through the mouth. The lung is already disabled. The violent pain in
the side and the dyspnoea are no longer found. Indeed, the exact time
of the rupture and commencement of the discharge is frequently unknown
to the patient himself. The symptoms of entrance of air into the
pleural cavity may not occur for some time. The patient who has had
empyema is made more uncomfortable; the discharge through the mouth is
offensive, and its quantity and its character call attention to the
chest, in which percussion shows the presence of air; auscultation
gives amphoric breathing, and succussion demonstrates the presence of
air and fluid in the pleural cavity. Very soon, however, the presence
of air produces putridity of the secretion, with loss of appetite,
fever, diarrhoea, and the other alarming symptoms of pyo-pneumothorax.
In some instances the pleura discharges its contents and heals over.
There is another variety of pneumothorax, which is ordinarily attended
with only temporary inconvenience, and which may soon disappear,
leaving the patient no worse than before the attack. This variety of
pyo-pneumothorax may be produced by the sudden rupture of emphysematous
vesicles, by coughing, or even without any unusual force in the
expiratory effort, the alveoli having become extremely thin and brittle
by degeneration of their walls. For the minute the pain is violent and
the dyspnoea great, but it soon subsides, and in a few days the gas may
be all absorbed, unless it is in large quantity. If the pleura is
healthy and the lung not otherwise diseased, the rupture may not cause
any inflammatory action, fever, or effusion. The rupture may heal over
entirely, or if some inflammatory effusion is produced it will probably
be rapidly absorbed. In exceptional cases pleurisy may be excited and
the case become prolonged. While the air remains in the pleura we have
the physical signs characteristic of pneumothorax--displaced heart, as
shown by palpation and auscultation, tympanitic percussion resonance,
amphoric breathing, and succussion.

DIAGNOSIS.--Ordinarily, there should be no difficulty in diagnosing
pneumothorax, no matter how it is produced. We have simply to consider
well the already-mentioned modes of the commencement of the disease,
and give due value to the characteristic physical signs, especially
displacement of the heart, hyper-resonance on percussion, absence of
vocal fremitus, amphoric respiration, succussion, and decided shifting
of flatness and resonance on change of position. When all these signs
are present, each being in itself almost characteristic, there can be
but little question. Obstruction of a large bronchus would be followed
by absence of health sounds and intense dyspnoea, but we should not
have the other physical signs of pneumothorax. Extensive emphysema
would produce some of the signs--exaggerated resonance on percussion
and enlargement of the side. Emphysema, however, is bilateral, and the
resonance over an emphysematous lung has not the same pronounced
tympanitic quality as in pneumothorax. The enlargement in emphysema is
more under the clavicle; the breathing not amphoric; the normal murmur,
although enfeebled, is never completely annulled; and the heart is not
displaced. Large superficial pulmonary cavities with firm but thin
walls give us several of the physical signs of localized pneumothorax,
such as amphoric respiration and metallic tinkling; but the succussion
sound is never heard over them. The tympanitic percussion is rarely so
pronounced in a cavity as in pneumothorax, and in the latter there is
never the cracked-jar sound. In phthisical cavities of large size there
probably would be depression instead of enlargement of the chest. The
situation will ordinarily enable us to make the differential diagnosis,
for localized pneumothorax is almost always low {581} down in the
thorax, and the pulmonary cavities but rarely below its middle third.
The progress of the case and clinical history would clear up the
diagnosis. If a circumscribed pneumothorax was present with phthisis,
the diagnosis might be difficult. Powell calls attention to the
similarity of some of the signs of acute congestion rapidly supervening
at the base of a comparatively sound lung to those of pneumothorax. But
in the former the resonance, although high-pitched, is not truly
tympanitic, and the heart is not displaced. There is no other disease
of the chest where we find in such close proximity the two extremes of
percussion sounds--flatness from the secondary effused fluid, and the
tympanitic resonance above. If delicate, slight percussion is used, the
line of demarcation can be clearly defined; if, however, the force of
the percussion stroke be even of moderate intensity, the flatness is
mingled with the tympanitic quality, as it is in percussing from the
left lobe of the liver to the stomach.

PROGNOSIS.--The prognosis is unfavorable and always uncertain. During
the first few days after the rupture of the pleura it is especially
bad, though it becomes less so as time goes by. There are cases where
the perforation and its results appear to prolong life. "If the
opposite lung be healthy, we may hope that arrest of the pulmonary
disease may convert the case into one of chronic empyema" (Powell).
But, unfortunately, the rupture often occurs when the patient is
emaciated and dying of chronic lung ulceration. Cases of
pyo-pneumothorax produced in advanced phthisis or by gangrene of the
lung are almost invariably fatal. The most unpromising cases at first
sometimes prove the least serious, and, again, those that appear at the
commencement slight, contrary to expectation, die. Much depends upon
the condition of the other lung and the position of the perforation. If
the other lung be healthy and the perforation low down, the chances of
recovery are better. The progress is most favorable in the cases where
the rupture occurs from emphysema. When from purulent pleurisy the
discharge passes through a bronchus, the orifice may heal and in due
time plastic material be thrown over it, and the air and fluid be left
in the pleura. Cases are reported where the orifice remains open and
pneumothorax lasts for a long time. Laennec reported one case where the
patient lived six years. Fuller[250] reports another where the orifice
was open at the end of eleven months, another nineteen months, and
another twenty-seven months. We have mentioned Demarquay and Marotte's
experiments of the innocuousness of air injected into the pleura. Air
is harmless, as they have shown, in the pleura, unless sulphuretted
hydrogen or sulphite of ammonia be developed. Fuller says the prognosis
is very unfavorable when the effusion is large, with great displacement
of the organs. Flint considers pneumothorax occurring as a complication
of phthisis as almost hopeless. It is important to ascertain promptly
the nature and direction of the opening, whether it be free or
valvular.

[Footnote 250: _Diseases of Chest._]

TREATMENT.--This is in a great measure palliative. Hypodermics of
morphia or opiates relieve the agony and lessen the shock caused by the
perforation. Alcoholic and diffusible stimulants may sustain the heart
in its struggle against the effects of dislocation and impaired
circulation. Care must be taken not to depress the powers of reaction
by too much morphia. Hot water in india-rubber bags applied to the
chest gives great relief. Alcoholic stimulants must be given to prevent
sinking from exhaustion. When the distension from air is excessive,
paracentesis gives marked relief, the lives of patients having been
prolonged for days by it. If the opening is valvular, to prevent the
air from accumulating in excessive quantity Reybard's protected
gold-beater's skin trocar may be used and kept in the chest. Otherwise
fine aspirators may be employed, which would seem to be harmless, and
the {582} operation be repeated whenever necessary. Larger points and
the trocar should never be used, as there is danger of making a
permanent fistulous orifice, as well as of injuring some blood-vessels
or the lung itself. After the excess of air has been removed by
aspiration the affected side should be strapped to control the
inspiratory movements on renewal of positive pressure. Anstie[251]
recommends drachm ss doses of ether every three or four hours.
Fernet[252] recommends inhalation of oxygen. If fluid should compress
the chest, some of it must be removed by aspiration, but care must be
exercised, for the presence of fluid is conservative in its effects.
Its pressure stops up the orifice and promotes its healing. If it
becomes fetid, pleurotomy, with detersive washes, ought to be resorted
to. Food should be frequently administered, with quinine and cod-liver
oil, and good hygienic surroundings prescribed.

[Footnote 251: _Reynolds's System of Medicine_, vol. iv.]

[Footnote 252: _Nouveau Dict. Méd._, vol. xxviii.]

Hæmothorax.

DEFINITION.--Accumulation of blood in the thoracic cavity unconnected
with inflammation of the pleuræ.

ETIOLOGY.--Hæmothorax may be caused by traumatic injuries, by the
bursting of an aneurism, from ulceration through the walls of the aorta
of the vena cava, or from the veins of the pleura. It may be caused by
laceration of the intercostal arteries in penetrating wounds. In very
rare cases a profuse bleeding takes place in caseous pneumonia or in
gangrene of the lungs, and bursts into the pleural cavity (Fraentzel).
Cancer of the lung or pleura may, by pressure, produce absorption and
destruction of the walls of the blood-vessels, and cause discharge of
their contents into the pleural cavity. Sir Thomas Watson[253] reports
a case where enormous hæmothorax caused enlargement of the left side,
pushing the heart to the right of the sternum from caries of two ribs
with ulceration through an intercostal artery. The blood never escapes
from the lung into the pleura when there is considerable pulmonary
apoplexy.

[Footnote 253: _Practice of Medicine_, vol. ii.]

PATHOLOGICAL ANATOMY.--Blood is found coagulated to a greater or less
degree in the pleural cavity, and the lesion producing the hæmothorax
can generally be found; the remains of blood may be found even after it
has been some time effused. If the hemorrhage does not prove fatal, it
may all be absorbed, or it may by its presence cause local inflammation
of the pleural membrane.

SYMPTOMS.--The symptoms are those of perforation into the chest--sudden
intense pain on the diseased side, with internal hemorrhage, great
pallor, feeble circulation, cold extremities, and syncope. Patients
often die in a few minutes. If the hemorrhage is moderate in quantity,
they revive and the circulation returns, but they complain of feelings
of suffocation and oppression. Slowly the general strength returns and
the patient recovers.

SEQUELÆ.--Most modern surgeons admit that serious hemorrhages into the
pleura come from the thoracic walls, or from the blood-vessels in the
neighborhood of the hilum, or from those which accompany the bronchial
diseases of the second or third order. Hæmothorax is always consecutive
to some primary lesion. Where it is caused by penetrating wounds or by
the bursting of blood-vessels in the lungs, air enters the cavity and
becomes mixed with the blood, producing a complication in the form of
hæmato-pneumothorax. This frequently gives rise to pyo-pneumothorax
with a collection of purulent and ichorous fluid.

DIAGNOSIS.--The previous history of the case, together with the
characteristic symptoms we have mentioned, enables us to diagnose
hæmothorax from {583} pneumothorax, which commences in a similar way.
The only other condition likely to be confounded with it is effusion in
pleurisy, the physical signs of which are somewhat the same. If the
blood remains uncoagulated we shall have absence of vesicular murmur,
with dulness on percussion, absence of fremitus, and no friction sound.
The introduction of a fine hypodermic needle enables us to be certain
of the nature of the fluid.

The PROGNOSIS is always serious. If the cause of the hemorrhage is the
bursting of an aneurism, death supervenes in a short time. Hæmothorax,
when caused by penetrating wounds, unless they produce hemorrhage, is
not necessarily serious. The blood may entirely disappear in a few
weeks. Entrance of air with the blood renders the prognosis more
serious. Secondary pleurisy is not ordinarily severe unless pus forms.

TREATMENT.--If time is allowed, every effort must be made by local and
general treatment to arrest the hemorrhage--ice-bags and hot-water bags
ought alternately to be applied to the chest and between the scapula;
the patient to be kept in the horizontal position and made to rest
quietly; ice taken by mouth; small doses of morphia and large doses of
ergotin must be given promptly hypodermically, as the stomach is in no
condition to absorb remedies readily. If the accumulation be excessive
and continues to embarrass the respiration very much, we recommend free
incisions to take out sufficient blood to relieve the pressure and
great dyspnoea. Unless danger is imminent, this is a hazardous
experiment, as letting in atmospheric air among blood-clots may
seriously complicate the condition. Should pleuritis or other
complications occur, they must be rationally treated.

Growths in the Pleural Cavity.

Some authors mention various tumors which are rarely met with in the
pleural cavity, and which are not peculiar to the serous membrane of
the pleura. Among them may be placed sarcomas, fibro-sarcomas, and
epithelioma. Their presence in other organs may assist in the
diagnosis. Other varieties exist more or less connected with chronic
pleurisies. Among these are fibromas, cartilaginous and osseous
formations. Rokitansky speaks of lipomas as deposited on the costal
pleura. The only varieties which we think it necessary to call
attention to are cancer and hydatids.

CANCER OF THE PLEURA.--Cancer of the pleura is not a very rare disease,
but ordinarily it is a secondary formation, coming from cancerous
disease of the mediastinum, of the lung, or of some abdominal organ.
Some authors doubt whether it is primary even in the lungs and
mediastinum. It certainly is not often met with as a primary disease of
those organs. Lebert[254] had only seen 6 observations, in 447 cases of
cancer, involving the mediastinum, the pleura, and the lungs.
Walshe[255] reported 29 cases of primitive cancer of the respiratory
organs; in 18 cases one lung was diseased with its pleura, and in 13
the right lung. Lépine[256] in 1869 communicated a very curious case of
primary cancer of the pleura in a child ten years of age. The right
pleural cavity was filled by a white scirrhous tumor. Darolles[257]
(1874) reported another example of primary cancer of the pleura, which
afterward spread to the lung. Andral, Vidal, and Lebert reported cases
where the tumors appeared to develop simultaneously in the pleura and
other organs. Primary cancer of the pleura may exceptionally occur, but
ordinarily the disease results from its extension step by step, or else
distant propagation, from lungs, breast, mediastinum, or the abdominal
organs. Most frequently the secondary {584} cancer appears more or less
independently of the primitive tumor, and is seen in the form of
disseminated points on the surface of one or both folds of the pleura.
This propagation of cancer is now generally admitted to be through the
intermediary of the lymphatic system; in fact, the lymphatics are
themselves attacked by the degeneration, and they are seen,
particularly on the surface of the pleura, in the form of white small
cords. Some modern pathologists consider that the serous cavities are
lymphatic cavities, which can, just as the vessels themselves, serve as
ways of generalizing the disease (Cornil and Ranvier, Charcot, Lépine,
and Virchow).

[Footnote 254: _Traité Prac. Mal. des Cancereuses_, Paris, 1851.]

[Footnote 255: _Nature and Treatment of Cancer_, London, 1846.]

