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of the heart and pericardium. In one of these instances the pericar-
dium was aspirated several times; in the other it was not considered
necessary or judicious to operate. The history of my first case was
read at a meeting of the Practitioners' Society, 1 October 11, 1901, and
the specimen shown. The case was discussed by the members.

During the past eighteen months I have also taken care of two other
cases of pericarditis. Of these, one occurred as a complication of
Bright's disease ; the other apparently of rheumatic origin. I shall
refer to these later in my remarks upon paracentesis.

In certain instances of tuberculous pericarditis it has been noted that
there was no evidence of tuberculous deposit in the adhesions which
were present. In those instances more numerous, where tubercles are
discovered in the adhesions, they may appear like grayish areas at the
line of union of the parietal with the visceral layer. In 1048 autopsies
Wells 2 found tuberculous pericarditis 10 times, which formed about 8
per cent, of all cases of pericarditis recorded by him. It is not limited
to adults, but may occur quite frequently in childhood or infancy. It is
more frequent among men than women. Baginsky reports 15 cases in
4500 autopsies, and of these 4 were purulent. In Osier's autopsies, 1000
in all, there were 7 instances of tuberculous pericarditis. 3

Welch, in his report from Johns Hopkins Hospital, states he has seen
6 cases. Although often spoken of as frequent, it is not shown by ref-
erences in Index Catalogue, Transactions of the Pathological Society of
London, etc. Up to 1893 Osier had seen only 17 cases, and yet he
writes tuberculous pericarditis follows hard upon the rheumatic form.
In Wells' cases, where the condition was miliary and chronic, there were
adhesions and no fluid. In acute miliary eruption, and in those where
there was caseous deposit, 4 there was also more or less effusion in the
pericardial sac.

1 Medical Record, November 23, 1901, p. 831.

» Journal of the American Medical Association, May 25, 1901.

8 The American Journal of the Medical Sciences, 1893, p. 20. * My second case.


In one instance, where no tubercles were shown in a case of acute
pericarditis, the inflammation was apparently due to toxins of tuber-
cular origin. This opinion was supported by the fact that tubercles
were found extensively in other viscera. The tuberculous cases, espe-
cially those which are acute, result fatally. This seems to be true, also,
of acute pericarditis following pneumonia or Bright's disease, but is not
true of this complication of acute articular rheumatism.

The forms of tuberculosis as they are found in the pericardium are
either of miliary form or cheesy masses. When effusion exists it is
serous, bloody, or purulent. It may be moderate or considerable in
amount. Whenever the condition has existed for some weeks, it is
probable that the pericardial sac becomes softened and dilated, and
offers a very insufficient support to the heart. The clinical evidence
of this softening and dilatation of the pericardial sac in disease is shown
by its greater capacity to contain fluid. Experimentally, this capacity
is limited to about 700 c.c. of liquid when forced into the sac. 1 In
disease we know much greater quantities of fluid may be contained.
Even when these larger amounts are present, we can only recover them
in part by paracentesis, owing, as will be shown later, to the position of
the heart in the fluid. Soon the heart would show signs of dilatation,
and this condition more surely and rapidly occurs if the heart walls are
subjected to any increased strain.

In some instances of tuberculous pericarditis, as we know, adhesions
with the chest wall have developed. These adhesions, if more than
usually taxed, are apt, sooner or later, to be stretched, and in some
instances to give way. Under these circumstances the heart shows
signs of insufficiency very soon.

As Sequira 2 points out, the dilatation of the pericardium is very
important from the standpoint of ultimate prognosis, and this we can
readily appreciate when we consider the immediate effects of hyper-
trophous dilatation where passive congestion of the viscera is more
than likely to occur. Sequira's observations are based upon the history
of 130 cases of acute pericarditis and observations of 1000 cases.

In occasional instances the pericarditis seems to be due to mere exten-
sion from adjacent parts in which tuberculous lesions clearly exist.
Under these conditions the pericarditis, curious to say, may occasionally
be simply inflammatory. This point is affirmed by Osier. Such in-
stances have also been noted where the extension came from a case of
non-tubercular pleuritis. Likewise they have been recognized as final
complications of chronic tubercular states, and as a result of terminal
bacteremia (Wells).

