diaphragm, flatness on percussion is first observed over the axillary
portion of the diaphragm, because, as explained by Calvin Ellis, the
conditions there are more favorable for percussion. As the effusion
increases the line of flatness, when the patient is in the upright
position, advances, not directly up the back and horizontally across
the chest, as was formerly supposed, but across the back in a curve
reaching its highest point in the axilla, from which it descends toward
the sternum.[30] R. Douglass Powell[31] says the upper margin of the
effusion in typical cases is not a water-level, but presents a curve
having its convexity upward and in the lateral region. Since the
attention of the author was first called to a careful examination of
the curve of flatness as ascertained by light and delicate percussion
(in the erect position), he has found it to be more or less of an Ellis
curve at an early stage of the effusion. The line is sometimes better
defined than at others. All observers, however, must acknowledge that
at the stage of the disease when cases of chronic fibro-serous pleurisy
are first seen the letter _S_ curve is not well marked. Mason states
that although in some of his 200 cases this peculiarity was observed,
in others the line was horizontal. When fluid fills the chest to excess
and overcomes the elasticity of the lung, it gives flatness on
percussion high up, even to the clavicle, and behind to the
supra-spinous fossa. The fluid filling the cavity, the line of flatness
becomes nearly horizontal. Then it is that percussion reveals the
displacement of the diaphragm and abdominal organs. On removing the
excess of fluid by aspiration or by absorption, this curved line
reappears, and continues as previously.
[Footnote 30: See section on Pathological Anatomy of Pleurisy,
distribution line.]
[Footnote 31: _London Med. Times and Gazette_, Oct., 1882.]
{501} Contrary to the general belief, when the fluid is moderate in
quantity change of position of the patient modifies but little the area
of flatness, owing to its being retained between the lung and
diaphragm. Woillez[32] noticed slight mobility (never more than to the
extent of one intercostal space) only in 5 of his 82 cases. He
concluded that the conditions were very different from what they were
in ordinary vessels outside the body. Woillez does not attempt to
explain what these conditions are. Skoda acknowledged that in the
majority of cases the fluid does not change its position as the patient
moves. Skoda and Wintrich attribute the non-movement of fluid to
adhesions. Garland, and subsequently W. H. Stone and Douglass Powell,
showed that the effusions were immovable when in moderate amounts,
because they were kept so by the retractility of the lung, and that the
large amounts were movable because the retractility had been overcome
by them. When in large quantities the fluid accumulates in depending
positions of the chest. Later on in the disease, adhesions and bands
mechanically interfere with the line of flatness; or if there be any
disease of the lung interfering with its retractive force, the fluid
may not take its usual line. These peripheral adhesions frequently
occur at the upper margin, and are sometimes wavy and irregular. They
often occur early in the disease, and prevent in a marked degree the
fluid from yielding to the negative lung-traction.
[Footnote 32: _Mal. Aigues des Org. Resp._, Paris, 1872.]
By these bands the pleuritic fluids become sacculated in different
parts of the thorax--between the lungs and the walls of the chest,
between the diaphragm and lungs and the pericardium, the mediastinum,
the vertebral column, and actually between the lobes of the lung.
Fraentzel holds that the percussion sound is dull over the thorax
whenever the effusion attains the depth of from one inch and a half to
two inches between the lung and the chest wall. Garland by his
experiments on dogs shows that the fluid does not thus rise between the
lung and parietes, except a very thin layer, by capillary attraction,
not sufficient to cause flatness on percussion or to interfere with the
expansion of the lung unless the amount is very excessive, and not
until the lifting power of the lung is completely overpowered. When the
effusion is very large, it fills up the posterior portion of the
thorax, compressing the lung against the uppermost portion of the spine
or the mediastinum. The percussion sound is absolutely flat, provided
the force of the blow be not too great; in that case the ribs are
thrown into vibration or the vibrations extend to the sound lung. This
materially impairs the dulness and may lead to error of diagnosis.
