side raised above that of the healthy chest. Subsequently, Peter,[24]
after a long series of researches, reported some very important results
as to the localized parietal temperature in cases of pleuritic
effusions: (1) He found that the {495} parietal temperature, as tested
by the thermometer, is always higher on the side of the pleurisy than
that of the body as tested in the axilla; (2) that the elevation of the
temperature increases as the effusion augments, the highest local
temperature corresponding to the period of secretory activity of the
inflamed pleura; (3) the rise affects both sides, but is greater over
the diseased pleura; (4) the temperature falls by degrees as the
effusion is reabsorbed--less on morbid side; (5) the absolute elevation
of local temperature is greatest in the sixth intercostal space; (6)
after paracentesis the parietal temperature is increased: this falls in
a few hours where the effusion is not re-formed, but when such is the
case it continues for some days. This local rise of temperature, he
considers, is from hyperæmia and cell-production, caused by the
traumatism from the needle added to the already-existing hyperæmia.
This excessive congestion, caused by the accumulation of blood
occurring when a large quantity of fluid is rapidly withdrawn, produces
the syncope, pulmonary congestion, consecutive albuminous
expectoration, the pain, and the oppression amounting sometimes to
suffocation, and occasionally ending in death.
[Footnote 23: _Thèse de Paris_, 1875.]
[Footnote 24: _La France médicale_, 4th May, 1878.]
At the commencement in acute cases the respiratory acts become very
frequent, even going to 40 or 50 per minute. They are short,
interrupted, and superficial. Their frequency makes up for their
incompleteness in furnishing sufficient air. The painfulness of each
act forces the individual not to expand the walls of his chest more
than he can avoid. Moreover, the high fever in itself produces frequent
respiration. As the temperature falls the respiration becomes less
abnormal. If the effusion forms rapidly, the patient may become
oppressed, even when the quantity is not large. If it is thrown out
gradually, the breathing is not so much interfered with until a large
quantity forms, the organism becoming accustomed to the interference
with the play of the lungs. The strength of the individual and the
activity of his nutritive functions are materially lowered. Sometimes
he breathes with difficulty, especially when he takes active exercise.
The dyspnoea is very painful and alarming. The aëration of the blood is
so materially interfered with that there results a large quantity of
carbonic acid, which irritates excessively the respiratory
nerve-centres.
During the acute stage the patient sometimes lies on his back, but more
frequently on the well side, and exceptionally on the diseased side. He
avoids lying on the side where the inflammation exists, because the
weight of his body increases the pain. I have, however, seen patients
who would persist in lying on the painful side and supporting it with
their hand. It sometimes happens that a patient lies on the affected
side, and will not move, because the movement gives him such acute
pain. Ordinarily, he prefers to lie on the healthy side, even after the
fluid has been poured out to a moderate degree, because his pain is
less. When, however, the effusion has become great enough to deprive
him of the use of the diseased side, he instinctively turns on that
side, so as to avoid the weight of the fluid pressing upon the lung on
the sound side. Moreover, he wishes to expand as much as possible the
side whose respiratory force now needs to do double work. This change
of position in patients has an unmistakable significance. It shows that
the sufferer is aware that he is more comfortable lying on the diseased
side. His physician's attention is drawn to the condition of the chest
as influenced by the increased quantity of fluid pressing the air out
of the lung.
Cough is not a constant symptom in pleurisy, but ordinarily it occurs
at some stage of the disease. It is short, dry, and suppressed in
character. It is painful, and therefore is avoided when possible,
especially previous to the effusion. It disappears generally about the
fourth or fifth day, when the effusion has attained a considerable
amount. The cause of the cough has been generally supposed to be the
exalted sensibility of the inflamed {496} pleura, but Nothnägel
maintains that such is not the case. Fraentzel holds that the cough is
caused by the strain on the lung-tissue and the finer bronchi when
there is a slight effusion. Cough brought on by change of position is
one of the characteristic symptoms of large effusions into the pleura.