In certain instances where the process in the pericardium is an acute

i Chatin. Kevue de Med., June 10, 1900. 2 British Medical Journal, June 17, 1900.


one, tuberculosis has not had time to develop there, but later we should
doubtless have discovered it if death from other organs affected with
tuberculosis had not occurred. Tuberculous pericarditis heals through
the formation of fibrous adhesions. In some forms, especially the caseous,
the healing may be accompanied with calcification. The thickening of
the sac wall may become very considerable. This is true of the parietal
wall particularly. These cases are often accompanied with a deposit of
numerous miliary tubercles. At the same time there is present more or
less effusion, which may present different characters. Often it is dis-
tinctly bloody. Still this is not sufficient to determine the diagnosis, as
it may take place in other conditions. Of the 11 cases found in liter-
ature by Sears, 1 6 occurred in scurvy, 3 in rheumatism, 1 in goitre,
1 idiopathic, in an alcoholic subject. 2

Bacilli may be found in this fluid, although sometimes it requires
several careful examinations to reveal them. 3 Osier reports 1 case,
quoted from Kast, in which tubercles have been found in the pericardial
effusion. F. C. Shattuck's 4 second case is another. Where this exami-
nation has remained negative the bacilli are revealed solely by means of
animal inoculations. 5

The proportion of successful inoculations is considerable. It is of
great value in fixing the positive diagnosis to be made. The drawback
to it is the time it takes to develop tubercles. 6 It is in the exudate, as
well as in layers of pericardium, that we find tubercle. When it
occurs in pericardial layers it oftener affects the parietal one and dis-
seminates to the left pleura. Serous effusion, when present, is fre-
quently surrounded by fibrous exudation, which in places becomes

The myocardium may be affected with tubercular infiltration at the
same time as the pericardium. The miliary form is relatively unim-
portant as compared with the caseous. The latter penetrates deeper and
sometimes perforates the cardiac walls, and may surround itself with a
fibrinous clot.

Formerly primary cases of tuberculous pericarditis were reported.
To-day, thanks to a more advanced knowledge of pathology, this
erroneous affirmation is rarely met with. One reason is because
lesions formerly considered of doubtful nature are now recognized to
be tuberculous. Hence, when such lesions are found elsewhere and by
their structure are known to be of old date, we can readily appreciate

1 Boston Medical and Surgical Journal, 1898, p. 293.

2 Churtan. The American Journal of the Medical Sciences, 1892, p. 84 ; also, Michailoff, loc,
<cit., 1878, p. 278.

8 Report of my first case.

* Transactions of the Association of American Physicians, vol. xii. p. 194.

' This was true in my second case.

■• About six weeks in guinea-pig.



that it is from them that the infection of the pericardium proceeds. In
very many cases, without doubt, the infection is carried by the blood-
vessels ; in others the lymph channels are the evident way of transport.

Simple carrying, as it were, by extension of a tuberculous process
through contact, although still admitted, is not so frequently allowed
as heretofore. The ordinary development of tuberculous pericarditis is
to run a subacute or chronic course. This course may be such an
insidious one that for a long while the disease is latent, and no obvious
symptoms indicate its presence. Indeed, Osier reports only a single case
in which, during life, " the diagnosis of tuberculous pericarditis was
made with a reasonable degree of probability." If, however, there is
no rheumatic history, and tubercles are discovered elsewhere with pre-
vious symptoms of pericarditis, we should think of the tuberculous form.
The protracted course of the disease and the more marked irregularities
of temperature may indicate its presence. Sometimes the symptoms
occur, but are concealed by grave symptoms of other organs which are
affected from general miliary tuberculosis as well as the pericardium.
It is a fact also worthy of remark that, as a result of experimental re-
searches about tuberculosis, while lungs, pleura?, and mediastinal glands
are usually attacked, it is a very infrequent circumstance to find the
pericardium involved ; indeed, it is doubtful if there be any well-authen-
ticated cases of it. The involvement of the pericardium through the
lymph channels and with transport of tubercle bacilli largely comes
from the lungs, pleura?, and peritoneum. This infection of cardiac
lymphatics is doubtless carried on indirectly, so far as the former
organs are concerned. Owing to the free anastomosis of the lymph
vessels across the diaphragm, it is readily understood how a tuber-
culous peritonitis may cause directly the development of tuberculous
pericarditis. Where the tuberculous pericarditis is of caseous form
brought from mediastinal glands, it is probable that later on this
matter is carried to and produces secondary infection of the lungs and

In regard to the question of the frequency with which one layer of
the pericardium is affected as compared with the other, this, it appears
to me, is difficult of solution, despite the statement of Wells, and, in any
event, of no practical moment.