The lung may be prevented from contracting by reason of various kinds
of adhesions or by means of widespread infiltrations, by emphysema, and
by laryngeal stenosis. In such cases, as the effusion increases, it
quickly rises in the thinner layers without displacing the organs.
Fraentzel warns us that sometimes, in left-sided effusions, the lung
having become adherent to the heart, the heart is drawn back with the
lung away from the wall of the chest, and then it cannot be felt
anywhere: the absence of the apex-beat and the feebleness of the
heart-sounds may lead us to assume, incorrectly, that there is effusion
in the pericardium. If the fluid collects between the external layer of
the pericardium and the mediastinum, the heart is surrounded and
pressed by the pleuritic effusion.
The Skodaic resonance is a remarkable tubular quality of resonance
heard on percussion when the effusion extends up to the fourth rib or
beyond it, nearly filling the pleural cavity. It is a high-pitched,
long vibration, semi-tympanitic sound, rarely absent when, from an
effusion, the lung is retracted to a very small size, but still
contains some air. It is most frequently found anteriorly under the
clavicle, near the sternum, because to that point the lung withdraws as
long as it has any retractility left. If the air be forced {502} out of
the lung by pressure, this sound is no longer heard. Flint called this
peculiar tympanitic sound, heard above the level of the fluid in
pleurisy, by the descriptive name vesiculo-tympanitic resonance. The
vesicular, though feeble, is combined with the tympanitic quality, and
the intensity of the resonance is abnormally increased. This
subclavicular tympanitic sound is not peculiar to pleurisy. It exists
in pneumonia preceding hepatization, and was noticed by Hudson, Graves,
and Williams before Skoda called attention to it in pleurisy. Skoda's
explanation of this phenomenon is now generally accepted--namely, that
it comes from diminished tension of the lung-tissue, caused by
diminution in the quantity of air, and consequently relaxation of
lung-tension. The residuary air in the alveoli does not mix properly
with the tidal column: it is indeed pent up by the narrowed diameter of
the minute bronchi. Thus it becomes surcharged with carbonic-acid gas;
this relaxes the air-sacs and lessens their tension. In fact, the
percussion sounds are invariably tympanitic when the parietes of the
organ which contains air are not stretched. When they are firmly
stretched, the sound elicited by percussion becomes less and less
tympanitic, and finally dull: such, we know, is the case in striking a
drumhead. The chief characteristic of the sign relates to the quality
of the sound; the resonance is nearly devoid of vesicular quality. A
resonance absolutely non-vesicular is always tympanitic (Flint). This
tympanitic sound is so constant under the clavicle that although it may
be from other causes, its appearance would lead us to suspect effusion,
especially in children. It is not only at the apex, but wherever the
lung shrinks from pleuritic exudation and loses in tension, the
percussion sound has the tympanitic quality. We find it occasionally
near the sternum, and sometimes in sacculated effusions we observe it
in different parts of the thorax. Traube, and subsequently Fraentzel
(_Ziemssen's Cyc._), called attention to the fact that sometimes a long
expiration would cause a temporary abolition of this tympanitic sound
at the apex. Their explanation is that the sound is heard over the
compressed lung. Garland urges that this explanation cannot be a
satisfactory one, for a certain amount of pulmonary expansion is
essential to the production of tympanitic resonance.
