manifestations of rheumatism in the texture of the lung itself, of the
bronchi, and of the pleura is of comparatively recent date. There had
been indefinite, loose statements, or rather suggestions, in some of
the writers in the early part of the century, such as Chomel and
Andral, as to the possibility of rheumatism appearing in the pulmonary
textures; but we believe that the first definite description of the
disease was made by T. H. Buckler of Baltimore in 1865.[190] He claimed
that the white fibrous tissue of the bronchi could be the seat of
rheumatism, as well as similar textures about the joints. He
illustrated his views by cases observed and reported by himself. He
showed how, as a result, there were symptomatic engorgements, more or
less solid, of the pulmonary parenchyma or rheumatic pneumonia. In
1854, Black[191] found crystalline particles of uric acid and of urate
of soda deeply imbedded in the thin white fibrous tissue of bronchi.
Buckler showed the metastatic character of rheumatic inflammation in
the bronchi and lungs as elsewhere. Buckler's subsequent papers[192]
published in connection with this subject, show remarkable success in
treatment of fibro-bronchitis and rheumatic pneumonia based upon his
views of their pathology.
[Footnote 190: _Fibro-Bronchitis and Rheumatic Pneumonia_.]
[Footnote 191: _Edin. Med. Journal_, 1854.]
[Footnote 192: _Boston Med. Journal_, 1882, and _Amer. Med. Journal_,
Oct., 1882.]
SYMPTOMS.--We find rheumatic pleurisy coming on in the course of {565}
rheumatic fever with the characteristic mobility of the points of
inflammatory action. Laseque[193] gives the symptom with accurate
details--the acute pain in the side of the chest without cough or
expectoration. He describes the pain as differing from that of ordinary
pleurisy, in that the extent of pain is greater and not so limited, due
to the fact that the rheumatism invades the aponeurotic tissue which
forms the covering to the intercostal muscles. It persists longer and
is wider spread. The dyspnoea is caused by the inability to move the
respiratory muscles and by the disease invading the aponeurotic centre
of the diaphragm.
[Footnote 193: "Pleurésie rheumatismale," _Arch. Gén. de Méd._, 1873.]
The rapidity of the inflammation causes the sudden pain and the
accompanying effusion in even a few hours. In a well-defined case
recently seen by the writer in a lady forty-seven years of age the
rheumatism literally jumped from a large joint to the pleura, giving
rise to a severe pain, without cough or expectoration, with an increase
of 2° of temperature and 20 beats of pulse. There was a moderate
effusion. In forty-eight hours, under the influence of an initiatory
dose of quinine (20 grains), followed by free doses of salicylate of
sodium, the attack subsided and the friction sound at the base of the
lung disappeared. This case did not follow the rule mentioned by
Senx,[194] that the disease, upon leaving the pleura of one side,
appears in the same manner on the other. It sometimes goes to the
pericardium and endocardium from the pleura. Chomel[195] insisted upon
the frequent examination of the heart to ascertain whether this had
occurred.
[Footnote 194: _De la Pleurésie rheumatismale_, Paris, 1878.]
[Footnote 195: _Art. Pleurésie Dict._, in 30 vols., 1842.]
Rheumatism of the pleura does not always appear and disappear suddenly.
It sometimes is gradual in progress and slow in recovery. It usually
occurs when we have manifestations elsewhere, but the pleura may be the
point first attacked, as is more frequently the case in pericarditis.
DIAGNOSIS.--The diagnostic signs are hereditary or personal tendency to
the disease, the character of the local pain, the mobility of the
disease, violence of pain and its rapid disappearance, and the
existence of profuse sweats. Suppuration rarely occurs.
PROGNOSIS is in its nature serious, not from the intensity of the
disease, but from its being a visceral rheumatic affection. It is,
moreover, frequently double, and may recur often in the same subject.
TREATMENT is that of rheumatism elsewhere--salicylic acid and its
salts, alkalies with opiates. Thoracentesis is rarely indicated,
because mechanically the effusion does not seriously impede
respiration: if the pericardium be involved, it may be necessary in
order to relieve the pleura or the pericardium.
Hemorrhagic Pleurisy.
DEFINITION.--Pleurisy complicated by hemorrhage. Hemorrhagic pleurisy
is the union of an ordinarily slight hemorrhage in the pleura with
inflammation of that membrane (Laennec).
