periods in the course of pleurisy, and from different causes in each
case: (1st) As soon as fluid forms in the pleural sac. At this period
the displacement is caused by the presence of the fluid which occupies
part of the pleural cavity. The lung by its elasticity retracts. It is,
consequently, of less volume and exerts less negative force upon the
mediastinum and its contents than the healthy lung. The two lungs
having by their equal tractile energy previously kept the heart in
situ, the healthy lung draws the mediastinum out of its position in a
transverse direction. Necessarily, the displacement of the heart from
this cause is in proportion to the amount of fluid effused. This is the
most frequent mode of displacement of the heart. It can be said to be
almost always present. (2d) When the quantity of fluid is great enough
to overcome the retractility of the lung and exert intra-thoracic
pressure, it forcibly expels the air from the alveoli of the lung and
by direct positive pressure pushes the heart aside. The displacement of
the heart in this case can only be produced when the pleural sac is
two-thirds or more filled by fluid. When this condition is met with,
the displacement is very great, because the heart has been already
displaced by lung-traction. Previous to the researches of Garland,
Stone, and Powell, this was supposed to be the only manner of
explaining the displacement of the heart from pleurisy. (3) Where, as
illustrated by Stokes',[40] Hunt's,[41] and Chew's[42] cases, the heart
is displaced toward the diseased side. This occurs more as a sequel of
pleurisy in the course of the absorption of chronic or suppurative
pleurisy, where by non-expansion of lung a partial vacuum is produced.
The external atmosphere presses in the thoracic walls of the diseased
side, and the internal atmospheric pressure from the healthy side is
exerted against the mediastinum and presses the heart in that
direction. Marked displacements from this cause are rare; slight
displacements are more frequent. Cicatrices from healing of large
cavities would have this effect. Mere consolidation of lung could not
cause it.
[Footnote 40: _Dis. of Resp. Organs_.]
[Footnote 41: J. W. Hunt, _Dub. Med. Journ._, _loc. cit._]
[Footnote 42: S. C. Chew, case reported to Med. and Chi. Soc. of Md.,
1883.]
Displacement of Lung.--The lung in cases of effusion is drawn up by its
own retractile energy. It has been demonstrated that this force is
considerable. As the effusion advances the lung recedes to a certain
point, when the fluid, having overcome the retractility of the lung and
having a fixed point below, actually exerts positive pressure upon the
lung (Garland), and compresses the air out of the alveoli and the
compressible bronchi. This compression cannot take place until the
diaphragm is no longer elevated into the thorax, but is bagged down by
the excessive weight of the fluid. There can be no compression of lung
until its elasticity has been exhausted. The gradual effect of the
continued contraction of the lung is to straighten out the letter _S_
curve. The force of lung necessarily diminishes gradually as it
contracts in volume. On the other hand, the immediate effect of
compression is to {507} obliterate that curve. So long, therefore, as
we are able to trace a well-marked letter _S_ on the chest, we may be
certain that the lung is well out of reach of compression (Garland).
Peyrot[43] showed by plaster-of-Paris injections into the chests of
cadavers, and then making cross-sections, that deformities of the chest
are not due to a development of one side, the other remaining normal,
but that they consist of a mutual adjustment of all parts. The
simultaneous movement of the sternum toward the left in left-sided
effusions makes the displacement of the heart appear greater than it
actually is.
[Footnote 43: _Arch. gén._, Juill., 1876.]
The Diaphragm and Intercostal Spaces.--The diaphragm is not depressed
below the edges of the ribs, nor do the intercostal spaces bulge until
the weight of the fluid exceeds the lifting force of the lung. The
admission of air into the pleural sac produces the same result. The
depression of the diaphragm is due in part to the weight of the fluid,
but chiefly to the diminished contractile energy of the retracted and
diminished lung. The displacement of the mediastinum depends upon
similar conditions. Since the traction of the lungs always affects both
sides of the thorax, the movable mediastinum must follow the lung,
which is still capable of contracting, and therefore with right-sided
exudations the left lung will draw the parts over to itself. Only with
excessive effusions in the pleural cavity does the pressure of the
fluid come into activity.
