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Another Random Scribd Document
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erysipelas, etc. The myocarditis accompanying acute endo- or
pericarditis may lead to dilatation, especially in the latter disease.
The cavities are usually large in fatty degeneration or infiltration
from the relaxed and atonic state of the walls. In anæmia,
leukæmia, and chlorosis the dilatation of the chambers may be
considerable. In fibroid degeneration the wall generally yields where
the process is most advanced, as at the left apex. The impaired
nutrition in coronary disease may lead to dilatation. Under any of
these circumstances the walls may yield with normal blood-pressure,
or if increased tension is present the effect is the more readily
produced.
65 Goodhart, Guy's Hospital Reports, Series iii. vol. xxiv.

66 Samuel West, Barth. Hospital Reports, xiv.

Pericardial adhesions are usually spoken of as a cause of dilatation,

acting by traction from without, and we generally find in a case of
extensive and firm union considerable hypertrophy and dilatation. In
this condition there is usually some impairment of the superficial
layer of muscle which may permit of over-distension.

MORBID ANATOMY.—Usually the condition exists in two or more

chambers, and is associated with hypertrophy, the appearances of
which have already been described. It is more common on the right
side than on the left. Perhaps the most general dilatation which we
see is in cases of aortic incompetency, in which all the cavities may
be enormously distended. In mitral stenosis the left auricle is often
trebled in capacity, and the right auricle and ventricle also are very
capacious. The former may contain eighteen to twenty ounces of
blood. In many chronic affections of the lungs the right chambers
are chiefly affected. Dilatation with thinning is often the result of an
acute process met with in the fevers. The walls may be very much
thinner than normal, almost membranous, and the dark color of the
blood may show through with distinctness. When the distension of
one ventricle is very great, there may be a distinct bulging of the
septum toward the other side. The shape of the organ is altered,
and when the right chambers are chiefly affected it is more globular
in shape. Distension of the left auricle may render it visible in the
front of the heart, and the appendix may be prominent. The right
auricle when enormously enlarged, as in some cases of pneumonia,
in emphysema, and in leukæmia, may form a large mass occupying
a considerable space in the antero-lateral part of the thorax. The
walls in dilatation with thinning are flabby and relaxed, and collapse
at once when cut, but in dilatation with hypertrophy they are firm,
especially those of the right ventricle.

The auriculo-ventricular rings are often dilated, and there may be an

inch and a half, or even two inches, of increase in the circumference.
Thus, the tricuspid orifice, the circumference of which is about four
and a half inches, may admit freely a graduated heart-cone of over
six inches, and the mitral orifice, which is about three and a half
inches normally, may admit the cone to five and a half inches or
even more. Great dilatation is always accompanied with relative
incompetence of the valves, so that free regurgitation into the
auricles is permitted. The orifices of the cavæ and of the pulmonary
veins may be greatly dilated.

The muscle-substance varies much in appearance according to the

presence or absence of degenerations. The endocardium is often
opaque, particularly in the auricles. The microscopical examination
may show marked fatty or parenchymatous change, but in other
instances of dilatation and heart failure in eccentric hypertrophy
there may be no special alteration noticeable. I fully agree with
Niemeyer's assertion, "that it is not possible by means of the
microscope to recognize all the alterations of the muscular fibrillæ
which diminish the functional power of the heart."67 We know too
little as yet of the changes in the ganglia of the heart in these
conditions: as centres of control they probably have more to do with
cardiac atony and breakdown than we generally admit. Degeneration
of them has been noted by Putjakin68 and others.
 67 Textbook of Medicine, vol. i., Am. ed.

68 Virchow's Archiv, lxxiv.

SYMPTOMS AND PHYSICAL SIGNS.—Dilatation produces weakness of the

cardiac walls, diminishes the vigor of their contractions, and is thus
the very reverse of hypertrophy. So long as compensation is
maintained the enlargement of a cavity may be considerable: the
limit is reached when the hypertrophied walls can no longer in the
systole expel all the contents, part of which remain, so that at each
diastole the chamber is abnormally full. Thus in aortic incompetency
blood enters the left ventricle from the aorta as well as the auricle,
dilatation ensues, and also hypertrophy as a direct effect of the
increased pressure and increased amount of blood to move. But if
from any cause the hypertrophy weakens, and the ventricle during
systole does not empty itself completely, a still larger amount is in it
at the end of each diastole, and the dilatation becomes greater. The
amount remaining after systole is a cause of obstruction, preventing
the blood entering freely from the auricle. Incompetency of the
auriculo-ventricular valves follows with dilatation of the auricle and
impeded blood-flow in the pulmonary veins. Dilatation and
hypertrophy of the right heart may compensate for a time, but when
this fails stasis occurs in the venous system, with dropsy. The
consideration of the symptoms of chronic valvular lesions is largely
that of dilatation and its effects. Acute dilatation, such as we see in
fevers or in sudden failure of an hypertrophied heart, is accompanied
by three chief symptoms—weak usually rapid impulse, dyspnoea,
and signs of obstructed venous circulation. Cardiac pain may be
present, but it is often absent.

