depending largely upon the primary cause, the intensity, the stage and
duration of the attack, the prior condition of the individual, and his
surroundings. The general prognosis is favorable to life: though some
of the older writers were disposed to look upon it as a highly
dangerous disease, it is clearly one from which recovery is frequent.
In many autopsies of individuals who have subsequently died of other
disease the evidences of cured pericarditis have been found. By cured
it is not wished to convey the idea that the pericardium was restored
to the condition it was in prior to the inflammatory attack, but that
the inflammation had ceased without injurious consequences. There may
be recurrent attacks, and they are frequently of a subacute character;
even when fibrinous deposit and attachments continue to exist, it often
happens that the movement and functions of the heart are not interfered
with. Unless the disease be exceedingly severe in the acute stage, the
prognosis is decidedly favorable. When the attack is very severe there
are strong reasons for believing that the structure of the heart is
also involved, and death ensues chiefly from the latter complication.
Should adhesions take place, the prognosis is unfavorable in proportion
to their extent, though to this rule there are decided exceptions. If
effusion rapidly develop, the prognosis becomes at once unfavorable,
death resulting in a short time from sudden pressure upon the heart and
its palsy. If, however, the effusion accumulate slowly, the parts
become tolerant, and a large amount of fluid may be thrown out without
fatal consequences. Where death occurs it usually comes on slowly, and
the immediate cause is from the pressure of the large effusion upon the
heart, preventing its free diastole. The lungs become engorged with
venous blood, and asphyxia of the heart ensues. There is apt to be
general dropsy in such cases, particularly oedema of the lower limbs
and accumulation of fluid in the serous cavities, as in the pleuræ, and
the patient becomes gradually exhausted. If effusion of serum be
accompanied by pus or by blood, or if there be pericarditis with pus or
blood alone, the prognosis is unfavorable. Balfour,[16] however, states
that recovery is not impossible in purulent pericarditis, "for the
elements of pus are more or less present in every pericarditis, and pus
may be only a transitional {782} stage, and may result in the breaking
down of cell-elements, the formation of a pathological cream, and its
complete absorption, and the perfect cure of the disease." The caseous
formation, or even the pathological cream, is rarely met with, and
cannot be detected prior to death. Burrows[17] records a case in which
there was a layer of concrete pus over a small space in a pericarditis
of seven days' duration. Pericarditis with large amount of membrane,
whether this be coated with pus or not, and even without liquid
effusion into the sac, is always of grave prognosis; so are cases with
high temperature, cases complicated with pneumonia, cases in which the
dyspnoea is of intensity disproportionate to the local symptoms, and in
which the pulse is not in unison with the impulse of the heart.
[Footnote 16: _Diseases of the Heart_, 1876, p. 299.]
[Footnote 17: _Disorders of the Cerebral Circulation_, London, 1846, p.
187.]
The pathological changes in pericarditis are such that it is quite
impossible to determine by the special signs or symptoms of the
affection between simple pericarditis and a pericarditis the result of
transmission from diseases in adjacent organs, as pleurisy or
pneumonia, or as a complication of rheumatism or Bright's disease,
except by the history and the general features of the case. Yet the
prognosis is vastly different. The prognosis of simple pericarditis
without carditis is good. Pericarditis in acute articular rheumatism is
generally favorable as to life, and is nearly as favorable as simple
pericarditis. Balfour[18] states that he has records of 1968 cases of
disease treated in the Royal Infirmary, 70 of which were cases of acute
rheumatism, with but 1 fatal case of rheumatic pericarditis. My general
experience of the favorable character of rheumatic pericarditis without
marked involvement of the deeper structures of the heart corresponds
with this. I except, however, the comparatively rare cases with high
temperature. A temperature of 105° is always grave. The prognosis of
pericarditis in Bright's disease is, speaking in general terms, as
unfavorable as that of the pericarditis of acute rheumatism is
favorable. The pericarditis of poisons, of pyæmia, or of scurvy is, as
a rule, a very serious malady. In the exanthemata recovery is the rule,
unless there be extensive pleurisy or pneumonia as a complication.
[Footnote 18: _Op. cit._, p. 288.]