This exaggerated resonance elicited by percussion has received its name
from the eminent German who wrote so much about it; but it did not
escape the accurate ear of the discoverer of percussion, Avenbrugger,
who clearly defined the subclavicular tympanitic resonance in
pleurisy.[33] Skoda's sign, however, is not unique, for observation
proves, when the lung is contracted with fluid below, that there are
several varieties of resonance. Notta,[34] who was not aware of Skoda's
ideas, describes the sound as hydroaérique where the lung is above the
level of the fluid. Roger,[35] who called especial attention to Skoda's
views, admitted that there were several varieties of tympanitic
resonance heard above the fluid. He compares them to those heard on
percussing over the stomach of the cadaver. Woillez[36] describes five
varieties or types of sonorousness, according to their intensity, their
tone, and their quality. He noticed these under the clavicle at
different points above the liquid--ordinarily on the level of the
second or the third rib. (1) The most common and the best defined was a
short sound, dry and superficial; the tone of this was acute, with
exaggeration of intensity. Williams[37] in 1841 called attention to
these peculiarities. With this variety we frequently have a
reverberation, pointed out by Stokes in 1837--a cracked-jar sound more
or less marked. Woillez noticed this variety in 11 of his 82 cases; of
this number 9 were in pleurisy of left side. (2) There was exaggeration
of intensity or tympanism with a grave tone: 7 of Woillez's cases
showed {503} this variety, of which 6 were on left side. (3) A
subclavicular resonance, unnaturally acute, but with exaggerated
intensity. (4) Exaggeration of intensity, with equal tone on both
sides; only 2 patients out of 82 showed this variety. (5) Exaggerated
abnormal resonance, more acute than healthy side, and with normal
fulness of sound. These are all modifications of percussion sounds
elicited in pleurisy and other pathological physical conditions
resembling it, where there are variations of tension together with
other modification of the structure of the lung. The bruit de pôt fêlé
is sometimes clearly marked, as it is also in hepatization of lung.
[Footnote 33: Avenbrugger, _Ouv._, ed. de Corvisart, 1808, Paris.]
[Footnote 34: _Arch. gén. de Méd._, 1850, t. xxii.]
[Footnote 35: _Ibid._, 1852, t. xxix.]
[Footnote 36: _Mal. Aig. des Org. Resp._, Paris, 1872.]
[Footnote 37: _The Path. and Diagnosis of Dis. of the Resp. Organs_,
1841.]
Traube's Semi-lunar Space.--There is a point on the left side where we
find normally a vesiculo-tympanitic sound, first pointed out by Traube
and enforced by Fraentzel. It is situated at the anterior base of the
left side, and is of a half-moon shape. It is bounded inferiorly by the
margin of the thorax, and superiorly by a curved line whose concavity
is turned downward. It begins in front, below the fifth or sixth costal
cartilage, and extends backward along the margin of the chest as far as
the top of the ninth or tenth rib. Its greatest breadth is from four to
four and a half inches. This tympanitic sound is caused by the air in
the stomach, which lies well up against the diaphragm. When the stomach
is pushed down by the falling of the diaphragm, from excessive fluid,
the tympanitic sound disappears. The value of this semi-lunar space in
the diagnosis of pleuritic effusions has been variously estimated.
Fraentzel considers it of great significance in the differential
diagnosis between pleurisy and pneumonia; Ferber and Garland do not.
Weil suggests that the area of this space may be diminished by filling
the stomach and colon with solid or fluid food. Garland shows that as
the diaphragm's depression depends upon the excess of fluid overcoming
the lifting force of the lung, we may have, with a vigorous, unimpaired
lung, a large amount of effusion in the pleural cavity, yet the
resonance of the semi-lunar space may remain tympanitic. The condition
of this semi-lunar space is of most diagnostic value in extensive
left-sided effusions. The more the diaphragm is pressed down by the
effusion, the smaller becomes the space of tympanitic resonance. It may
gradually disappear altogether.
Auscultatory percussion may sometimes be advantageously employed to
detect fluid in the pleura, especially in the younger subjects, for
intercostal fluctuation may frequently be appreciated when we press
carefully with the palm or surface of the finger between the ribs while
the percussion shock is applied to another part of the same side. If we
auscultate with a stethoscope, the chest extremity of which is made to
fit in between the ribs, while another person percusses the chest, we
can sometimes detect the fluctuation within the cavity of the chest.
We thus see that in the diagnosis of pleuritic effusions percussion is
very valuable, perhaps the most valuable of the physical signs. We must
not, however, forget that its significance may deceive us if the fluid
is prevented from gravitating by pre-existing adhesions, or if it is
encapsuled between the diaphragm and lung or between the lobes. Cases
occasionally occur where, from fibrinous bands, the fluid is kept in
the posterior part of the thorax, consequently there is pronounced
clearness and fulness in front. Percussion does not enable us to
diagnose the consistence of the contents of the pleura, or its nature,
whether it be fibro-serous or purulent. To do this we must resort to
Bacelli's method, or, still better, to exploratory punctures by the
hypodermic syringe.