The physical signs of dilatation are those of a weak and enlarged

organ. The impulse is diffuse, often undulatory, and is felt over a
wide area, and an apex-beat or a point of maximum intensity may
not exist. When it does it may be visible, and yet cannot be felt—an
observation of Walshe's which is very valuable. An extensive area of
impulse with a quick, weak maximum apex-beat may be present.
When the right heart is chiefly dilated the left may be pushed over
so as to occupy a much less extensive area in the front of the heart,
and the true apex-beat is not felt; but the chief impulse is just below
or to the right of the xiphoid cartilage, and there is a wavy pulsation
in the fourth, fifth, and sixth interspaces to the left of the sternum.
In extreme dilatation of the right auricle a pulsation can sometimes
be seen in the third right interspace close to the sternum, and with
free tricuspid regurgitation this may be systolic in character. Whether
the pulsation frequently seen in the second left interspace is ever
due to a dilated left auricle is not satisfactorily determined. I have
sometimes thought it was presystolic in rhythm, though it may be
distinctly systolic. Post-mortem, it is rare in the most extreme
distension to see the auricular appendix so far forward as to warrant
the belief that it could beat against the second interspace. The area
of dulness is increased, but an emphysematous lung or the full
distended organ in a state of brown induration may cover over the
heart and limit greatly the extent. The directions of increase were
considered when speaking of Hypertrophy with dilatation.

The first sound is shorter, sharper, and more valvular in character,

and more like the second. As the dilatation becomes excessive it
gets weaker. Reduplication is not common, but occasionally
differences may be heard in the joint sound over the right and left
hearts. Murmurs very frequently obscure the sounds; they are
produced by incompetency of the valves due to the great dilatation,
or are associated with the chronic valve disease on which the
condition depends. The aortic second sound is replaced by a murmur
in aortic regurgitation; the pulmonary is accentuated in mitral
regurgitation and pulmonary congestion, but with extreme dilatation
it may be much weakened. The heart's action is irregular and
intermittent, and the pulse is small, weak, and quick.

The DIAGNOSIS is generally easy when the physical signs, the history,
and the general condition are taken into account. In a case of
valvular disease with hypertrophy the onset of dyspnoea and venous
stasis with dropsy tell unmistakably of cardiac dilatation. Increased
præcordial dulness, with a weak, diffuse impulse, is not simulated by
many conditions, and one only, pericardial effusion, need be
specially mentioned. This may present very serious difficulties, and
indeed a dilated heart has been aspirated under the belief that
effusion was present. The points to be attended to are—the greater
lateral dulness in dilatation and the wavy impulse which may extend
over a great part of it; in effusion the dulness extends upward and is
more pear-shaped, the impulse is not so extensive, and may be
tilted up an interspace or may not be visible. The sounds in
pericardial effusion are muffled and distant over the dull region, but
at its upper limit may be clear. The absence of friction is an
important negative sign. In some cases it is extremely difficult to
determine between the conditions, and I have known a weak,
feeble, irregular heart, with cyanosis, and oedema lead to the
diagnosis of dilatation when effusion was present.

The PROGNOSIS depends upon the cause of the dilatation. In anæmia

and fevers the temporary dilatation may undoubtedly pass away with
the improvement of health; but when the cause is not remediable
the danger must be measured by the presence or absence of
compensation. In the majority of the cases which we see the
dilatation occurs in valve disease, and no symptoms of importance
arise so long as the compensation is perfect. Failure of this, which
may result from many causes, as already mentioned, is always
serious. It may be only temporary, and with care the compensation
can be re-established and the symptoms pass away. We constantly
see this in the eccentric hypertrophy of the right heart from mitral
disease; an attack of bronchitis suffices to disturb the compensation,
and with the relief of the catarrhal trouble the dyspnoea and heart
symptoms disappear.

The TREATMENT of dilatation is virtually that of chronic valvular

disease, and we shall only refer to general indications. With the
earliest symptoms of failure the work of the heart should be reduced
to a minimum by placing the patient at rest. This in itself may suffice
without any other measures. Time and again I have seen,
particularly in cases of aortic insufficiency, the dyspnoea relieved and
the oedema of the feet disappear and the compensation re-
established by placing the patient in bed, enjoining absolute quiet
and carefully regulating the diet. The importance of rest in the early
stages of heart failure cannot be too much insisted upon.69 Quiet
and careful dieting may suffice for the milder attacks, but we have
usually even in these to resort to heart tonics. Digitalis is the most
powerful remedy we possess in restoring and maintaining
compensation. Under its use the irregular, feeble, and frequent
contraction becomes regular and stronger, and the embarrassed
circulation is relieved. In hospital practice the same chronic heart
cases may return year after year with attacks of cardiac failure,
dyspnoea, dropsy, etc., and each time the rest in bed and digitalis
may suffice to restore compensation. A fourth or fifth, even a sixth,
attack may be safely weathered, and then the final breakdown
occurs when nothing avails to combat the dilatation. Of substitutes
for digitalis, caffeine and convallaria have been much used of late.
Caffeine in some cases acts more promptly, which is an advantage,
but its action is not so certain and not so enduring. Convallaria is
very variable in its action; it has succeeded in some instances in
which digitalis has failed, and in others has been quite without
effect. In extreme cardiac failure with great dilatation, lividity,
orthopnoea, and feeble pulse, stimulants must be freely given; ether
may be employed hypodermically. In this condition of final
asystolism digitalis seems to have lost its influence. In the heart
failure of pneumonia I have found camphor a valuable adjuvant to
the diffusible stimulants. To improve the general nutrition, and with
it that of the heart-muscle, iron and arsenic are most valuable
adjuvants, especially in the dilatation of anæmia. The treatment of
special symptoms, dropsy, dyspnoea, etc., is considered under
Valvular Affections.
69 In Ortel's system (Ziemssen's Handbuch der Allgemeine Therapie, Bd. iv.) of
treating heart disease exercise, particularly climbing, forms a very important part, but
an analysis of his cases shows that most of them were instances of fatty heart in
obese persons. It would scarcely be applicable to valvular disease. The severe
exercise, he thinks, stimulates the heart-muscle and helps in the restoration of the
hypertrophy. His other suggestion, the reduction of the liquids ingested, seems much
more reasonable, as in this way the volume of blood to be circulated may be
considerably reduced.
 Aneurism of the Heart.