[Footnote 256: _Bull. de la Soc. Anat._, 1869.]

[Footnote 257: Quoted by Fernet, _Nouveau Dict. Méd._, vol. xxviii.]

PATHOLOGICAL ANATOMY.--Primary cancer of the pleura is ordinarily
encephaloid and multiple. Extended infiltration is very rarely found.
Lebert reports one case in an infant of seven months. The multiple
masses are ordinarily soft and pulpy, varying in volume from the size
of a grain of millet-seed to that of a small nut. The aspect is
yellowish-white. The juice is rarely pressed out of them. Under the
microscope we see large cells and multiple cells with their nuclei. The
small granulations or the lenticular masses are flat, resembling drops
of wax. We may have solid bodies possessing all the characters of
scirrhous, encephaloid, and colloid, grayish, or gelatinous structure.
These cancerous productions are generally vascular, especially in the
encephaloid variety. Their rupture frequently produces hæmothorax and
hemorrhagic pleurisies. The bronchial glands, and finally the cervical
glands, often become involved.

SYMPTOMS.--The symptoms of pleural cancer, especially of the smaller
and secondary deposits, are often obscure and indefinite. They are not
sufficiently definite to attract attention during life. If the masses
are scirrhous and large, they press upon the lungs, impede respiration,
and give rise to dyspnoea. If the disease is propagated from the lungs
or breast, we may suspect cancer where we have a dull pain with some
cough. Pain, indeed, is constant, but not violent, unless the nodules
excite local inflammation. When scirrhous tumors press upon the
intercostal nerves, the pain is very persistent. External pressure over
the points gives rise to pain. The dyspnoea increases as the size of
the tumor increases. The expectoration is occasionally bloody. The
physical signs are sometimes characteristic--dulness on percussion,
absence of respiratory murmurs, friction sounds, no vocal fremitus.

DIAGNOSIS.--Generally very difficult. The progress of the disease is
ordinarily slow, and follows its development in other portions of the
body. Cancerous cachexia, degeneration of the glands above the
clavicle, hæmothorax, and hemorrhagic pleurisy, together with dry cough
and persistent intercostal neuralgia, are, when present, valuable aids
to diagnosis. Extensive caseous pneumonia and pleuritic effusions may
be confounded with cancer of the pleura. These tumors may not be at the
base, but in the middle of the thorax; dulness may not exist at the
base as is invariably the case in pleurisy. The position of the body
does not affect the limit of dulness in cancer.

The PROGNOSIS is always very serious, the disease being invariably
fatal. In Walshe's cases the duration of the disease was from three and
one-half months to twenty-seven months; average duration, thirteen and
one-fifth months. One-fourth of his cases occurred between the ages of
fifty and sixty years.

The TREATMENT is palliative--opium and other narcotics, and locally
chloroform and aconite for the intercostal pains. When effusion results
from cancerous inflammation the aspirator may be used to relieve the
great oppression caused by the quantity of fluid.

{585} Hydatids of the Pleura.

Trousseau[258] considered hydatids of the pleura a comparatively rare
disease. He believed that when found in the cavity it was frequently
caused by cysts of the lung which had fallen into the pleural cavity.
Vigla[259] mentions 3 cases. Davaine[260] met with 25 cases of
hydatids, only 1 of which he believed originated in the pleural cavity.
The acknowledged greater frequency of these hydatids in the right
inferior lobe of the lung, gives probability to Dolbeau's[261] view
that "they frequently proceed from cysts on the convex surface of the
liver." Hearn[262] reports 75 cases collected from various observers as
intra-thoracic, 15 of which were in the pleura, in the subserous
tissue, between the parietal pleura and thoracic wall.

[Footnote 258: _Clin. Med._, vol. i., Philada. ed.]

[Footnote 259: "Des Hydàtides intrathor.," _Arch. gén._, 1855.]

[Footnote 260: _Traité des Entozoaires, etc._, Paris, 1860.]

[Footnote 261: _Thèse de Paris_, 1856.]

[Footnote 262: _Thèse de Paris_, 1875.]

PATHOLOGICAL ANATOMY.--In the greater number of cases, as examined at
autopsies in Hearn's reports, the tumor was formed by a voluminous
pocket occupying a large part or the whole of the cavity of the pleura.
The walls of the envelope were formed of a transparent or slightly
opaline and whitish membrane composed of numerous thin layers,
containing on its interior surface the echinococci. In the interior of
the cyst there was a limpid hyaline liquid with living parasites.
Nothing different was noticed in cysts from those found elsewhere,
except the absence of the usual adventitious membrane--a fact
previously noticed by Davaine. When the cysts are very large they press
upon the lung and adjoining organs just as is the case with large
effusions in the pleural cavity. The heart, moreover, is pushed to one
side, out of its normal position; the lung is compressed and diaphragm
depressed.

SYMPTOMS.--The first appearance of cysts of the pleura causes but
little disturbance of the functions of the lung. It is scarcely
appreciable until it interferes with the play of the other organs. The
three prominent symptoms are the pain, the dyspnoea, and the cough. The
pain occupies the exact point where the tumor is situated, and radiates
from that point. Once developed, it persists with tenacity throughout
the duration of the disease. This persistence of the pain is indeed an
important characteristic of the disease, and is a sign of value in the
diagnosis between hydatids and pleuritic effusions. The dyspnoea
increases progressively with the volume of the tumor. The cough is not
heard as frequently as when the cysts occur in the lungs. It is dry,
and does not cause hæmoptysis.

DIAGNOSIS.--Physical signs must be marked to enable us to distinguish
fluid cysts of the pleura from cysts in the lung or effusions in the
pleural cavity. When the hydatid tumor has attained sufficient size to
cause pain and dyspnoea it generally presses outward the walls of the
chest after the lung has been compressed. It does not occupy the base
of the cavity, as the effusions do, and the dilatation has a globular
form. Trousseau[263] has given several examples in which this shape
determined the diagnosis. With this arching of the chest the immobility
of the chest is an important sign. Vocal fremitus is diminished or
totally abolished, and percussion elicits absolute flatness. These two
physical signs assist us in making the diagnosis between hydatids and
pleurisy. The auscultatory phenomena, from similar physical conditions,
closely resemble those of pleuritic effusions. It must be borne in mind
that sometimes hydatid cysts are complicated by pleuritic
inflammations, caused by their presence. The diagnosis is
unquestionably complicated by difficulties that are not removed unless
the cysts burst through a bronchial tube and discharge a transparent
and clear fluid in which the microscope shows the presence of
echinococci. Such hydatid expectoration is a pathognomonic {586} sign
of the existence of an intra-thoracic cyst. Hydatids of the liver may
press the diaphragm far up into the pleural cavity without bursting
through it. Trousseau maintained that without bursting they may make a
passage for themselves through the distended, attenuated fibres of the
muscular portion of the diaphragm, for the progress of these cysts is
necessarily slow. We must not hesitate to make an exploratory
aspiration to determine with certainty the nature of the fluid.

[Footnote 263: _Loc. cit._]

PROGNOSIS.--The prognosis is certainly very serious, but not so bad as
when cysts of the same nature are situated in the lungs. Their
spontaneous cure may be effected by bursting through a bronchus or even
through the walls of the chest. The patient may, however, die from
asphyxia during the discharge through the lungs. When not evacuated
they may produce death by compression of the lungs.

TREATMENT.--If the disease is recognized previous to its making an
opening through a bronchus, it can be treated safely and effectively by
aspiration. Bird[264] reports a number of cures by this operation in
Australia. Trousseau advises extreme caution, even in regard to
exploratory punctures, unless adhesions have taken place between the
tumor and the walls of the chest, for he fears the escape of fluid into
the cavity of the chest and consequent purulent pleurisy. It is well to
remember that this great practitioner was not aware of the
innocuousness of capillary punctures and aspiration. If the bronchus
has been perforated, we must hope for spontaneous cure. If empyema be
caused by the tumor pleurotomy must be used as recommended by
Moutard-Martin[265] and Vigla,[266] and constant washing of the pleuræ
must be used. This treatment gives us reasonable assurance of success.

[Footnote 264: Quoted by Hearn.]

[Footnote 265: _Purulent Pleurisy_.]

[Footnote 266: _Loc. cit._]

History of Thoracentesis.

Thoracentesis ([Greek: thôrax], chest, and [Greek: chentein], to
pierce) is the operation for the evacuation of collections of fluid,
serum, pus, or blood from the pleural cavity.

Among the ancients, dating back to the time of Hippocrates, it was
practised, and was known as the operatio empyematis. Hippocrates uses
the word [Greek: empyon], signifying, literally, an internal collection
of pus just above the cavity of the peritoneum, above the diaphragm.
Subsequently he speaks of empyema of blood, empyema of serum, empyema
of gas, but not of pus, applying the term to the operation, which he
employed principally for empyema necessitatis. Subsequently the name
empyema was used, as now, to designate a purulent collection in the
pleural cavity.

If we may credit the story which has descended from mythological times,
the operation for empyema had its origin in an accident. It is related
that a certain Phalereus, who was attacked with what was denominated an
ulcer on the lungs, was pronounced by all his physicians to have an
incurable disease. In his despair he exposed himself in battle so that
he might be slain; the enemy's weapon, however, pierced his side,
making an opening through which the pus escaped, and he recovered.[267]

[Footnote 267: Cicero, _De Naturâ Deorum_, lib. iii. cap. 28.]

It is certain that from the most remote periods the chest was opened
when collections of pus were formed. Galen states that the ancients
employed actual cautery for that purpose. He reports that Euryphon de
Cinde by this means saved the life of Cinesias, son of Evagoras.[268]
The details into which Hippocrates and his school entered in regard to
the operation show that it was frequently performed in their day. It is
very remarkable that many of the more important precautions in the
operation were observed by {587} Hippocrates. We find from the
_Aphorisms_ that the operation was considered the only means of
cure,[269] and that when these precautions were observed, and the fluid
was white and of good quality, the patients recovered.[270] The
principal precautions were not to delay the operation after the
existence of pus was recognized, and to draw off the liquid. He further
states that if the serous fluid in dropsy of the chest or pus in
empyema should be drawn off too rapidly the patient would die. So
impressed were the disciples of Hippocrates by this view that they
adopted the operation of perforating a rib instead of cutting through
the intercostal space, because they could with more ease stop up the
orifice and regulate the outward flow of the fluid. The later
Hippocratians preferred cutting instruments to actual cautery.
Hippocrates, if unable to discover the locality of the fluid in the
thorax by succussion, applied over the walls of the chest a linen
compress which he soaked in earth of Eretria and warm water, and
concluded that the collection existed at the points where the earth
commenced to dry!

[Footnote 268: _Comm. in Aphor. Hipp._, lib. vii.]

[Footnote 269: _Aphorisms_, lib. vii., Aph. 44.]

[Footnote 270: _Ibid._, lib. vi., Aph. 27.]

When these signs failed, he cut through the most prominent rib at the
base of the chest and toward the back. He made a large incision through
the rib, but only a small one the size of a thumb-nail through the
tissue beneath the rib. After allowing a small quantity of pus to
escape, he introduced a tent of undressed flax, with a piece of thread
attached to it. This he withdrew twice daily, to allow the pus to flow.
At the end of two days he permitted the remaining pus to be discharged,
and inserted a tent of linen. To prevent the lung, habituated to the
presence of fluid, from drying too rapidly he injected wine and oil
through a canula. When the excavated fluid was thin (serous?) he
replaced the tent by a tube of tin, and when it ceased to secrete fluid
he shortened each day the length of the tube, so that the cicatrization
of the wound extended from the inner end of the orifice.[271] The
genius of Hippocrates cannot but excite our admiration, as it did
Laennec's, who selected as the subject of his thesis "The Doctrines of
Hippocrates as applicable to the Practice of Medicine." Can it have
been Hippocrates's modes of physical explanation that suggested to
Laennec the idea that led to his great discovery of auscultation?

[Footnote 271: _De Morbis_, lib. i. p. 448.]

Hippocrates's operations were made by boring through the rib or with a
red-hot iron or a bistoury cutting through the intercostal space. Galen
(A.D. 150) had his pyulcon with which to draw out the fluid. Galen and
Roger of Parma bored through the sternum. Many of the ancient surgeons,
such as Eumphon of Cnidos, Paul of Ægina, Celsus, Solinger, divided the
soft parts by caustics and the knife after laying bare the pleura.
Blunt instruments were sometimes used, such as sounds. Celsus in his
latter years lost confidence in the operation, and it fell into
discredit among the Greeks and the Romans, by whom it seems to have
been nearly abandoned. In the Middle Ages the question was discussed
whether it was better to open the chest by steel or by fire in
traumatic pleurisies. Trousseau states that about the sixteenth century
the operation of trepanning the ribs was revived. About the same time
the detersive injections which had been recommended by Galen were again
advocated, especially by Fabrice d'Aquapendente. The operation was
unpopular among the greatest surgeons, and but seldom resorted to
except in extreme cases. Notwithstanding the servile obedience to
tradition in those days, some important points were advocated in regard
to the propriety of allowing the openings for empyema to remain
unclosed for an indefinite period. From the seventeenth to the
eighteenth century the operation of paracentesis was the topic of many
surgical treatises.

Early in the seventeenth century practitioners became less distrustful
of {588} puncturing the chest, and were led to believe in the
harmlessness of the operation (Trousseau). As a consequence of this
tendency, physicians began to study the question of puncturing the
chest in hydrothorax. In 1624, Gérome Goulée alleged that he succeeded
more frequently in hydrothorax than in abdominal paracentesis. Twenty
years later, Zacutus Lucitanus asserted that paracentesis was as
necessary in cases of serous effusion into the chest as incision in
empyema. In 1663, Robin and Duval recommended thoracentesis as the best
treatment for hydrothorax. Some time afterward this practice was put in
force by Willis. Lower also mentions a case, and subsequent authors
quoted these cases as an encouragement to the performance of
paracentesis of the chest for the removal of serous effusions. Jean de
Vigo brought out again the pyulcon. Druin about the year 1665 proposed
the use of the trocar as a substitute for the actual cautery in opening
the chest.