In injuries, such as in rupture or puncture, the prognosis must depend
upon the extent and the character of the injury, the condition of the
patient, and whether or not the puncturing body has been removed from
the wound. Generally, these must be regarded as unfavorable cases,
although paracentesis of the pericardium is now accepted as a proper
operation and is attended with comparatively little risk. The cerebral
symptoms occurring in pericarditis can hardly in themselves be regarded
as unfavorable to life, but they are unfavorable when associated with
high temperature and when considered in connection with full recovery
of the mental powers. Relapses and recurrences of pericardial attacks
have strongly fatal tendencies. Age and sex contribute materially to
the prognosis. The very young and the aged are unpromising subjects;
and Sibson[19] has shown that while females are somewhat more liable
than males to acute articular rheumatism, males are more often attacked
with rheumatic pericarditis; also that endocarditis accompanies
pericarditis more frequently in males than in females, while simple
endocarditis is more frequent in the female than in the male. He also
shows that while pericarditis affects the two sexes below the age of
twenty-one in nearly equal proportions, after the twenty-fifth year
males are three times oftener subject to it than females. The disease
is greatly modified by occupation as well as by age. Thus, Sibson has
pointed out that female domestic servants under twenty-one years of age
are extremely prone to acute rheumatic pericarditis, endocarditis, and
carditis, as they are often unequal to labor and fatigue, and are
easily affected by draughts and by exposure to wet and cold.
[Footnote 19: _A System of Medicine_, by Reynolds.]
{783} The causes of death in pericarditis are various. Death may occur
in a few hours after the attack by the rapid effusion of a large
quantity of fluid, compressing and causing mechanical paralysis of the
heart; or it may happen from syncope due to the patient making sudden
exertion, as in getting out of bed, more especially if there be a large
amount of fluid in the pericardium; or, again, it may be owing to
paralysis of the heart from disturbance of the cardiac centres, or to
fatty degeneration of the cardiac walls largely induced by the
inflammatory condition. Again, a fatal termination may be caused by
pneumonia or extensive congestion of the lungs, or by a large quantity
of fluid in the pleura, having its origin really in the pressure
exerted on the veins and the other structures by the pericardial
effusion; or death may result from non-aëration of the blood and from
general exhaustion.
TREATMENT.--In the treatment of acute pericarditis the first thing to
insist upon is absolute rest--rest of body, rest of mind; all effort,
all fatiguing conversation, is to be avoided. The diet should be of an
easily-digested kind, nourishing, but given in small quantities at a
time, so as not to distend the stomach. Milk, eggs, animal broths, with
occasionally just enough solid food to gratify the wish of the patient,
constitute the best diet. Further, from the very outset the cause of
the malady should be clearly kept in view and the treatment directed in
accordance. As so many cases have their origin in rheumatism, an
antirheumatic treatment has usually to be carried out. But here let me
at once record the more than uselessness of the salicylates. They have
no influence when pericarditis has arisen, and if salicylic acid or its
compounds are being given, they should at once be stopped. The alkalies
have a far better action. Again, speaking in general terms, opium in
moderate doses, to keep the nervous system quiet and to moderate the
general discomfort, is of wide applicability and signal use; few are
the cases which its steady, judicious employment will not benefit.
Especially is this witnessed in the earlier stages and before marked
effusion occurs.
The treatment of acute pericarditis is much influenced by the stages of
the malady--whether it is seen in the stage with plastic exudation;
whether this exudation markedly persist and but little liquid effusion
takes place; whether the effusion is copious. Now, in the earlier
stages and before decided effusion bloodletting was at one time much in
vogue, but it has been by general consent abandoned, at least general
bloodletting has. Local bloodletting is still employed by some, and I
am sure I have known a few cups to the præcordial region or leeches
there applied relieve the pain and make the action of the heart more
regular. It is, I think, in robust subjects and in the early stages
decidedly to be recommended. Mercurials, like general bloodletting,
have fallen into disuse. Cases of pericarditis have been seen to
originate in those whose gums were touched by mercury, and it does not
prevent effusion. Certainly, in pericarditis with Bright's disease the
remedy must not be thought of; but under other circumstances, in
lingering cases with extensive plastic deposits, or in effusions that
remain uninfluenced, it is worth a trial.