This term is now restricted to local or partial dilatations of the wall of

one of the cardiac cavities. Formerly, dilatation of the heart or of one
of its chambers was spoken of as aneurism. This rare condition70 is
most frequently associated with fibroid degeneration, but other
causes of local weakness of the walls, as ulcer, acute myocarditis,
and fatty degeneration, have been present in a few cases. An
instance is on record where the aneurism followed a stabbing wound
of the chest.71 The left ventricle is usually involved; very few cases
occur in the other chambers. The condition may be acute or chronic.
70 In the index catalogue there are references to only 18 cases by American authors.
In the museums of Philadelphia there are only 5 specimens—3 in the museum of the
College of Physicians; 1 each in the University and Pennsylvania Hospital cabinets.

71 Quoted by Legg, Bradshawe Lecture on Cardiac Aneurisms, London, 1883.

Acute aneurism is met with occasionally in ulcerative endocarditis,

more rarely as the result of local softening due to myocarditis or
plugging of a branch of a coronary artery. In severe endocarditis
perforation is, I think, more common than the production of
aneurism. In one case I saw a deep excavation at the upper part of
the septum produce a bulging the size of a marble in the wall of the
left auricle, and in another ulceration in one sinus of Valsalva had
extended into the septum, the upper part of which presented an
aneurismal dilatation which had ruptured into the left ventricle. Legg
considers the production of acute aneurism by the rupture of
abscesses or cysts as doubtful.

Chronic aneurism is almost confined to the left ventricle, and, as

Cruveilhier pointed out,72 is the result of fibroid degeneration of the
muscle. In a few instances fatty degeneration appears to have been
the cause. The monographs of Thurnam,73 Pelvet,74 and Legg75 give
the most complete account of the disease. They are more common
in men than in women, and the majority of the cases occur after
middle life.
72 Anatomie pathologique, Paris, 1835–42.

73 Medico-Chirurgical Transactions, vol. xxi., 1838.

74 Des Aneurysmes du Coeur, Paris, 1867.

75 Loc. cit.

The situation of the aneurism is most frequently at the apex—59 of

90 cases collected by Legg. They are usually rounded in shape, and
may vary in size from a marble to a cocoanut. The sac may be
double, as in a case described by Janeway,76 or, as in a specimen in
Guy's Hospital Museum, the whole wall of the ventricle may be
covered with aneurismal bulgings. In the simplest form there is a
rounded dilatation at the apex, and the lower part of the septum is
lined with thrombi. Often the tumor is distinctly sacculated, and
communicates with the ventricle by a very small orifice. The
pericardium is usually thickened, and calcification may occur in the
walls. Rupture seems rarely to occur—in only 7 of the 90 cases
collected by Legg. Of other parts of the ventricle, the septum and
the undefended space at the highest part of the septum just below
the aortic ring are most often involved. This latter situation is
sometimes the seat of a congenital dilatation, usually a small, thin,
smooth sac without thrombi, which has no pathological significance.
76 N.Y. Med. Journ., 1875, xxi.

Cardiac aneurisms rarely produce any symptoms, and in the majority

of cases have been found accompanying other conditions which
have proved fatal. At the left apex the increase in dulness and area
of pulsation could scarcely be distinguished from hypertrophy unless
associated with marked bulging. They seldom perforate the chest-
wall. Berthold (quoted by Legg) has described one connected with
the right auricle which produced a pulsating tumor beneath the skin,
the region of the second and third ribs.

Adventitious Products in the Heart.

Tubercle.—In general tuberculosis and in tuberculous pericarditis

there may be nodules in the heart-substance, but, as a rule, this
organ is very rarely the seat of tubercle. Large caseous masses
sometimes occur, but unless associated with tubercle in other organs
they are not to be regarded as necessarily tuberculous. Miliary
granulations have been seen on the valves.

Cancer and sarcoma rarely are primary, and are not often met with
as secondary growths. Sometimes a mediastinal sarcoma penetrates
along the veins and involves the auricle, with or without great
involvement of the pericardium. The secondary tumors may be
single or multiple. In a case of cancer of the uterus I found a large
mass in the wall of the right ventricle, involving also the anterior
segment of the tricuspid, and partially blocking the orifice. The
surface was eroded, and the pulmonary arteries contained numerous
cancerous emboli. In another instance the heart was considerably
enlarged by the presence of many rounded masses of colloid cancer
throughout the walls. In a remarkable case of sudden death in a
child I found the tricuspid orifice firmly blocked with a sarcomatous
mass which I thought at first had originated in the heart, but
dissection showed to have come from the renal vein, which was
filled with sarcoma extending from a large tumor of the kidney.
Melanotic cancer, fibromata, and myomata have occasionally been
seen, and a secondary epithelial growth has been described by
Paget.

