Extracted from the 
TRANSACTIONS OF THE COLLEGE OF PHYSICIANS OF 
PHILADELPHIA. 
THIRD SERIES, VOLUME IV. CASE 
OF 
ULCERATIVE ENDOCARDITIS WITH PYAEMIA; 
DEATH FROM PERFORATION OF 
THE HEART. 
By 
JOHN M. KEATING, M.D., 
PHYSICIAN TO THE PHII.ADEPHIA HOSPIT 
[Read June 5, 1878.] 
M. S., set. 34 years, was admitted to the Medical Ward of 
the Philadelphia Hospital on a Monday in April, 1878. 
The patient had the appearance of being well nourished; 
was a washerwoman; was married ; had had two children; 
and stated that she had never been sick before in her life. 
Rheumatic history was carefully searched for, but none ob- 
tained ; she denied ever having had syphilis, and no eruption 
nor scars were found to disprove her statement. She com- 
plained of obscure pains in the joints, and of muscular pains, 
but when questioned closely stated that the feeling was one 
of stiffness rather than pain, the symptoms all being of very 
moderate intensity. There was a rise in temperature. She 
was seen that evening shortly after admission by the resident 
physician, who, thinking the case to be one of muscular rheu- 
matism, ordered her a dose of jaborandi. The following 
morning she expressed herself as feeling perfectly well, she 
had sweat profusely, and the temperature was nearly normal. 
Owing to my absence, my colleague, Dr. Edward T. Bruen, 
who had temporary charge of the ward, and to whom I am 
indebted for the following notes of the case, after instituting 28 
KEATING, 
rigid inquiries which elicited the above history, made a care- 
ful examination. 
Upon percussion the heart was found in its normal posi- 
tion, and not hypertrophied; the apex beat was normal. The 
pulse was regular, rather small, resembling that found in 
cases of mitral regurgitation. Auscultation revealed a basic, 
systolic murmur, but this murmur w7as transmitted down- 
wards to the ensiform cartilage, and was heard louder at that 
point than at the base. There was also a murmur at the 
apex, and this was slightly transmitted to the axilla. The 
murmur was not found in the arteries of the neck, nor wras 
either murmur heard in the back. The first murmur was 
blowing, low in pitch, and occupied the whole of the systole. 
At times the radial pulse became more feeble for one or two 
consecutive beats, and then the murmur wras faint or entirely 
absent. The venous system was moderately engorged 
throughout, but there was no venous pulse. This moderate but 
still marked engorgement was more than could be accounted 
for by the apparently slight valvular lesion. The second 
sound of the heart was impaired ; it was hut feebly accentu- 
ated, and had not the clear, defined characteristics of health. 
The lungs were normal throughout. There was no dys- 
pnoea. There had never been hemorrhages. There had 
never been dropsy, nor had the patient suffered from head- 
ache. The urine was not albuminous. The patient stated 
that she had of late suffered at times from gastric irritability, 
and that this still remained. She was ordered the Tinetura 
Ferri Chloridi, and a pill of Digitalis gr. ss, Quiniae Sulphat. 
gr. ss, Extract. Gentianse gr. j, thrice daily. 
The report on Thursday morning stated that the patient 
had vomited all through the night. The temperature on the 
previous evening had been very high, but wras now, as will be 
seen by the temperature chart (Fig. 1), lower than normal. 
There was slight joint pain, no tenderness, and no other bad 
symptoms. Heart the same as before. Medicine discontinued. 
During the day the vomiting ceased, the pain disappeared, ULCERATIVE ENDOCARDITIS. 
29 
and the patient felt comparatively well; in the evening the 
thermometer again sliowTed a rise. 
Friday morning.—Patient seems perfectly well. She asked 
to get up, but this was forbidden. In the evening the tem- 
perature again rose. She was unusually bright. 
Saturday morning.—The patient sat up in bed about six 
o’clock to arrange her hair, when she complained of sudden 
and great dyspnoea, and intense pain. Shortly afterwards 
she became almost collapsed; the feet and hands were cold, 
and the body blue and covered with sweat; the facial expres- 
sion anxious; and the radial pulse almost imperceptible. 
