration. Others in their desperate struggle for breath
spring from the bed, throw open the window, and, regardless of
everything save what they believe to be impending suffocation,
recklessly gasp in the cold night air. Sometimes the sufferer prefers
to kneel before a table or some other article of furniture, supporting
his head with his hands. Whatever posture he assumes, he is actuated by
the one impulse of placing himself in the position that will enable him
to use to the greatest advantage the muscles of respiration and their
auxiliaries. The sterno-cleido-mastoid muscles are contracted to the
utmost, and, projecting like hard cords, with the aid of other muscles
draw the chest upward. The patient instinctively avoids every
unnecessary exertion as having a tendency to aggravate his dyspnoea; he
speaks but little, and when questioned usually replies with a motion of
the head.
In ordinary respiration the inspiratory movement is twice as long as
the expirium, the latter, except in forced expiration, being a purely
passive act. In asthma this rule is reversed, the expiratory movement
being four or five times as long as the inspirium, and is often so slow
that it fills the whole of {187} the pause which usually intervenes
between the completion of one respiration and the beginning of another.
It is sometimes so slow "that it seems as though the lung would never
empty itself." In the desperate struggle for breath the respiratory
muscles are exerted to the utmost in futile endeavors to expand the
chest; with each inspiration there is an elongation of the thorax, but
no lateral movement. The chest moves up and down, but there is no
expansion; "the muscles tug at the ribs, but the ribs refuse to rise"
(Salter), the walls of the chest remaining immovable.
Notwithstanding the all but tetanic contraction of the diaphragm, there
is during each inspiration a sinking in of the epigastrium, and in
severe cases also of the spaces above and below the clavicles. During
expiration the abdominal muscles, especially the recti, are hard and
tense, the pressure thus exerted being sometimes sufficient to expel
the contents of the lower bowel and bladder.[3] The transversus is also
tightly contracted, and a cross furrow above the umbilicus indicates
that the contraction of its upper half is opposed to the contents of
the abdomen forced down by the distended lung (Biermer). Although the
dyspnoea is great, there is no increase in the frequency of the
respirations so long as the patient remains quiet, but, on the
contrary, they are often less frequent than in health. This slowing of
the respiration is also observed in the dyspnoea from laryngeal
stenosis in croup, etc.; but in these cases we do not have the
prolonged expiration which is so characteristic of asthma (Biermer). At
every breath which the patient takes there is a peculiar wheezing sound
which may be heard distinctly all over the room; it is usually heard
only during expiration, but some authors (Biermer) claim that it is
also audible during inspiration.
[Footnote 3: Bamberger's case, as quoted by Riegel, _Ziemssen's
Pathologie u. Therapie_, Leipzig, 1875, Band iv. 2, S. 282.]
On auscultating the chest it will be found that the ordinary vesicular
murmur is either entirely absent, or if heard it is only over very
limited areas. In the place of it we have an endless and ever-changing
variety of dry sounds, such as whistling, cooing, mewing, snoring,
etc., technically styled sibilant or sonorous ronchi. They are usually
equally diffused over both lungs, but are sometimes confined to one.
The sibilant râles afford an index of the degree of spasm, being in
mild cases equally audible during both inspiration and expiration,
while in severe attacks they are louder during expiration (Biermer).
That the vesicular murmur cannot be heard is due not only to its being
masked by the louder ronchi, but also to the absence of the condition
necessary for its production, the spasmodic constriction of the
bronchial tubes or their plugging with tough, viscid mucus preventing
the entrance of sufficient air to produce the sound. Sometimes a
hitherto occluded tube becomes pervious, and we have vesicular
respiration where a moment before only dry sibilant râles were heard.
Usually at the close of the attack, when cough sets in, there are
occasional moist râles. These become more frequent as the expectoration
becomes more abundant. Frequently, however, the paroxysm terminates
much more abruptly, the spasm relaxes, and the air rushing through the
tubes gives rise to puerile respiration.
During the paroxysm there is, even in the early stages of asthma, more
or less distension of the lungs, measurement of the chest showing that
its circumference is four to eight centimeters greater than before the
attack (Beau). This transitory emphysema, which must not be confounded
with that due to structural changes observed in old cases, disappears
with the attack, and the lung returns to its normal condition. This
distension causes the exaggerated resonance obtained by percussion
which is one of the most constant symptoms. At the base of the lung,
especially posteriorly and laterally, there is a peculiar modification
of the percussion sound to which Biermer has applied the name
Schachtelton, from its resemblance to the note produced by striking
{188} an empty pasteboard box. Besides this exaggerated resonance, it
will be found that the line of dulness on the right side, which marks
the upper border of the liver, is fully two inches lower during the
paroxysm than before, and that the area of cardiac dulness is somewhat
diminished by the overlapping of the distended lung-tissue (Riegel).
