{770} cold and injuries to the thorax to those diseases of which it
becomes a companion, whether the seat be remote from, or in immediate
juxtaposition to, the pericardium. Simple cold as a cause of
pericarditis is, as has already been indicated, very much questioned.
Though a very rare, I believe it a possible, cause. Other causes of
simple pericarditis may be blows upon the breast, as with the fist;
crushing or compression, as in railway accidents; penetrating wounds,
as from gunshot or knife; and injury from foreign bodies in the
oesophagus, such as pins, false teeth, etc. Buist[1] records a case of
a man who swallowed a plate with artificial teeth attached. The plate,
becoming lodged in the oesophagus, finally penetrated the pericardium
posteriorly and produced fatal pericarditis. A similar case is recorded
by Flint.[2]
[Footnote 1: _Charlestown Medical Journal and Review_, Jan., 1858.]
[Footnote 2: _Diseases of the Heart_.]
By far the most common form of pericarditis may be termed secondary,
which, like simple pericarditis, may be divided into the acute and
chronic forms. It is termed secondary or consecutive, because it
follows as a result either of impoverishment of the system or a
pre-existing disease, constitutional or local. There are, however,
exceptions to this rule; for we meet with cases of secondary
pericarditis in which pericarditis preceded the onset of, and then
continued associated with, the other manifestations of the disease
which determined it. We see this sometimes in the history of acute
rheumatism.
The disease of the pericardium is often the result of contiguity, but
is much oftener determined by constitutional causes. Why the
pericardium should be the particular membrane selected to take on
inflammation as a complication to other affections has baffled the best
endeavors of the most careful inquirers to determine. The diseases
affecting the pericardium by continuity or contiguity of texture are
chiefly myocarditis, tubercle of the lung and mediastinal glands,
cancer of the same structures, pleurisy, pneumonia, and cancer of the
oesophagus. On fibroid disease of the heart pericarditis is a frequent
attendant.[3] The diseases affecting the pericardium by a special
election, and which are remote from the membrane, are, principally,
acute articular rheumatism, Bright's disease, inflammation and other
diseases of the liver, phlebitis, typhus, typhoid and eruptive fevers,
scurvy, and acute alcoholism. Without doubt, by far the most frequent
cause of pericarditis is acute articular rheumatism. Pericarditis does
not occur in chronic rheumatism, and it is doubtful whether it may be
occasioned by gout, notwithstanding the decided and weighty opinion of
Hayden that this is an efficient cause.
[Footnote 3: It was found in more than half the cases published by
Fagge in _Transactions of the Path. Soc. of London_, vol. xxv.]
Acute pericarditis resulting from acute articular rheumatism has some
peculiarities which it is well to bear in mind. It comes on early in
the disease. We also know of its great frequency as a result of
rheumatism, although the rheumatism be mild; for the intensity of the
rheumatic inflammation is no measure of the extent or severity of the
pericarditis. Nor does the number of joints involved nor their location
give any idea of the greater or lesser liability of the pericardium to
participate in the inflammatory action. Neither does the frequency of
the rheumatic attacks bear any direct relation to the pericardial
involvement; although experience has shown that the first attack
usually is the one most likely to be the cause of pericarditis, while
succeeding ones may or may not produce fresh seizures of pericarditis,
or an aggravation of the disease where it has remained as the result of
previous attacks of rheumatism.
Clinical literature is notably deficient in the reports of pericarditis
ending in recovery, while the recorded cases of death from the disease
as verified by autopsies are most numerous. Yet, although pericarditis
is a serious malady, it is not commonly fatal; and this is especially
true of the pericarditis of acute rheumatism. But it is a frequent
disorder. Sibson,[4] with large experience {771} and patient
observation, has collected and tabulated facts from many sources. In
that particular variety of pericarditis which is the accompaniment of
acute articular rheumatism he found that in 326 cases of acute
rheumatism admitted into St. Mary's Hospital, about one-fifth of the
cases (63) had pericarditis, which was accompanied in 54 cases by
endocarditis; and only in one-fourth of the whole number (79) was there
neither pericarditis nor endocarditis. One-third of the whole number of
cases (108) had endocarditis, and a fourth (76) had threatened
endocarditis, the signs being transient or imperfect. It is notable
that the majority of the cases, regardless of sex and occupation,
occurred prior to the twenty-fifth year of age; and what is equally
notable is that the severity both of the joint and the heart affections
was greatest at or before the same year. Of the 63 cases of
pericarditis in rheumatism, there were 35 males and 18 females; of
these, 11 males and 14 females were from sixteen to twenty years of
age, and the fatal cases were all under the twentieth year.