ETIOLOGY AND PATHOLOGY.--These must be studied together, because the
pathology of the disease explains its etiology. While hæmothorax
designates hemorrhage into the pleural cavity without inflammation,
hemorrhagic pleuritis involves necessarily the idea of inflammation
accompanied by effusion of blood, whether this occurs before, during,
or subsequently to the inflammation. We cannot assign the name
hemorrhagic pleurisy simply because there may be slight red coloration
of the effusion. Microscopic researches have shown that all effusions,
even the simplest, contain more or less white and red blood-corpuscles.
The presence of a certain number of the red discs no more justifies us
in calling the pleurisy hemorrhagic than the presence of {566} the
leucocytes would entitle us to call it purulent pleurisy.
Dieulafoy[196] states that there can be from 500 to 4000 red globules
to the cubic millimeter without producing any coloration. They must
reach 5000 before they will really attract attention. He says, however,
that when the number of red corpuscles reaches 2000 the effusion is
"histologically hemorrhagic," because the presence of blood is
analogous to the state of engorgement or congestion of the first stage
of pneumonia or other phlegmasia, and constitutes a particular phase of
pleurisy which must produce purulent matter. The name hemorrhagic
pleurisy ought to be used when the number of red blood-corpuscles is
sufficient to enable us, by the unaided vision, to detect the presence
of blood. We may, however, find a fluid in the pleural sac which is red
and yet does not contain blood-discs, but their coloring principle, the
dissolved hæmatin. Jaccoud[197] designates this condition
pseudo-hemorrhagic pleurisy. Vulpian and Charcot explain the slight
discoloration by the presence of hæmatin crystals, which, having been
imbedded in the false membranes, escape into the flow of the chest.
Nolais[198] included both of these discolored effusions among the
varieties of hemorrhagic pleurisies: "Hemorrhagic pleurisies include
all those of which the liquid borrows the red coloring matter of the
blood." Moutard-Martin (R.)[199] divides hemorrhagic pleurisy into
three varieties: simple, as produced in simple, acute, or subacute
pleurisy; tubercular; and cancerous. Trousseau[200] considered all
hemorrhagic pleurisies as caused by cancer. Beigel[201] states
positively that in cancerous pleurisy the effusion is limpid with a
yellowish tinge. Walshe[202] held the same views. Nolais,
Moutard-Martin (R.), and Fernet satisfactorily demonstrated that such
is not the case, but that the hemorrhagic effusion may be simple and
independent of any organic disease. It may be produced by acute
inflammations of the pleura as well as by cancer of the lung or pleura.
It may be connected with pleuro-pneumonia or miliary tubercle. It
comes, although more rarely, from fevers, such as measles, and from
certain dyscrasiæ due to renal, hepatic, or even splenic lesions. When
hemorrhagic pleurisy follows hæmothorax, the blood, after remaining
liquid at least one or two hours, initiates the inflammatory action
which has, according to Ch. Nélaton,[203] for its object the encystment
of the clot. Cornil and Ranvier[204] claim that the cyst is caused by
the retracted clot, and that after absorption of the serosity this cyst
may become organized. The presence of air causes fetidity of the blood
and purulent pleurisy.
[Footnote 196: _De la Thoracentèse par Aspiration dans la Pleurésie
aigue_.]
[Footnote 197: "De l'Humorisme ancien comparé à l'Humorisme moderne,"
_Thèse de Concours_, 1863; _Gazette Méd._, 1860, quoted by Nolais.]
[Footnote 198: _Thèse de Paris_.]
[Footnote 199: _Thèse de Paris_, 1878.]
[Footnote 200: _Clin. Méd._]
[Footnote 201: _Reynolds's Syst. of Med._, 1871.]
[Footnote 202: _Dis. of the Chest_.]
[Footnote 203: _Thèse de Paris_, 1880.]
[Footnote 204: _Path. Anatomy_.]