In 1658, Bontius for the first time took up in a precise manner the
subject of the introduction of air into the pleural cavity. He declared
there was no danger from it. Bartholin maintained the opposite opinion.
The indications for the operation were laid down, but they were
necessarily very imperfect. In proportion as attention was directed to
the question of the admission of air, the manner of operating was
modified. In 1669, Scultetus discussed thoracentesis in his work
_Armamentarium Chirurgicum_. He made use of a trocar, with a bladder at
the external orifice, principally to prevent the introduction of air,
as Reybard later used a piece of cat's intestine and a bladder of
gold-beater's skin. Scultetus used the sypho, a common syringe, for
injecting the chest, and also the [Greek: pyoulchon] ([Greek: pyon],
pus; [Greek: elchô], to draw out), or pyulcon, for drawing out matter,
as its name indicates. This was practically the syphon. Scultetus
describes the operation by incision with his gladeolo salicet longo,
and by puncture with the canula et acus, both figured in his plates; so
also his drainage-tubes, with directions for shortening them as the
cavity heals, and the long tubes, which probably acted by gravitation
after the manner of the syphon. Aspiration was made by the mouth, by
cups, and by syringes affixed to a canula or catheter.[272]

[Footnote 272: These facts were kindly furnished me by Morrill Wyman,
who carefully examined Scultetus' work (edition 1672) in the Harvard
Library.]

It is thus evident that more than two hundred years ago aspiration was
used to evacuate fluid from the pleural cavity. Trousseau says that "at
that period aspiration and suction were used for this purpose--timidly
pursued, in accordance with Scultetus' example; and that it became
afterward in vogue with the masters of surgical art."

Palfin preferred the trocar to incision for treatment of hydrothorax.
In 1707, Anel wrote a book on the art of sucking wounds without using
the mouth. Bourdelin (1742) rejected the trocar for fear of injuring
the lung. That Scultetus' practice was continued is evident from the
work of Laurence Heister (1742), who described puncture of the chest,
with drawings of exhausting syringes for the removal of pus or serum.

In 1765, one hundred years after Druin's use of the trocar, when
perforation by actual cautery was abandoned, Lurde timidly advocated it
on account of his fear of wounding the lung. He advised the operator to
close the canula with the finger at each inspiration, leaving it open
during expiration, so as to prevent the entrance of air. Chopart and
Desault opposed the use of the trocar as a coarse mode of operation,
involving the risk of wounding the intercostal artery and lung
(Trousseau). Van Swieten at the end of the last century questioned the
advisability of using the trocar. Later, in 1796, Benj. Bell,[273] in
cases of thoracentesis, used india-rubber bottles fitted to the opening
for the same purpose, first compressing them and then allowing them to
expand by their elasticity. He strongly recommended paracentesis {589}
of the pericardium when the amount was so excessive as to cause death.
He gives exact directions how and where to operate.

[Footnote 273: Vol. v.]

Isbrand de Diéonerbrock[274] plunged a bistoury between the fifth and
sixth ribs, and introduced into the wound a silver canula large enough
to fit the orifice, and stopped the canula with a tent which he
withdrew each day. Jean Scultetus[275] recommended several different
canulas, some of silver, some of gold. He also invented syringes,
straight and curved, to absorb the pus or make injections into the
chest. Scultetus operated in the sixth intercostal space; he raised a
piece of skin, so that it might lap over the orifice after the
operation. He used a tent until the eleventh day, when he inserted a
canula. After Scultetus, Lamzweerden[276] used suction, and contended
that it was very successful. Paul Barbette[277] considered
thoracentesis as indispensable in empyema and hydrothorax. He
maintained that it was less dangerous than the puncture for ascites. F.
Hoffmann at the commencement of the eighteenth century[278] gave his
full and complete approbation to the operation performed according to
the accepted rules. Dominique Anel[279] was an avowed partisan of the
suction of the effused fluids in the chest. He had seen soldiers very
successfully suck, with the mouth, wounds of the chest. He invented
different syringes and other machines to pump out the effused fluids,
some of which were very large, with canulæ whose orifices were very
wide and of different shapes.

[Footnote 274: _Medic. Morb. Pectoris Hist._, 2.]

[Footnote 275: _Armam. Chir._, Paris, vol. i. p. 20, quoted by
Sprengel.]

[Footnote 276: _Appendix ad Sculpt. Armen_, 1671, quoted by Sprengel.]

[Footnote 277: _Chirurgia_, lib. iii. cap. 2, Geneva, 1688, quoted by
Sprengel.]

[Footnote 278: _Medicina consultatoma_, vol. i., 1721.]

[Footnote 279: _L'art de Sucer les plaies sans se servir de la bouche
d'un Homme_, Amst., 1707.]

Laurence Heister[280] (1742) acknowledged that Anel's syringes were
valuable in pumping out the fluid from the middle or lower part of the
chest, but not when paracentesis was performed in the higher portions
between the second and third ribs. Heister gives[281] drawings of
exhausting syringes for the removal of pus or serum. C. G. Ludwig
published[282] a new apparatus invented by a surgeon named Bucer to
pump out the fluids contained in the chest. This machine was composed
of canulæ, to which was adapted a bowl to receive the liquid as it was
withdrawn. Ludwig claimed that the especial advantage of this
instrument was that it pumped all the fluid out at one time, without
the operator being annoyed by any disagreeable odor. Leber[283]
proposed a similar instrument which was easier of application. A. T.
Richter demonstrated the inutility of all these inventions; the blood,
he said, would be drawn out with the fluid and by coagula stop up the
canula. Valentin (1772) objected to the use of these pumps as applied
to chest fluids.

[Footnote 280: _Chirurgie_, Th. i. Buch. i. Kap. 10, p. 89.]

[Footnote 281: _Ibid._, p. 72.]

[Footnote 282: _Diss. de Vul. Pectoris_, Leip., 1768.]

[Footnote 283: Quoted by Sprengel, p. 60, vol. ix.]

In the latter part of the eighteenth century there were numerous
English and continental writers on the subject of paracentesis. Among
them were J. W. Belquer, Sharp Mohrenheim, Richter, Ponteau, Callisen,
Pierre Cooper, Allemoth, Zellar, and Audouard. Some of these preferred
the trocar to the bistoury. Some were in favor of prompt action, and
others objected to the operation unless there were threatening
symptoms. Valentin urged that the presence, on the surface of the
chest, of oedema and ecchymosed spots was a certain indication of fluid
effusion.

During the first twelve years of this century the operation seems to
have fallen into disuse. In 1808, Audouard objected to the Hippocratian
method, which had been practised for centuries, of drawing out small
quantities at a time, for fear that the sudden withdrawal of a large
quantity would produce a vacuum in the chest. He maintained, and
proved, that sudden and {590} complete evacuation had no such result.
In 1811, Corvisart[284] drew attention to thoracentesis. In 1812,
Larrey discussed its merits. Charles Bell[285] preferred the trocar to
the other methods in hydrothorax when he could be positive of the
presence of fluid, but he stated that he preferred first to introduce
the bistoury. He operated in the sixth intercostal space, but in
empyema he preferred to make the puncture higher up. Samuel Cooper[286]
recommended as small an orifice as possible for the evacuation of
serum, but larger and wider ones for pus and blood.

[Footnote 284: _Maladies du Coeur_, 1811.]

[Footnote 285: _System of Operative Surgery_, vol. ii. p. 194.]

[Footnote 286: _Dictionary of Surgery_, p. 749.]

In tracing the history of this important operation we have shown that
it has been performed from the time of Hippocrates, and that it has
been held in different degrees of estimation by the numerous authors
who have discussed it--that sometimes it has been popular, and again
regarded unfavorably.

Récamier operated, but unsuccessfully. Up to the period we have now
reached (1816) great difficulty of accurate diagnosis existed, and
crude notions of physiology prevailed. Errors of diagnosis as to the
character of the fluid when present, and still more as to its existence
in the chest, frequently led to unpleasant results. Laennec's genius so
completely cleared up the differential diagnosis of all diseases of the
chest, including pleurisy, that men grew less timid. Laennec[287]
himself was a strong advocate of the operation; he advised it in acute
pleurisy where dyspnoea, threatening life, supervened, and in chronic
cases where other remedies failed. He proposed to apply a piston
cupping-glass over the wound after the discharge of liquid, and to
produce a vacuum in the chest more or less quickly, continuously, and
completely according to effects.

[Footnote 287: _Traité d'Auscultation mediate_, 1818.]

As Bowditch[288] states, "We should be groping in the same dark way,
and perhaps getting into the chest by caustic pastes or by actual
cautery, had not Laennec discovered for us auscultation, with all its
admirable powers of diagnosis of thoracic affections."

[Footnote 288: Unpublished communication to the writer, 1882.]

In 1815, Blondel practised puncture of the chest with a bistoury.
Gendrin performed the same operation in acute pleurisy in 1831, but
with only bad results. Townsend[289] (1833) acknowledged that the
operation had fallen into disuse, as much from uncertainty of diagnosis
as from any experience of its general danger. He gives the results of
Thomas Davies's operations--8 out of 10 successful cases in empyema,
with 9 fatal cases in pneumothorax with effusion (probably tubercular),
and 3 fatal cases in hydrothorax. Davies used a grooved needle to
determine the presence of the liquid, its quality, and the thickness of
the walls. After the operation his practice was to inject a weak
solution of chloride of lime, which he found to have the effect of
diminishing the discharge and correcting its character. Crompton[290]
(1834) had 3 successful cases out of 10.

[Footnote 289: _Cyc. Prac. Med._, vol. ii. p. 43.]

[Footnote 290: _Ibid._, vol. iii. p. 400.]

Robert Law[291] pronounced paracentesis more successful in chronic than
in acute pleurisy. Townsend doubts whether the admission of air was
hurtful; he quotes Nysten and Spies's experiment, showing that air
introduced into healthy pleuræ was invariably absorbed in a few days.

[Footnote 291: _Ibid._, 1834.]

Townsend[292] and Law, as well as C. I. B. Williams,[293] speak of the
different kinds of syringes that have been proposed to draw off the
fluids.[294] Dupuytren proposed (1814) the introduction of a small
canula with a very flexible substance at its outward extremity, such as
the bladder of some domestic animal, which would allow fluid to escape,
and at the same time would oppose the entrance of air into the chest.
Becker (1834) published a work in which he investigated the nature of
the false membranes in pleurisy, and showed that the {591} access of
air did not produce unpleasant results. He reported 2 successful cases
out of 3 of operation.

[Footnote 292: _Ibid._]

[Footnote 293: _Library of Pract. Med._, 1841.]

[Footnote 294: Boyson, _Thèse de Paris_, 1814.]

R. Townsend[295] wrote an elaborate paper in 1833 on empyema, in which
he applied the principles of physical diagnosis. He cites numerous
cases of thoracentesis, and speaks of the operation as easy of
execution, productive of little pain to the patient, generally followed
by immediate relief, and as having been in numerous instances crowned
with complete success. Robert Law[296] (1834) speaks discouragingly of
the operation in consequence of the "unavoidable admission of air into
the inflamed cavity." He considered the operation of tapping the chest
more likely to be successful in chronic than in acute pleurisy.

[Footnote 295: _Cyclop. Prac. Med._, vol. ii., 1833, London.]

[Footnote 296: _Ibid._, vol. iii., 1834.]

In 1835, Faure[297] read his paper on thoracentesis before the Academy
of Medicine of Paris, which attracted a great deal of attention.
Contradictory opinions were given by prominent members as to the value
of the operation. The debate was prolonged, and no definite conclusion
was reached. Laennec, although he had recommended the operation in
excessive effusions and in chronic cases, was yet timid, and his advice
had not the overwhelming influence that it should have had. Becker of
Berlin in 1834 wrote his paper on chronic pleurisy, in which he also
laid down the principles of diagnosis by means of auscultation and
percussion. He detailed 5 cases which he had operated upon. To Thomas
Davies is due the credit of having in 1835 recommended the use of the
exploring-groove needle to ascertain the nature of the pleuritic
effusions, but Powell claims that Sir Benj. Brodie first suggested it.
Ringer first recommended the use of the hypodermic syringe for that
purpose. Stokes[298] insisted upon the evils attending paracentesis,
among which he mentions the converting of serous into purulent
effusions.

[Footnote 297: _Bullétin de l'Académie de Médecine_, 1838, tome i. p.
62.]

[Footnote 298: _Dis. of Chest_, Dublin.]

Watson's lectures on practice, delivered in 1836-37, show that while he
was much interested in the operation, the necessity of which he
discusses with his characteristic ability, yet his conservatism led him
to put prominently forward the dangers and evils connected with it.
According to these two prominent English practitioners, only imminent
peril to life justified the operation. Guérin[299] in 1841 applied his
subcutaneous method of operation to empyema. He drew fluids from the
chest by a suction-pump applied to a canula, using a curved trocar and
canula to prevent injury to the lung.[300]

[Footnote 299: _Essai sur la Méthode Sous-cutanée_, Paris, 1841.]

[Footnote 300: Drawings of the trocar and canula, with the aspirators,
are shown in Jacob and Bongeré, _Med. operatoire_.]