The respirations were very rapid. 
Fig. 1. 
When seen by Dr. Bruen, at ten o’clock, these symptoms 
continued unabated. He at once examined the heart, and 
found upon percussion a dulness reaching from the second to 
the sixth rib on the left side, and from the right sternal bor- 
der four inches to the left. This broad area of dulness ex- 
tended over the whole region of the pericardium. Surround- 
ing this area of dulness, pulmonary resonance was clearly and 
sharply defined. Palpation revealed no apex beat. The 
sounds of the heart were scarcely audible, and were distant; 
but when distinguished, as they occasionally were, an absence 30 
KEATING, 
of murmur was noted. The respiratory murmur was harsh, 
but was heard distinctly everywhere. The diagnosis of ex- 
tensive pericardial effusion of course was clear. The very 
sudden onset explained the gravity of the symptoms. 
It will now be seen that as the temperature and vomiting 
indicated pyaemia, and the murmurs revealed an endocardial 
roughening, the diagnosis of ulcerative endocarditis with 
rupture of the heart seemed plausible. On this account 
paracentesis was deemed unnecessary. During the day the 
severity of the symptoms decidedly ameliorated, and at 5 
P. M., when again seen, the patient expressed herself as feel- 
ing better; she was, and had been, perfectly conscious; the 
pulse could be felt at the wrist; the general surface of the 
body was warmer; and the heart sounds more audible, and 
with no murmur. The precordial pain had entirely disap- 
peared. 
The patient continued to do well till ten o’clock that night, 
when suddenly the above-mentioned symptoms returned with 
all their previous intensity, and she died in a few minutes. 
A post-mortem examination was made fourteen hours after 
death. Body well nourished ; no scars anywhere to be seen, 
and no evidence of specific disease. 
When the sternum was removed, the pericardial sac was 
found distended to a very great degree. The lungs appeared 
somewhat engorged, but there was no oedema, and otherwise 
they were perfectly healthy. When the pericardium was 
opened, about twelve ounces of fluid blood were removed, 
with a lairge amount of clots of various sizes. Adherent to 
the heart was a stringy clot, which, when traced to the point 
of its apparent origin, was found attached to a process 
springing from the base of the aorta posteriorly, at the junc- 
tion of the aorta and the cardiac muscle. An opening was 
carefully searched for at the place where the clot was adhe- 
rent, and one was found so small as scarcely to deserve the 
name, being merely large enough to allow the passage of a 
No. 8 needle. The process mentioned above was teat-like in ULCERATIVE ENDOCARDITIS. 
31 
shape, and about half the size of an ordinary nursing-bottle 
nipple ; it was composed of the outer sheath of the aorta. 
Fig. 2. 
The left ventricle being opened, presented a healthy ap- 
pearance as far as the size of the muscular structure and its 
condition were concerned. There was no fatty degeneration, 
and no hypertrophy. The mitral valves were healthy ; the 
aortic were sufficient; and the general appearance of the en- 
docardium was healthy with the exception of a spot below 
the origin of two of the aortic valves, where there wTas a 
crater-like mass about the size of a dime, which with jagged 
edges surrounded an orifice communicating by a narrow sinus 
with the teat-like process before mentioned. This ulcer 
opened by a larger opening, probably big enough to transmit 
a lead-pencil, into the right auricle, just inside the attach- 
ment of the internal leaflet of the tricuspid valve. A mass 
of fleshy granulations, resembling in size that found in the 32 
KEATING, 
left ventricle, surrounded the opening here also, and that 
portion of it nearest the right ventricle had no doubt inter- 
fered so with the proper closure of the tricuspid valve as to 
give rise to the systolic murmur there heard. Otherwise the 
right cavities of the heart were normal in every respect. The 
pulmonary valves were not in the least affected, even by thick- 
ening, nor were the tricuspid valves at all diseased. No athe- 
roma was anywhere visible. All the other organs were in 
perfect health. 