[Footnote 4: _Reynolds's System of Medicine_, vol. iv.]
Pericarditis happens most frequently between the first and second weeks
of acute rheumatism, although there are instances in which it occurs
later, and occasionally it follows a sudden subsidence of the disease.
It may be observed coincident with the onset of the rheumatic attack,
and even preceding it by several hours. Latham has pointed out how
acute pericarditis is more to be looked for when acute rheumatism is
shifting and inconstant in its seat than when it is fixed and abiding.
Having now looked at rheumatic pericarditis, we may examine the
pericarditis of some other disorders. In that class of affections known
as Bright's disease of the kidney the serous membranes are liable to
take on inflammatory action. A particular preference for the
pericardium seems to exist, and the affections are the cause of
pericarditis next in frequency to acute rheumatism. The tendency
varies, however, with the particular kind of disease of the kidney
which may be present. Pericarditis is common in the contracted kidney;
in amyloid degeneration it is rare.[5] Where uræmia happens, it is apt
to be developed. In warm climates it is less usual as an accompaniment
than it is in cold and damp. But whether this be the full explanation
of the varying frequency of pericarditis as an attendant upon Bright's
disease in different countries is doubtful. There is, however,
certainly, as we learn from the elaborate inquiry of Sibson, a varying
ratio. The complication is, he proves, more frequent in Germany than in
England, least frequent in France.
[Footnote 5: _Ziemssen's Cyclopædia_, vol. xv. p. 629.]
Let us now take into consideration other diseases which in their course
have strong, although less-marked, tendencies to involve the
pericardium. As a class, the eruptive fevers, especially scarlet fever,
may present a pericardial lesion. This is owing to the fact that the
serous membranes generally are liable to become inflamed in these
conditions; but another element in the production of acute pericarditis
may probably be found in the congestion of the kidneys which is apt to
occur. Pericarditis is not commonly present early in these diseases,
but rather in their later stages, when the body is enfeebled by the
specific poison and the skin is susceptible to the slightest variation
of temperature. It is then that the weakest and most vulnerable part
will be attacked, and the pericardium may prove to be the most
vulnerable part.
Other diseases which will cause pericarditis are those dependent upon
dyscrasia of the blood, as in the diatheses, injuries attended by
shock, and those conditions in which there is a great drain from the
system. Perhaps the diathesis most apt to induce pericardial
inflammation is the scorbutic, in which the impoverished and relaxed
state of the system frequently manifests itself by inflammatory lesions
of a low grade. In injuries or diseases {772} where there is excessive
suppuration the system is so weakened that a low form of pericarditis
is prone to develop itself. Diseases of the respiratory organs, as
phthisis, pneumonia, or pleurisy, also enteric inflammations, will
sometimes produce pericarditis. Indeed, any disease dependent upon or
attended by a greatly deteriorated condition of the blood may cause
pericarditis; for the health of the heart itself is determined by the
quality of the vital fluid from which it draws its own sustenance in
common with all other structures of the body, and any vitiated state of
the blood seems to make a special impression upon the heart itself, its
membranes as well as its structure.
MORBID ANATOMY.--In acute pericarditis the serous membrane first
becomes injected with blood, and the injection, starting at a single or
at several points, may become diffuse. If the engorged vessels do not
relieve themselves, infiltration of lymph into the transparent serous
layer follows, producing thickening and opacity as well as slight
roughness. Consequent upon this there is further congestion, the
membrane becomes red, with possibly here and there points of
inflammation of greater intensity than that surrounding the original
lesion; and at these places the vessels may give way and cause a
hemorrhage into the sac or there are little spots of ecchymosis in the
membrane. Usually there is a drying up or a partial suspension of the
serous secretion from the turgid membrane, but before long the
secretion generally recurs, and is even increased in quantity. Upon the
surface of the serous membrane patches of coagulable lymph, more or
less extended, are at the same time exuded. Under the microscope the
bundle of fibres of connective tissue of the membrane appear swollen
and broken up, and the proliferation starts which, as it progresses,
determines the new growth and the villosities. Portions of the exuded
lymph may be washed off and be found as shreds in the serum. The
appearance of the lymphous deposit, as just indicated, is not always
that of a plain smooth layer, but may be velvety and villous, like the
lining of the small intestine, or it may be more roughened, or it may
be honeycombed, as the interior of the stomach of the calf, or be in
ragged shreds of varying sizes, either single or in bunches. Again, it
may assume a lace-like texture, as of fibres coarsely woven together,
or it may appear as if the threads were attached at one end to the
pericardium and at the other floating free. All of these various forms
are largely due to the heart, which in its action presses and rubs the
lymph-covered surfaces together and keeps the softish exudation in
constant agitation. One layer of lymph may be superimposed upon another
until the deposit becomes very thick. It is this lymph which, existing
before fluid is effused to any extent, determines what clinicians
recognize as the dry or plastic stage of pericarditis.