Reybard in 1837 took up Dupuytren's suggestion, and used gold-beater's
skin as a valvular means of excluding air at the mouth of the canula;
this is now known as Reybard's canula apparatus, and was the one used
and highly recommended by Trousseau. Stanski in 1839 invented an
apparatus for drawing off air from the chest, working on the principle
of aspiration. Bowditch states[301] that while in Paris from 1832 to
1835 he never saw a case of pleurisy in Louis's, Chomel's, Andral's, or
Trousseau's wards where thoracotomy was performed or even suggested.
Medical opinion was either indifferent or in actual opposition at that
time. H. I. Bowditch of Boston relates[302] that he saw 2 cases of
effusion in the pleural cavity in 1839, in which he proposed
thoracentesis, but the surgeons would not operate: both of these
patients died. He was convinced at the time that their lives might have
been saved. Schuh of Vienna published his work on the _Influence of
Auscultation and Percussion on Practical Surgery_, in which he boldly
maintained that paracentesis was a radical cure in cases of chronic
thoracic effusion, no matter how originating. This work had a great
influence in advancing {592} the popularity of the operation of
thoracentesis. Subsequently, Schuh and Skoda, both professors at
Vienna, published[303] a monograph on the treatment of pleurisies,
especially by surgical means, which, as Trousseau acknowledged, has
become a classical work in Germany, and occupies a distinguished place
in the history of paracentesis of the chest. They admitted that when
the effusion is not excessive in quantity, and there are no
complications, recovery generally takes place. When the effusion is
excessive even, it may in time disappear, but it may prove a matter of
months or years. They advised that the operation should be performed
when there was no marked improvement for three weeks. These authors
refuted the arguments urged against the operation, and gave details as
to the mode of operating. The Germans were the first to consider the
puncture as a means of radical cure in pleuritic effusions: Becker,
Schuh, and Skoda gave it a decided impulse. Hope's[304] paper
endeavored to prove that pleuritic effusions did not require surgical
interference, but would yield to general treatment.

[Footnote 301: Unpublished MS., 1883.]

[Footnote 302: _American Journal Med. Sciences_, April, 1852.]

[Footnote 303: _Medicinische Jahrbücher der K. K. Oesterreich Staates_,
1841.]

[Footnote 304: "Notes on the Treatment of Chronic Pleurisy," in
_Medico-Chir. Review_, London, 1841.]

Thus we see that up to 1841 these unsettled controversies over the
dangers and advantages of the operation were still going on. Fred.
Bird's results in 1843 proved the possibility of its successful
employment, doubted up to that time in England. Trousseau's attention
was strongly drawn to the necessity of the operation of thoracentesis
as early as 1832, when he attended a case at the Hôtel Dieu that died
from excessive pleuritic serous effusion. Louis, from the observation
of 150 cases of simple pleurisies that had recovered, had enunciated
the law that pleurisy is never the immediate cause of death. This fact,
together with Récamier's want of success, had so prejudiced the minds
of French practitioners against the operation that it was loudly
condemned in acute cases of effusion and in all cases of hydrothorax.
Having no fears of fatal termination in pleurisy, they saw naturally no
necessity for surgical interference. Trousseau states that it was not
until after he had witnessed three patients die from acute pleurisy
that he ventured to operate (Sept. 11, 1843). He did not summon a
consultation, for fear of being thwarted. It was so successful that he
was emboldened to operate without hesitation. After his third operation
he read his memoir to the Academy of Medicine in 1843. Trousseau in
these memoirs maintained the proposition which extensive observation
has now after forty years fully sustained, that dyspnoea and orthopnoea
may occur when the effusion is in moderate quantity, and that they may
be absent when the effusion is considerable, especially if it has
formed slowly. Furthermore, that the signs that constantly indicate the
gravity and imminent danger of effusions, and which consequently demand
the operation, are the displacement of the heart (whence results
syncope), displacement of the mediastinum, depression of the spleen and
of the liver, acceleration and feebleness of the pulse, and an anxious
countenance.

The next year (1844) Trousseau read another memoir on the same subject.
He used the trocar with Reybard's gold-beater's skin at the orifice.
While he was popularizing the operation and laying down the indications
which called for its performance, several English observers[305] were
turning their attention in the same direction. The paper by Hughes and
Cock[306] showed that they had been operating in Guy's Hospital for
four or five years, and with great success, using a simple trocar and
canula of the diameter of one-twelfth of an inch. They imputed their
success to the small size of the instrument used, which allowed the
fluid to flow slowly and never permitted air to enter the chest during
respiration. They gave a tabular account of 20 operations. Hamilton
Roe[307] at that time was operating successfully with the trocar. {593}
Roe's paper was replete with information and with practical
suggestions. He tabulated 39 cases where syncope (one great objection
which had been urged against the operation) did not occur even once. He
disproved another popular objection, that there was great danger of the
admission of air into the pleural sac. Owing to the size of his trocar,
a considerable quantity of air entered the pleura during his
operations, and in some of them so freely as to produce all the
physical signs of pneumothorax, but in none of them did it produce any
permanently evil effects. In one instance only was even temporary
inconvenience caused. When the fluid was ascertained by the
exploring-needle to be purulent, he advised the immediate performance
of the operation. In acute cases he recommended a delay of three weeks
as the time for testing nature's powers of absorbing the fluid. He
advised the closing of the orifice after operation. This author gave an
account of his 24 cases. He concluded by stating that the operation is
not more dangerous than any other which is performed upon the human
body, and that the evil consequences supposed to attend it are
imaginary rather than real, inasmuch as it was only fatal in 1 out of
24 cases, and does not produce even temporary inconvenience. Thompson
in the same year justly condemns the practice of leaving the canula in
the orifice--a proceeding he considers as capable of converting a
serous into a purulent fluid. In 1848,[308] at the request of H. I.
Bowditch of Boston, J. M. Warren operated by the usual method
recommended in the works on surgery. Partial relief was obtained, but
the amount of suffering undergone by the patient during the operation,
and the fact that an aperture was usually left open by this method,
decided Bowditch that he would never recommend it unless under very
urgent circumstances. Soon after this, Stone operated with the common
trocar and canula, by the advice, in consultation, of Bowditch. In
1849, Bowditch saw another death resulting from effusion where he had
advised the operation, but the consulting surgeon would not consent.

[Footnote 305: _London Medical Gazette_, 1847.]

[Footnote 306: _Guy's Hospital Reports_, vol. ii., 1844.]

[Footnote 307: _London Lancet_, 1844, copied into _Amer. Journal Med.
Sciences_, Oct., 1845.]

[Footnote 308: Bowditch, _Amer. Journal Med. Sciences_, April, 1852.]

To illustrate the opposition Bowditch found in the United States, he
quotes[309] a remark of W. W. Gerhard, the distinguished auscultator of
Philadelphia, "that he should be as willing to have a bullet shot
through his chest as to have paracentesis performed on one of his
patients."

[Footnote 309: Unpublished MS., 1882.]

About 1850,[310] Bowditch saw the paper published by Hughes and Cock,
and it determined him in future to try the trocar they had used or
something like it.[311] "Fortunately, a few weeks before (April 10,
1850) M. Wyman had a sudden and severe case with large effusion and
intense orthopnoea. Death was threatening, yet Wyman felt called upon
by public opinion, medical and lay, to summon a prominent practitioner
from Boston. They both agreed that the patient was in extreme danger,
and Wyman urged tapping with an exploring-trocar. It was decided to
postpone surgical interference until next day, when another meeting
would be held, the consulting physician returning to Boston to advise
with the ablest men of the faculty and render their decision the
following forenoon. That was done, and it was found that no prominent
practitioner in Boston would consent to the idea of tapping.
Nevertheless, the oppression was so severe, and death so imminent
unless the patient could be relieved by some means, that the country
physician agreed to Wyman's proposal that an exploring-trocar should be
introduced. The fluid flowed out imperfectly, but some relief and no
harm resulted" (Bowditch). Two days after this, Wyman operated again
with the exploring-trocar and a suction-pump. Wyman[312] demonstrated
to John Homans on the 23d of February, 1850, that the chest could be
safely punctured with his instrument and the serum evacuated in acute
pleurisy.

[Footnote 310: _Ibid._]

[Footnote 311: _Ibid._]

[Footnote 312: Private letter to author, 1883.]

Although suction, as we have shown, was used as far back, probably, as
Galen (second century), by Scultetus in 1662, and was in use in 1707,
as {594} shown in Anel's work, in 1742 in Laurence Heister's work, by
Ludwig and Lehren in 1768, again in 1796 (Benj. Bell), yet it had been
abandoned and lost sight of, with the exception of Laennec's suggestion
of its application in the form of a cupping-glass over the orifice of
puncture, until Guérin (1841) used it. The author followed Trousseau's
clinics in 1849 and 1850, and saw him repeatedly operate with Reybard's
canula guarded by gold-beater's skin, but never with Guérin's suction
apparatus. The French seemed to have lost sight of it until 1865, when
Guérin, at the French Academy, recalled attention to it, showing how he
aspirated liquids, instead of allowing them to flow outward after the
puncture. His apparatus consisted of a curved trocar, the end of which
was made tapering and sharp enough to puncture the thorax through the
skin and the muscles; of a pump, the piston of which was perfectly
adjusted to produce a vacuum; and of an adjuster at the extremity of
the pump, consisting of a stopcock which enabled the operator
alternately, without removing the instrument, to aspirate the fluid and
evacuate it into a basin. Wyman's pump, invented in 1850, was arranged
very much in the same way, only it contained valves which were opened
and closed by the movement of the barrel, to enable the operator to
suck out the fluid and then force it out of the pump. After the
operation the skin, being drawn over and closing the orifice, acted as
a valve which prevented at the same time the entrance of air and the
escape of fluid. Dieulafoy, in November, 1869, invented his aspirator,
which is based upon the same principles as those used by Guérin (1841)
and by Wyman and Bowditch (1850)--namely, pneumatic aspiration, which
the vacuum of the air-pump supplies. Guérin's instrument was large and
costly. Wyman's trocar was of a very small diameter, being only
one-twenty-fourth of an inch, and the canula but little larger. This
was attached, at first, directly to the aspirating syringe, afterward
by means of a flexible tube. With this apparatus Wyman demonstrated
that tissues could be safely punctured and cavities evacuated without
the admission of atmospheric air, that the wound, causing but a drop or
two of blood, was followed by no inflammation, and that no dressing was
required. The smallest trocar used previously to Wyman's was that of
Roe, which was one-twelfth of an inch in diameter. From 1850, Bowditch
appreciated the great value of Wyman's invention, as shown in one of
the first operations on a patient of his. He adopted and practised it.
His position as professor of diseases of the chest, and his great
reputation in that branch, gave him an extensive practice and brought
him many cases of pleurisy. He met with great opposition from the
surgeons and prominent practitioners of the country, but his results
were so favorable that he forced an unwilling and an unbelieving
profession to accept, as he expresses it, "the beautiful thought of
Wyman of thoracentesis or aspiration with a fine needle." "I considered
the operation so simple, and yet so effectual, and never harmful, that
I deemed it my duty to print cases illustrative of its value." Bowditch
had been for eight or ten years endeavoring to get some effective plan
of opening the chest without risk. He readily caught at Wyman's plan,
and he operated so frequently and successfully as to demonstrate its
value to the medical public both of this country and of Europe. As he
states,[313] it was, in fact, what he had been for years longing
for--viz. a simple and painless, or almost painless, operation for
removing fluids from the thorax--one that could be done without danger
and leave no open wound. Bowditch relates[314] that when he visited
Europe, nine years after his first publication of cases, he showed the
instrument in England, Scotland, France, and Germany, and that he met
with very indifferent recognition of its value. Only W. T. Gardner of
Edinburgh and Budd of London seemed to appreciate the plan. They had
instruments made after the American pattern. All others had no faith in
the operation. In Paris his old master, Louis, smiled {595}
incredulously at his enthusiasm for it and doubted its necessity. At
Vienna Skoda turned with apparent scorn and left the room as Bowditch
was demonstrating its employment. The Parisian authors, Woillez, Peter,
Moutard-Martin, Peyrot, and others, do not even mention Bowditch, but
give Trousseau alone the credit of popularizing thoracentesis.

[Footnote 313: Unpublished MSS., 1883.]

[Footnote 314: _Ibid._]

Trousseau's first publication was in 1843, and yet in 1859 there was no
general adoption of the operation, nor was there until 1869, when
Dieulafoy rediscovered Wyman's wonderful improvement of the application
of negative force to draw out fluids from the chest.

In estimating the value of the substitution of aspiration for the
trocar-and-canula method, we must bear in mind that with the latter
there was danger of the introduction of air into the thoracic cavity,
of the production of fistulous orifices, and the too rapid, and
therefore dangerous, evacuation of the fluid. Moreover, there are cases
where the trocar and canula is not effectual, although the quantity
effused be considerable--where, indeed, the fluid cannot flow out,
although the canula be pushed in actual contact with the fluid. The
explanation of this is now understood. The fluid is kept in the pleural
sac by a negative pressure of from 4 to 5 inches of water (Stone), 6
millimeters mercury (Donders), 5 millimeters mercury (M. Foster),
exercised by the lung in its elastic contraction, and by the passive
tension of the arched diaphragm. The fluid has no tendency to flow out,
and this suctional pulmonary force must be antagonized by an external
suctional force, that of aspiration, before the fluid can be withdrawn.

The invention can best be appreciated from the standpoint reached by
modern investigations of the physics of the living mechanism of the
chest. The principle of applying suctional force in pleurisy is in
imitation of nature's gentle methods in connection with respiration. We
have shown that most of the dangers connected with aspiration are
caused by not taking into consideration the adjustment of lung-tension
with thoracic resilience, and consequently of using too great negative
force and withdrawing the fluid too rapidly and in too great quantity.

Thoracentesis by aspiration, with greater or less force as may be
necessary, is now placed upon a scientific basis. We claim that this
modern method is an American invention--that Morrill Wyman was the
discoverer and H. I. Bowditch the utilizer of the discovery. As such
they may be regarded as benefactors of the human race.