Death from perforating ulcer of the heart is cer- 
tainly of great rarity. But few cases are found on 
record, with an ante-mortem history so complete as 
to permit of, at least, a supposition of the origina- 
ting cause of the occurrence. The symptoms re- 
corded in the many reports of cases of heart-rupture, 
are very vague and obscure, relating as they all do 
simply to the rupture, not to the cause; the data that 
we have to base our clinical studies upon, are, the 
verdict of the coroner’s jury and such information as 
can be gathered from the statements of friends. 
Intrinsic diseases of the heart,1 such as fatty degene- 
ration, etc., are the usual causes of rupture, and as 
such pathological changes are found in persons past 
middle life, rupture of the heart is usually found at 
that age. Markham’s2 report of twelve cases of heart 
rupture, excluding those of traumatic origin, taken 
from the first seven volumes of the London Patho- 
logical Society’s Transactions, shows us that the 
youngest patient was 52 years of age, the oldest 79. 
Seven were men, five women. In nearly all, if not in 
all, the coronary arteries were diseased. Quain3 reports 
1 Sehroetter. Ziemssen’s Cvclopoedia of Medicine, vol. vi. 
2 Medical Times and Gazette, 1859. 
3 Lancet, vol. i. 1872. ULCERATIVE ENDOCARDITIS. 
33 
88 cases—G3 in persons over sixty, 33 between sixty 
and seventy, and the remainder between seventy and 
eighty years of age. He states that in many cases no 
symptoms whatever were noticed antecedent to the 
death agony. Out of 100 cases, death occurred in one 
or two minutes in 71; one patient lived eight da}7s; 
one six days; one three days; and five over forty- 
eight hours. The heart was fatty in 77 cases, and in 
0 “ softened.” In one case there was bursting of an 
aneurism, and in one the rupture was due to an ab- 
scess. Acute disease of the endocardium or of the 
heart substance may lead to the same result, h}r the 
formation of an aneurism through the yielding of the 
endocardium at any point, in the former case, or by 
localized myocarditis with the formation of an abscess, 
in the latter. In interstitial inflammation of the heart, 
the pus formed, following channels, may burrow in 
various directions. As the foci of inflammatory ac- 
tion are occasionally discrete, and oft-times limited 
in number, they have been called cardiac abscesses.1 
When they ulcerate through the endocardium or begin 
in that tissue, they form ulcers. 
Senac,2 in 1719, first pointed out that ulcers or ab- 
scesses of the heart were more frequently found 
at the base, referring at the same time to diseases of 
the pericardium and neighboring organs as their im- 
mediate cause. Deitrich in 1852 made the same ob- 
servation. They usually occur between the ages of 20 
and 40.:i According to Schroetter, “primary disease 
of the heart substance is very rare. There are only a 
1 See an interesting article on this subject in Hayden, Diseases of the 
Heart and Aorta. 
2 Schroetter, loc. cit. 
s Ibid. 34 
KEATING, 
few cases described where no possible cause could be 
ascertained.” Syphilis is stated by the same writer 
to be a cause. The acute fevers, especially typhus, are 
among the many causes that have been assigned for 
abscess of the heart and ulcerative endocarditis, but 
rheumatism, according to most authors, is the most 
frequent. The puerperal state has an equal tendency 
to this result, and the so-called metastatic abscesses 
are found in all active muscular organs having poor 
nutrition. Pyaemia is then the most prolific cause. 
But ulcerative endocarditis, according to Lance- 
reaux,1 is not always an off-shoot of the rheumatic pro- 
cess; the high temperature, vomiting, and chills, with 
sudden syncope, which may disappear or may be fol- 
lowed by death, are really the symptoms of the con- 
current pyaemia. Lancereaux believes that purulent 
ulcers of the endocardium may be the result of intense 
malarial poisoning, but that they are then never situ- 
ated on the valves themselves, but occupy the heart 
lining at the valvular attachments, and produce death 
either by perforation or by pyaemia. In support of 
his view he quotes the observations of Winge and 
Heiberg, verified in one case by Virchow, where vibri- 
ones of filiform shape were found in the ulcers. 