Palpation.--The sense of touch gives valuable physical signs in
pleurisy. At the commencement, before there is any effusion of fluid,
even of fibrinous deposit, we notice by palpation the decreased
movement of the walls of the chest, and also the sensitiveness of the
walls. When the eye cannot {504} notice modifications of the expansion
and elevation movements or movements of the ribs, correct views may be
formed by palpation, especially in regard to the amount of local
expansion in the upper part of the chest. In the lower part, by
inserting a finger in the intercostal space we notice the modification
of local expansion, also the convergence of the ribs taking place
coincidently with the continuance of the elevation movement. We are
thus furnished with additional presumptive proofs of the impermeability
of the pulmonary tissue. When fibrinous effusion exists, the hand,
early in the disease, recognizes the pleuritic friction or grazing.
Later on, palpation perceives the rubbing when the muscles have
recovered from their temporary paresis.
As soon as the effusion begins to form we detect a lessening of the
delicate vibrations of the voice as communicated to our hands, always
guarding ourselves against error by remembering that the normal sound
is greater in the infra-clavicular region of the right side, and that
it is always weaker in children and women, unless they have shrill,
weak voices, in which case it may be entirely absent. It, indeed,
requires a certain sonority of voice to be felt through the walls of
the chest. When we find that both sides convey the vocal vibrations to
our touch, we may be sure there is no effusion of fluid. Errors are
often made by applying palpation over too extensive a surface, thus
reaching beyond the fluid. It is important to use light, delicate
palpation, employing the finger-tips instead of the whole hand, in
order to exclude the vibrations from above as we approach the confines
of the effusion. This vocal fremitus is entirely lost from the base up
to the point to which the fluid reaches, and later on when it separates
the two pleural surfaces. This absence of vocal fremitus is one of the
most valuable physical signs of pleuritic effusion. It enables us to
diagnose it from nearly all cases of lung-consolidation except when
caused by malignant disease. When there are considerable pleuritic
adhesive bands, they interfere with the complete absence of fremitus;
but in children this sign is not so reliable. With them vocal fremitus
is often scarcely perceptible in health. In dry tubercular pleurisy
palpation gives us the characteristic friction. Palpation detects also
the rubbing of the two lymph-covered surfaces after the absorption of
the fluid. When there are thick fibrinous bands extending between the
parietal and pulmonary pleuræ, there may be a vocal fremitus
notwithstanding the presence of a quantity of fluid in the pleural
cavity.
Displacement of Adjacent Organs.--The displacement of the heart as a
physical sign indicating the presence of fluid in pleurisy is one of
great significance. It is indeed a cardinal sign, second only in value
to percussion flatness. It is almost invariably met with. Stokes[38]
stated that it was observed at an early period, and was one of the very
first signs of effusion; "that it may exist even before the upper
portions of the chest have become dull, and is a circumstance of
constant occurrence long before any yielding of the muscular portions
of the thoracic walls." The heart is displaced at the very commencement
of the effusion, and its dislocation increases pari passu with the
effusion. The absence of the displacement, unless it can be explained
by some special circumstance which rarely occurs, such as the retention
of the pericardium by old adhesions or consolidation of the opposite
lung, would negative the diagnosis of unilateral effusion. In this
condition there is a marked contrast with the displacement and
depression of the diaphragm and the resulting alterations of position
of liver, spleen, and stomach. These only occur when the effusion is in
great excess--not until from the large quantity of fluid the
retractility of the lung is overcome, and it is consequently unable to
lift up the fluid and the diaphragm. This altered position of the
diaphragm drags the heart {505} downward by means of the ligamentous
attachment of the pericardial sac to its tendinous portion. The
deviations from the normal positions of the heart in slight effusions
can always be noticed if the exact point of the apex-beat is sought for
by palpation and listened for with the stethoscope. Careful percussion
will show the shifting area of flatness.