It is extraordinary that Trousseau never alluded to Bowditch's
operations, and that Dieulafoy should never have heard of them.
Fraentzel acknowledges that Bowditch was the first to introduce
aspiration into practice. The Germans have been very slow in
appreciating its value. Fraentzel states that he did not use it until
1871, and that it was not until 1879 that it had in Germany any ardent
supporters. Bowditch[315] has now operated 387 times upon 246 patients
without any unpleasant result.[316] The distinctive points in
Dieulafoy's ingenious modification of the aspirator are that the
needles are very fine, even one-half of a millimeter in diameter; that
the barrel of the exhausting pump is of glass; that there is a
pre-existing vacuum; that we are not compelled to jar the side of the
patient by the process of pumping, and moreover by turning the cock we
produce at once a vacuum in the needle itself, and know with certainty
the moment the fluid is reached, and can see it flow through the glass
index in the tubing, even if it be in drops. We can judge of the nature
of the fluid, whether it be serum, pus, or blood. The minuteness of the
needle is a great cause of safety, because it allows the fluid to flow
so gradually that the lung has time to expand slowly. We can in an
instant arrest the flow of the fluid by turning the stopcock, and if
necessary by drawing out the needle. By giving the needle a downward
direction after it {596} enters the cavity, we prevent the point from
pricking the lung. So small an orifice is made that even if the needle
does touch the lung, there is no danger, for the orifice closes over at
once. As Dieulafoy claims, "the fineness of the needle guarantees the
harmlessness of the puncture." Castraux's concealed point (invented in
1873), and Fitch's (of Nova Scotia) protected canula (invented in
1873), are valuable additions to the aspirator-needle. These
dome-trocars, as they are called, prevent the possibility of injuring
the lung, for the sharp-pointed needle, after it has penetrated the
pleural cavity, is at once, by a slight movement, converted into a
blunt-pointed needle with an orifice near the end. With these very fine
needles the force is sufficient to draw up the thickest fluids. We are
compelled to admit that Dieulafoy's instrument is a great advance on
any other that has been invented. Its simplicity, its easy application,
its safety, have rendered paracentesis a harmless operation and one of
great value in serous effusions. While Guérin and Wyman may both claim
priority of invention, all must admit that Dieulafoy has improved upon
their ideas and given us a beautiful and effective instrument. There
have been proposed, since Dieulafoy showed his instrument in 1869, no
less than forty other aspirators, modifications in form or dimensions
of his apparatus. Of these, to us the most valuable is Potain's bottle
aspirator, with which aspiration can be so easily and effectually
employed. It is simple and cheap. An india-rubber cork accurately
fitting a strong bottle is perforated for two tubes each having a
stopcock. One of the tubes fits on the end at the exit in the basin,
and the other is adapted to an aspirating syringe.

[Footnote 315: _London Lancet_, vol. ii., 1879.]

[Footnote 316: Letter to author, 1883.]

One of the most important of the improvements to the aspirator-canula
is the addition--first suggested in 1858 by Charles Thompson,[317] and
afterward adopted by Potain, Powell, and Fraentzel--of a lateral tube
for the outflow connected with the main canula through which the trocar
passes. By this improvement, in case the canula is clogged up, the
trocar can be pushed down to remove the obstruction without danger.

[Footnote 317: _Med. Times and Gazette_, 1858.]

The principle of aspiration is now well established, and the
indications for its use are becoming more defined and more accurate.
New applications as a means of diagnosis, as well as of treatment,
daily render it more valuable.

To guard against the dangers shown by modern experience to be sometimes
attendant upon the operation of aspirating the pleura (see Dangers of
Thoracentesis), it is now generally admitted that the removal of the
contents of the chest should be slow and gradual; and that, ordinarily,
it is safest at one operation to remove only a portion of the effused
liquid. Our object should be to remove pressure and allow nature by
absorption to take away the remainder, for positive pressure is an
urgent indication for thoracentesis. It is therefore of primary
importance to properly estimate the quantity present, and thus to test
the intra-thoracic pressure. Great care and caution must be used,
because if we extract too much the operation may be followed by serious
results.[318] Large-sized canulæ should never be used, for fear of too
rapid withdrawal of fluid. It has been demonstrated that even with a
capillary perforated needle we can exercise more negative pressure than
is safe, especially toward the close of the operation, when there
supervenes a negative pressure exerted by the fluid remaining in the
pleural cavity. It is from these well-known facts that we recognize the
great value of Potain's ingenious addition to the aspirator of a
manometer of extreme simplicity, a kind of barometer or cuvette, which
is placed along the tube which withdraws the fluid. If we are not
satisfied with this new safety improvement of the aspirator, we may
adopt Douglass Powell's suggestion (_On Consumption, etc._) {597} of
fitting into the bottle a pressure-gauge, so as to know at any moment
what degree of aspiration is being used.

[Footnote 318: _Trans. de l'Assoc. pour l'Adv. des Sciences_, 6th
Session, 1877.]

The syphon method has been of late years very extensively used,
especially by Southey, W. H. Stone, and Garland, A. T. H. Waters,
Wilks, Oxley, and habitually by Douglass Powell. It is a feeble
aspirating force, which has very decided advantages. It is effective,
and acts slowly and uninterruptedly with a gentle and uniform negative
pressure. Its action allows the lung gradually to expand and the
displaced organs slowly to resume their normal position. It thus in
many cases furnishes us with a safe means of thoracentesis. (See
Surgical Treatment, in Pleurisy.)

{598}

{599}

DISEASES OF THE CIRCULATORY SYSTEM.

DISEASES OF THE SUBSTANCE OF THE HEART.

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

CYANOSIS AND CONGENITAL ANOMALIES OF THE HEART AND GREAT VESSELS.

CARDIAC THROMBOSIS.

NEUROSES OF THE HEART.

DISEASES OF THE PERICARDIUM.

THE OPERATIVE TREATMENT OF PERICARDIAL EFFUSIONS.

DISEASES OF THE AORTA.

DISEASES OF THE CORONARY, PULMONARY, SUPERIOR MESENTERIC, INFERIOR
MESENTERIC, AND HEPATIC ARTERIES, AND OF THE COELIAC AXIS.

DISEASES OF THE VEINS.

THE CAISSON DISEASE.

DISEASES OF THE MEDIASTINUM.

DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM.

DISEASES OF THE BLOOD AND BLOOD-GLANDULAR SYSTEM.

DISEASES OF THE SPLEEN.

DISEASES OF THE THYROID GLAND.

SIMPLE LYMPHANGITIS.

{600}

{601}

DISEASES OF THE SUBSTANCE OF THE HEART.

BY WILLIAM OSLER, M.D.

Malpositions of the Heart.

We shall consider only such alterations as affect the whole organ;
faulty position of individual parts comes under the section upon
Malformations. It may, however, be mentioned that cases are known of
complete transposition of the chambers, the pulmonary artery and cavæ
being connected with the left, the aorta and pulmonary veins with the
right side, the valves being also transposed.[1]

[Footnote 1: Pazannuzzi, _London Med. Record_, 1877.]

Malpositions of the heart result either from errors of development, or,
more commonly, from changes in contiguous organs, usually the effect of
disease.

Of the congenital anomalies only a few are of practical interest. The
heart may be placed vertically in the chest, as in the foetus, the apex
beating at the lower end of the sternum; or, more rarely, the organ
lies transversely. Dextrocardia, the condition in which the heart is on
the right side of the body, is much more important, and is usually
associated with the transposition of the abdominal viscera--situs
inversus viscerum. In these cases the apex-beat is in the region of the
right nipple; a distinct area of dulness can be obtained to the right
of the sternum, in which situation the heart sounds are loudest; and,
lastly, there is pulmonary resonance in the place of normal cardiac
dulness. In the great majority of cases--70 out of 78[2]--the abdominal
organs are also transposed, the liver on the left side, the spleen on
the right; but in a few instances the heart alone has been misplaced,
and under such circumstances care is needed to diagnose the condition
from dislocation of the organ due to old-standing lung disease with
retraction.

[Footnote 2: Gruber, _Virchow's Archiv_, 1865.]

More serious congenital malpositions, but of less practical importance,
are the cases of ectopia cordis, which may exist in all grades, from
simple failure of closure in the sternum--fissura sterni--to the most
extreme condition, in which the naked heart lies outside the
chest-wall. Hodgen[3] and March[4] have each described remarkable
examples of the latter condition. In other instances the heart lies
free in the neighborhood of the neck, or it may be in a congenital
umbilical hernia.

[Footnote 3: _American Practitioner_, xviii. p. 107.]

[Footnote 4: _Trans. of the New York State Medical Society_, 1859.]

The malpositions with which we are more immediately concerned arise
from disease of the heart itself or its membranes, or from disease of
contiguous organs.

We judge of the situation of the heart by the site of the apex-beat, by
the position and extent of the area of dulness, and by the character of
the sounds. So constant in health is the position of the apex-beat in
the fifth intercostal {602} space that in our examination of the heart
we seek first to determine its existence as affording the most
important information of the normal situation of the organ. The area of
dulness is a much more variable guide, depending as it does so greatly
on the degree of distension of the lungs. When, as sometimes happens,
neither apex-beat nor area of dulness can be obtained, the position of
maximum intensity of the heart sounds becomes an important indication.

In regard to the effect of respiratory movements in the position of the
heart, with each inspiration it is drawn down slightly by the descent
of the diaphragm, and it is separated from the chest-wall by the
inflation and descent of the left lobe of the lung--in deep inspiration
to such a degree as to obliterate the area of dulness and to prevent
the systolic impulse from reaching the intercostal space.

The effect of gravity on the position of the heart is well illustrated
by the more forcible and extended beat when the chest is bent forward
or when the person is turned toward the left side--procedures
frequently resorted to when from any cause the apex-beat is obscure.

Of diseases of the heart itself, dilatation and hypertrophy are very
common causes of displacement, and in general enlargement the organ may
occupy a very considerable part of the left side of the chest, and the
apex-beat in the seventh or eighth space in the axillary line.
Hypertrophy of the left ventricle alone pushes out the apex-beat, while
enlargement of the right ventricle gives a stronger impulse toward the
left border of the sternum and a more marked pulsation below the
ensiform cartilage. Hypertrophy and dilatation of the auricles increase
the width of the cardiac dulness, and may cause marked pulsation in the
second and third spaces on either side of the sternum.

In pericardial effusion the heart is pressed backward and the apex
slightly raised.

To understand clearly the effects upon the position of the heart of
disease of contiguous organs, we must bear in mind their mutual
relations. Situated in the mediastinum between the lungs on either
side, it is subject to the elastic traction of these organs, which
counterbalance each other, but if from any cause the elastic tension of
one lung is suppressed, as in pneumothorax or in pleural effusions,
then the other lung may also collapse to a slight degree, and pull over
the mediastinum and with it the heart. The pericardium is firmly fixed
below to the diaphragm, chiefly to the central tendon, to a slight
extent also to the muscular substance, but the union with the diaphragm
is so intimate that there can be but little movement of the attached
portion. The mobility of the heart is measured by that of the
mediastinum and pericardium, and through these alone the displacing
forces act. The limits of dislocation are determined by the attachments
of the central tendon, of the inferior cava, and the great vessels at
the root. Within the pericardium the heart has a certain degree of
mobility, but this is confined, as regards pressure or traction
effects, to rotation upon its axes.

Of the malpositions due to changes in contiguous organs, the following
may be considered:

Changes in the Chest-wall.--The gradual incurvation of the ribs and
costal cartilages in some cases of rickets may alter the position of
the heart.

Curvature of the spine, particularly cases which narrow to a great
extent the upper outlet of the thorax, may produce very considerable
displacement of heart and great vessels. There may be areas of
extensive pulsation on either side of the sternum, and the condition
may simulate aneurism of the aorta, as in a case reported by
Bramwell.[5]

[Footnote 5: _Lancet_, 1878, i.]

In certain affections of the lungs the position of the heart is much
altered. {603} In emphysema, when extensive, the apex is directed more
to the right, and the organ is somewhat lower than normal, on account
of the depressed condition of the diaphragm. The heart may also occupy
a more transverse position. The area of cardiac dulness may be greatly
reduced by the distended left lung, and there is usually forcible
epigastric pulsation, due to the lower position of the organ and the
hypertrophy of the right ventricle which almost always accompanies
emphysema.

The most marked displacement is produced by fibroid induration of the
lung, with contraction--cirrhosis. As the process of condensation goes
on, the chest-wall is gradually flattened, and the mediastinum, with
the heart, drawn toward the affected side. When the left lung is
involved, the heart may be completely to the left of the median line,
and is usually drawn upward as well. There may in such cases be a very
wide area of impulse, as the heart occupies the position of the left
lung in front. In cirrhosis of the right lung the organ is drawn toward
the right side, and the area of visible impulse may be in the third and
fourth interspaces to the right of the sternum. In the process of slow
traction the heart revolves upon itself and the left chambers come
uppermost. In many cases of chronic phthisis, when the anterior margin
of the left lung is involved, the retraction from induration may leave
a large portion of the heart exposed and increase the area of visible
pulsation; sometimes, when there is much contraction of the upper lobe,
the organ is drawn up and to the left, and the apex-beat may be in the
fourth interspace.

The pressure of a pneumonic lung may depress the diaphragm and draw
down the heart.