The liver and spleen may be pushed below their normal position by
excessive effusion after the diaphragm yields to the weight of the
fluid. Woillez found the liver displaced downward in the abdominal
cavity in one-fourth of the right pleurisies and only once in left-side
pleurisies. The extent on the right side was from two or three
centimeters to three fingers' breadth, even as far as the umbilicus.
The stomach, when the diaphragm sinks, may be pushed downward; thus the
so-called semi-lunar space of Traube may be obliterated. Ferber noticed
a peculiar displacement of the stomach in two cases where he had
produced an artificial hydrothorax of the left side. The fundus was
pushed to the right, and the stomach was folded over on itself to a
certain extent. A second and marked folding-in of the greater curvature
occurred near the pylorus. This condition of stomach, with left-sided
pleural exudations, has been hitherto entirely neglected by authors.
May not the vomiting which is often observed with excessive effusion,
and which has been attributed to violent acts of coughing, be due to
this doubling over of the stomach?
Auscultation.--At the commencement of acute pleurisy, when hyperæmia
exists with dryness of the pleural surfaces, auscultation shows a
respiratory murmur lessened in intensity and duration. There is also a
jerking unevenness in the rhythm of respiration, and weakness or
indistinctness of the vesicular murmur consequent upon the imperfect
and irregular expansion of the lung. On the healthy side the
respiratory murmur is hypervesicular, and becomes puerile and noisy in
character. In from twelve to eighteen hours the plastic fibrinous
deposit on one or both pleuræ causes us sometimes to hear, over
circumscribed spots, at the end of inspiration and the beginning of
expiration, a fine friction sound, which varies in intensity over the
points of contact of the surfaces. This is especially the case in the
infra-mammary, infra-axillary, and infra-scapula regions. Woillez heard
friction sounds in 52 of his 82 cases. The pain in respiration makes it
very jerking and irregular. The contact of the surfaces pushes aside
the lymph, and thus we hear the sound at a given point at one
inspiration and not at another. It is heard more distinctly during
inspiration than expiration. The reason of our not hearing the friction
sound at the early stage of pleurisy continuously, but with
interruptions in inspiration and expiration, is because the opposed
rough pleural surfaces do not continuously rub against one {508}
another, but remain adherent for a few moments, until a deeper
inspiration tears them asunder. The effusive stage comes on so rapidly
in acute pleurisy that often when patients are examined the friction
sound of the first stage has disappeared. It has been generally taught
that the cause of the disappearance of the friction sound, and its
subsequent reappearance as convalescence commences, are owing to the
fluid separating the surfaces and its reabsorption. We have seen, from
Garland's experiments and from careful clinical percussion
explorations, that the fluid does not come between the two surfaces
unless in very great effusion, but that it occupies the cavity between
the lung and diaphragm. Stokes long since showed that there was
temporary paresis of respiratory muscles, and consequently loss of
movement of the surfaces over each other, which movement was necessary
to produce friction sound. The reappearance of friction sounds
indicates recovery of this muscular power. When heard, the friction is
of the grazing variety--the most delicate form. Walshe designates it as
the attrition species, and says it is audible over a limited extent of
surface, occurring with occasional respirations, dry, and limited
strictly to inspiration. As the effusion appears, we find, beginning
with the lower border, that the respiratory murmur disappears, becoming
less distinct as the effusion advances in the pleural cavity.
Ordinarily, we hear no breath sounds. The absence, however, of breath
sounds as a sign of pleuritic effusion is by no means a constant one.
When the fluid contains many fibrinous bands, binding the lung down to
the costal pleura, or when the effusion is very large and forces the
air nearly out of the pulmonary tissue, pressing it into a firm mass
against the vertebral column (at a point corresponding to the spine of
the scapula), or when the lung is solid simply from the residual air
being pressed out of it, diffused bronchial tubular breathing is heard.