If the lung is completely compressed by the pleuritic effusion, then no
actual strain on the alveoli or the bronchi can exist. In such cases
there is no cough, but it returns when the effusion decreases in
quantity, and quite violently, if this occurs suddenly, as, for
instance, in puncture of the chest (Fraentzel). In the latter case the
cough is probably caused by the rush of blood and the sudden expansion
of the chest.
Slight frothy expectoration may exist, but ordinarily there is none
whatever, unless from bronchial catarrhal complications. In that case
sero-mucous fluid is expectorated in small quantity. If it becomes
viscid and tinged with blood, it is caused by pulmonic involvement.
In empyema, if the expectoration becomes purulent, we ought at once to
suspect the presence of some circumscribed spots of necrosis of the
pleuritic covering of the lung, which have allowed the pus from the
pleural cavity to filter through the lung-tissue. By careful physical
examination of the chest we can ascertain whether there has been any
diminution in the quantity of fluid. When, as sometimes occurs, there
is actual perforation of the lung, the pus from an empyema comes in
quantity, through the bronchial tubes, out of the mouth. Patients may
sink from exhaustion following this discharge, or if the discharge be
excessive it may fill up the bronchial tubes too rapidly for its
removal by expectoration, thus causing suffocation. This danger is
increased if the discharge takes place during sleep.
Cyanosis is a symptom which should cause serious alarm, for it shows
that the effusion is so great as to interfere very materially with the
due arterialization of the blood. When the cyanosis is accompanied by
pallor, coming on suddenly in the course of a pleurisy, we may infer
with considerable probability that there is a hemorrhagic exudation.
But if the paleness comes on slowly during weeks or months, it may also
be dependent on a simple sero-fibrinous effusion (Fraentzel).
Protracted cases of effusion, especially if purulent, are associated
with emaciation and loss of strength. There may exist more or less
oedema of the lower extremities and of parts of the body where the
patient lies down, as we have in the chronic diseases of the chest.
When this oedema is limited to the affected side of the chest, whether
it be extensively developed and spread over the entire half of the
chest or confined to certain spots, it almost invariably justifies the
diagnosis that the effusion is purulent. The effusion may, however, be
purulent without the presence of this localized oedema. Occasionally,
cases are met with of effusion in the left pleura where there are
visible and palpable systolic pulsations in the intercostal spaces
arising from the impulse of the heart or of the larger blood-vessels
passing through the fluid.
Physical Signs.--Perhaps in no other disease of the chest are physical
signs so important for purposes of diagnosis as they are in pleurisy.
Even at the very beginning of the attack they give us valuable
information. In later stages, when the effusion is in the pleural sac,
they furnish, as we shall hereafter show, trustworthy data for
diagnosis, prognosis, and also very valuable indications for treatment.
There is no other disease of the chest where the physical changes made
by the inflammatory process are so pronounced and so accessible to the
senses of hearing, sight, and touch. The physical signs are so marked
that, almost by themselves, they give us the pathological condition.
They have been so carefully studied, and their correlative value
insisted upon, that they are readily interpreted. One is often tempted
to rely too much upon them to the exclusion of the proper consideration
of the general symptoms.
{497} As the physical condition of the pleuræ varies much in the
several stages of the disease, the physical signs must necessarily vary
accordingly.
At the very beginning of the attack the sensibility of the pleuræ is
augmented by the inflammation. Consequently, on inspection, it will be
observed that the patient is careful to avoid the pain caused by the
inflamed pleuræ rubbing together. He not only tries to avoid using the
ordinary muscles (especially the intercostals) for enlarging the
capacity of the lower portion of the chest, where the disease is
generally found, but he retracts his chest and keeps the pleuritic side
almost motionless. The well side has double work to do, and is seen to
expand more fully. The patient will frequently press the lower ribs in,
on the affected side, with his hand, or he will lie on that side, so as
to control the expansion of the chest, or he will lie on the healthy
side and bend his body over.