Abnormal conditions of the pleuræ are frequent causes of cardiac
displacements. In pneumothorax there is collapse of the lung on the
affected side, and the elastic traction of the sound lung draws over
the mediastinum and heart. It is not that the heart is pushed over, as
so often stated, but the tension of the other lung, being unopposed,
pulls the mediastinum toward the sound side. Later, when, as usually
happens, effusion takes place, the pressure assists in the
displacement. In pleuritic effusion dislocation of the heart to one
side is almost constant if the amount of fluid is at all considerable.
Here pressure plays the most important part, and the heart is gradually
pushed over by the effusion; but the elastic tension of the lung on the
sound side is also concerned in the result. In right-sided effusion the
whole organ may be to the left of the median line, and from the
depression of the diaphragm it is usually lower in the chest, so that
the apex-beat may be in the sixth, rarely the seventh, interspace in
the axillary line. When the exudation is on the left side, the
dislocation is more marked, and there may be a cardiac impulse at the
right nipple or even beyond it. A common error is to regard the
pulsation as due to the apex, but it is invariably caused by some
portion of the right chambers, usually the ventricle. Even in the most
extensive effusion the apex is probably never pushed beyond the right
border of the sternum, and the relative position of apex and base is
not changed. This I have carefully noted in several autopsies.[6]

[Footnote 6: Fig. 76 of Sibson's article on "Displacements of the
Heart" in _Reynolds's System of Medicine_ gives an incorrect idea of
the position of the organ in these cases, as the apex is represented as
beating beneath the right nipple.]

In the gradual absorption of a pleuritic effusion, serous or purulent,
the heart may not only regain its normal position, but is in many
instances drawn toward the affected side by the contracting false
membranes.

Of conditions of the mediastinum producing displacement, two only need
be mentioned--aneurism and tumor. Very large aneurisms of the arch
usually press the heart downward, and its axis may be transverse; but
much depends on the direction of growth, and a slight lateral and
downward dislocation is most frequently met with. Tumors do not
necessarily {604} cause displacement, but when large there may be some
dislocation in the direction of the growth of the mass. Most extensive
masses of mediastinal cancer may occur without any disturbance of the
position of the heart.

Diseases of the abdominal viscera not uncommonly produce dislocation of
the heart, generally upward. Extensive peritoneal effusion, gaseous or
fluid, forces up the diaphragm, and with it the heart, which may assume
the transverse position, and the apex beat as high as the third
interspace. Gas much more readily than fluid rapidly lifts the
diaphragm and produces upward dislocation of the heart. Diaphragmatic
hernia of intestines or stomach may push the heart up or to one side.

Conditions of the liver not infrequently affect the position of the
heart. Abscess or hydatid cysts of the left lobe may push the organ up
and to the left. More rarely large hepatic tumors drag the diaphragm
down, and with it the heart. Very great splenic enlargement, as in
leukæmia, may push up the diaphragm and lift the heart.

Other abdominal growths, as large retro-peritoneal and ovarian tumors
or aneurism of the abdominal aorta, may occasionally produce the same
effect. Knowsley Thornton has given in Fothergill's work on the _Heart_
an excellent account of the upward displacement of the heart in ovarian
disease.

As a very rare circumstance, the heart is displaced by accidental
injury to the chest-walls. The case which Stokes relates of this kind
was probably, as he subsequently suggested, due rather to the effects
of the pleuritic effusion which followed the accident.

The dislocations of the heart when gradually induced rarely disturb to
any serious extent the functions of the organ.

Myocarditis.

Inflammation of the heart-muscle is rarely primary; usually it is
associated with endo- or pericarditis, strain,[7] embolic processes,
disease of the arteries, or the presence of certain
poisons--diphtheritic, rheumatic, etc.--in the blood.

[Footnote 7: Some French writers refer specially to the occurrence of
myocarditis from strain or prolonged muscular exercise--myocardite des
surmenes. Peter (_Maladies du Coeur_, Paris, 1883) gives two cases
(without autopsy), and quotes a case from Revilliod, whose work (_La
Fatigue_, Lausanne, 1880) I have not been able to consult.]

We may recognize three forms--acute suppurative, acute interstitial,
and chronic myocarditis. By many writers the parenchymatous
degeneration so frequent in fevers is regarded as an inflammation, but
it is the result of a process which we can scarcely term inflammatory.

Acute suppurative myocarditis is almost invariably associated with
pyæmia or with malignant endocarditis, and in most instances may be
regarded as embolic. In severe pyæmia from any cause foci of
suppuration are not infrequently met with in the walls of the
ventricles. There may be multiple abscesses or a single purulent
collection varying in size from a pea to a walnut. Numerous miliary
abscesses are not so often met with in ordinary pyæmia as in
endocarditis. If large, the abscess may burst into the heart or into
the pericardium and excite inflammation of this membrane; or, indeed,
without perforation, as I saw in one instance. The calcareous nodules
occasionally found in the muscle-substance have been regarded as healed
abscesses. Suppurative myocarditis is a frequent result of malignant
endocarditis, and we meet with it either in the form of miliary
abscesses, scattered in numbers through the substance, or as large
solitary abscesses at the bases of vegetative outgrowths or in
connection with excavating ulcers of the endocardium, valvular or
mural. The small embolic abscesses vary in size from {605} a pin's head
to a pea, and may occur in extraordinary numbers in the
muscle-substance of all the chambers. They present usually a central
grayish-white focus of suppuration surrounded by a zone of
deeply-congested and hemorrhagic tissue. Microscopically, there is a
central infiltration of leucocytes with destruction of the
muscle-fibres, and in every instance colonies of micrococci can be
readily discovered. These abscesses are identical in character with
those occurring in the kidneys, intestines, and brain. Sometimes at the
base of large endocardial outgrowths, particularly of the aortic
segments, abscesses are found extending deep into the muscle-substance,
and even perforating the wall. These occur most often in the left
ventricle, but occasionally in the right, as in a case of stenosis of
the pulmonary valves at the Montreal General Hospital, in which there
was an abscess cavity in the wall of the right ventricle the size of a
marble, situated at the base of some endocardial vegetations. The acute
ulcer of the heart is of the nature of a suppurative myocarditis,
having its starting-point, in the great majority of cases, in the
endocardium. It may perforate the wall of the ventricle, as in the
cases of Mackenzie[8] and Keating.[9] The blood-pressure in the
abscess-cavity may dilate the wall, and form what is known as acute
aneurism of the heart.

[Footnote 8: _Path. Soc. Trans. London_, xxxiii.]

[Footnote 9: _Trans. of the College of Physicians of Philadelphia_,
1879.]

Acute interstitial myocarditis occurs in connection with the infectious
fevers, and also with pericarditis, more rarely endocarditis. It is
characterized by the presence of numerous round cells in the
interfibrillar tissue, multiplication of the corpuscles, and
degeneration, granular or fatty, of the muscle-fibres. The coarse
appearances are--a relaxed state of the cardiac walls, pale or turbid
condition of substance, in extreme instances a sodden, soft friable
state, so that the muscle readily tears on pressure. In acute
pericarditis the superficial myocardium, for a line or two beneath the
membrane, frequently presents this condition in a typical manner; it
looks pale and turbid, contrasting strongly with the deeper parts, and
on examination presents infiltration of leucocytes, swelling of the
interstitial tissue, sometimes effusion of blood-corpuscles, and a
swollen, granular, or fatty state of the muscle-fibres. Although the
process may be intense, suppuration rarely occurs, whereas in
myocarditis supervening upon inflammation of the endocardium it is, as
we have seen, not uncommon. A similar diffuse interstitial process is
met with in many of the fevers. In rheumatism, typhus, scarlet fever,
small-pox, and diphtheria the myocardium may be found relaxed and soft,
the chambers dilated, the substance pale, easily torn, in some
instances extremely soft; and this condition has been variously
described as inflammatory or degenerative. While not denying that such
a state of the muscle-fibre may be brought about by the action of the
fever or the influence of some specific poison without any signs of
inflammatory action, yet in other instances changes have been found
which are evidently of the nature of a myocarditis. In these cases the
intermuscular connective tissue is swollen, infiltrated with round
cells and nuclei, the vessels are dilated, and often there are minute
extravasations and the muscle-fibres are granular and fatty, with
indistinct striæ and nuclei. As Leyden[10] has pointed out, this
condition probably affords an explanation of some of the cases of
sudden death in diphtheria. It may occur without the coarse or
microscopic appearance of degeneration of the muscle-fibres, and when
of any duration may produce areas of atrophy. Though usually diffuse,
it may be patchy and limited in distribution. Martin[11] has described
in cases of sudden death in diphtheria and typhoid fever an acute
endarteritis of the small branches of the coronary arteries, which
probably has a close relationship with this acute interstitial
myocarditis.

[Footnote 10: _Zeitschrift für klinische Medicin_, Bd. iv.]

[Footnote 11: _Revue de Médecine_, 1881.]

{606} The SYMPTOMS of acute myocarditis are those of cardiac weakness
and irritability, and it is the conditions under which these occur
which make us suspect involvement of the myocardium rather than any
special features pertaining to the disease. We may reasonably suspect
its presence in a case of rheumatism, puerperal fever, or other
specific fever when the patient complains of cardiac distress or actual
pain, with shortness of breath, and on examination we find a weakened
impulse, feeble, indistinct first sound, and a small, irregular pulse.
The area of heart-dulness is increased, and there may be a murmur due
to muscular incompetence. There is usually fever, but this is generally
due to the primary affection. The symptoms are those of a weak and
dilated heart, and are peculiar only in the mode of onset and the
circumstances under which they arise. A point of note observed by
Stokes is the weakening or disappearance of organic murmurs during an
attack of acute myocarditis. In acute pericarditis grave implication of
the myocardium may be suspected when the pulse gets small and rapid,
dyspnoea urgent, and the cardiac pain is increased. Such symptoms, in
the absence of copious effusion, would appear to indicate extension of
the inflammation to the heart-muscle. Even the occurrence of
suppuration has no distinctive symptoms, as it almost invariably occurs
as part of a pyæmic process, and the cardiac weakness which supervenes
may be regarded as an outcome of the septic or febrile condition. The
bursting of an abscess into the pericardium will excite violent
pericarditis. In the case of Kortüm, referred to by Friedrich,[12] an
abscess in the septum burst into the ventricle; the symptoms, which
developed suddenly during a lecture, were a sense of constriction in
the chest, dyspnoea, and lividity, and death occurred in six hours.

[Footnote 12: _Virchow's Handbuch_, Bd. v.: "Herzkrankheiten," S. 275.]

The DIAGNOSIS can rarely be made with certainty; at the best we can
suspect its presence under the conditions above mentioned.

The course of suppurative myocarditis is always unfavorable, but the
fatal termination of the case is usually dependent on concomitant
causes. The possibility of recovery in some instances of abscess of the
heart is suggested by the occurrence of caseous and cretaceous masses,
probably the remnants of collections of pus.

The chief danger in interstitial myocarditis is heart paralysis and
sudden death, as occur in diphtheria and occasionally in rheumatism.
From mild grades of the disease recovery may take place, and even when
general and severe it has often been some indiscretion which has
induced the collapse, as sudden sitting up in bed or getting out to
attend to the calls of nature. Possibly the slight intramuscular scars
and spots of atrophy furnish evidence of past acute myocarditis.

When suspected, the TREATMENT should consist of absolute rest, muscular
and mental, with careful feeding and stimulation. If a rheumatic case
upon the alkaline or salicylate treatment, the remedies should be
stopped. I saw sudden death from heart failure in a case of acute
rheumatism in which during four days the full alkaline treatment of
Fuller was followed, and in which, by mistake, a much larger quantity
of the bicarbonate of soda was given each day than had been intended.
Strychnia and small doses of quinine may be given. Shall digitalis be
employed in acute myocarditis? Upon this point authorities differ. If
we regard it as simply increasing the force of the muscular
contractions, we can understand the fear of straining a weakened heart;
but digitalis has important trophic influences, and, while it
stimulates the vigor of the contraction, improves the nutrition of the
heart-muscle and renders it better able to contract. After all, the
question amounts to the giving of digitalis in dilatation, and with a
weak first sound and feeble action the careful administration, in
conjunction with stimulants, will be found beneficial. Peter[13] speaks
highly of the application of a blister in the region of the heart.

[Footnote 13: _Loc. cit._]

{607} Chronic Myocarditis (Fibroid Heart).

A condition characterized by the substitution in areas of variable
extent of a fibrous connective tissue for the muscular substance. It is
an interstitial growth, comparable to the cirrhosis of other organs,
and the muscle-elements in the affected regions are wasted or entirely
destroyed. The process may occur in a mild grade throughout the organ,
but it is more common to find it distributed in certain parts which
seem specially prone to this form of degeneration.

The conditions under which it is most likely to occur are those which
we find in connection with arterio-sclerosis. It is an affection of
adult and advanced life, and is met with most frequently associated
with disease of the coronary arteries. In chronic valvular affections
it is very common, and may be part of the so-called cyanotic induration
or an extension from the thickened endocardium. Sometimes it seems a
part of a general arterio-capillary fibrosis. In a few cases there is
direct extension from the pericardium. Rheumatism is in this way
indirectly responsible; possibly some of the cases are directly
traceable to acute interstitial myocarditis occurring in this disease.
Chronic alcoholism, syphilis, and gout are prominent factors in the
etiology. Some of the most marked cases give no clue in the history or
habits of any conditions which we could reasonably connect with the
disease. Males are more often affected than females. The tendency to
arterio-sclerosis seems to run in some families. Mental anxiety is not
without influence, and when the disease is established seems very
liable to bring on the anginoid attacks. The situation and extent of
the fibrosis are very variable. The papillary muscles and the columnæ
carneæ of the left ventricle are most frequently affected, less often
the corresponding structures on the right side. The middle portion of
the muscular bundles and the apices of the papillæ are first involved.
In the latter the process may extend almost to their bases, but on
section it will be found that it is more advanced in the superficial
than the deep parts. This change is very common in cases of valvular
disease with hypertrophy, especially mitral stenosis, but it often
occurs in elderly persons who have had no special heart symptoms.