What is affirmed with authority is that a large proportion of cases
show tuberculous deposit in mediastinal lymph glands and pericardium
at about the same time, and frequently this is true where no tuberculous
deposit exists elsewhere. We are more likely to notice this dual condi-
tion where already the process has become somewhat a chronic one.
Effusion into the pericardium is more likely to occur, it is stated, where
caseous masses exist on its surface than where we find the small gray


Where the myocardium is affected the disease comes primarily, as a
rule, from the pericardium. The muscle of the heart is, however, rarely
thus diseased. This is especially true of the ventricle ; the auricle is
oftener invaded.

Tuberculous pericarditis may recover, it is stated. This is rare.
In general, we may say it is not directly fatal, and death subse-
quently occurs from tuberculous deposit in some other important organ.
At this time that of the pericardium may have become quiescent.
This, of course, occurs only in the relatively chronic forms. If it does,
we may find fibrous nodules in the exudate or pericardial walls as the
only direct evidence of a tuberculous lesion. It may be inferred, how-
ever, by considering the evident tuberculous condition of the mediastinal
glands, and through the fact that this is the sole efficient cause of tuber-
culous pericarditis which can be brought to light.

The most important effects, clinically, are those which are seen upon
the heart. In some instances there is no valvular lesion or structural
defect of the heart muscle, and yet there is dyspnea, cyanosis, and weak-
ness of pulse — all pointing to cardiac distress. The effusion, by its
mere pressure, seems to be the explanation of these symptoms, and its
prompt removal is therefore the essential and urgent indication, so as to
re-establish, as far as may be necessary, functional power. If this con-
dition is allowed to remain, even though life may not be imminently
imperilled, the heart soon shows the results of the external pressure
against which it contends by becoming enlarged with hypertrophous
dilatation, and by growing weaker progressively and constantly. Where
adhesions exist with the thoracic walls, which is often true in these cases
whenever they tend to chronicity, the duration of life is notably short-
ened. It is equally true, only more so, where the two layers of the
pericardium have also become adherent and the effusion has become
resorbed or been removed by paracentesis. In these instances life may
be measured by a few months. This is eminently true in pericarditis
affecting children. Lee Dickinson 1 reports " one solitary case in which
adhesion, certainly contracted in childhood, proved ultimately harmless."
The late Dr. Sturges showed in these cases that acute carditis is present,
usually of rheumatic origin. Peck 2 has ably described in several such
cases a condition of " pericarditic pseudocirrhosis " resembling precisely
the mixed form of cirrhosis 3 of the liver, which is due to latent pericar-
ditis. The differential diagnosis is based upon : (1) Absence of etiologic
factor of cirrhosis ; (2) a history of pericarditis supported with the evi-
dences of it from physical signs.

i The American Journal of the Medical Sciences, 1895, p. 692.
2 Ibid., 1896, p. 221.

8 A case of pseudo-atrophic cirrhosis of the liver, secondary to adherent pericardium, is
reported by Dr. R. H. Babcock, of Chicago, in the Medical News, December 14, 1901, p. 924.


We should not ignore the difficulty of explaining why pericardial
adhesions are occasionally followed by such changes. Wells gives sev-
eral good aud sufficient reasons why tuberculous synechia is less to be
feared than that which occurs in purely rheumatic cases. Among these
may be regarded slowness of growth, no valvular defects, no toxemia
affecting heart muscle. Moreover, he states heart dilatation occurs in
rheumatism at period of inflammation or later, when effusion is being

In the latter instance, as I have already pointed out, the pericardium
becomes dilated and softened, and thus fails to give the heart proper
support. In addition to this, however, if the pericardium is attached to
the chest walls it simply cannot follow the heart, owing to mechanical
conditions. For this reason, again, the heart yields more and more to
internal pressure, and consequently becomes more and more dilated,
weak, inefficient, and ultimately powerless.