Syphilis of the heart is met with in the form of gummata or as a

specific arteritis leading to patches of fibroid induration. The
gummous growths form tumors of variable size, which usually
occupy the septum or the ventricles. Possibly many of the caseous
and calcified masses not infrequently met represent obsolete
gummata. The syphilitic myocarditis probably originates in an
affection of the arteries, and leads to patches of fibroid induration
more or less extensive. Many authors hold that syphilis plays a very
important rôle in the production of fibroid heart.

Cysts.—Simple cysts are rare in the heart. I have met with two
instances—one, the size of a marble, situated in the wall of the right
auricle near the septum, was filled with a brownish fluid; the other,
the size of a small walnut, occupied the base of the posterior
segment of the mitral, and was filled with a clear fluid. Blood-cysts
occasionally occur.

Parasites.—The Cysticercus cellulosæ, the larva of Tænia solium, and

the hydatid or echinococcus, the larva of Tænia echinococcus of the
dog, are sometimes found in the heart. The former, usually single, is
extremely rare; in the hog and calf the measles, as the cysts are
called, very often exist in the heart-muscle. In the recent paper by
Mosler77 references are given to 13 cases of cysticerci in the heart.
The greatest number present was 19. The hydatid is more common:
25 instances are mentioned in the statistics of Devaine and Cobbold,
and Mosler's more recent figures only give 29. They occur in the
right ventricle more frequently than in the left. Occasionally they
attain a larger size and compress the heart and push back the lungs.
The cyst may burst and the contents be discharged into the
pulmonary artery or aorta, as in a case given by Osterlen,78 in which
gangrene of the right leg followed the plugging of the femoral by
hydatid vesicles discharged into the blood by the bursting of a cyst
in the left auricle.
77 Zeitschrift für klinische Medicin, Berlin, Bd. vi., 1883.

78 Virchow's Archiv, xlii.

 ENDOCARDITIS AND CARDIAC VALVULAR
DISEASES.

BY ALFRED L. LOOMIS, M.D.

Endocarditis.

DEFINITION.—Endocarditis is an inflammation of the endocardium, and

may be either exudative, neoplastic, or ulcerative in character. While
its different varieties are closely connected in their etiology, they are
distinct in the extent, duration, character, and course of their
pathological changes. They cannot be classified as acute and chronic
in the ordinary acceptation of these terms, for they often so merge
into each other as to render it difficult, if not impossible, to
determine when they cease to be acute and become chronic; and
some cases are at no time acute. It has been claimed that an acute
endocarditis becomes chronic when its course is prolonged, but the
advanced changes are only a stage of the acute process.

So-called acute endocarditis is accompanied by a fibro-cellular

exudation into the substance of, and underneath, the endocardium,
causing elevations of its surface. The better term for this variety is
exudative endocarditis, it being borne in mind that the exudation
does not take place upon the free surface of the membrane, but into
its substance and underneath it. This form of endocarditis may be
entirely recovered from, or it may lead to interstitial changes in the
endocardial and myocardial tissue which will correspond to the
changes usually described as those of chronic endocarditis.
Interstitial endocarditis is a better term for these changes. The
disease may be the sequela of exudative endocarditis, or may be
interstitial from its commencement, for the valvular changes of
interstitial endocarditis are often found in those who never have had
either acute articular rheumatism or exudative endocarditis, but have
been the subjects of chronic rheumatism or gout.

Acute exudative endocarditis may, in certain cases, be stamped with

an ulcerative process, the result of septic infection, giving rise to
those pathological changes which have been described as acute
ulcerative endocarditis.

HISTORY.—The history of endocarditis is restricted to modern

pathology. It is not spoken of by the older medical writers. Before
the sixteenth century knowledge of the structure and functions of
the heart was imperfect and scanty, and its diseased conditions were
altogether unknown.

The history of the pathology of cardiac disease commenced with

Harvey, Lancisi, Vesalius, and Vieussens. They investigated not only
the normal structure of the heart and the mechanism of the
circulation, but accurately described a few of its valvular diseases.

There is little doubt but that Laennec, Senac, and Morgagni were
quite familiar with the valvular diseases of the heart, but Kreisig first
traced the relationship between valvular diseases and inflammation
of the lining membrane of the heart.

The term endocarditis was first used by Bouillaud, who had the
advantage of Laennec's discovery of auscultation. Corrigan first
discovered the physical signs of aortic insufficiency. The most
important advance in the pathology of endocarditis is due to the
investigations of Virchow and Luschka, the former developing its
sequelæ or results, the latter its histological changes. Ulcerative
endocarditis is of modern date, and its literature scarcely extends
back twenty years. The labors of Kirk, Virchow, Charcot et Vulpian,
Moxon, Eberth, and Lancereaux are all connected with the etiology
and anatomical changes of ulcerative endocarditis.

The relationship of interstitial endocarditis to valvular diseases of the

heart and to cardiac murmurs is a subject which at present is
engaging the attention of many medical observers.

I shall describe endocarditis under three heads:

1st, Exudative endocarditis;
2d, Ulcerative endocarditis;
3d, Interstitial endocarditis.

That the pathological changes which I shall describe may be readily

appreciated, I will briefly review the anatomical structure of the
endocardium.

The endocardium consists of connective tissue, with numerous

elastic fibrils, covered by and continuous with a layer of flattened
cells. Upon this lies the endothelial layer, which disappears in twenty-
four hours after death.