[Footnote 38: _Dis. of Heart and Aorta_, 1854, Dublin.]
Powell calls attention to a fallacy with reference to cardiac
displacements in the earlier stages of effusion--that, as the base of
the lung retracts, the left or the right margin of the heart, as the
case may be, becomes uncovered. This may lead to an apparent delay in
the displacement of the organ, the more extreme left or right boundary
being now within reach of palpation. The axis of the heart is not
greatly changed by an ordinary degree of effusion. It becomes a little
more vertical, and in extreme cases it may become slightly twisted.
Only in rare and extreme cases does the axis of the heart become
altered in direction beyond the vertical line. Powell[39] found at a
post-mortem a heart that had become so twisted as to present itself
obliquely edgeways in front. Sibson had previously pointed out this
disposition of the heart to turn over and to present its posterior
surface forward in cases of effusion.
[Footnote 39: _Consumption and Dis. of Lung_, London, 1878.]
In examining into the cause and significance of the displacement of the
heart in pleurisy we find that until within a few years, it was, and
indeed very generally now it is, believed that the sole cause was from
direct pressure of the fluid actually pushing the heart away from its
normal position. Skoda, Traube, Stokes, Powell, and Garland were, we
believe, the first authors to show that such was not the case,
certainly in moderate effusions. The displacements take place when the
amount is very small--too small to exert any positive pressure. It is
true that nature places the heart in such a position that it can yield
readily to slight forces. It hangs in the pericardial sac, which is
suspended by the aorta, and which is bound by ligaments to the body of
the third dorsal vertebra. Every change of position of the body causes
certain anatomical alterations of the heart's position. Wintrich,
Skoda, and Braune think that the heart swings like a pendulum from its
base, and that its apex is therefore elevated with every deviation to
the right or left. Lebert says the heart is first depressed by the
sinking of the diaphragm, and then elevated by being pushed to the
right. Fraentzel says that in displacements to the right the heart is
simply pushed over, and is never elevated as Wintrich describes it. The
mediastinum offers but slight resistance, and is very easily pushed to
the right side, where there is no compact organ to resist, and where
the cavity is larger; whereas it is with more difficulty pushed to the
left, where the heart occupies so large a space.
It has been satisfactorily demonstrated that until the pleura is about
two-thirds full of fluid no positive pressure is exercised upon the
lungs or heart. According to Rokitansky, the lung cannot be compressed
until seven-eighths of the pleural cavity is occupied by fluid. The
fluid cannot be drawn off by a canula unless air enters to replace the
fluid. Unless the pressure on the fluid from within the cavity is
greater than that of the atmosphere we cannot draw off a large
quantity: if the pressure balances that of the atmospheric air, only a
few drops of fluid are discharged externally, except by forced
expirations and coughs. This is the case even when the quantity reached
several liters. The feebler the expiratory force the less fluid
escaped. Yet the heart is displaced as soon as the effusion appears.
The significance of the displacement is that it shows the presence of
fluid, but does not show the measure of intra-thoracic pressure
(Powell).
Garland's explanation is that the heart, with the sac and its
connections, "is placed between two highly elastic bodies (the lungs)
which are striving to retract in opposite directions. The heart,
therefore, being acted upon on {506} either side by opposing forces,
occupies a position where these forces just balance each other; and
this is the status of physiological repose in the vertical position of
the body. Now, when an effusion is poured into either chest, the lung
of that side contracts, and thereby exhausts a certain amount of its
retractile energy. The opposing lung, however, still remaining normal,
immediately begins to draw the heart toward itself, and the degree of
displacement thereby induced will be proportional to the diminution of
energy in the compromised lung." Stokes divided displacements of the
heart into excentric and concentric. The former he considered due to
direct pressure of the fluid, and the latter, when from any cause there
was diminution in volume of one lung, the other lung, by its increased
volume, forced it over. The concentric displacements, he thought, were
generally the result of some chronic disease producing atrophy of lung.