Generally, however, there is effusion of considerable liquid,
occasioning what is termed the stage of effusion. The fluid poured out
is serous, alkaline, and albuminous, of a pale-yellow color, and
transparent, but it may be opaque and milky. It may have flocculi
floating in it, be stained any shade of color from red to brown by the
coloring matter of the blood or by exuded blood-corpuscles, and may
also contain pus. The quantity of fluid varies from a few ounces to
several pints, but the latter amount is rare. The fluid is usually
composed of the watery and saline elements of the blood, with a small
quantity of albumen and a trace of fibrin. If the amount of fluid be
small, the opposing surfaces of the pericardium come together, and the
lymphous layer, becoming more or less organized by the presence of
blood-vessels in it, makes attachments to the opposite wall; in this
manner adherent pericardium is produced. The adhesion may vary in
extent from the slightest filamentous attachment to complete
obliteration of the pericardial sac; and it may be readily peeled off,
or it may be so closely united as to become a part of the tissue upon
which it lies. As the disease progresses the serum and, in exceptional
cases, the fibrinous deposits may be entirely reabsorbed and leave
{773} but little evidence of the previous inflammation. The white
milky-looking spots often found in autopsies are regarded by many as
the remains of cured pericarditis, but they are more likely the result
of nutritive changes and consequent tissue-alteration. Fibrinous
deposits are not always entirely removed. In complete adhesion of the
pericardium they may be considerably reduced, but the sac never regains
its normal appearance, and when the adhesions are partial they remain
permanently.
The formation, density, and organization of the lymph depends largely
upon the cause of the pericarditis. The more acute the attack and the
greater the constitutional disturbance, the more likelihood there is of
rapid effusion of lymph and of its speedy organization, whether it form
adhesions or not. Where the fibrin is exuded under the influence of a
subacute or chronic disease, the formation will be slow, paler, less
highly organized, softer, and if adhesions form they will be less
strong.
The heart participates in the inflammation of the pericardium, and if
it be for any time subjected to the presence of the fluid effusion its
walls degenerate and a granular atrophy occurs. Besides this, in
extensive and firm adhesions there is likely to be primary hypertrophy
followed by dilatation, the walls being enfeebled by degeneration, and,
it may be, becoming thinner. At first, the effort to overcome the
pressure of the pericardial effusion produces the hypertrophy; then the
more or less complete binding down of the walls of the heart,
preventing complete systole and weakening their inherent elasticity,
and the pressure upon the coronary vessels, depriving the heart of the
blood necessary for its healthful existence, are the causes of the
degeneration and wasting of the walls and of the dilatation of the
cavities.
Pus in the pericardium, as a result of pericarditis, may appear very
early in the inflammatory attack, or it may occur after the effusion of
lymph and serum. It may happen but in small amounts smeared over the
surface of the membrane, or be profuse in quantity. Pus may also arise
from small abscesses in the tissue of the heart bursting through the
pericardium. It may be the result of injuries to the pericardium or to
the inflamed membrane, or it may originate in the migration and
proliferation of the leucocytes of the blood. The microscope in
doubtful cases gives us the best idea of their prevalence and quantity,
as well as of the amount of blood-corpuscles present. Where pus alone
exists it is yellow and creamy; but with an excess of serum or fibrin
it may be thinner or thicker in consistence, the entire heart being
bathed in the fluid.
The lesions of chronic pericarditis differ but little from the acute,
except as to their inception or the initial stage. The change from the
acute to the chronic form may occur in a very few days, or even in less
time, and an autopsy would not reveal anything to determine the fact.
Pericarditis in any form is apt to be associated with pleurisy, and
adhesions between the pericardium and adjacent pleura are common. In
some instances the distended sac is adherent to the back of the chest.
By its pressure on the lung and the oesophagus it may produce secondary
lesions in them as well as in the phrenic nerves.
SYMPTOMS.--The symptoms of pericarditis may be so slight as not to
attract attention. Where they are noticeable we find pain or a sense of
uneasiness or of pressure, with or without tenderness in the
pericardial region. The pain or uneasiness is not infrequently
accompanied by pain or tenderness in the epigastric region when
pressure is made upon it. This arises from the contiguity of the part
and the pressure of the diaphragm against the inflamed and tender
pericardium. The pain is sometimes preceded by a chill of varying
severity, and is followed by febrile symptoms of greater or less
intensity; but these may be so slight as to escape observation
altogether except by taking notice of the markings of the thermometer.