Another peculiarity elicited by percussion, and to which Bamberger was
the first to direct attention, is that in some rare cases instead of
moving vertically the line of hepatic dulness remains unchanged during
both acts of respiration.
Toward the close of the attack the congested mucous membrane of the
bronchi begins to secrete, and there is more or less cough. The matter
expectorated consists at first of little balls of tough,
semi-transparent mucus not much larger than a pea. It is exceedingly
tenacious, and is raised with great difficulty. Examined under the
microscope, the sputum is found to consist "of a great number of
corpuscles, some of which are polyhedral in form with rounded angles;
they are pale, homogeneous, and slightly granular. At first sight they
resemble pus-corpuscles, but they are much larger, less circular in
form, and have no nucleus. In addition to these corpuscles there are
others which are oval, elongated, fusiform, and sometimes linear in
shape, but all of them appear to be of the same nature and possess the
same refracting power as the corpuscles first mentioned. They are all
of them agglomerated in a sort of viscous matter."[4] The expectoration
often contains blood, and in some rare instances profuse hemorrhages
have been known to occur. Sometimes the matter has particles of soot
and coal-dust intermingled with it, the so-called carbonaceous sputum
(Sée). In addition to the cells above described, the sputa contains
small yellowish-green masses or threads in which are imbedded the
peculiar octahedral crystals which Leyden has ingeniously connected
with the etiology of asthma, and to which we shall again have occasion
to refer.[5] Ungar has recently also discovered crystals of oxalate of
lime in the sputa.
[Footnote 4: Germain Sée, _Nouveau Dictionnaire de Médecine et de
Chirurgie_, pp. 612, 613; also, Salter, _Asthma, its Pathology and
Treatment_, Am. ed., p. 944.]
[Footnote 5: Riegel, in _Ziemssen's Handbuch d. Pathologie u.
Therapie_, vol. iv. 2, pp. 268, 285.]
Laryngoscopic examination reveals more or less congestion of the
air-passages. "In ordinary respiration the glottis is widely open
during inspiration, and at each expiration the arytenoid cartilages
approach each other so as to narrow the glottis; but in the labored
respiration of asthma the glottis is fixed in the condition of
expiration; that is, the glottis is narrowed, and the air enters and is
expired through the same narrow space."[6]
[Footnote 6: Steavenson, _Spasmodic Asthma_, p. 23.]
The embarrassment of respiration and the pressure of the air in the
distended alveolæ by impeding the capillary circulation of the lungs
prevent the left auricle from receiving its full supply of blood; hence
the pulse is small and weak during the paroxysm, but regains its
natural volume as soon as its immediate effects are over. The action of
the heart, like every other phenomenon of asthma, is subject to
constant variation. At one moment it beats tumultuously, while at the
next its action may be so feeble as to cause temporary syncope (Sée).
The venous blood, unable to overcome the obstacles to its passage, is
forced back into the vessels, causing distension of the cervical veins
and the jugular pulse sometimes observed in severe attacks. The bluish
hue of the face in bad cases is due to cyanosis resulting from
insufficient aëration of the blood. The paroxysm is unattended with
fever, the temperature, if altered at all, being rather below than
above the normal. Coldness of the face and hands is quite a common
symptom in protracted cases.
In addition to the nervous sensations described among the premonitory
symptoms, patients have been known to suffer from disturbances of a
more {189} serious nature during the paroxysm. In some instances there
is complete loss of consciousness, and Riegel[7] states that such cases
have been known to have tetanic convulsions of the trunk and
extremities.
[Footnote 7: _Loc. cit._ p. 285.]
The course of an attack of asthma is in most cases quite typical, the
paroxysms recurring nightly for an indefinite period, and usually
increasing in severity until, as in epilepsy and other nervous
diseases, it finally exhausts itself. On awaking from the sleep which
usually succeeds the final paroxysm the patient, unless the attack has
been very mild and of short duration, feels weak and exhausted, but
there is no tendency to the recurrence of the dyspnoea; on the
contrary, he may expose himself with perfect impunity to the causes
which at other times would be certain to produce an attack. The chest
feels stiff and sore, the cough and expectoration diminish, and in a
few days disappear, and if the disease has produced no organic lesion
the patient returns to his usual state of health.
