auscultation, and it is the interpretation of these signs which enables
us to distinguish the various stages. We must bear in mind that,
roughly speaking, there is first a stage of suspension of the serous
secretion, and consequent dryness of the pericardium; secondly,
effusion of lymph or fibrin; thirdly, effusion of serum or sero-pus.
Now, the question arises whether we can distinguish the first effect of
the inflammation on the serous membrane, which, indeed, may be
exceedingly short in duration, limited to a few hours. From the fact of
there being a suspension of secretion and absorption of that which has
been normally secreted, it becomes evident that, the parietal
pericardium coming into direct contact with the visceral layer, certain
sounds will be caused by the friction of the heart in its action. Can
we discern them? Great differences of opinion have been expressed with
reference to this; indeed, it has even been questioned whether sounds
would be or would not be produced. Stokes doubted the competency of
simple dryness of the pericardium to generate friction phenomena.
Collin, on the contrary, held that this is actually the condition of
the pericardium indicated by the new-leather sound. To this Walshe
makes assent. Hayden[9] says: "I have never met with a case which would
warrant me in asserting that a state of simple dryness and vascularity
of surface may give rise in the pericardium to veritable friction
sound. I do not, however, deny the possibility of an occurrence which,
theoretically, would seem not improbable. In every instance, without
exception, in which I have had the advantage of determining by
post-mortem examination of the body the condition of the serous surface
of the pericardium, where friction sound of indubitable pericardial
origin had existed during the patient's last illness, I have found
lymph in greater or less quantity effused upon the surface." My own
experience is entirely in accord with this. Theoretically, I grant the
possibility. Practically, I have never seen it; and in the suspected
cases lymph has always been found, with the single exception of a case
in which the friction sound had disappeared nearly a week before death,
which resulted from kidney lesion, and where it was reasonable to infer
that the lymph had been absorbed.
[Footnote 9: _Diseases of the Heart and Aorta_, Philada., 1875, vol. i.
p. 327.]
The friction sound, then, is the sign of exudation. Since it was
originally described by Stokes in 1833 it has been likened by different
observers to familiar objects, such as the crackling of parchment and
the new-leather sound. It is generally most evident at the base of the
heart, is considerably influenced by pressure, is more often double
than single, frequently resembles a double cardiac murmur, and
justifies the name of a to-and-fro sound given to it by Watson. The
friction sounds change from time to time according to {776} the
character, quantity, and stage of the exudation, ceasing altogether
when adhesions have taken place or fluid has been effused, to return
again as the fluid is absorbed, and to cease when recovery has taken
place. They exhibit an inspiratory rhythm very much intensified by full
inspiration. Although, as the place of election of the inflammation is
at the base of the heart, we are apt to find the friction there
earliest as well as longest, this is not invariable; for, as above
stated, the morbid process may begin anywhere in the continuity of the
pericardium.
Next to the friction sound, the most valuable signs in pericarditis are
derived from the muffling of the cardiac sounds. This is particularly
valuable in the stage of effusion, for prior, notwithstanding the
friction phenomena are somewhat obscure, they do not render the sounds
of the heart fainter to any material degree. The cardiac sounds become
less and less distinct as the fluid increases. The heart sounds cease
to be audible, just as is the case with the friction sound, from below
upward, beginning to be indistinct at the apex of the heart. Gradually
and lastly, the sounds of the aorta and pulmonary valves are lost, but
not entirely, unless there be a large amount of fluid pushing up the
pericardium at its attachment around the roots of the great vessels,
and the second sound at these valves is scarcely ever wholly gone.
Sudden effusions of large quantities of fluid are so rare that the
progressive extinction of the cardiac sounds becomes an important
element in diagnosis and prognosis. It has already been noted that the
friction sounds linger around the base of the heart; this may happen
with even considerable effusion. As regards the character of the fluid
influencing the distinctness of the cardiac sounds, I think it may in
general terms be stated that if the effusion be dense, sero-purulent,
or purulent, the sounds of the heart are, in proportion to the size of
the effusion, relatively more obscured than when this is thin.