{774} Yet the thermometric record, although indicative of fever, has
nothing characteristic. It is, I think, more influenced by the
conditions under which pericarditis happens than by the pericardial
inflammation itself. Often the fever-curve is marked by decided
remissions, and as the result of the pericarditis alone does not attain
a high degree. In the aged, Charcot has pointed out that the
temperature of the body is lowered in some instances of acute
pericarditis. The setting in of pericarditis in acute rheumatism was
observed by Lorain to depress the thermometric marking, and Brouardel
has noted the same effect at the onset of pericarditis in typhoid
fever.[6]
[Footnote 6: Constantin Paul, _Maladies du Coeur_, Paris, 1883, p.
130.]
The action of the heart is increased in frequency and force, as
indicated by observing the impulse and the pulse at the wrist. There
may be present, in different degrees, difficulty of breathing or a
sense of suffocation; difficulty in swallowing; also cerebral
disturbance, as headache, dizziness, sleeplessness, mental depression,
fear of impending death. Besides these we may meet with hiccough and
nausea and vomiting. But any or all these symptoms may also occur in
myocarditis and in endocarditis, and are therefore not of themselves
diagnostic; they only serve as indicators of the direction in which to
seek the cause of disturbance. Some of the latter symptoms may be so
aggravated, particularly those manifested by the nervous system, that
attention is absolutely diverted from the seat of the disease. Indeed,
they are often very misleading; and I cannot even agree to Hayden's
statement[7] that with few exceptions the symptoms of pericarditis take
precedence of the physical signs, though they cannot be regarded as
sufficiently distinctive to warrant a positive diagnosis. Doubtless
these symptoms, however suggestive of pericarditis, may be found to
depend upon other causes. With so little, then, of a positive nature to
assist us in our search, we should be always at great loss were it not
for the physical signs.
[Footnote 7: _Diseases of the Heart and Aorta_.]
PHYSICAL SIGNS.--The chief of these are determined by inspection of the
chest, by palpation, by auscultation, and by percussion.
Inspection.--In inspection of the chest the age of the patient is to be
regarded in the interpretation of the appearances. In pericarditis with
effusion we are apt to find a change in the shape of the chest--a
bulging in the region of the heart, even though the effusion be
somewhat small in quantity. This change is more apparent when it occurs
in young persons, where the chest-walls are very elastic. In those
advanced in years, in whom the costal cartilages are more or less
ossified and the elasticity of the rib materially altered, or where the
chest-walls are bound down by pleuritic adhesions, the shape of the
chest may be materially altered and yet not be very apparent. The
intercostal distension is in any case a matter for investigation. The
chest shows a bulging in the pericardial region, slightly diminished by
a dorsal decubitus and but little influenced by the acts of
respiration.
Palpation.--This gives us an idea of the amount and outline of the
tenderness, which is often found to correspond with that of the
inflamed pericardium. It also enables us to determine to some extent
the limit of distension of the pericardium, the location of the heart,
and the shape of the sac. We also ascertain the impulse of the heart.
Now, at first this is somewhat increased, although it is apt to be
irregular. As effusion of liquid takes place, the heart is displaced
generally backward and upward, and the impulse becomes indistinct or
imperceptible. A slight wavy, irregular motion diffused over
considerable part of the cardiac region may take its place.
Percussion.--During the dry stage, unless a very considerable amount of
lymph be extravasated, the natural percussion dulness in the cardiac
region is not appreciably altered. When the pericardium becomes
distended with fluid the cardiac dulness increases markedly,
particularly in a transverse {775} manner; and as the pericardium is
conoidal in shape, but its position the reverse of that of the heart,
its base resting upon the diaphragm, with its distension a roughly
pyramidal outline of dulness is found, the apex being near the root of
the vessels, the base upon the diaphragm. A great deal of stress has
been laid on this shape of the percussion dulness--much more, I think,
than in point of fact is warranted, for it is not always to be
distinctly made out. Rotch[8] has called attention to the dulness being
early manifest in the fifth intercostal space of the right side, and in
all large effusions it is sure to extend across the sternum. It may,
when the sac is much distended, reach as high as the first rib, as low
as the seventh rib, and below the ensiform cartilage, and the line of
the lower dulness may become continuous with that of the displaced
liver. The dulness may extend on the left side backward almost to the
spinal column and across the sternum to the right nipple. The dulness
is somewhat influenced by position; changing from side to side alters
the line of the fluid.
[Footnote 8: _Boston Medical and Surgical Journal_, 1878, vol. xcix.]