The respiratory movements are marked by an irregular and jerking
rhythm, and are quickly made. The pain felt on inspiration is of a
catching or stabbing character, and produces dyspnoea, the subject
struggling for air. The diaphragm is held as fixed as possible, so as
to prevent the movement of the inflamed surfaces over each other. The
patient restrains as far as possible the respiratory movements,
especially those of expansion and retraction. This is the condition not
only at the initiation of the disease, but at the next stage, that of
effusion. We meet with the same painful respiration also in dry
tubercular pleurisy. Mensuration shows that the sound side of the
thoracic cavity is slightly enlarged by the extra work it has to
perform in the first stage. The elevation movement is noticed to be
restrained when the effusion has increased to the extent of overcoming
the retractility of the lung, for the diaphragm is no longer drawn up
by the lung, and the effusion rises and separates the parietal and
pulmonary pleuræ. The diaphragm bags from the quantity of fluid, and
contracts but feebly. This condition forces the liver and the spleen
down in the abdominal cavity. Gradually the jerking rhythm ceases as
the effusion advances, and the characteristic stitch in the side
disappears. If the effusion increases until it reaches as high as the
second rib, the respiratory movements are scarcely perceptible to the
eye. When it reaches its maximum, the clavicle, they appear to be
arrested, but the vertical diameter is slightly altered by the action
of the intercostal muscles as they endeavor to elevate the ribs, and of
the diaphragm as it feebly contracts and relaxes. The pleural cavity,
which in health is lubricated by about two drachms of moist serous
secretion, is frequently filled to the extent of seventy, eighty, or
more--even to one hundred and twenty--ounces. We cannot wonder that it
should be changed in shape and diameter. All available space is filled
with the fluid, and yet the serous membranes continue to throw out the
secretions. The lung must lose in size by its retractile force, and
when that is overcome the fluid must press in all directions. The fluid
gradually rises from the surface of the pleura over the diaphragm, and
the lung, by negative pressure, draws it and the fluid upward. As long
as the diaphragm is arched, although the lung recedes before the
effusion, it is not really compressed. When, however, the diaphragm
yields and falls from the large quantity of fluid, then the fluid
conquers the lung. Ordinarily, the fluid, when in excessive quantities,
presses upon the lung and the bronchi until it forcibly expels the air;
the lung is compressed against the vertebral column, occupying a very
small space corresponding to the surface under the scapula, often not
larger than from three and a half to four inches square. Inspection
shows that the spaces between the ribs become flattened out, that the
ribs are more widely separated, and that the spaces themselves
frequently bulge. The first observable indication of great distension
of the pleural cavity, sufficient to cause intra-thoracic pressure, is
the depression of the diaphragm, and next the flattening of the spaces
between {498} the ribs. This last is followed by increased pressure,
which causes more general and marked enlargement. "This levelling of
the intercostal spaces is due partly to paralysis of the intercostal
muscles from serous inflammatory infiltration, and partly to the
limited range of movement now possessed by the lung, which is reduced
in volume by the effusion, and is no longer in contact with the
thoracic parietes" (Guttman). This is especially noticed in children
and young persons before the ribs become firm and resisting, the
negative pressure exerted by the lung being in part annulled by the
presence of the fluid. The diaphragm is notably depressed, and pushes
the liver, the spleen, and the stomach below their usual point. So
great is this centrifugal force that the heart's impulse may be felt in
the epigastrium. The heart, when the effusion is on the left side, is
frequently found over to the right of the sternum, and, in extreme
cases, even in the right axilla. When the effusion is on the right
side, the mediastinum is drawn over with it, and the heart is forced to
the left until the apex-beat is perceived as far as one and a half
inches to the left of the line drawn through the nipple, or, in some
cases, to the left axilla. This rarely occurs unless we have fluid
intra-thoracic pressure on the diseased side in addition to
lung-traction of the healthy side. Even the costal pleura, projecting
above the clavicle, may yield to pressure. Inspection reveals to the
observer these striking physical alterations. Hippocrates did not fail
to notice them.