Luschka regards the endocardium as continuous with all the arterial

tissues, but the majority of histologists consider it a continuation of
the internal membrane. Some regard the endocardium and inner
coat of the arteries as analogous, since both are non-vascular and
have an endothelial covering upon a connective-tissue base. As
endocarditis is, for the most part, limited to the valves of the heart,
a knowledge of their anatomical arrangement is important.

A transverse section of a segment of an auriculo-ventricular valve

shows that upon the superior or auricular surface and upon the
inferior or ventricular surface there are flattened cells and
endothelium, and that next to each lies a fibro-elastic layer, the
superior being the thicker. These two layers are separated by
connective tissue.
The layer of flat cells is thickest on the ventricular surface. The fibro-
elastic tissue is thickest at the base of the valve. The semi-lunar
valves have endocardium on one side and the tunica intima on the
other.

Although the endocardium has no vessels of its own, the capillaries

upon the cardiac walls are in contact with it. The arrangement in the
valves is different, as only a few vessels ramify between the layers of
the mitral valve, and none are found, normally, in the sigmoid
valves.

Acute Exudative Endocarditis.

This variety of endocarditis is met with most frequently in connection

with acute articular rheumatism.

In adults it usually has its seat in the left heart; in intra-uterine life it
occurs in the right heart. The inflammation commences in, and
seldom extends beyond, the valves and the valvular orifices, but it
may involve the whole or any part of the ventricular or auricular
portions of the endocardium.

MORBID ANATOMY.—The endocardium becomes infiltrated with young

cells, the process beginning in the layer of flat cells. The new
formative cells are developed not only from the cells of the layer
immediately underneath the endocardium, but also from leucocytes.
This hyperplasia, this heaping up of embryo-plastic cells, is
accompanied by softening of the deeper layers of the intercellular
structure, and as the softening goes on the intercellular substance is
destroyed.

The endothelial elements also play an active part in the processes.

The masses of new cells push out the endocardium, and papillary
elevations are formed, filled with a fluid whose chemical properties
resemble those of mucin, since it coagulates into threads when
acetic acid is added. The cone-like vegetation is surrounded in the
deeper layers of the endocardium by a zone of proliferation which is
never distinctly limited, but which exhibits progressive hyperplasia
from the periphery toward the centre.

All these changes may have taken place in non-vascular tissue.

Where the capillaries are most numerous a punctuate or arborescent
vascularity is seen, and this is followed by opacity of the part which
is the seat of the inflammation. After death the endocardium and
lining membrane of the vessels are often stained; this staining is
produced by the coloring matter from the red corpuscles, and is the
result of post-mortem change.

There is no exudation upon the villous projections; the coagula

found upon them are a deposit of fibrin from the blood, the
projections acting as foreign bodies in the blood-current. The
fibrinous deposits occur chiefly on the surface which is opposed to
the current of the circulation, and sometimes they are distinctly
conical; at others they have the shape of a raspberry. They occupy
the parts most exposed to the friction of the blood, and are arranged
on the borders of the aortic valves at a little distance from their
edges, the seat being determined by the limit of the vascular
network. The band of tissue which passes from the attached border
of the valve to the Arantian body in the centre shows the
inflammatory granulations most distinctly. They consist of a
cauliflower-like bulbous extremity, connected by a constricted neck
with a firm, hard base that is intimately blended with the subjacent
tissue. A thin hyaline layer covers each mass. At first these
granulations or vegetations are very small and numerous, so that the
membrane presents a granular appearance. Later, they become
larger, reaching oftentimes the size of a small pea.

Near the insertion of the tendons upon the auricular surface of the
mitral valve are found irregular wreaths of vegetations which enclose
the attachments of the chordæ tendineæ. Moxon has shown that the
friction of the vegetations or of fibrinous clots that gather upon the
vegetations may, by the irritation it produces, excite endocarditis at
points remote from the valves.

The tendon of the mitral valve may show the effects of endocarditis
by becoming soft and friable, and even rupturing, or the chordæ
tendineæ may adhere to one another. When such adhesions occur
either with agglutinations of the flaps to each other or to the heart-
walls, stenosis or regurgitation may result.

In connection with these changes new vessels are developed in the

substance of the mitral valve, or those that already exist become
more apparent. In the semilunar valves new vessels are formed or
neighboring capillaries send out prolongations into the parts
destitute of vessels. This, according to Charcot, is one way in which
arborescent vascularity occurs. These changes are most marked in
those forms of exudative endocarditis which run an acute course.

In some instances the hyperplasia is so extensive as to interfere with

nutrition, and may lead to fatty metamorphosis. A cavity is then
formed filled with granular fat-cells, discrete fat-globules, and blood-
pigment, whose endocardial covering ruptures, and the contents are
carried into remote capillaries to cause capillary embolism and
septicæmia. This has been called ulcerative endocarditis.

Ulcerative Endocarditis.

Ulcerative endocarditis occurs in those diseases where there is great

vital depression. It is met with oftenest in pyæmia, puerperal fever,
scarlatina, and diphtheria. It has been called septic, diphtheritic, and
infectious endocarditis.1
1 Jaccoud, Klebs.