The tubular sound is conveyed, not ordinarily through the fluid, but by
the parietes of the chest and by the solid plastic linings and
adhesions. The fluid, if in large quantity and filled with fibrinous
bands, may also feebly conduct the sound, which, being produced on
solid surfaces, is best conducted by solids. We hear, in fact, a
respiratory sound of low pitch, but tubular in quality. It is
bronchial, but it differs widely from the familiar bronchial
respiration observed when the lung is consolidated in pneumonia. It is
a diffused distant tubular sound unaccompanied by moist sounds, soft in
its quality and muffled. It has not the brazen, harsh character of
pneumonic bronchial respiration. In pneumonia this sound is immediately
under the ear, the lung being in contact with the inner surface of the
ribs, and rendered a good conductor by its solidity, and the sound
rendered louder by the increased consonating properties of the walls of
the bronchi; whereas, in pleurisy, the lung is contracted above the
level of the fluid, or, when the effusion is excessive, is removed from
the walls by an indifferent conductor of its sounds, and the sounds are
conveyed from the compressed lungs at their base by the walls of the
chest, and, in a degree, by the deposits on the pleural surfaces. The
bronchial breath sound which we hear over the lung, compressed by
fluid, near the vertebra continues sometimes a long time after the
absorption of the fluid, because the lung, deprived of air, expands
slowly. If the effusion be small, we do not hear bronchial respiration,
because there is sufficient air in the alveoli to prevent the
conduction of the sound, the air not being compressed out by the
effusion, but the whole lung being lessened in volume. If, again, the
mass of fluid be very large, it prevents the free transmission of the
waves of sound, and we do not hear them.
The auscultatory phenomena necessarily vary according to the amount of
fluid in the cavity, the extent of the adhesions, the retraction, and
the compression of the lung-parenchyma. If the compression be
sufficient to prevent the air from passing down the bronchi, we do not
hear bronchial respiration, {509} because where, as in health, it is
not communicated to the ear (owing to its non-conduction by the
lung-tissue), it cannot be produced. Douglass Powell[44] calls
attention to another unusual pressure effect--altered quality of voice
and cough, a husky voice, and a laryngeal quality of cough
undistinguishable from that so often heard in cases of mediastinal
tumor or aneurism. These disappear after paracentesis.
[Footnote 44: _Consumption and Dis. of Lungs and Pleura_, 1878.]
Above the level of the fluid, and again as absorption of fluid takes
place, we have a return of the characteristic friction sound as the
muscles of the chest recover their normal power. With care this sound
will not be confounded with intra-pulmonary râles, which are moist
sounds removed or modified by cough or expectoration. These convey to
the ear the sound of bubbles of air as they pass through the mucus and
the secretions of the bronchi; whereas the friction sounds are
superficial noises from rough surfaces moving over each other. The
mucous râles which are sometimes heard are not from the pleurisy, but
from bronchial catarrh. The friction sounds heard in the stage of
absorption are ordinarily coarser and more abrupt. They are unequally
jerking in character, and in quality resemble osseous crepitation. In
chronic pleurisy, and for a long time after the fluid is gone in acute
pleurisies, we have pleuritic rubbing sounds when the walls of the
chest are drawn out in full respiration. At the absorption stage we
ordinarily hear the lung gradually expanding. The respiratory sounds
are feeble, and frequently moist subcrepitant râles are heard in the
bronchial tubes. If the effusion has been of long duration, we find the
pleural surfaces so thoroughly coated with fibrinous deposit, and the
lung so separated by bands from the costal pleura, that the expansion
of the lung is very much impaired and the percussion dulness does not
subside. Leaming and Camman of New York give numerous cases where there
might well be difference of opinion as to whether the signs heard were
intra-pulmonary or pleuritic. In cases where the intra-pulmonary
adventitious râles resemble the extra-pulmonary frictions, the
diagnosis is assisted by considering the length of the sound. The
character and intensity of the friction murmur varies very much. It may
be a slight grazing sound or a coarse, sharp creaking-of-leather noise.
Walshe gives no less than six modifications of the friction sound,
ranging from a feeble, scarcely audible noise to one of extreme
loudness. Friction sound is mostly an isolated phenomenon--that is, it
is not accompanied by any unnatural quality of respiratory or vocal
sound. Advanced type friction consists of a series of jerking sounds,
rarely exceeding three or four in number.
We must remember that sometimes, notwithstanding a considerable
quantity of fluid, the lung expands, and, pushing the fluid aside,
causes the rubbing of the pleural surfaces together. When unmistakable,
these respiratory friction phenomena are pathognomonic of the results
of pleurisy. Thus they are properly considered of great value in the
diagnosis.