It may be interesting to glance over the cases re- 
ported that bear upon this intricate subject, and en- 
deavor to gather what we can to complete its etiology. 
As an example of secondary abscess of the heart 
caused by metastasis or thrombosis, may be cited the 
case reported by Dr. Moxon,2 of a child at Guy’s Hos- 
pital with suppurative periostitis, where death resulted 
‘ De l’Endocardite vegetante ulcerease; Archives Generates, 1873. 
2 Medical Times and Gazette, vol. ii. 1872. ULCERATIVE ENDOCARDITIS. 
35 
from multiple cardiac abscess. There were abscesses 
in the kidneys also. 
Dr. Inman1 reports the case of a man of 35, who 
had complained of “ague-shakes” for three or four 
hours daily, during seven or eight months. There 
was no malarial history. Nothing wrong could be 
detected with the heart or lungs. The patient’s intel- 
lect seemed affected as in the early stage of typhoid 
fever, and he had a yellow, jaundiced complexion. 
The man died suddenly. After death there was found 
an extensive abscess at the base of the pulmonary 
artery, and this abscess communicated with the right 
ventricle behind one of the valves of the artery. 
Around this opening a fleshy vegetation existed about 
the size of a horse-bean. The lungs contained dif- 
fused and infiltrated pus. This patient’s case was 
evidently one of primary suppuration of the gland in 
that vicinity, from which pus had been thrown into 
the venous current for some time. 
The most interesting case, and the only one that I 
can find analogous to that which I have had the honor 
to report, is one given us by Heslop,2 of a girl aged 18. 
There was no heart murmur, but the action of the organ 
was tumultuous and irregular. On the patient’s admis- 
sion to the hospital, she stated that she had had rigors, 
followed by flushes of heat, but never any rheumatism. 
She was a weak, anaemic girl, and died in convulsions. 
The part of the endocardium immediately beneath the 
semilunar valves (in the left cavity5), presented an 
1 Ibid. vol. i. 1862. 
2 Medical Times and Gazette, vol. ii. page 245, 1856. 
3 Hanska (Medical Times and Gazette, 1855) is quoted to have shown, 
by 300 examinations of hearts, that there was in the normal septum a spot 
varying iu size from a beau to an almond, entirely destitute of muscular 36 
KEATING, 
irregular, eccliymosed surface, and had the appearance 
of being undermined, leading to the base of the aorta. 
At the attachment of the middle and anterior segment 
of the valves, was a mass of fibrinous deposit the size 
of a small walnut, surrounding a cavity containing a 
recently formed coagulum, pus, etc.: it did not perfo- 
rate. It was noticed that two days before death a 
continuous blowing sound was heard, accompanying 
and masking both first and second sounds. The pa- 
tient had vomited at the commencement of the attack, 
and there was epigastric tenderness; rigors set in 
early, and the skin was jaundiced. Death took place 
in all probability from pyaemia.1 
Greenfield notes, for Dr. Murchison,2 a man aged 
56, in whom the temperature from May 7 till June 1 
varied, with nightly exacerbations, from normal to 105° 
Fahr. The rigors occurred at irregular periods, some- 
times more than once daily. The mitral valves were 
thickened, and the aortic slightly affected; the tricus- 
pid valves also were thickened. There was a granu- 
lating, white mass, an eighth of an inch thick and a 
quarter of an inch long, on the border of one flap; the 
heart was the seat of fatty degeneration. 
substance, the two chambers being there separated only by the layers of 
endocardium that line them. Examining the septum from the left, after 
slitting up the aorta, we may remark a thin diaphanous spot under the angle 
formed by the convex borders of the right and posterior semilunar valves of 
the aorta, being closed above by a thin musculoid bundle, coursing along the 
contour of the ostium arteriosum sinistrum. In the right ventricle, the de- 
privation of muscular substance is covered by the end of the tricuspid valve, 
and so thin is the duplicature of the endocardium that the lines and mark- 
ings of the fingers held under it can be seen through. 
1 In Watson’s Practice I find it stated that “ a Duchess of Brunswick died 
of rupture of the heart. In her case an ulcer penetrated the parietes of the 
right ventricle, which in other respects was healthy.” 