DIAGNOSIS.--The diagnosis of pericarditis, as before remarked, cannot
be determined by any but physical signs, and even these signs may not
be sufficient for us to come at once to a positive conclusion: the
refinement of perception necessary to detect and properly interpret the
delicate changes which occur in some cases is still lacking to us. In
reviewing the general diagnosis of pericarditis we must bear certain
facts in mind. The acute malady has a very dissimilar origin. It
usually sets in with a fever, ordinarily not of high grade, which may
be preceded by a chill of differing intensity; the pulse is decidedly
accelerated and of varying regularity, not uncommonly strikingly
irregular; on the other hand, the nervous phenomena may be the most
prominent. Craigie[10] observed long ago in a case of pericardial
inflammation in a girl of fourteen that the only prominent symptom
besides the symptom of fever was constant tossing of the extremities
and person, jactitation similar to the motions of the dance of St.
Vitus. Roeser of Bartenstein observed the same symptom in a child of
nine years. There is at times early delirium, very frequently
considerable restlessness, with more or less of an anxious expression
of countenance. Quickened rather laborious breathing is often early
observed, and so is pain in the præcordial region directly under or
near the sternum, perhaps extending to the left shoulder, acute,
severe, and shooting, increased by pressure and motion, and, as
Peter[11] has pointed out, associated with pain in the phrenic nerve,
elicited by pressure between the two insertions of the sterno-mastoid
and also found on each side of the xiphoid appendix. But the pulse may
be regular, the breathing not perceptibly accelerated or laborious, and
even the important symptom, pain, may be wanting from the beginning to
the end of the disease. This occurs in the so-called latent cases.
[Footnote 10: _Elements of the Practice of Physic_, Edinburgh, 1837,
vol. ii. p. 151.]
[Footnote 11: _Clinique Médicale_.]
Since pericarditis is frequently attendant upon certain classes of
diseases, {777} as acute articular rheumatism, Bright's disease of the
kidneys, the eruptive fevers, it behooves the physician to be on the
alert and examine the heart, even though nothing point to its
involvement. Reminded of this fact, we must seek for those signs which
will enable us to diagnosticate early the cardiac disease. And in any
case the first sign of importance detected will be, in all probability,
the friction sound, generally, but not invariably, first heard at the
base, and prone to mask the natural sounds of the heart. At all events,
this is the case when the friction sound is localized at the apex of
the heart, as it occasionally is, before there is very marked
development of the lymph-deposit; it is then, too, that from its
softness the friction may be mistaken for a regurgitant mitral murmur.
The friction may at times be felt by applying the hand to the region of
the heart. This friction fremitus is, however, far from constant, and
can hardly be considered of much diagnostic value, notwithstanding the
high authority of Stokes, who looked upon it as distinguishing
pericarditis from valvular disease. Prior to the existence of the
friction sound we may suspect pericarditis by the sense of general
distress and the dropping of pulse-beats or the otherwise altered
cardiac rhythm. But the diagnosis is presumptive; the friction
phenomena make it positive. Until the quantity of fluid is sufficient
to separate the two walls of the sac the rubbing sound will be
apparent. The friction sound never disappears suddenly, and this
gradual disappearance points to the formation of fluid and may be
regarded as a truly diagnostic sign. The fluid, following the laws of
gravitation, seeks the most dependent portion of the sac, which it more
or less fully distends; in consequence, the disappearance of the
friction begins at the bottom of the sac and at the apex of the heart
and gradually extends upward to the base. Adhesions of the pericardium
will modify and may entirely prevent the formation of the friction
sounds. If the adhesions be local, and if no lymph-deposit be present
between them, there can be no friction; so also where the adhesion is
general the friction sound is destroyed. Where local adhesions and
portions of free surface more or less covered by the lymph exist, the
heart, being allowed sufficient motion, produces friction sounds which
may be found anywhere over its surface except at the points of
adhesion. From the character of these sounds the location and the
extent of the adhesions and of the cardiac movements may be determined,
for "the rhythm of the pericardial friction sound is as the natural
movement of the portion of the heart engaged and the mobility of the
opposed surfaces," says Hayden[12] very truly.
[Footnote 12: _Diseases of the Heart and Aorta_.]