1st. Mensuration shows that the semicircular, antero-posterior, and
vertical measurements of the side are generally increased. According to
Douglass Powell, the total circumference of the chest is always
increased in effusion. 2d. Except in children, the bulging of the
intercostal spaces does not occur until after the adjacent organs have
been displaced by the fluid. When the effusion is large, it becomes
evident, by inspection and by pressing the hand over the sides of the
chest below the armpits, that there is almost immobility of the
diseased side. We insist upon the importance of daily and repeated
comparative measurements of the two sides as aids to diagnosis and
prognosis in pleurisy. A full inspiration or a prolonged expiration
will sometimes show a marked difference by measurement when it is not
discovered during ordinary breathing. Woillez's cyrtometer, as
perfected by Samuel Gee, is the best instrument for testing the
circumference of the chest, and a pair of callipers for the diameter.
The cyrtometer tracings give us the altered shape as well as
circumference. It is especially valuable in the diagnosis of local
empyema from basic pulmonary cavities. Care should be taken not to
confound congenital deformities in the shape of the chest, such as the
alar, flat or pigeon-breasted, or rachitic, with alterations produced
by internal disease. It must also be borne in mind that the
semi-circumference of the right side is normally greater by one-quarter
to half an inch than that of the left side. By inspection of cases
where large effusions have remained for long periods of time slowly
absorbing--often, perhaps, not recognized--we discover marked
unilateral retraction of the chest-walls, with torsion of the spine and
shoulders. The adhesions preventing the lung from expanding, the
alveoli become obliterated, and we have, in fact, atelectasis of the
lungs. This is particularly the case in children, where the disease
prevents the proper development of the side, the healthy side becoming,
from supplementary work, more enlarged. Care must be taken not to
confound with these the anatomical depressions met with sometimes in
the anterior wall of the chest, especially at the lower portion of the
sternum. The amplification of the chest takes place, to a greater or
less degree, at its lower portion as soon as an appreciable quantity of
liquid collects, long before it is possible to have any intra-thoracic
pressure. The lung by its elasticity collapses, and the fluid is drawn
upward in contact with the lung. The thoracic wall, consequently, has
not, at that point, the retractile force of the lung to {499}
counteract its excentric resilience. It is not then drawn in in
expiration by the lungs, while it is continually being drawn outward in
inspiration. The lung-traction of the parietes of the chest is feeble
from the diminished size of the lung. The greater the amount of fluid,
the less lung-tension; consequently, the greater the enlargement of the
chest, as shown by the cyrtometer. If the lung is contracted to its
utmost limit (one-third of its size, according to Powell; one-eighth,
according to Rokitansky), then there could be no suction force
exercised by it upon the parietes of the chest, for, being disabled in
its elasticity, it literally has no power. The whole parietes of the
chest on the diseased side have nothing to antagonize their elasticity,
so it is kept enlarged. In addition, at this stage the fluid of itself
presses against the walls of the chest in all directions.
The elastic pulmonary tissue is always, to a certain extent, on the
stretch. It is striving to pull asunder the pulmonary from the parietal
pleura; but this it cannot do, because the air can have no access to
the pleural cavity. The five mm. of mercury elasticity of the lungs can
be increased by a distension of the chest from a forcible inspiration
to thirty mm. of mercury. Anything which lessens this elasticity of the
lungs takes off so much from the force which interferes with the
rebound of the thoracic resilience, and consequently increases the
circumference of the chest. Such is the case in emphysema, oedema of
the lungs, pulmonary congestion, and, curious to relate, at the outset
during the pyrexial stage of acute diseases, such as pneumonia,
variola, bronchitis. The enlargement of the thoracic circumference is
appreciable. It, however, gradually decreases and becomes normal. This
yielding of the thoracic walls is attributable to temporary engorgement
of the lungs, lessening their retractile force.