MORBID ANATOMY.—Ulcers may form in endocarditis in either one of

three ways: 1st. The exudative process may be so rapid and
extensive as to cut off the nutrition of the endocardium covering the
apices of the papillary elevations, and ulcers result in non-septic
inflammation. 2d. Degeneration of the neoplastic tissue, due either
to deficient blood-supply or other causes of impaired nutrition, may
so soften the villi or efflorescences that their apices will be swept
away by the blood-current and ulcers thus be formed. Charcot
especially insists that the ulceration of these elevations is the
consequence of granular degeneration, and not of fatty
metamorphosis, with which it is often confounded. 3d. The
exudative process may be purulent in character, and form minute
abscesses in the substance of the valves beneath the endocardium,
which, rupturing, leave comparatively deep ulcers. Acute multiple
abscesses in the aortic valves are of frequent occurrence in
ulcerative endocarditis.

The margins of the ulcers are irregular, but well defined; the edges
are swollen and thick, and their floor (the muscular substance of the
heart or the fibrous layer of the valve) is infiltrated with pus.

Where there is extensive loss of substance perforation of the valve

may occur. These perforations are sometimes closed or hidden by a
fibrinous exudation.

The soft and friable vegetations may be torn into long shreds by a
forcible blood-current, and subsequently may excite endocardial
inflammation where they come in contact with the walls of the
heart-cavity, or they may break off and form emboli. A fibrinous
string upon a flap of the aortic valve is not infrequently driven down
and back by a regurgitant current, so as to excite endocarditis in the
mitral valve.

Some observers state that micrococci and bacteria are found in

ulcerative endocarditis of a septic or diphtheritic origin, and they
have given to it the name of mycosis endocardii. It is probable that
these minute organisms are developed by the septic ulcerative
process rather than that they are the cause of such processes. They
appear as spheres, highly refractive, motionless, cohering in groups,
without any stroma. Acids, alkalies, ether, and chloroform have no
effect on them, so that they are not to be regarded as vegetable
products.

The valvular ulcerations in this form of endocarditis give rise to the

most diverse lesions. Masses may be detached from the diseased
cardiac orifices, either from the fibrinous deposits on the valves or
from ulcerations of the valves themselves, and, having entered the
circulation, they will produce various symptoms in the organs and
tissues to which they are carried.

It is important to make a distinction between the results produced

by displacements into the blood-current of large masses and those
arising from the entrance of molecular fragments. It is also to be
remembered that the masses from the vegetations or ulcerated
valves in ulcerative endocarditis are often stamped with a septic
element which leads to the development of suppurative infarctions in
different organs.

The size and site of the emboli are important, for they may be so
large as to obstruct vessels of large size.

The femoral and even the external iliac may suddenly become
impervious to the circulatory currents, on account of the presence of
a large embolus from the heart.

When the arteries in the limbs are thus plugged, the result is
generally an ischæmia, terminating often in gangrene. Capillary
embolism may occur in a number of organs at the same instant, and
give rise to a variety of lesions. When the cutaneous capillaries are
obstructed ecchymotic spots are produced, followed by cellulitis.
When the cerebral vessels are obstructed softening may occur,
which, if the vessels are very small, may be developed without any
evidence of obstruction to the cerebral circulation. If the obstructed
artery is of large size, instantaneous hemiplegia and secondary
softening will result.
Capillary emboli may have their seat in the vessels of the spleen,
giving rise to infarctions and suppuration.

The kidneys may also undergo analogous changes. Rayer, without

knowing the origin of these changes, has given an excellent
description of them under the name of rheumatic nephritis.

In addition to the local lesions arising from these arterial or capillary

emboli, the septic phenomena are most important. When typhoid
symptoms, deep jaundice, and symptomatic intermittent fever are
associated with acute endocarditis, it establishes its ulcerative
character. In acute exudative as well as in ulcerative endocarditis,
when the inflammation progresses rapidly, the valves soften and
become less resistant than normal. As a result, they are stretched,
bulged, or torn by the stream of the circulating blood-current.

A rupture of the mitral valves will open into the auricular, and that of
the aortic into the ventricular, cavity. The reason for this is to be
found in the fact that when the valves are closed the blood-pressure
is exerted from the left ventricle toward the mitral valve, and from
the aorta toward the semilunar valves. If the blood penetrates a rent
in a flap of the valves, the endocardium is puffed out, and a valvular
aneurism is formed, and round or funnel-shaped aneurismal sacs
may project from the valves. The bottom of one of these sacs may
be perforated, and long, ragged, gray shreds, covered with fibrin,
may be found hanging in the ventricular cavity.

Microscopically, the torn shreds from a valvular aneurism, the result

of acute endocarditis, consist of nuclei and round cells imbedded in a
mass of granular matter. There is neither connective fibrilla nor
elastic tissue. When the ulceration is localized in the ventricle, the
pressure of the blood may bulge out the heart-wall, and thus give
rise to a so-called partial cardiac aneurism. By rupture of such
aneurism communication between the different heart-cavities may
be established, which will vary with the seat of the ulceration.
Acute exudative endocarditis may involve the muscular structure of
the heart. Such myocarditis (or carditis) may involve the deeper
structures, weaken them, and so alter their consistence that bulging
and the formation of a ventricular aneurism may result. Usually such
myocarditis is so slight that incomplete organization of the new
embryo-plastic cells occurs and the tissue undergoes fatty changes.
The results of all forms of acute endocarditis are best studied in
connection with the morbid changes of interstitial endocarditis, into
which they so often gradually merge.

Interstitial Endocarditis.