In these cases we often find beneath a very thick pericardium a con-
siderable growth of connective tissue, together with a deposit of fat in
the superficial parts of the heart muscle. 1 In rare instances are we able
to demonstrate the existence of gray tubercles in the myocardium.
Where caseous deposits are found at the autopsy they are more impor-
tant because they have penetrated the heart wall deeply, and in the
event of perforation they serve to explain the transport of numerous
bacilli in other organs and the signs of general miliary tuberculosis,
which are easily recognized, even during life.

The usual termination of tuberculous pericarditis is death. This
may be brought on directly by the recurrence of a large effusion, fre-
quently hemorrhagic, which repeated tapping has failed to relieve. Of
course at times the adhesions which have formed to chest walls, lungs,
and diaphragm seem greatly to shorten the duration of life ; but these
again may never occur, and the heart may simply float freely in the
fluid which surrounds it more or less on all sides. 2 Often, as I have
said, the fatal ending is immediately attributable not to the heart itself,
but to the general miliary tuberculosis of different viscera with which
the cardiac condition is associated.

Death may occur from an embolism, but this is extremely rare. 3
" Tuberculous pericarditis is generally unaccompanied by any symptoms
referable to the heart, and is almost always an autopsy finding." * With
this statement of Wells, corroborated by Osier, 5 judging by my two
recorded cases, I should be inclined to differ.

For the cases which are slowly and insidiously developed there is little
or no local treatment to be advocated. This is true of the cases which

1 Second case reported by me. 2 See my first case— pathologic report.

3 Case 8, reported by Wells. 4 Loc. cit, p. 1458.

6 Already cited.


terminate in synechia and where the symptoms are frequently very
obscure. The systolic retraction of the nipple in these instances is a
deceptive sign, as more than once I have been able to observe. In this
connection Lee Dickinson states we may have pulling in of lower ribs
with systole, but adds that cases with this indication are seldom avail-
able. The most characteristic of all indications " are rapid progress of
the case to the fatal end and the signal failure of all known means of
relief in heart disease." 1

Inasmuch as there is small effusion and no obvious inflammation,
these two conditions may not require active interference. In those
instances in which the onset of the disease is acute it is indicated at
first to limit the amount of inflammation. Personally, I favor the local
use of poultices or hot flannel stupes. To the former mustard may be
added ; the latter may be sprinkled with turpentine. Equal parts of
soap liniment and turpentine applied for several hours on warm flannel
are recommended. If cold be employed I much prefer Leiter's coil to
an ice-bag. The latter is difficult to keep in place and causes distress
from cold at times, which we cannot regulate easily. 2 A small quantity
of morphine hypodermically may be called for to allay pain. In the
cases that I have seen I have not thought the cautery or blisters were
required in the beginning of the attack. Later, I am confident, repeated
small fly blisters may limit the amount of the exudate formed. It is
also possible that an effusion already formed may thus be made to dis-
appear, in part or wholly, and more rapidly than it otherwise would.
Despite what has been said, it is far wiser in many cases not to attempt
to influence the pericardial condition by any local application. When-
ever the effusion becomes considerable or excessive, paracentesis should
be thought of. If the lips and fingers become cyanosed — if there is
marked dyspnoea, and weak, frequent, irregular pulse — prompt with-
drawal of fluid is necessary to preserve life. If, before paracentesis is
performed, the exploring needle shows the presence of pus, it is more
judicious, in many instances, to incise the sac freely and introduce a
drainage-tube. Of course, if the condition of the patient is imminent,
paracentesis may first be performed and subsequently the more radical

The position of the heart with respect to pericardial effusions is fre-
quently undetermined. In purulent fluids the heart is supported by or
floats upon the fluid, and is carried directly against the chest walls.
This has been proven experimentally. In fluids containing some blood,
or in pure serum, the heart is surrounded by fluid, as a rule, of which
the larger quantity is in the lower and left lateral portion of the peri-
cardial sac.