We may have hemorrhagic effusions occurring simultaneously with acute
pleurisy, with pulmonary congestions, pneumonias, and apoplexy of the
lung. They are caused by the violence of the inflammation with local
plethora, producing a sanguinary stasis--a mechanical result of intense
congestion. Moutard-Martin (R.) states that in these cases the red
globules come through the walls of the blood-vessels, as do the
leucocytes, by diapedesis. Jaccoud[205] admits that the blood-vessels
are altered by the inflammation, perhaps also by the derangement in the
vaso-motor innervation. The tissue of the pleura is penetrated by both
red and white blood-corpuscles, and the blood-vessels and lymphatics
are dilated, red corpuscles being found in lymphatics. By far the
greatest number of hemorrhagic pleurisies are secondary to pleural
inflammations, either resulting from acute causes or from cancerous or
tubercular disease, or from diseases causing a dyscrasia of the blood,
such as nephritic diseases, hepatic, cardiac, scorbutic affections, or
alcoholic excesses. The secondary result of these pleurisies is the
formation of neo-membranes, fibrous {567} in their nature, which
pathological anatomy shows contain, as they become organized, abundant
blood-vessels with thin and brittle walls. A slight exciting cause is
all that is necessary to produce their rupture. The primary cause is
the false membrane, and, in some cases, vascular granulations, which
have rapidly formed, perhaps in twenty-four hours--conditions eminently
favorable to the production of hemorrhage. In cancerous, tubercular,
and dyscrasial conditions of the blood, the blood-vessels are
especially weak and easily give way, owing to the defective nutritive
properties of the blood itself, just as, in typhoid fever, we have
nasal and intestinal hemorrhage, and in typhus, petechiæ. In 200 cases
collected by Moutard-Martin[206] there was found intra-pleural effusion
in three-eighths of the cases. Only one-third of that number were
hemorrhagic. In 42 cancers observed between 1872 and 1876, 35 were
without pleural effusion, 1 only was hemorrhagic. M. Moutard-Martin
reports 34 observations of hemorrhagic pleurisy produced by cancer, 19
by tubercle, and 31 following simple pleurisy. Of these last there were
7 cases of effusion complicated with a pneumonia, 3 with a cirrhosis, 6
with a cardiac affection: all except 12 of these cases had some
complication. Most of these (12) recovered, so he had not the autopsies
to verify his diagnosis. Rayer[207] cites 4 cases of bloody effusion in
the pleura occurring in the course of a nephritis. Poutin[208] reports
1 in renal sclerosis. M. Natalis-Guyon[209] reports an epidemic of
measles where many infants died of hemorrhagic pleurisy. Marguerite
cites 13 cases complicating pneumonia, granulations, chronic pleurisy,
small-pox, etc.
[Footnote 205: _Clin. Méd._]
[Footnote 206: _Loc. cit._]
[Footnote 207: _Traité des Mal. des Reins_.]
[Footnote 208: _Soc. Clin. de Paris_, 1879.]
[Footnote 209: _Soc. Méd. des Hôpitaux_.]
Rilliet and Barthez[210] say that it is common to find in infants
considerable discoloration of effused serum in variolic and other
organic poisons. It seems fair to conclude that hemorrhagic pleurisy
may occur in a large number of cases where the blood has undergone
alterations, but to produce it, it is necessary that the pleura should
have been rendered vulnerable by pre-existing causes, because it
ordinarily resists, better than many other membranes, the hemorrhagic
tendency. If we admit the existence of tubercular or cancerous
hemorrhagic pleurisies, we ought not to consider those as simple which
are produced under the influence of the other causes that we have
mentioned. The tubercular granulations are deposited either on the
pleural surface or in the parenchyma of the lung near the surface, the
most frequent locality being in the thickest parts of the organized
false membranes. The rupture of their blood-vessels causes the escape
of blood into the pleural cavity. The effusion, more or less
discolored, rarely exceeds a liter in quantity. Effused blood from
cancerous origin may either come from rupture of the vessels in the
growths themselves by ulceration, or from the neo-membranes in their
vicinity.
[Footnote 210: _Traité des Mal. des Enfants_, t. iii.]
The primitive seat of the cancer is rarely in the pleura, but most
frequently in the lung, the cancer being of secondary formation arising
primarily from ganglions of the mediastinum. Hemorrhagic pleurisy may
be caused by laceration of the newly-formed blood-vessels in the
neoplasms by aspiration or by the lung expanding too suddenly. We
conclude that hemorrhagic pleurisy is generally owing, directly or
indirectly, to vascular neo-membranes which are produced in simple, in
tubercular, and cancerous pleurisies.