MORBID ANATOMY.—Interstitial (or chronic) endocarditis may be a

continuation of a process which commenced in an acute exudative
endocarditis, or it may be interstitial from its commencement, and
be so insidiously evolved as to escape notice. The anatomical
changes may sometimes be confined to the edges of the valves, at
others to their base, or they may involve the entire valves, which
become thickened, indurated, contracted, degenerated, and
adherent. It is more closely allied to rheumatism, gout, and chronic
interstitial changes in other organs than either of the other varieties.

There is no part of the endocardium which is exempt from interstitial

inflammation. The favorite place for its development is the
endocardium of the valves and that at the apex of the left ventricle.
The thickening at first may be either translucent or opaque, and the
valves may become three or four times thicker than normal. In some
instances, although the valves are thickened and indurated, their
functional activity is not interfered with, and they offer no
obstruction to the blood-current.

White, thickened, opaque spots are often irregularly scattered over

the internal wall of the heart. The vegetations met with in interstitial
endocarditis differ from those of the acute exudative variety in that
they are less prominent and firmer. They rest upon an indurated
base. Their cartilaginous consistency is due to the fact that their
cellular elements are not round (as in acute exudative endocarditis),
but elongated and flattened, possessing an abundant intercellular
fibrillated tissue.

In and underneath the endocardium there is an increase of tissue,

and upon any prominence arising from the thickening of the
endocardium occur fibrin deposits. These fibrinous efflorescences
assume a variety of forms, and sometimes string out into the
adjacent vessels and cavities for half an inch or more. Their usual
form is globular or wart-like, and their seat is on the ventricular
surface of the aortic and upon the auricular surface of the mitral and
tricuspid valves.

In interstitial endocarditis the cell-development is far less rapid and

abundant than in the acute exudative form, and this very slowness
accounts for the greater induration and thickening.

A microscopical examination of a cross-section of an indurated valve

shows a number of flat cells arranged in irregular layers, having
between them a fibrinous material which has in it here and there a
few elastic fibres. The new formations always originate in the layer
of flat cells. These changes are best marked in the fibrous zone at
the valvular orifices, upon the surfaces of the valves themselves, and
in the chordæ tendineæ. The new tissue, whether developed rapidly
as in acute exudative, or slowly as in interstitial endocarditis,
becomes fibroid and contracts, and this contraction is progressive.

As a consequence, the rigid valves, whose edges are round and

hard, are drawn toward their base, and thus are made to assume a
puckered appearance. A similar process in the chordæ tendineæ
causes them to become hypertrophied, rigid, and cartilaginous, while
they are diminished in length. In this way the valves are not only
diminished in depth, but not infrequently have their free edges
approximated to the cardiac walls, so that extensive valvular
insufficiency is the result. This, however, does not always happen,
for a thickened cartilaginous valve may have such abundant fibrinous
or papillary excrescences upon it that the onward current is
obstructed and extensive stenosis results.

As the thickening and rigidity of the flaps of a valve increase, their

mobility is diminished, and adhesions take place between their edges
which begin at their bases and progress toward their apices: so
thoroughly do they become adherent that in some cases all evidence
of a valvular outline is lost, and a fibrinous diaphragm is formed
across the valvular orifice having only a small slit at its centre,
looking and feeling like a buttonhole; hence the term buttonhole slit.
The mitral opening, which will usually admit the ends of three
fingers, may be so narrowed that the end of the little finger will
scarcely pass through it, and the aortic opening may become so
diminished as not to admit a small quill. These retractions and
adhesions cause the mitral valves, with their columns and cords, to
assume the form of a perforated cone.

Long stringy masses of fibrin, when located on the aortic valve,

sometimes form adhesions with the aortic walls, and thus is induced
a sudden and extensive regurgitation.

Insufficiency and stenosis are often found at the same valvular

orifice as the result of the thickening, adhesion, and retraction.

Changes at the aortic orifice usually occur after middle life, and
induce more insufficiency, retraction, and adhesion than those which
are limited to the mitral valve. The mitral valves are the most
frequent seat of interstitial endocardial changes in early and adult
life. These lesions are analogous to those characteristic of
endarteritis deformans. The tendency of the lowly-organized tissue
which results from interstitial endocarditis is to undergo fatty and
calcareous changes.

The minute patches of fatty degeneration in the imperfectly

organized tissue underneath the endocardium sometimes form
atheromatous masses containing more or less granular débris. The
endocardium over these patches may be destroyed, or the patches
may soften and ulcerate and cause extensive destruction of the
valves. Valvular aneurism may form in the same manner as has been
described in exudative endocarditis. The formation of calcareous
granules and plates is a very frequent termination of interstitial
endocarditis.

The aortic orifice is the most frequent seat of calcareous

degeneration. It is rarely associated with mitral stenosis. So
extensive may this process be that little beads of chalky material
may be seen studding the free edges of the valve and even
extending into the cardiac cavities.

When interstitial endocarditis has its seat in the endocardium of the

cardiac cavities, the endocardium will undergo changes similar to
those of the valves, and the muscular walls of the heart will be the
seat of interstitial myocarditis. As a result, the walls of the heart
become thinner and less resistant than normal, and depressions are
formed on its inner surface. The process is in reality a fibrous
overgrowth, which occurs in spots varying in size from half an inch
to one inch in diameter. When it extends through the entire heart-
wall the columns and cords may be so shortened as to cause
valvular insufficiency.