1 The American Journal of the Medical Sciences, 1896, p. 696.

2 Of course we can put a towel or flannel compress underneath.


Whenever puncture of the heart is indicated, some hesitancy arises
in performing the operation on account of the danger incident thereto.
There is risk of wounding the mammary artery, of entering the left
pleural cavity, of puncturing the liver, of wounding the peritoneum, or,
indeed, of going through the diaphragm. Perhaps the latter is of no
special moment, as it is the way by which entrance to the pericardium
is occasionally suggested or taken by the surgeon in a radical operation.

The classical site for aspiration of the pericardium may be regarded
as the left fifth interspace, near the sternal margin. 1 Other regions,
however, have been tried more or less successfully — i. e., beyond the left
nipple and near the outer line of cardiac dulness ; in the right fourth
intercostal space ; in the angle of the xiphoid cartilage and the margin
of the left costal arch. The right interspace is specially indicated by
Dr. Rotch, of Boston, in those cases where he has found dulness over
this area. 2 Dr. F. C. Shattuck, in his able paper before the Association
of American Physicians, Washington, 1897, has tried different points
for aspiration of pericardium, with satisfactory and sterile results.

On one occasion where a small quantity of fluid was withdrawn, later
the autopsy showed at least one pint of fluid in the sac. It may be
inferred in such cases that the fluid thus discovered was produced
during the agony or after death. It seems to me more probable that it
was in the pericardial sac during life, but could not be aspirated on
account of the position of the heart and the wrong point of puncture.
In this connection I am glad to be able to refer to a recent able article
by Dr. O. Damsch, 3 which settles definitely, it may be, most points
hitherto questionable about the position of the heart, that of the effu-
sions, and the point where we should always try paracentesis. Dr.
Damsch made injections experimentally into the pericardium, the sub-
ject being in the upright position, for the purpose of determining the
position assumed by the pericardial exudate. Small amounts, he found,
collect in the lower and anterolateral portions of the pericardium, caus-
ing approximation of the right anterior portion of the pericardium to
the chest wall. The heart, when of normal size, was always found
pressed against the posterior portion of the pericardium, the fluid occu-
pying the anterior portion. In cases in which the heart was hyper-
trophied it was pressed upward and anteriorly, Its increased size,
according to Damsch, causes it to fill the whole space between the
anterior and posterior chest walls, and therefore, since the fluid collects
in the lower part (pericardium), the heart must be pressed upward.

1 Roberts states (Trans. Surg. Assoc.) that this point of election " will not assure safety to
the pleura."

2 The clinical conclusion from Damsch's experiments was that "first sign of pericardial
effusion would be an area of dulness in heart-liver angle, as taught by Rotch." (Lot. cit.)

3 Gould's Year-book, 1901, pp. 178, 179.


" From his experiments he decides that the best position for puncture is
well down toward the lower part of the pericardium." He also decides
that puncture in the fifth or sixth intercostal space (left) next to the
sternum, directing the trocar somewhat inward, is the safest method and
location of paracentesis. Thus performed there is no danger of wound-
ing either heart or pleura. If the heart is normal the fluid is in front
of it and at lower part of pericardium ; if the heart is enlarged, which
it usually is, it is floated upward and out of danger.

Aspiration of the pericardium relieves, without doubt, for a while
imminent symptoms, and, as an operation of urgency, should be em-
ployed unquestionably. When we come to consider it as a curative
means it is of less value. I have seen the fluid recur several times
after it has been removed, and that, too, in a relatively short period.
This statement is true of instances in which the pericarditis, either at
that time or subsequently, was known to be tuberculous. One is thus
led to ask whether in these instances it is not preferable to perform a
radical operation with proper surgical technic and thorough drainage
of the pericardium. In purulent cases the general consensus of good
surgical judgment is to that effect. In tubercular cases where the
effusion is not purulent it may be also a wiser procedure than simple
puncture, because through the open wound the finger may be intro-
duced and large masses of fibrin extracted. These masses, if allowed to
remain in situ, inevitably delay cure by allowing fluid to re-form rapidly.
After a reproduction of fluid on one or several occasions, adhesive peri-
carditis may and does develop, and, sooner or later, we have to do with

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