Pneumo-pericardial Friction Sounds.--On the left side the uneven
pleural surfaces are sometimes forced together by the impulse of the
heart; of course, the resulting friction sounds are cardiac in their
rhythm. Then, again, fibrinous deposits on the outer surface of the
pericardium are forced against those of the covering pleural layers,
both by respiratory and heart impulses. Close attention to the rhythm
and the positions where these sounds are heard will prevent their being
considered pericardial in their nature.
The fluid may be nearly removed and yet the condensation of the
superficial strata be sufficient to produce extensive and marked
dulness. Under such circumstances the production of friction phenomena
is inevitable. The retention of some portion of the lung surface in
tolerably close proximity to the costal pleura by means of adhesions
also renders the production of {510} friction sound possible, although
a considerable quantity of fluid be present in the pleura. It is common
to find effusion signs in the back and friction signs in front. We most
frequently have friction at the base when there is absolute flatness.
If the walls be separated by fluid, there can be no friction from
contact. But it rarely happens that the fluid rises between the
surfaces. To produce friction sounds we must have motion of rough
surfaces which are in contact.
If the patient talks while we are listening in cases of small effusion
we hear over the scapula, toward the spine, and between the scapula and
the spine, bronchophony, as we do also when the lung is nearly deprived
of air, in which case the sound sometimes has the bleating, nasal
resonance designated by Laennec ægophony. In his opinion this was of
constant occurrence and of great diagnostic value, but now it has been
demonstrated that this sound can be heard when there is no fluid
whatever, but consolidated lung. Anstie calls it one of the fancy signs
of pleurisy. Ægophony is an unimportant variety of bronchophony, and
not a characteristic phenomenon of pleuritic effusions. Of itself, it
is not diagnostic of effusion, yet it is none the less true that it is
a modification of bronchophony, and is commonly met with in cases of
moderate pleuritic effusion, usually toward the upper margin of the
fluid. It is difficult to state definitely the amount of fluid which
usually produces it. Guttman thinks it is probably produced by the
vibration of the walls of the flattened, compressed bronchi; this
vibration is excited by the voice and transmitted to the thin layer of
fluid which, at the upper part of the exudation, lies between the lung
and the chest-wall. This tremulous movement of the sides of the bronchi
gives the voice sounds a quavering, interrupted character; and, as they
have to pass through a fluid medium to reach the surface, they lose in
clearness and precision and acquire a nasal twang.
When the effusion is large, and we have full dilatation of the chest,
all vocal resonance ceases, because the vocal vibrations go through
media of such different kinds that they are lost before they reach the
ear. During absorption, before the lung recovers its normal volume, we
again hear bronchophony. Pleural adhesions and thickening cause the
sound to be heard through the effusion when we least expect it. It is
not unusual to find ægophony and bronchophony in the same lung. They
are also found in some cases of pneumonia, and in some individuals,
especially in children, we have between the scapula a normal resonance
of the voice, with an ægophonic resonance.
Bacelli's Sign (Pectoriloquie aphonique).--This, the reverberation of
the whispered voice through the fluid, is a sign of considerable value.
If well marked it indicates fibro-serous fluid; its absence, however,
does not show that the fluid is not of this character. (See Purulent
Pleurisy.)
Auscultation is of great value as indicating with definiteness the
position occupied by the effusion as it is being reabsorbed.
Heart Murmur.--From excessive accumulation of fluid in the pleural sac
a systolic murmur over the base of the heart is very often heard. That
it is produced by pressure or twisting of the aorta is evident from the
fact that it ceases when the fluid is withdrawn.
Phonometry we have found of but little value in the diagnosis of
pleurisy.
COURSE AND DURATION. Acute pleurisy is essentially a unilateral
disease. It does not pursue a regularly-defined course, nor have we any
critical stages, as in pneumonia. In mild cases of acute primary
pleuritis the disease advances slowly and recovery is tardy. The
febrile movement may be four or five days in reaching its height. It
remains at this point for several days--from four to seven days; in
rare instances as long as ten days.
The effusion sometimes comes on very rapidly, but ordinarily is one or
two days in forming. When it appears it may be divided into (1) the
stage of {511} progress, (2) stationary period, and (3) resolution. For
the examination of both of these we must employ percussion, and
mensuration by means of the cyrtometer, which give us exact results.