Beneath patches of pearly-white thickened endocardium local fibrosis
may occur, often seen at the upper part of the septum in left
ventricle, and in the dilated and thickened left auricle of mitral
stenosis, and occasionally in other parts. This is usually regarded as
an extension from a chronic endocarditis. More rarely the fibrosis
extends from a thickened pericardium, but cases are on record of the
conversion of the outer layers of the muscular fibres into a firm, hard
tissue. We frequently meet with scattered areas of fibrosis in septum
and ventricular walls without any implication of peri- or endocardium.
During foetal life an endo-myocarditis may occur in the conus of the
right ventricle, less frequently in the left, and produce very great
narrowing by the gradual contraction of the newly-formed tissue. But
the condition to which the term fibroid heart can be most properly
given is an extensive affection of the left ventricle, involving most
commonly the anterior wall near and at the apex and the lower part of
the septum. In these cases there may be marked bulging at the apex, and
on section the wall cuts with great resistance, and a dense fibrous
tissue of a grayish-white appearance occupies the position of the
myocardium. In extreme cases a large part of the septum and anterior
wall is in this state, and may present only traces of muscular tissue.
There is usually thinning, sometimes thickening, of the affected
portions, and the septum bulges toward the right ventricle. The
endocardium is opaque, often much thickened, and directly continuous
with the fibrous tissue. The columnæ carneæ may be narrow and
flattened, and the lacunæ {608} between them very small. The chamber is
usually dilated. The upper third of the septum and the base and
posterior wall of the ventricle in such cases present a marked contrast
to the affected parts, and may look natural, but more commonly are
hypertrophied. The other chambers may not show any special change or
there may be scattered areas of fibrosis. The thinning and dilatation
at the apex and septum are the conditions which precede and lead to the
formation of cardiac aneurism. The valves may be normal, but in many
cases there is sclerotic endocarditis and retraction. The histological
appearance varies much with the stage of the process. When early or
where advancing, the muscle-bundles are seen separated by round and
elongated cells. The process is usually more marked about groups of
fibres, which gradually become isolated by the increase of the growth,
and in this way one often sees streaks or patches of muscle-tissue
surrounded by the fibrous elements. The destruction of the muscle-cells
is apparently by pressure; they gradually waste and present the
condition of brown atrophy, the pigment of which remains and indicates
the position of the fibres. The intimate pathology of the process is of
great interest. Doubtless in some instances we may attribute the
fibrosis to an extension of an indurative process from the endo- or
pericardium, but the researches of Tautain,[14] Martin,[15] Huber
(Karl),[16] and others have thrown a new light on the subject, and it
seems probable that in most instances the fibroid degeneration is
associated with changes in the coronary arteries. The former describes
an endarteritis and a periarteritis of the small vessels, leading to
disturbance of nutrition and increase of the connective tissue
(sclérose dystrophique). Huber in a considerable number of cases has
traced the connection between the arterio-sclerosis, chiefly of the
smaller twigs, and the indurative process. The region supplied by the
obliterated arteriole is in the condition of an infarct and undergoes
an anæmic necrosis, and subsequently by a proliferating myocarditis is
transformed into a fibroid area. The condition is well described and
figured by Ziegler.[17] Why this obliterating endarteritis should be so
limited in the majority of cases to the vessels of the left ventricle
is not very clear. The parts most distant from the aorta seem most
liable to the process, as the apex and the tips of the papillæ; and it
is interesting in this connection to note that the left coronary artery
is more frequently diseased than the right.

[Footnote 14: _Thèse de Paris_, 1878.]

[Footnote 15: _Revue de Medicine_, 1883.]

[Footnote 16: _Virchow's Archiv_, Bd. lxxxix.]

[Footnote 17: _Pathologische Anatomie_, Lief. ii., 1884.]

In the milder grades of fibrous myocarditis, when only the apices of
the papillæ and thin layers beneath the endocardium are involved, the
heart does not appear to be seriously affected; but when of any extent
the vigor and force of the contractions are impaired, and the ventricle
is unable to do the work of a healthy muscle. Compensatory hypertrophy
is not readily established, possibly on account of the arterial
sclerosis on which many of the cases seem to depend, although in rare
instances, as in a specimen referred to by Quain,[18] there may be very
great muscular hypertrophy. Dilatation of the left ventricle is much
more apt to follow, as the fibroid walls have not the resisting power
of muscular tissue, and the patients finally present a clinical picture
of heart failure. The gradual yielding of the fibroid region may result
in aneurism.

[Footnote 18: "Lumleian Lectures," _Lancet_, 1872, i.]

There are no characteristic symptoms to indicate the condition. The
fibroid heart is a weak heart, and it is scarcely possible to
distinguish it from fatty degeneration. A feeble, irregular, sometimes
slow, pulse, dyspnoea on exertion, and painful anginoid
attacks--symptoms which may have persisted for many years--are special
clinical features in many cases. In a patient I examined some years ago
for Palmer Howard of Montreal--a typical instance of the condition
under consideration--the first symptoms began eight years before death
with angina, and there were repeated attacks of cardiac asthma. {609} A
careful study of the case was made by Howard[19] extending over several
years, and weak heart, dyspnoea on exertion, and anginoid attacks were
the prominent symptoms.

[Footnote 19: "Fibroid Disease of the Heart," _Canada Med. and Surgical
Journal_, vol. viii., 1880.]

Several very careful studies of the disease have been made within the
past few years.[20] Among the symptoms the following may be specially
considered. The first place seems accorded by all to the cardiac
weakness, and in consequence the pulse is feeble. By some (Rühle)
irregularity is regarded as a special feature (delirium cordis), but
Ebstein refers to three cases in which the pulse was always regular.
Juhel-Renoy also speaks of it as frequent and regular. In many cases
the number of beats appears about normal; in others there is a great
increase; while in a third set the pulse may be very slow, sinking to
40 or 50 per minute. It is evident that in regard to regularity and
frequency of the pulse there are very great differences. In this
connection it is interesting to refer to the case of thrombosis of the
coronary artery reported by Hammer,[21] in which the pulse sank to 8
per minute.

[Footnote 20: Rühle, "Zur Diagnose der Myocarditis," _Deutsches Archiv
f. klin. Med._, Bd. xxii.; Ebstein, _Zeitschrift für klinische
Medicin_, Bd. vi.; Leyden, _Ibid._, Bd. viii.--a most important and
exhaustive article; Welch, in a paper read before the Medical Section
of the American Medical Association, Washington Meeting, 1884;
Juhel-Renoy, _Archives gén. de Médecine_, Juillet, 1883.]

[Footnote 21: _Wiener Med. Wochenschrift_, 1878, No. 5.]

Angina is a most important symptom; attacks may recur for years, and
death may take place in a paroxysm. Asthmatic attacks are very common:
a feeling of impending suffocation, and gasping for breath amounting in
some instances to urgent dyspnoea. Oedema of the lungs may occur in
these attacks. Fainting and pseudo-apoplectic attacks are frequent
symptoms. The physical signs are not very definite or constant. The
apex-beat may be displaced and weak, perhaps unrecognizable. With an
increase in the area of dulness this is a sign of dilatation. A
systolic murmur at the apex is not infrequent. There may be the bruit
de galop; gradual heart failure, with general dropsy, is the mode of
termination in a considerable number of cases.

The DIAGNOSIS can rarely be made with certainty. The combination of
weakened heart, atheromatous arteries, and angina attacks occurring in
a person above fifty years of age is certainly suggestive of the
existence of this condition; but, as will be seen, this group of
symptoms occurs also in fatty degeneration, although the anginoid
attacks are probably not so frequent.

In spite of the admirable clinical memoirs above referred to, we are
still in need of careful studies of an extensive series of cases,
whereby we can get information which will enable us to distinguish more
clearly than we can at present the diseases of the myocardium from one
another. In this respect our pathological knowledge is in advance of
our clinical.

The TREATMENT is largely that of cardiac dilatation and angina, which
will be elsewhere considered. The condition is a chronic one, and often
associated with hypertrophy, and many of the symptoms are dependent
upon failing compensation. Under such circumstances digitalis is
indicated, but when there are attacks of angina caution must be
exercised in its use.

The Degenerations of the Heart-Muscle.

Under this division we shall consider the following conditions, all of
which are characterized by an alteration in the quality and an
impairment of function in the affected tissue: 1. Anæmic necrosis; 2.
Parenchymatous degeneration; 3. Fatty changes, infiltration and
degeneration; 4. Brown atrophy; 5. Amyloid degeneration; 6. Hyaline
degeneration; and 7. Calcareous degeneration.

{610} 1. Anæmic necrosis is a condition which results in the
heart-muscle when a branch of the coronary artery is blocked either by
a thrombus or an embolus, or is obliterated by a progressive sclerosis.
The region supplied by the affected vessel is deprived of blood and
undergoes a process of infarction. In some instances the tissue is not
infiltrated with blood, as in an ordinary infarct, but has a pale
yellowish color and is very soft. When there is extravasation the color
is more reddish-brown. Histologically, the muscle-cells are found in a
state of granular degeneration, and on staining the nuclei do not take
the tint, and the whole tissue ultimately assumes the homogeneous
granular aspect of coagulation necrosis. There may be fatty
degeneration in the contiguous muscle-fibres, and finally, as with
infarcts in other organs, fibroid induration takes place. This process,
as before mentioned, plays an important part in the production of the
fibroid patches scattered through the myocardium. When fresh, the
softening of the affected region may be marked, and the name myomalacia
cordis which Ziegler[22] has suggested is so far suitable, but it seems
more appropriately applied to that condition of general softening of
the organ met with in severe fevers. This process most frequently
affects the left ventricle, and if extensive may lead to rupture.

[Footnote 22: _Loc. cit._]

The clinical aspects of this condition, as induced by sclerosis of the
coronary arteries, have been recently studied with great care by
Leyden.[23] In acute cases death occurs in a few hours with symptoms of
intense angina pectoris and heart failure. The subacute cases are
characterized by recurring anginoid attacks lasting from a few minutes
to half an hour. There may be attacks of asthma with heart weakness,
and signs of oedema of the lungs. The clinical picture is that of
angina pectoris, and the patient may have had similar attacks on
previous occasions.

[Footnote 23: _Zeitschrift f. klin. Med._, Bd. vii., 1884.]

2. Parenchymatous Degeneration.--The relation of inflammation of the
heart-substance to this degeneration is still somewhat indefinite. I
have under Myocarditis described an acute interstitial form
characterized by inter-fibrillar swelling with exudation and
proliferation of corpuscles, and often granular or fatty degeneration
of the muscle-cells. These changes may certainly be regarded as
inflammatory, and they are met with either in association with endo- or
pericarditis or in connection with specific fevers. Under the term
parenchymatous degeneration or cloudy swelling Virchow described[24] a
change of frequent occurrence in the heart-muscle and elsewhere, which
I think should be distinguished from myositis, although the two
processes may lead to alterations difficult to distinguish
macroscopically. It is characterized by a pale, turbid state of the
cardiac muscle, general, not limited, and a relaxed, soft, brittle
condition of the walls. The turbidity and softness are the special
features; there are no peri- or endocardial changes--simply the loss of
color and consistence. It is the softened heart of Laennec and of
Louis; and Stokes speaks of an instance in which "so great was the
softening of the organ that when the heart was grasped by the great
vessels and held with the apex pointing upward, it fell down over the
hand, covering it like the cap of a large mushroom."[25]
Microscopically, the fibres are indistinct, the protoplasm occupied by
fine granules which obscure the striæ, and sometimes the nuclei.
Proliferative changes rarely occur, although swelling and
multiplication of the nuclei and the interstitial cells have been
described. The granules may be extremely minute, or so large that they
are mistaken for fat. They are generally uniform in size, and are
scattered irregularly through the fibres. In extreme grades the entire
fibre may be occupied by them, and no trace of structure can be seen.
Dilute acids and alkalies dissolve the granules, but they resist the
action of ether, indicating their albuminous nature. This condition is
met with in the infectious diseases--typhoid, {611} typhus, small-pox,
pyæmia, remittent fever, etc.--particularly when the disease is
protracted and the temperature high. Apparently, we must regard it as
an expression of the effect of the poison upon the metabolism of the
fibres, inducing a separation of albuminous particles in a granular
form. That the high temperature alone does not produce it is
demonstrated by its absence in many other diseases in which this
condition prevails. The relation to fatty degeneration is not clear. It
would appear to precede the development of this change.

[Footnote 24: _Archiv_, vi.]

[Footnote 25: _Diseases of the Heart_, Am. ed., p. 373.]

The effect of this degeneration is virtually the same as that of
myocarditis, already described. It produces the weak heart of fever so
well described by Stokes,[26] with indistinct impulse, feeble or
imperceptible first sound, and progressive diminution of contractile
power. There is often a great reduction in the number of beats, which
may sink to 40 or 50 per minute. In severe cases of typhoid fever we
often have an opportunity of studying the progressive enfeeblement of
the heart with weakening or disappearance of the first sound.

[Footnote 26: _Loc. cit._, chap. vii.]

To Stokes we are indebted for the suggestion of the use of alcohol in
this condition, and the experience of the past forty years has fully
confirmed this practice of the Dublin school.

3. Fatty Heart.--Two conditions of the heart are recognized under this
heading--viz. fatty infiltration and fatty degeneration.

Fatty Infiltration.--Cor adiposum, Lipomatosis cordis, and Fatty
hypertrophy or overgrowth are synonyms found in the older and more
recent works.

A condition in which there is an excess of fat beneath the pericardium
and a growth of the same between the fibres of the myocardium. There is
normally a certain amount of fat in the cardiac groves, particularly
the auriculo-ventricular, and along the coronary arteries. An excess is
not infrequently met with in connection with general atrophy, whether
the result of disease or the natural decay of old age. Here it serves
as padding, and has no pathological significance. In very corpulent
persons there is always much subpericardial fat; it forms a part of the
general obesity, and in this state an excessive accumulation may lead
to a dangerous or even fatal impairment of the contractile power of the
heart. Obesity is the expression of a morbid tendency, generally
hereditary, to the deposition of fat in the connective tissues. A
sedentary life and the consumption of food rich in carbohydrates favor
this tendency, but we see it arise under conditions just the opposite
when the predisposition to polysarcia is marked. Males are more usually
affected than females, at least in Great Britain and Germany.