2 Lancet, vol. i. 1873, page 909. ULCERATIVE ENDOCARDITIS. 
37 
Cases have been recorded where friction was sug- 
gested as a cause of endocardial nicer, by Dr. Hodg- 
kin, Dr. Hilton Fagge, and others. Coupland1 records 
a case with an aneurismal pouch starting from a nod- 
ule on an aortic valve which directly faced it. 
In this short resume of a subject about which 
really so little has been written, it will be seen that ulce- 
rative endocarditis is looked upon as secondary to vari- 
ious affections and diatheses; as a 'primary disease it 
must be looked upon as rare, particularly when limited 
to one spot, as it was in Heslop’s case and in that which 
I have reported; in fact, in the above cases it may even 
be attributed to a cachexia, where a focus of inflamma- 
tion started either in the connective tissue of the heart, 
or in the endocardium, resulting in an ulcer which, 
small as it was, induced pyaemia. Suppurating pro- 
cesses near the heart may involve it in their progress, 
as we have already seen; again there is no reason why 
metastatic infiltration or infectious embolism, may not 
occur and give rise to phenomena so intense as to 
mask the primary irritation; or thrombosis of the car- 
diac veins or of atheromatous coronary arteries, may 
be a cause, in persons advanced in years. Malaria, 
from pigmentous deposit or otherwise, may give rise 
to embolism, or, if the germ-theory be accepted, the 
emboli may be charged with bacteria. But notwith- 
standing all these varied causes assigned by authors, 
undoubtedly some cases exist unaccounted for, and 
that which I have had the honor to report stands boldly 
forth as an example. 
In a strong, healthy woman, bearing evidence of no 
1 Lancet, vol. ii. 1875. 38 
KEATING, 
previous disease, with all the other organs in perfect 
health, a small ulcer situated in healthy tissue demands 
an explanation which none of the cases I have cited 
throw light upon. The process without doubt had 
been going on for some time. Could some congeni- 
tal malformation, some previous strain, or the puerpe- 
ral state, have laid the foundation of disease at a point 
where the blood current was directly and forcibly im- 
pinging; or shall we attribute the rupture to an ab- 
scess of a lymphatic gland within the heart substance? 
But take it as we may, it serves to prove that, as 
far as we know, such cases can occur spontaneously, 
or rather idiopathically. 
Among the many points of interest in these cases, 
we have the temperature. A small quantity of pus, 
measured by the drop alone, gave rise in this case, and 
in others I have cited, to the most marked symptoms 
of pyaemia, viz., hectic, vomiting, and, in some, jaun- 
dice, chills and convulsions. 
In the patient spoken of by Dr. Inman, the pyaemic 
symptoms had lasted many months, and the fleshy 
vegetation at the cardiac opening of the abscess 
showed that pus had been intermingling with the 
blood for some time. The same existed in Heslop’s 
case, and also in mine. 
The only symptom then that marks this disease is 
pyaemia—pyaemia coming on suddenly, and usually 
associated with some cardiac disturbance, or else with 
embolic infarction of other organs. Of course the 
symptoms of pyaemia are severe1 in proportion to the 
amount of pus entering the circulation, or to the non- 
resisting power of the nerve centres to its poisonous 
1 Medical Times and Gazette, October, 1877. ULCERATIVE ENDOCARDITIS. 
39 
action. Chance1 speaks of a boy aged 13, who, ap- 
parently in perfect health but with a scrofulous dia- 
thesis, was attacked one day immediately after eating 
with nausea and vomiting. The next day he became 
drowsy, and complained of feeling very sick with pain 
in the stomach. Finally, complete coma set in, with 
rapid and fluttering pulse, and occasional convulsive 
movements. lie died in two days from the beginning 
of the attack. There were multiple abscesses of the 
heart, with perforation and pericarditis. Here nothing 
was observed until perforation into the pericardium 
had taken place. But in all cases where ulcerative 
endocarditis has been found, a rise in temperature has 
been noticed. 