The application of cold to the cardiac region, either in the shape of
cold compresses frequently changed or of a bladder of ice, is very much
lauded by some of the French and German physicians. Gendrin's method
consists in keeping a bladder of ice over the heart for from one to
three hours until the pulse and temperature come down to about a normal
condition. As these rise it is from time to time reapplied, although
for a shorter period; and it is thought to influence both the pain and
the inflammation. I have not seen the latter effects from it; and for
the pain it is less trustworthy than the more commonly employed
hot-water applications and poultices. Digitalis is in the earlier
stages an admirable remedy. Its use in small, frequently-repeated doses
will render the action of the heart more regular and reduce {784} its
frequency. Friedreich[20] and Bauer[21] both recommend its employment
in large doses, to be suspended when the pulse becomes slower or
irregular. Notwithstanding it might be thought particularly valuable in
marked effusions alike from its tonic action on the heart and its
diuretic powers, my clinical experience is against it under such
circumstances. It is far inferior to the free use of stimulants.
[Footnote 20: _Die Krankheiten des Herzen_.]
[Footnote 21: "Diseases of the Pericardium," _Ziemssen's Cyclop._]
When there is decided effusion diuretics are our main dependence, and
squills and tartrate or acetate of potassium are most employed. The
acetate of potassium is very serviceable--half an ounce or more in
twenty-four hours in broken doses. Nor need we wait for the occurrence
of the effusion to begin with this remedy. An occasional hydragogue
cathartic is also indicated where the strength of the patient permits;
but care must be enjoined not to let him rise to go to stool. In
lingering effusions iodide of potassium, not less than forty grains
daily, and repeated blisters are employed. The latter remedy may also
be used early in the case where the friction sound is extensive, and a
large blister then is better than a small one.
A state of things is at times met with in which the pulse is weak, the
extremities cool, the effusion large, the impulse of the heart very
faint, the heart evidently struggling. There is but one remedy for
this--the free use of stimulus, whiskey or brandy or wine, whichever is
best taken. Nor do cerebral symptoms contraindicate--on the contrary,
they more decidedly indicate--stimulants. Tonic doses of quinine and
hypodermics of brandy aid in this stage. Should the symptoms still
prove unyielding and the effusion large, the question of puncturing the
pericardium will arise; and as a means at least of gaining time the
operation is strongly indicated. Its manner of performance and its
general results have been carefully studied by John B. Roberts, and to
his remarks in this volume the reader is referred. We cannot be too
careful to be on the lookout for the pulmonary complications, pleurisy
or pneumonia, which are so apt to be found in acute pericarditis. They
require prompt treatment, but they ill bear depressants. They demand,
among other means, often quinine, and the greatest attention in
sustaining the action of the heart and in keeping the kidneys actively
at work. When the dyspnoea is very great, and there is considerable
pleural as well as pericardial effusion, it is best to tap the pleura.
I have several times given this advice in cases in which it was under
discussion to tap the pericardium, and after the relief afforded to the
lung the pericardial affection has yielded to remedies.
Chronic Pericarditis.
Chronic pericarditis, as such, requires but little consideration here,
since its main features have been discussed in this article under other
heads.
Chronic pericarditis is divided from the acute by a very shadowy line:
a few hours of the acute disease may terminate in the chronic form, as
in acute inflammatory affections elsewhere, or the malady may follow an
attack of acute pericarditis of several weeks' duration, or it may be
chronic from the beginning. In the first case the pericardium is the
organ primarily affected, generally from cold, or the lesion is
dependent upon some acute inflammatory disease adjacent or remote, as
carditis, pleurisy, mediastinitis, or upon rheumatism. In pericarditis
the result of the exanthemata, of Bright's disease, of scurvy, of
tuberculosis of the lungs or elsewhere, of profuse drainage from
abscesses or injuries--of, in fact, any wasting disease or fault in the
economy associated with malnutrition--the pericarditis may be subacute
at first, and is then apt to become chronic.