SYMPTOMS.--The symptomatology of this form of pleurisy does not differ
materially from that of other varieties. We cannot attach much
importance to the initiatory symptoms nor to the march of the disease.
If the quantity of blood be great, we must expect general weakness,
pallor, and even fainting. We may have oedema of the walls, as in
purulent pleurisy, and exceptionally in serous pleurisy. Ordinarily,
however, hemorrhagic pleurisy is more extensive, and limited to the
inferior part of the chest, owing to the interference with the venous
circulation. If cancerous in its origin, we shall have dyspnoea {568}
and violent intercostal neuralgia from pressure of the tumor. When the
effusion is formed in the pleural sac, the physical signs already
enumerated indicate its presence. Some authors, especially Fernet,
Moutard-Martin, Alcoud, and Guéneau de Mussey, attach considerable
significance to Bacelli's whisper-pectoriloquy as showing that the
effusion is not serous in character. Nolais questions this view, and
says that this sound ought to be heard whenever there is blood, whereas
they state it is heard only at the base or summit of fluid. When
hemorrhagic pleurisy results from tuberculosis, it is never from the
ordinary ulceration form, but always from the acute miliary,
non-ulcerating variety. We must not, therefore, expect to be aided in
our diagnosis by the progress and symptoms of pulmonary phthisis. We
may, however, detect uncertain, indefinite symptoms which are hard to
interpret as indicative of tuberculosis. The effusion is rarely
excessive in this variety, whereas when resulting from cancer it is
often very abundant and is rapidly reproduced.
DIAGNOSIS.--We may suspect the presence of hemorrhagic effusions, but
only by exploratory punctures can we arrive at certainty of diagnosis.
We must bear in mind that we may withdraw with the aspirator-needle
some drops of blood at its insertion and at the close of the
exploration from the highly vascular neo-membranes or from the lung
itself. Having ascertained the nature of the fluid, the differential
diagnosis must be made as to the cause, simple, tuberculous, or
cancerous. We must study the manner of access of the disease, and
especially ascertain if its invasion was violent, with a quantity of
blood (d'emblée), or whether it came from the neo-membranes. In the
simple variety there are the ordinary acute or subacute symptoms of
pleurisy, without any preceding symptoms. In cases of tubercular origin
we have to aid us a small quantity of fluid effused and the insidious
character of symptoms. In cancerous cases we must expect to find traces
of hereditary or of personal taint which may have affected the general
health. We must look for cancer elsewhere, and examine carefully to see
if there be any tumor of the mediastinum or intra-thoracic pressure, or
any infiltration of the lymphatic glands, especially above the
clavicle. The fluid drawn in the exploration ought to be examined
microscopically, for we may detect evidences of cancer. Walshe[211]
cites a case where encephaloid débris was thus discovered. Other
authors also give similar cases.
[Footnote 211: _Diseases of the Chest_.]
PROGNOSIS.--This depends upon the nature of the disease producing it.
When caused by the newly-formed membranes connected with simple serous
pleurisy it is ordinarily not serious, for the mere presence of blood
in the pleura has no bad influence over the restoration of health. It
is more the intensity of inflammation, with the quantity of blood
effused, that indicates gravity of prognosis. Dieulafoy[212] considers
the prognosis as unfavorable in the hémorrhagie d'emblée form, drawing
the distinction between this and the histologically hemorrhagic. He
thinks that every purulent pleurisy was at first hemorrhagic, and the
presence of pus shows greater intensity of inflammation. Homolle[213]
also states that the pleurisies rich in red globules are ordinarily
very acute, and, in consequence of that fact, predisposed to purulence.
Purulency is not the sole cause of danger. We fear compression of the
lungs, and still more septicæmia. In the tubercular and cancerous forms
the prognosis must be very serious. When the hemorrhagic pleurisies
arise in the course of organic diseases of the heart, kidney, and
liver, they are of grave import.
[Footnote 212: _Loc. cit._]
[Footnote 213: _Rev. des Sci. Méd._, 1880.]
TREATMENT.--If the quantity is excessive, local applications and ergot
ought to be employed to arrest the flow. If the dyspnoea and oppression
are great, it is best to draw off at least some of the fluid. If the
quantity be not large enough to embarrass respiration, we must expect
nature to absorb {569} it, or by local inflammation to encyst it.