Jaundice may be said to be dependent on the length 
of the attack; in those where pus was pouring into 
the circulation for some time, it was always noticed, 
but not otherwise. 
Vomiting has always been present, both in the 
very acute and in the more prolonged cases, though 
usually it has been more frequently seen in the former, 
as tolerance seems to have been established in the 
latter cases. I would call attention to the fact that in 
Heslop’s case there was no stupor characteristic of a 
typhoid state, nor septicaemia, but that the patient 
died in convulsions. In the case reported by me there 
was consciousness to the very last. Patients dying 
of puerperal pyaemia also exhibit this peculiarity. 
As regards physical signs, there is nothing that 
will aid us in diagnosis until perforation takes place. 
If the abscesses are numerous or confluent, irregularity 
1 Lancet, vol. i. 1846. 40 
KEATING, 
and tumultuous action of the heart may aid us. If 
ulceration takes place, murmurs will he produced, dif- 
fering in character and position from those of valvular 
lesions, unless the action of the valves should he inter- 
fered with. It may be well to state here that old val- 
vular deposits, from rheumatism or other causes, may 
become caseous and break down,1 causing at times 
pyaemia or embolic infarction in other organs (second- 
ary ulcerative endocarditis). The murmurs heard in 
such cases would of course be limited to the valves 
affected. The corporeal endocarditis of acute specific 
fevers, such as puerperal or searlet fever, or pyaemia, 
may lead to ulceration, and ulcers will then form on 
the papillary muscles, often eroding them.2 
In Greenfield’s case, there was heard at the ensi- 
form cartilage and over the lower part of the sternum, 
a loud, systolic murmur which became fainter towards 
the left, but was replaced on that side by a rough, sys- 
tolic murmur, apparently distinct and conducted to 
the angle of the scapula; all the valves, as we have 
seen, were affected more or less, and hence the mitral 
regurgitant murmur; the tricuspid murmur was aided 
by the fleshy mass spoken of. In Ileslop’s case there 
1 See case by Pepper, Transactions of the Philadelphia Pathological 
Society, vol. iv. 
2 Dr. Harrison Allen, in answer to a note from me, kindly gives me his 
opinion on this subject, as follows: “The researches of Schweigger-Seivel 
show that lymphatic vessels are in abundance beneath both pericardium 
and endocardium, and from these two localities freely communicate by ir- 
regular spaces in the muscular structure of the heart-wall. I presume that 
an analogous arrangement exists in the septum between the endocardial 
surfaces of the right and left hearts. The glands are outside the cardiac 
figure, at the base. I could not localize an abscess at the base of the ven- 
tricular septum by reason of any known disposition of lymphatic glands or 
vessels.” ULCERATIVE ENDOCARDITIS. 
41 
was no murmur, but the action of the heart was “ tu- 
multuous and irregular.” In my case, the aortic 
valves showed no insufficiency, but at times there was 
slight systolic roughening; the tricuspid murmur was 
well marked, but the feeble mitral-systolic murmur 
was not transmitted to the back, and may have been 
due to the granulations changing the course of the 
blood current. 
In conclusion, then, I think that we can safely assert 
that primary abscess of the heart, or primary ulcera- 
tion, if it proceed far enough, independent of general 
myocarditis, is occasionally found.1 I cannot offer any 
explanation except that it may be due to disease of the 
lymphatic channels or the glands. I have no doubt that 
many of the cases recorded as secondary ulceration, 
and attributed to multitudes of causes, were in reality 
cases of this kind occurring in persons of strumous 
diathesis. Can we proceed farther, if we accept this 
theory, and give credit to small abscesses of lymphatic 
origin, in the heart or arteries, in early life, for the 
starting point of many of those obscure cases of aneu- 
rism where the absence of atheroma is noted? 
Of course little is to be said under the head of treat- 
ment. When the cases come to us they are usually 
beyond our aid. Cases have gotten well, and, after 
death from other causes, calcareous nodules have, it is 
said, been found imbedded in the heart muscle. 
1 Hayden, Diseases of the Heart and Aorta ; Article on Myocarditis.