{785} The symptoms are slow of development, and are not usually rapidly
productive of discomfort. They are in the main the same as those of the
acute affection, although less decided, and the thermometer may mark a
normal degree or but little above the normal. The physical signs of
effusion of fluid, the presence of pus and blood or of adhesions, have
all been discussed under their proper heads. The prognosis is,
generally speaking, not as favorable as in the acute form; it depends
very much upon the cause, the duration of the case, and the character
of the fluid. In the treatment great attention must be paid to the
cause as well as to getting rid of the effusion and relieving any
direct oppression of the heart the result of the pressure of the fluid.
If this cannot be done by medical means, or if there be reason to
believe that the collection is purulent, paracentesis is indicated.
Adhesions are not, or are but very seldom, removed by any special
treatment directed to them. Indeed, it is by adhesions that most of the
cases of pericarditis with lymphous effusion get well. When adhesions
have disappeared after these attacks of inflammation, it has been
through the efforts of nature, and nothing is left but the milk spots
to testify to the previous condition of the membrane. But these, it
must be remembered, are also the result of altered nutrition in the
membrane, and do not in themselves bespeak a chronic pericarditis.
Adherent Pericardium.
Early in this article adhesions were mentioned as one of the results of
pericardial inflammation, and it was stated that the exudation may
appear in spots or extend over the visceral or parietal layers of the
pericardium or over both, and become organized tissue filled with
blood-vessels, gluing the walls together, and completely obliterating
the sac. Limited adhesions are much more common than those which are
extensive or complete. The intensity of the inflammation offers no
indication of the probability of the formation of adhesions. The
position of the body will materially assist in the adhesion of one
point in preference to another, more especially if the body should
retain a certain posture for any length of time; for the heart
naturally gravitates to the most dependent part, and these portions
coming into apposition will form attachments. If these are not too
large and firm they may become broken, their torn ends being absorbed
or remaining as pendent shreds or patches.
When the adhesions are long and flexible, the motion of the heart is
not interfered with; but when they are short, firm, and extensive, the
heart labors to perform its duties, without hope of relief. If the
adhesions do not contract, the heart retains its shape, and diastole is
easy; but in its systole the difficulty is marked, for besides the
effort to expel the blood there is restraint of motion, with great loss
of energy in drawing to itself the unyielding pericardium. If the
pericardium be adherent to the pleura and other surrounding parts, the
obstacle is increased and the sternum and costal cartilages are drawn
inward and the diaphragm upward. It is to this effort of the heart in
systole that the hypertrophy which is often found with pericardial
adhesions has been attributed; and in the main I believe this view to
be correct. But a number of distinguished observers have denied that
the pericardial adhesion is the cause, and think that the cardiac
hypertrophy is more probably accidental or dependent upon valvular
disease the result of endocarditis, or upon a condition of myocarditis
which, however slight, may coexist and lead to inflammatory deposit in
the walls, and consequent hypertrophy. It is not difficult to
understand how with altered walls dilatation, another consequence of
pericardial adhesion, may be caused. Adhesions to the more resisting
chest-wall and diaphragm prevent the approximation of {786} the cardiac
walls and also the complete closure of the valves. The weakened cardiac
walls begin to yield: this will be assisted by the traction of the
adhesions on the walls and by the persistent engorgement of the
cavities of the heart resulting from inability to empty themselves as
completely as when in the normal condition. Another element will be
that of shrinkage of the heart-walls, which comes on when the adhesions
become so firm and produce so much pressure by contraction that the
nutrition of the organ is materially interfered with. But the problem
is by no means an easy one to solve, and it seems to me that there is
more than one factor influencing it, and that in cases with predominant
dilatation the altered heart-walls play, most likely, the prominent
part.
Now, even as to the fact of hypertrophy occurring there is far from
unanimity. To cite, by way of illustration, the opinion of a few
observers. This condition has been asserted by Chevers[22] and by
Barlow[23] to be the usual and normal result of complete adhesion of
the pericardium to the heart and consequent obliteration of the sac.
Hope[24] very emphatically states: "I have never examined, after death,
a case of complete adhesion of the pericardium without finding
enlargement of the heart, generally hypertrophy with dilatation."