Woillez in a large number of observations found that the first period
lasted from eleven to twenty-four days, most frequently from fifteen to
twenty days. The stationary period he found varied from twenty-four
hours to several days. Frequently the reabsorption commences suddenly
without any interval. Resolution is initiated from the eleventh to the
twenty-fifth day, and lasts over fifteen days.
As the effusion advances the acute symptoms--rapid pulse, the elevated
temperature, acute pain, and superficial dyspnoea--are materially
lessened. If, however, the effusion be very great, we shall have at
first painful dyspnoea, especially when the patient makes unusual
exertions. This dyspnoea is ordinarily in proportion to the amount of
the effusion. If there is much displacement of heart or distortion of
larger blood-vessels, there is imminent danger to life. After the first
few days we are often surprised at the tolerance of the whole system of
the excessive amount of fluid. Absorption, after the effusion has been
thrown out, is at first rapid, then it occurs more gradually; part of
the liquid portion disappears, and the fibrinous portion undergoes
fatty degeneration previous to absorption. The physical signs of
flatness, vocal fremitus, together with the return of the displaced
organs, the heart, liver, and diaphragm, to their normal positions,
give us accurate means of judging of the progress toward cure. The
general health shows unmistakable signs of improvement. The appetite is
better, as are also the color and strength. If the effusion remains
undiminished in quantity, or if it becomes purulent in character, the
general appearance will show evidences of weakness and lowered
vitality.
The average duration of acute primary pleurisies varies, when the
effusion has not reached any considerable height, from two to four
weeks. It may continue thirty or thirty-eight days--minimum duration
twenty days. The absorption requires many weeks if the effusion is
large or if it becomes chronic. Two months may elapse before the fluid
entirely disappears. In some cases it continues, unless thoracentesis
be performed, for many months. We have given the symptoms manifested
when there is any renewal of the inflammatory process. In pleuritis
acutissimus death may occur in ten days or two weeks from syncope, or
from thrombosis caused by pressure upon the large venous trunks and
consequent twisting, especially of the ascending cava, where it
perforates the central tendon of the diaphragm to reach the
pericardium, or by torsion of the aorta. When the effusion remains for
a long time, the lung may be permanently prevented from expanding by
pleuritic thickenings resulting from inflammatory products. In acute
primary pleurisy the tendency is toward resolution. Louis went so far
as to state that pleurisies never caused death. Trousseau, Lacaze, and
others give cases where sudden deaths were produced by the quantity of
fluid pressing upon the heart and blood-vessels. In subacute pleurisy
(latent pleurisy of the older writers) the course of the disease is so
gradual, so unattended by pain or even discomfort to the patient, that
he goes perhaps weeks with considerable fluid in the cavity without
being aware of it. He has probably been able to continue his occupation
without intermission. It is only when he begins to feel weak and to
lose flesh, and finds that his respiratory force is impaired, that he
consults a physician. The rational symptoms scarcely point to pleurisy,
but the physical signs of the presence of fluid are very distinctive.
In this form the effusion is ordinarily greater in quantity than in the
acute variety, and unless some of the fluid be taken away by
aspiration, absorption is very sluggish. In these cases, if the fluid
remains long in the cavity, the lung may become permanently disabled by
the long continuance of the compression.
{512} In chronic pleurisy the effusions from the acute or subacute
pleurisies remain unabsorbed. They ordinarily are purulent in
character, but sometimes they remain sero-fibrinous many months.
Purulent pleurisies may be primary as well as secondary. (See Purulent
Pleurisy.)
TERMINATIONS.--Pleurisy of a fibro-serous nature terminates in (1)
convalescence, (2) becomes chronic, or (3) ends fatally. Among those
who are cured there are some instances where the disease is of short
duration and the recovery prompt and complete. With others the disease
itself is of a severer type and lasts longer. If the attack of pleurisy
be secondary to another disease, especially if the latter be of a
nature to profoundly affect the nutrition, convalescence is very
tedious.
Acute pleurisies which are primary but rarely become chronic, but when
secondary they frequently are chronic from the beginning. Heyfelder
states that chronic pleurisies are three times more frequent on the
left side than on the right side.