At the very commencement immediate results of percussion are negative,
but by delicate taps over a pleximeter there is a sound at the margins,
owing to the deficient expansion, of impaired resonance and of higher
pitch, and the vibrations are less full. There is also a sense of pain,
owing to the increased sensibility of the costal pleuræ. As the
fibrinous coatings form, the sound becomes less and less full and the
normal vibrations of sound are less diffused, more circumscribed,
giving to the finger, used as a pleximeter, a sense of resistance from
the diminished elasticity of the lung. This is especially the case at
the base over the attachment of the diaphragm. As the effusion rises
from the base, the sound on percussion becomes flat. The fluid being a
non-resonant body, the vibrations of the percussion taps do not extend.
The sound is of high pitch, but not resonant. It has been properly
designated by Skoda an empty sound, for it conveys to the ear the
condition beneath, which is one of perfect airlessness. It is not
simply a dull sound or one where there is not the normal resonance, but
it is destitute of all resonance: it is absolutely flat. The confusion
of dulness with flatness has in the past led to erroneous conclusions
as to the line showing the level of the fluid in pleurisy. As high an
authority as Woillez, in reference to fluid flatness, speaks of dulness
as complete, absolute, or very incomplete sub-dulness! The muscular
coverings of the walls of the chest or unusual amount of adipose tissue
or pleuritic coatings or bands produce impairment of resonance, and
sometimes marked dulness on percussion. But when the percussion wave
penetrates to the lungs, there is more or less resonance. When the lung
is solid from pneumonia or tubercular deposits, the sound is often very
dull, but rarely flat, because it seldom happens that all of the
alveoli are filled up, and even when they are the vibrations are
communicated to the bronchial tubes which contain air, and in this way
there is some resonance. We call particular attention to the importance
of these distinctions and to the necessity of light and delicate
percussion in order to test the resonance or non-resonance of the
thoracic cavities. If the percussion be strong, the vibrations are
conveyed {500} by the thoracic walls to the portions where there is no
fluid, and thus we have impaired air-resonance, and not flatness. We
have frequently seen errors of diagnosis in cases of pleurisy owing to
the physician percussing with too much force. To secure accuracy,
Garland[25] lays down the simple rule of percussing with great care and
always in straight lines, and of percussing each line to its terminus
before taking up another. Powell[26] compares the peculiar flat
percussion sound of pleuritic effusion to that elicited on striking
against a brick wall. The flatness is characteristic and more marked
than the dulness of lung-consolidation. If we are not careful to make
the distinction between impaired resonance and non-resonance, we may
easily draw erroneous conclusions as to the rise and extent of the
fluid in the chest. We have shown elsewhere (Pathological Anatomy of
Pleurisy--Distribution of Fluid) that, as the fluid collects in the
cavity, the lung contracts before it. The border above the level of the
liquid contains less air, the capillary circulation is less active, and
frequently there is more or less oedema, owing to its being the most
dependent portion. These physical conditions impair, to a greater or
less extent, the pulmonary resonance. Thus at the base above the fluid
we might, on reflection, naturally expect some dulness on percussion,
lessening as we recede from the fluid. Several observers have called
attention to the impaired resonance over the lowest portion of lung
posteriorly when the person is standing. Garland[27] termed it the dull
triangle. Heitler[28] of Vienna observed this same condition in that
locality, and likened it to a monk's hood cut longitudinally through
the centre and hanging apex down. Rosenbach[29] of Breslau noticed that
this non-resonant triangle in pleurisy would often clear up on exercise
or by breathing; this fact he considered distinctive between pleurisy
and pneumonia.
[Footnote 25: _Loc. cit._]
[Footnote 26: _Med. Times and Gazette_.]
[Footnote 27: _Ziemssen's Supplement_.]
[Footnote 28: _Wien. med. Wochenschr._, 1878, quoted by Garland.]
[Footnote 29: "Ein Beitrag zur phy. Diag. der Pleur.," _Berlin klin.
Wochenschrift_, 1878, No. xii.]