In weighing the value of friction sounds in diagnosis, especially in
determining whether they are produced in the pericardium and not in the
adjacent pleura, we have the simple, though not infallible, method of
discrimination of letting the patient cease breathing for a moment and
then ausculting the heart: they persist if pericardial. This test will
fail, however, in case a portion of the pleura adjacent to the
pericardium also be covered with lymph: then the heart's motion,
transmitted through the pericardium, may produce pleuritic friction
even while the lung is at rest. In such a case if a friction fremitus
be felt it will pass beyond the cardiac area, while in pericarditis
without associated pleurisy it will not be likely to extend farther
than the normal limit of cardiac dulness. The pericardial friction
sound may be sometimes noticed more or less extensively over the whole
chest in children, and also in adults with hypertrophy of the heart,
but this is far from being usual. There may be a friction sound
produced by the action of the normal heart in an inflamed roughened
pleura. This is very difficult to distinguish except by the attending
symptoms. The sound is perceived near the apex of the heart. It is not
apt to occur with each beat of the heart, and may be absent in held
expiration.
{778} In the diagnosis of pericardial effusion, when at all extensive,
we have, in judging of the amount of fluid in the pericardium, to take
into account the increasing dyspnoea with a decided suffocative
tendency, the dizziness, the pallor or lividity of the countenance, the
swollen cervical veins, the bluish nails, the heart flutterings, the
weak, rapid, and irregular pulse, the drowsiness or tendency to mental
wandering. But the physical signs of the effusion above detailed are of
the greatest value, although they give us but little information as to
the character of the fluid. Even in large effusions the friction sound
may not disappear from the base. Indeed, Balfour[13] records as the
result of his observation that "however large may be the effusion,
basic friction, if it have once existed, is never effaced." It is
stated that when the amount of fluid does not entirely fill the
pericardium there may be a splashing sound, and the location of the
sound, as well as that of the percussion dulness, will be changed by
changing the position of the patient's body. I have never observed this
splashing sound. The extent of percussion dulness is no absolute sign
of the extent of effusion. The area of cardiac dulness may be
materially influenced by the following circumstances: the anterior
margins of the lungs which overlap the front of the heart may, from
emphysema, give rise to percussion resonance over the heart, even
though considerable effusion have taken place; the anterior margin of
the lungs, becoming solidified and having strong pleuritic attachments
to the pericardium and anterior chest-wall, may increase the dulness
over the heart and prevent the recognition of the effusion in the
pericardium; effusion in the pleural cavity of one or both sides may
produce similar results. Balfour[14] in fact mentions a case of his own
in which the pericardial dulness was merged in the pleuritic dulness,
and careful auscultation failed at any time to detect friction sound;
the coexistence of pericarditis was surmised, but could not be
detected. After death the pericardium was found to be distended with
reddish serum, and both its surfaces were coated with shaggy,
blood-stained lymph. Such cases are unusual, yet I have met with a
similar instance. Lastly, a growth in the anterior mediastinum may be
the means of masking or being mistaken for pericardial effusion by
changing the dulness in the cardiac region and altering the cardiac
sounds, or it may, by obstructing the circulation, cause effusion. When
an effusion of fluid takes place into a partially adherent pericardium,
the area of cardiac dulness may be irregular or restricted, or both,
the shape and size depending on the length and strength of the
adhesions.
[Footnote 13: _Diseases of the Heart_.]
[Footnote 14: _Ibid._]
Some of the results of large effusions show themselves on other organs.
The backward pressure of the fluid upon the bronchi, trachea, aorta,
and oesophagus interferes with their functions and actions. There may
be bronchial or blowing respiration heard over the lung, due to
compression of the parenchyma. The fluid around the heart prevents free
motion of the organ, although not to so great an extent as in adherent
pericardium; complete diastole does not occur; the auricles and
ventricles are not completely filled; the systemic and pulmonary
circulations become engorged, and pressure is exerted upon the coronary
arteries, thus disturbing the nutrition of the heart. The irregular
action of the heart occasions at times a vibration which is more or
less apparent to the touch. Percussion of the liver shows enlargement
of the viscus; this is due to the obstruction of the ascending vena
cava, which prevents a free emptying of its blood into the right
auricle, and consequently causes a backing up of the blood in the
gland. If the pericardial effusion press upon the anterior portion of
the chest, it may produce pain and aggravate all the other symptoms,
such as the pulmonary oppression, the dizziness, the hurried
respiration, the increase of pulse. Water, blood, or pus in the
pericardial sac gives rise to the same physical signs as serous
effusion, and {779} cannot be distinguished from it with any degree of
certainty, although a careful consideration of the general symptoms
presented may enable us to make a guess which can only be proved or
disproved by an autopsy.