DURATION.--The duration of asthma, except in young persons and in those
rare cases in which the cause can be discovered and removed, is very
indefinite, the disease lasting for years, if not for life. As the
patient grows older the attacks become less severe, but are more
frequent. Sometimes a case which has recurred for years and defied the
most energetic treatment will all at once recover of itself.
SEQUELÆ.--Although bronchial asthma is essentially a neurosis, and
therefore purely functional in its character, it is rare for it to
continue for any great length of time without causing some organic
affection of the lungs or heart.
The most common sequel of asthma is emphysema. The bronchial tubes
being more or less completely closed, either by contraction of their
muscular fibres or by plugs of thick, viscid mucus, the air pent up in
the parts beyond the obstruction is subjected to the negative pressure
produced by the exaggerated inspiratory act, becomes rarefied, and, in
obedience to the diminished resistance induced by the partial vacuum in
the thorax, causes distension of the air-cells. This condition
continues until, the tubes having again become pervious, the natural
elasticity of the lung-tissue, aided by the expiratory muscles, forces
out the air and permits them to return to their natural size. This is
the transitory emphysema to which we have already alluded. Germain
Sée[8] regards it as analogous to the paralytic emphysema which occurs
the moment the pneumogastric is divided. With repeated attacks the
air-cells lose their elasticity and remain permanently dilated. Owing
to the constant distension, the walls of the alveolæ become more and
more attenuated, until, finally giving way, two or more of them
coalesce, forming one large cell. The symptoms of this condition are
the same as those of ordinary vesicular emphysema.
[Footnote 8: _Op. cit._, p. 637.]
Owing to partial occlusion of the afferent bronchi and the altered
conditions of pressure mentioned, the blood accumulates in the
capillaries during the paroxysm, the lung-cells do not receive their
adequate supply of air, and oxygenation is imperfect. In the early
stages of the disease this congestion is only temporary, and disappears
with the removal of the obstruction, but in those cases in which the
attacks are severe and frequent the vessels lose their contractility
and remain permanently congested.
The state of chronic congestion just mentioned is occasionally attended
with serous exudation into the interalveolar tissue, which by pressing
upon the adjacent air-cells causes their obliteration. This oedema,
with the remains of the compressed air-cells and the viscid mucus
stagnating in the finer tubes, forms the little islets of carnified
tissue known as lobular pneumonia.
The most frequent change observed in the bronchial tubes in old cases
of asthma is hypertrophy of their muscular fibres, causing thickening
of their {190} walls and diminished calibre. In other cases they are
dilated, but this condition is due more to the concomitant bronchial
catarrh than to the asthma.
Obstructed in its course through the lungs, the venous blood
accumulates in the pulmonary artery, and, pressing back upon the right
ventricle, excites it to increased action, which in the course of time
leads to hypertrophy of its muscular fibres and dilatation of its
cavity.
In the early stages of asthma, the face is usually pale during the
intervals between the paroxysms, but when the latter become more
frequent the impeded circulation causes stasis in the peripheral
vessels. The imperfectly-oxygenated blood gives the face a dusky hue,
and in severe cases it may become bluish or even violet-colored. The
eyes are prominent, owing to the enlargement of the orbital veins
(Sée), and the conjunctivæ congested and watery.[9]
[Footnote 9: For a description of symptoms of the above-mentioned
secondary affections the reader is referred to the articles on
EMPHYSEMA and HEART DISEASE.]
ETIOLOGY.--Predisposing Causes.--Every one is not liable to asthma, and
the fact that out of a large number exposed to its exciting causes only
a few are attacked justifies the assumption that there is an inherent
tendency to the disease. That this tendency is hereditary in its nature
is conceded by every prominent writer on asthma except Lebert, who
believes this to be only occasionally the case. Thus, of 35 cases
collected by Salter, heredity could be traced in 14, of whom 7
inherited the disease from the father, and the remainder from
grandparents and other relations. Ramadge gives an instance in which
the disease appeared in four generations: an asthmatic father had four
children, three of whom inherited the disease; one of the daughters
married, and of her two children one became asthmatic; the other
escaped, but the disease reappeared in one of her children.[10]
[Footnote 10: Germain Sée, _op. cit._, p. 668.]