If the cardiac walls yield so that a well-defined pouch is produced, a

condition results which is called aneurism of the heart. Cardiac
aneurism, thus induced, is usually seated at the apex of the left
ventricle; the aneurismal sac may vary in size from that of a marble
to that of a closed fist, and may communicate with the ventricle by a
funnel-shaped or ring-like aperture. The walls of the sac are solid
and rigid; the internal surface is smooth, but it may be anfractuous.
In the latter case clots adhere to its wall. Cardiac muscular fibres are
found here and there in the aneurismal walls. They are mostly,
however, made up of layers of flat cells, their flatness being the
result of pressure.
Aneurisms at the base and in the inter-ventricular septum may result
from the extension of a valvular aneurism.

ETIOLOGY.—In most instances endocarditis depends upon a

constitutional dyscrasia characterized by alterations in the vital,
physical, or chemical properties of the blood.

Acute exudative endocarditis rarely, if ever, occurs as a primary or

idiopathic affection. It seems to have a direct connection with those
diseases and dyscrasiæ in which the blood is altered either in the
relative proportions of its constituents or in its physiological
elements. So frequently is acute exudative endocarditis associated
with acute articular rheumatism that they have often been described
as one disease.

It is generally stated that acute endocarditis occurs in 50 per cent. of

those who suffer with acute articular rheumatism, but the statistics
of Bellevue Hospital show that endocarditis complicates rheumatism
in only 33 per cent. of the cases. From these statistics it is evident
that a majority of the cases of acute rheumatism run their course
without endocardial complication.

The irritant action of the blood, the salts of which are changed or
which contains excrementitious products or a specific poison, is
shown most markedly upon the valvular surface of the endocardium;
and it is for this reason that the parts which are most exposed to
friction of the blood-current are those which first and most
extensively exhibit the pathological changes of endocarditis.

Charcot records a large number of observations in which

endocarditis developed in patients with chronic rheumatism and in
which it never assumed an acute form. It therefore seems evident
that organic lesions of the valves from endocarditis may occur in the
course of chronic as well as of acute rheumatism.

There is no disease in which a morbid blood-state exists in which

endocarditis may not occur. The essential fevers, the exanthemata,
diphtheria, septicæmia, pyæmia, and Bright's disease, are all
conditions in connection with which endocarditis is frequently
exhibited. It is met with occasionally in secondary syphilis.

Acute and chronic Bright's disease are often complicated by it. When
an individual who is already the subject of valvular disease of the
heart is attacked with acute rheumatism, the liability to endocarditis
is much increased.

Even when rheumatism and chorea are absent, endocarditis is liable

to occur when valvular disease exists. Some regard myocarditis,
pericarditis, pleurisy, and pneumonia as capable of exciting
endocarditis by the extension of the inflammatory process from the
surface of the heart; it is questionable if it ever results from such
extension. That it can be the result of traumatism is possible:
Bamberger records two cases of traumatic endocarditis. Wunderlich
ranks measles, next to rheumatism, as a cause of endocarditis.

In estimating the etiological importance that any disease bears in

the production of endocarditis, we must remember that not every
blowing sound or murmur is indicative of an inflamed endocardium.
Bamberger and Niemeyer think that the excited and irregular action
of the heart in children, by inducing irregular tension of the valves,
may bring about a blowing sound during the course of acute
rheumatism.

Acute ulcerative endocarditis is met with in pyæmia, puerperal fever,

and endometritis, scarlatina, and diphtheria: it may occur as a
secondary affection to some inflammatory focus located in the body
—septic endocarditis.

Again, this form of endocarditis may appear without obvious cause—

spontaneously or in connection with some specific form of
inflammatory disease, as croupous pneumonia. Wilks calls it then
arterial pyæmia. Primary ulcerative endocarditis is a name recently
and perhaps more aptly given it.
Finally, ulcerative endocarditis may appear as a graft (recurrent
endocarditis) upon a valve the seat of interstitial endocarditis, and
have all the pathological appearances of the septic form, but none of
its clinical aspects.

The majority of cases of interstitial endocarditis are the sequelæ of

the exudative form. It is far more frequently associated with articular
rheumatism than with any other condition. In a certain proportion of
cases the process is interstitial from its onset, especially when it
occurs with gout, chronic rheumatism, in alcohol-drinkers, or in the
aged.

SYMPTOMS.—The subjective symptoms of acute exudative endocarditis

are more obscure than those of any other disease. They are not only
few and ill-defined, but they have no regular order of development.
When the muscular tissue of the heart is not involved the disease
may run its entire course without exhibiting a single subjective
symptom.

The urgent symptoms of acute rheumatism, the different phases

assumed by the dyscrasiæ and acute infectious diseases in which
this condition is liable to occur, so mask those of the endocardial
inflammation that they are often overlooked.

When the endocardial inflammation is extensive and the muscular

tissue of the heart is involved, the patient will complain of palpitation
and a sense of discomfort in the region of the heart; not infrequently
cardiac palpitation is accompanied by dyspnoea, and decubitus on
the left side is noticed. In a small percentage of cases the palpitation
is appreciable to the physician. The heart may beat with great force
and its action be tumultuous, and yet the pulse not be altered in
character.

The pulse, at first, is usually strong and forcible; later, it becomes

rapid, small, feeble, and irregular. In some cases it is very frequent
from the onset of the disease. As a rule, the force of the pulse will
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