Having endeavored to show the most prominent features characterizing
pericarditis in its various stages and bearing in a general way on its
diagnosis, we shall examine some of the special maladies which are
liable to be confounded with it. The diseases most likely to be
mistaken for the acute inflammatory stage of pericarditis are
inflammation of the pleura and of the endocardium. They are liable to
occur from the same causes, and may be--indeed, often are--concurrent.
Pleurisy gives rise to many of the symptoms of pericarditis. The chief
difference is in the physical signs, some of which, however, are alike
in kind, although different in locality; for in pericarditis they are
confined to the region of the heart: in pleurisy they are spread over
the whole side of the chest and are most perceptible at the back. This
is true of the dulness, and for the most part of the friction sound,
which when of pericardial origin is very rarely heard posteriorly. Then
stopping the act of breathing if the sound be pleural suspends it. At
times, however, as above described, we meet with cases in which a
friction sound discovered over the heart may in reality be produced in
the adjoining pleura. To confound the dulness on percussion caused by
liquid in the pericardium with that due to liquid in the pleura is,
from the different site of the liquid, not likely to happen unless the
effusion be extremely large; for ordinarily a pericarditis
uncomplicated with pleurisy or with pleuro-pneumonia does not change
the clear sound at the back of the chest nor enfeeble or abolish there
the breath sounds and the vocal fremitus. Besides, effusion into the
pleura, if it give rise to a flat sound anteriorly, does not occasion
the special præcordial bulging, and shows the sounds of the heart
unaltered unless the pericardium contain fluid also.
Acute pericarditis is likely to be confounded with acute endocarditis.
The chief difference consists in the physical signs--the friction
sounds and signs of effusion in pericarditis, the blowing sounds, the
slight alteration of percussion dulness in endocarditis, and the fact
that in this disease the abnormal murmurs are often transmitted beyond
the cardiac region and heard in the carotids and subclavian, and are
far less changeable in character and in pitch.
There are other affections with which pericarditis is likely to be
confounded, such as gastric irritation and acute inflammation of the
brain. When pericarditis resembles gastric disorder the thoracic
symptoms may be latent, but the disease produce the manifestations of
extreme gastric irritation or inflammation. There are nausea and
vomiting, and tenderness on pressure in the epigastric region, yet no
disease of the stomach may be present. An examination of the cardiac
region for the physical signs of pericarditis should be made in every
case of persistent vomiting or of hiccough.
Where the symptoms are chiefly cerebral, the cardiac disease may be
overlooked; indeed, in both endocarditis and pericarditis the insomnia
and the active delirium may throw all the other symptoms into the
shade. The violent disturbance of the brain may have its origin, in
part at least, in the contaminated state of the blood which occurs in
the affections, as rheumatism or Bright's disease, with which
pericarditis is often associated. But it is possible also that it may
be due to a coexisting endocarditis of which the products are washed
into the brain. In ulcerative endocarditis cerebral manifestations are
especially common, and there may be acute mania of the most violent
type, as in the case reported by Sioli.[15] Sibson in his exhaustive
analysis points out what I have known to happen in more than one
instance, that the desponding and taciturn--or, as he calls it,
sombre--delirium of pericarditis lasts from two to three weeks to as
many months. Indeed, it may terminate {780} in confirmed insanity. Any
form of nervous disturbance having its centre of disorder in the
cerebro-spinal axis and of any degree of intensity may be seen in cases
of pericarditis, whether produced as a consequence of rheumatism, of
albuminuria, or by other causes. The cases with marked nervous symptoms
are apt to present high temperature, 105° or more.
[Footnote 15: _Archiv für Psychiatrie_, Bd. x.]