Stokes,[25] on the other hand, writes: "Without denying that generally
adhesion may induce hypertrophy and dilatation, experience leads me to
doubt that such an effect necessarily or even commonly follows the
condition indicated. I have often found the heart in a perfectly normal
condition with the exception of an obliterated pericardium." He adds:
"It has been stated to me by Smith that he has found general adhesion
of the pericardium coinciding with atrophy or with hypertrophy of the
heart in nearly equal frequency. In some of the cases of atrophy the
change was simple, consisting essentially in a diminished volume, with
perhaps a paler color of the heart, while in others a true fatty
degeneration had commenced." Bauer[26] records that "as a rule the
heart is found in a more or less marked condition of degeneration and
atrophy. The bundles of muscular fibres show evidences of fatty
degeneration, or even of hyalin and pigment degeneration, or the
appearances are those of an interstitial myocarditis, with its
results." To my mind, I repeat, the state of the muscular walls seems
of great importance, and it may explain the varying condition of
hypertrophy and dilatation found in association with the pericardial
adhesions in such a differing manner.
[Footnote 22: _Guy's Hospital Reports_, vol. vii. p. 421.]
[Footnote 23: "Gulstonian Lectures," _London Med. Gazette_, 1844, pp.
755, 756.]
[Footnote 24: _Diseases of the Heart_.]
[Footnote 25: _Diseases of the Heart and Aorta_.]
[Footnote 26: _Ziemssen's Cyclopædia_, vol. vi. p. 634.]
It is strongly held by some that hypertrophy is occasioned more by the
valvular disease that may coexist than it is by adherent pericardium.
Sibson[27] tells us that "when pericardial adhesions are associated
with valvular disease the heart is always enlarged. It was so in
twenty-five out of twenty-six cases, and in the remaining instance, a
case of mitral constriction, the heart was rather large." Undoubtedly,
this combination is not unusual, but there may be the most marked
hypertrophy with adherent pericardium without valve affections. I have
met with several such instances, and Blache[28] has recorded three of
striking character.
[Footnote 27: _A System of Medicine_, by Reynolds, London, 1877, vol.
iv. p. 440.]
[Footnote 28: _Maladies du Coeur chez les Enfants_, Thèse de Paris,
1869.]
Adherent pericardium may occur at any age. It has been found by Behier
as the result of chronic pericarditis in an infant of eleven
months.[29]
[Footnote 29: Constantin Paul, _Maladies du Coeur_, Paris, 1883.]
The SYMPTOMS of adherent pericardium are uncertain; the physical signs
are the only means we have of determining its existence, and even these
signs are far from invariable or well defined. In marked cases, on
inspection of the præcordial region, it will be noticed that there is
more or less complete {787} absence of the heart's impulse against the
chest-wall. This is due to the fixed or restrained condition of the
heart, particularly of its apex, and to the interposition of a layer of
plastic lymph, and possibly of some fluid. There is sometimes a
prominence of the costal cartilages over the heart, and the organ
itself may be abrupt and jogging in its motion. The intercostal spaces
to the left of the sternum are indented, and there is a drawing in of
the lower portion of the sternum and attached cartilages with each
systole of the heart, giving rise to a wavy movement in the
epigastrium.
The application of the hand over the heart detects the impulse, but
this is diminished in force and extends over a larger area than in
health. The pulse is usually accelerated and irregular in its rhythm.
When palpitation of the heart occurs--and this is far from a constant
sign--it is dependent upon pressure at the origin of the great vessels.
In some cases there is pulsation in the liver, also pulsation in the
epigastrium, and venous pulsation in the vessels of the neck. The
regularity of form of the chest in its rise and fall during the acts of
respiration will be interfered with if the adhesions be extensive.
The position of the heart is but little changed from the normal, though
of necessity the organ is more or less fixed in its position by the
adhesions. No matter what posture the patient may assume, the apex-beat
of the heart remains unchanged where bound by the adhesions; this is
especially the case if the adhesions have extended to the pleura. The
apex-beat may be entirely masked; but if it be in its normal site, a
depression of the intercostal space during the systole of the heart
occurs, caused by traction upon the intercostal muscle at that point.
If the pleura be implicated, greater expansion of the upper and outside
portion of the left side of the chest in inspiration takes place. In a
certain proportion of cases the position of the heart is more oblique
than normal.