In the inspection of the bodies of very corpulent persons we find the
mediastinum occupied by masses of fat which may completely cover the
pericardium. The entire heart may be enveloped in a thick sheeting of
fat, through which not a trace of muscle-substance can be seen. Along
the groves, the regions of normal deposit, the layer may be an inch or
more in diameter. In some cases the muscle-substance beneath seems but
slightly involved; there may be superficial infiltration and
penetration of columns of fat between the bundles, but the thickness of
musculature is normal, and apart from the excessive deposition there is
not much amiss. In other instances the muscle-substance is seriously
affected; on section of the ventricular wall the fat is seen to
infiltrate the entire muscle, separating strands of fibres and reaching
almost to the endocardium. There may be places, indeed, in the thinner
parts of the ventricular walls in which there appears to be complete
substitution of the muscle by fat. Even the papillary bundles may
contain adipose tissue. The chambers are usually dilated and the entire
organ soft and relaxed. Microscopically, the fat-cells are everywhere
{612} seen infiltrating the muscle-tissue, separating the fibres and
inducing atrophy. In some cases, even when the condition is advanced,
the muscle-fibres appear normal, but in the majority fatty degeneration
is also present. Often in these cases the coronary vessels will be
found atheromatous.

The SYMPTOMS of fatty overgrowth will depend greatly on the degree of
infiltration, the state of the muscle-fibres--whether normal or
degenerated--and on the presence or absence of coronary atheroma. Many
very fat persons enjoy excellent health and have actively beating
hearts, which fail them only on severe exertion, when they get out of
wind and experience cardiac distress, perhaps palpitation. The pulse is
good and the heart sounds are clear. The signs of heart failure (which
may be due either to excessive infiltration or secondary degeneration
of the muscle, or both combined) in obese persons are generally very
marked--breathlessness on slight exertion, amounting oftentimes to
dyspnoea; attacks of asthma of a distressing nature coming on without
cause or after a full meal; cough, with or without bronchitis;
dizziness and pseudo-apoplectic attacks. Sudden death from syncope or
rupture of the heart is common. Dropsical symptoms and cyanosis may
supervene. The physical signs are those of heart weakness; impulse
imperceptible or very diffuse; area of dulness increased, but often
hard to delimit, with fat chest-walls and fatty mediastinum; sometimes
a soft systolic murmur at apex; radial pulse rapid, weak, and
irregular, in some instances very slow.

The DIAGNOSIS of the condition with such a series of symptoms in an
excessively stout person can offer but little difficulty.

The TREATMENT in the early stage should be directed to reducing the
general obesity, and such persons should be warned against taking too
violent exertion or subjecting the heart to unusual strain. Moderate
exercise, mental quietude, and careful dieting may do much toward
postponing heart failure, which, when established, calls for the
treatment which shall be described under Dilatation.

Fatty Degeneration.--An anomaly or disturbance of nutrition in which
minute particles of fat accumulate in the protoplasm of the
muscle-fibres, and impair the functional activity of the organ.

This is one of the most common of post-mortem conditions, and in mild
grades is met with in a great variety of diseases. The fat is a product
of the metabolism of the protoplasm of the muscle-fibres, and in a
normal state it (or its immediate antecedents) is oxidized; but when
either there is increased transformation or reduced oxidation the
products accumulate in the protoplasm, and are evident as minute
molecules or as distinct fine oil-droplets. The condition of cloudy
swelling or parenchymatous degeneration appears in many cases to
precede that of fatty degeneration, and sometimes the granules are of
such a size, so abundant, and resemble fat so closely that chemical
tests alone can distinguish between them.

A practical division of fatty degeneration is into--1, cases in which
the process has attacked a normal heart; and 2, cases in which we find
it associated with valvular disease and hypertrophic states of the
muscular walls.

In the first group we have _(a)_ The degeneration which accompanies the
failing nutrition of old age, of wasting diseases, and of cachectic
states. _(b)_ The fatty change in the heart-muscle so often a sequence
to, or coexisting with, the parenchymatous degeneration of fevers.
_(c)_ The extreme fatty degeneration so constantly associated with
profound anæmia. _(d)_ Certain poisons, particularly phosphorus;
arsenic, lead, and antimony also act in the same way. The slow
poisoning by alcohol is a very frequent cause of a gradually fatty
degeneration of the heart. And _(e)_ some local causes are important in
inducing this change in the previously normal organ. Pericarditis is
almost invariably associated with involvement of the superficial
myocardium, {613} either inflammatory or degenerative. Disease of the
coronary arteries is a frequent and important cause of fatty
metamorphosis. When due to the general conditions above mentioned, the
affection is widely distributed in the organ; when the result of
gradual narrowing of the vessels by atheroma, the distribution is in
the regions supplied by the affected vessels.

The second group comprises those cases in which the fatty degeneration
involves the muscle-substance in a condition of hypertrophy, and is an
important element in inducing the disturbance of compensation upon
which so many heart symptoms depend. Here the process may be more
local, affecting, for example, the left ventricle chiefly, as in the
hypertrophy from aortic valve disease or in association with contracted
kidneys, or the right ventricle in chronic lung affections and mitral
stenosis. More rarely we find the process confined chiefly to the
auricles, but there may be advanced changes of this nature in the
hypertrophied left auricle in mitral stenosis. The fatty degeneration
of an hypertrophied heart may be induced by any of the general causes
above referred to, but there are also special ones to which it is
liable. The chronic congestion which accompanies a dilated heart
affects the walls of the organ as well, and diminishes the vigor of the
coronary circulation. In emphysema and in mitral stenosis, and other
diseases which induce a dilated state of the right heart, fatty
degeneration, sometimes combined with fibroid change, is, as Jenner
pointed out,[27] very common. This state of the right chambers also
interferes with the proper oxygenation of the blood in the lungs, and
so acts in a double way. Degenerative changes in the coronary arteries
are specially prone to accompany valvular diseases, on which the
majority of cases of hypertrophy depend, and we have here one of the
most serious causes of fatty degeneration in this state. And, finally,
we see this change in some hypertrophied hearts without being able to
ascertain any exciting cause: a nutritive breakdown occurs, of which
the fatty degeneration is the expression. Possibly in such cases the
trophic nerve-influences may be at fault.

[Footnote 27: _Medico-Chirurgical Transactions_, xliii.]

Defective oxidation, in whatever way brought about, seems the common
factor in all forms of fatty degeneration. The process may be almost
confined to the heart or be more or less general in the solid viscera
and voluntary muscles. The diaphragm is sometimes much involved with
the heart, even when the other muscles show no signs of the change.
There certainly seems to be a special proneness to fatty degeneration
in the heart-muscle which may perhaps be associated with its incessant
activity. So great is the need of an abundant oxygen-supply that it
early feels any deficiency, and in consequence is the first muscle to
show nutritional changes.

Fatty degeneration is met with at all ages. I have seen it in the
hypertrophied right ventricle of a new-born infant, with stenosis of
the pulmonary artery. The cases dependent upon vascular changes are
most frequent after middle life. Males appear more frequently affected
than females. The form associated with anæmia is an exception to this
rule. Stout persons are not more liable to be affected than thin ones;
indeed, it is often, to use Paget's phrase, "a lean degeneration."
Sedentary habits, worry, grief, and other depressing emotions are
believed by some to have a predisposing influence. Persons with gouty
and arthritic tendencies are more prone to this change.

The anatomical condition is very characteristic even to the naked eye,
and the microscope may be required only in corroboration. It may be
local or general. In the former case the left ventricle is most
frequently affected, the right ventricle more rarely, and the auricles
very seldom. The amount of subpericardial fat may be slight. If the
process is advanced and in all the chambers, the heart looks large and
is flabby and relaxed. It is pale, of a light yellow-brown tint, buff
color, or, as it is sometimes expressed, a {614} faded-leaf color. The
consistence is greatly diminished, and the substance tears easily and
the finger can be readily thrust through the wall. Extreme grades are
met with in profound anæmia and in phosphorus-poisoning. The fatty
degeneration of coronary disease and of valvular affections is usually
more local, and the heart has often a brownish-yellow tint from the
coexistence of brown atrophy. In the left ventricle the papillary
columns and the layers of muscle just beneath the endocardium are most
affected, and in a curious streaked or patchy way--the tabby mottling
of some authors. A similar change may be seen in the right ventricle,
particularly in the hypertrophy from mitral disease. In the auricles
the right may show patches on the musculi pectinati, but on the left,
which is most often affected, the thick endocardium usually obscures
it. Chemically, it has been shown that in fatty degeneration the heart
may contain from 3 to 5 per cent. more fat than normal.

On microscopical examination of teased portions of the muscle the
fibres are broken and irregular, and there is much free fat, in form of
droplets, among them. The appearance of the fibres will vary with the
intensity of the process; in mild grades there are minute scattered
droplets in the protoplasm, not obscuring the nuclei or the striæ; but
in an advanced condition the fibres seem occupied completely with
minute globules, and no trace of structure can be seen. The patchy
distribution of the fatty degeneration in many cases, usually evident
to the naked eye, is corroborated by the microscope, and one may obtain
portions of the muscle with scarcely a normal fibre, while in a
contiguous bit the fibres are little if at all affected. In some
instances of general fatty degeneration in anæmia, and even in fevers,
as diphtheria, the process is so advanced that it is difficult to find
any normal-looking fibres. Brown atrophy is a frequent accompaniment of
fatty degeneration.

The effect of this change upon the heart is seen in a diminution of its
functional power; the contractile force is weakened and the organ
rendered incapable of doing its work efficiently. If the change occurs
in a previously normal heart, much will depend on the rapidity with
which it has supervened. Repeated hemorrhages or poisoning by
phosphorus will induce in a few days an extreme degree of weakness
rarely seen in the fatty degeneration of chronic anæmia--perhaps
equally extensive. As a consequence of the enfeebled action of the
heart, the arteries are not well filled during the systole, and there
is anæmia of the organs. The mural weakness readily permits of
dilatation, with imperfect emptying of the chambers and distension of
the venous system. In hypertrophy the failing compensation is
frequently due to the onset of fatty degeneration. During a sudden
strain or a more continued effort than usual there may be heart
failure, asystolism, or the walls may tear and sudden death occur from
rupture.

The SYMPTOMS of fatty degeneration of the heart are by no means
definite, being those of defective cardiac power. It is often met with
post-mortem when not expected, and on the other hand we may fail to
find it even when the symptoms seem to point very clearly to its
existence. In chronic anæmia, in chlorosis, in fevers and wasting
diseases the process may be extreme, without leading to any more marked
symptoms than feeble action of the heart, palpitation on exertion or
excitement, with signs of slight dilatation, and a soft mitral systolic
murmur from incompetency of the valves. In cases of idiopathic anæmia,
in which the fatty degeneration is perhaps more marked than in any
other condition except phosphorus-poisoning, the pulse is frequently
full, though soft, and regular so long as the patient is quiet. The
symptoms of fatty degeneration in cases of valvular disease with
hypertrophy are simply those of failing compensation, and we see the
same process in the non-valvular hypertrophy of chronic Bright's
disease. But, apart from these conditions, fatty degeneration occurs as
part of a process of general failure {615} of nutrition, premature or
senile. These form the cases of idiopathic fatty heart which seem so
constantly to be associated with atheromatous changes in the coronary
vessels. English writers have dealt specially with this form, which
certainly appears to be more prevalent in Great Britain than on this
continent or in Europe. In these cases there may be general obesity,
but as often the subjects are of spare habit, with full atheromatous
arteries, and other indications, perhaps, of early senility. They are
usually persons who have lived freely and taken stimulants in excess.
Among the symptoms believed to indicate fatty degeneration in these
cases are--weak, irregular action of the heart, with a small
intermittent pulse; cardiac pain, sometimes anginoid in character;
dyspnoea, particularly on exertion, as in ascending an incline; signs
of cerebral anæmia, indicated by vertigo or pseudo-apoplectic attacks
and loss of mental power; the presence of an arcus senilis; and, as a
final symptom, Cheyne-Stokes respiration.

Persistent irregularity in the action of the heart in a person with
atheromatous arteries, and dyspnoea on exertion, without signs of
valvular affection, are certainly suggestive of degeneration of the
muscle-fibres of the heart. In some instances there has been noted a
greatly diminished number of beats, 40 or 50 per minute, or even
slower. Irregular action of the heart may, however, persist for years
without indicating any serious mischief.[28] The yellow fatty arcus
senilis is believed by many physicians to indicate a weak fatty heart,
and it does occur in many persons of soft flabby habit of body with
degenerated arteries and evidences of premature decay; but by itself it
is of no value as a sign of vascular degeneration. It must not be
confounded with the opaque white calcareous arcus not uncommon in
elderly people, and met with occasionally in middle-aged persons. The
Cheyne-Stokes breathing so often referred to as specially associated
with fatty heart is, in my experience, a much more frequent concomitant
of uræmic states.

[Footnote 28: In the spring of 1882, I saw, for Geo. W. Campbell, a
gentleman aged eighty-two, a man of remarkable vigor, mental and
bodily. He had an extraordinarily irregular yet full pulse, with
atheromatous arteries--a condition which he assured me had been
constantly present for close upon forty years, and had been a source of
needless anxiety to many physicians, and for some years to himself.]

The physical signs of fatty degeneration of the heart are a weak
impulse, often diffuse, and if the patient is thin the area of dulness
may be found increased. In stout persons it is difficult to determine
dilatation on account of the fat inside and out. The sounds on
auscultation are generally weak, distant, and muffled, but in the fatty