The diagnosis of pericarditis from hypertrophy of the heart is made by
remembering that in pericarditis we find friction sound, præcordial
bulging, peculiar enlargement of percussion area, enfeebled impulse and
heart sounds, besides the presence of pain, of fever, of dyspnoea. In
hypertrophy the area of percussion dulness is enlarged, but the shape
is normal; the impulse and heart sounds are strong; no pain or fever,
no friction sounds exist. The chance of mistaking dilatation of the
heart for pericarditis is much greater. In the early stage of
pericarditis the area of percussion dulness is generally similar in
size and shape to the dulness in dilatation. But soon the difference
both in size and shape of the cardiac area becomes marked, the shape
being pyramidal or pyriform in pericardial effusion, while in
dilatation the increase is lateral and does not extend beyond the point
of impulse. There is no friction sound in dilatation; and if the first
sound be weakened, though it may be also sharp and short, the second
sound is everywhere distinct, unlike the muffling of the cardiac
sounds, except at the base, in pericardial effusion.
Tumor of the anterior mediastinum, whether solid or fluid, may become a
source of perplexity in determining the diagnosis of pericarditis; for
by the interposition of the morbid mass between the chest-wall and the
heart the cardiac dulness is increased and the heart sounds are
lessened in distinctness and perhaps in force; though if the tumor be
solid and very dense the sounds may be intensified. Pericarditis may
also be associated with a tumor, and a diagnosis under such
circumstances is attended with great difficulty. A tumor of the
anterior mediastinum is comparatively rare, and seems to be more
frequent in females than in males, although the statistics are meagre
and not conclusive. There may be displacement of the heart in any
direction as the result of pressure from the growth. Should this be
equable in front of the heart, the diagnosis becomes one of doubt, for
the same alteration of the shape of the chest may be present as in
pericarditis with effusion. If the tumor be malignant or scrofulous,
tumors of a similar character may be found in the neck, axilla, or
elsewhere, and aid us in arriving at a correct conclusion.
The differential diagnosis of pericarditis from inflammation of the
anterior mediastinum will cause at times no slight difficulty. However,
inflammation of the anterior mediastinum is infrequent. It may come on
without assignable cause or as the result of injuries. It may be
produced by extension of inflammation from adjacent parts, as in
pericarditis; it does not appear in association with, or as a
consequence of, other diseases, such as rheumatism, renal diseases,
scurvy, or the exanthemata, as is so largely the case with
pericarditis. The symptoms resemble those of pericarditis, and there is
likely to be chill, followed by fever, substernal pain and weight, pain
on pressure over the sternum, accelerated action of the heart.
Respiration is more or less difficult and painful, on account of the
movements of the cartilages and intercostal muscles. The disorder in
respiration becomes the more decided when the inflammation has extended
to the pleura; there is also pain on pressure in the epigastrium. The
physical signs of mediastinitis may be precisely similar to those of
pericarditis. The extension of the inflammation to the adjacent parts
produces the characteristics of uncomplicated inflammation of these
parts, and under such circumstances the distinction is far from being
easily made; the pleuritic and pericardial friction sounds which are
developed will naturally be ascribed to affections of the pleura and
pericardium alone. In accumulation of pus in the mediastinum no little
uncertainty {781} will exist in determining the difference between this
and pericardial effusion. The percussion dulness may extend beyond the
area of the heart, and take the form of the area in effusion into the
pericardial sac. It is true, however, that in purulent collections in
the mediastinum the shape of the percussion dulness is often more
elongated, extending upward to the sterno-clavicular articulation.
Should the accumulation be large, we meet with difficulty of
respiration and of deglutition from pressure, as in pericarditis with
effusion or in hydropericardium; and there may be elevation of the
sternum and intercostal bulging. Abscess of the mediastinum tends to
point at an intercostal space; it may also do so in the scrobiculus
cordis: the impulse of the heart is weakened or entirely lost and the
heart sounds are distant and obscured. There is apt to be hectic, with
headache, delirium, and syncope. In fact, there is no symptom of
pericarditis or of hydropericardium which may not also be found in
acute mediastinitis or in the accumulation of pus in the mediastinum.
Where the inflammation can be traced to an injury, as a blow upon the
sternum, or where there exists caries or necrosis of the sternum, the
diagnosis is greatly facilitated. The inflammatory symptoms, while of
all grades of intensity, are, as a rule, more intense in the forms of
mediastinitis than in any of the acute stages of pericarditis. In cases
of fibrinous mediastinitis associated with fibrinous or fibro-purulent
pericarditis, Kussmaul has called attention to the diagnostic value of
a pulse intermitting at regular intervals simultaneously with
inspiration, the pulsus paradoxicus.