Lacaze[214] reports a case where a fistula was established, and the
case was cured. Dieulafoy gives another case where six punctures were
made, and no less than 6 liters, in all, were withdrawn. He injected
afterward a solution of 4 grammes of sulphate of zinc to 400 grammes of
water, and the patient was cured. In the first stage of the disease we
use palliatives--morphia hypodermically, bromides, and chloral--if
indicated. During febrile symptoms of acute cases we refrain from
withdrawal of fluid unless it is excessive. The question of
thoracentesis has been discussed in regard to simple pleurisies. The
same rules apply, a fortiori, when the nature of the fluid is
hemorrhagic. Ordinarily, the abundance of fluid, and the dyspnoea which
results therefrom, indicate the operation. We prefer not to draw off
the fluid completely--only enough to relieve the embarrassment of
respiration--because we destroy the equilibrium of pressure on one side
against the neo-membranes and the compressed lungs on the other.
Congestion of the lung may thus be produced with albuminoid
expectoration. Moutard-Martin (R.) coincides with Dieulafoy in limiting
the amount to be withdrawn to one liter. Of course the fluid is slowly
aspirated. After part of the fluid is withdrawn, what remains is
absorbed, remains stationary, or increases in quantity. We repeat the
operation, and slowly draw off greater quantities of fluid if it
returns; especially in cancerous cases, where the effusion is often
very large, the operation gives great relief. It is rarely large enough
in tubercular cases to justify thoracentesis.
[Footnote 214: _Thèse de Paris_, 1851.]
Tubercular Pleurisy.
Tubercular pleurisy may be acute or chronic. It may occur during the
course of ordinary tubercular disease of the lung, by extension of the
disease from the lung to its serous covering, or it may proceed from
tubercular deposit on the pleura independently of any previous disease
of the lung. Acute tubercular pleurisy may be dry and situated at the
summit of the chest, or may be what is called accidental pleurisy. Dry
pleurisy is almost constant in tuberculosis of the lung. Its existence
is, in itself, a powerful presumption of pulmonary phthisis, especially
when it is situated at the apex. In tuberculosis pleuritic inflammation
is lighted up by slight and scarcely appreciable causes. Its
commencement is insidious, with little or no pain or fever: indeed, it
is with subacute symptoms that the disease slowly advances. The first
intimation the patient has of the disease is the impairment of his
breathing-power by the presence of fluid. The fluid is not generally in
large quantities, and is serous or sero-fibrinous, and sometimes
sero-purulent. Latent pleurisy of the older writers was frequently
tuberculous in its origin. This form of tuberculosis may precede or
follow the deposit of tubercles in the lung-tissue. The tubercles may
be deposited to a slight extent in the tissue of the lung, and their
presence is shown by an irritating cough only when the pleurisy
approaches insidiously. The tubercular granulations over the visceral
pleura are extended to the parietal surface also, and notably to the
circumference of the fibrous leaflet of the diaphragm--an especial
point of elevation for the secondary products.
This disposition of tubercular lesions of the pleura is one of the most
striking examples of what is called infection from contiguity, and is a
powerful proof of the infective property of tubercular products which
from an initial nucleus is propagated from point to point. Acute
tuberculosis of the pleura is one of the most common manifestations of
acute phthisis. It more frequently causes acute than subacute pleurisy.
Chronic tuberculosis almost always produces purulent pleural effusions.
It is much {570} more common in infants than in adults, and is
sometimes met with in children from three to ten years of age (Barthez
et Rilliet[215]). Tubercles may be developed in the intra- or
extra-serous membrane. Among old people the tubercle sometimes appears
first in the recent false membranes produced by pleuritis (as
associated with caseous pneumonia, or genuine tuberculous processes in
the lungs), or in connection with tubercles of other organs
(Fraentzel[216]). The advance of this disease is habitually slow, or at
least not accelerated by the development of other tubercular diseases.
The diagnosis is often accompanied with great difficulties, for the
disease may be confounded with chronic or with purulent pleurisy,
especially if these are developed in a tuberculous subject. In both
cases we have hectic, night-sweats, emaciation, etc. Thoracentesis
alone can give definite results when the effusion is in considerable
quantity. When suppurative pleurisy supervenes in tuberculous subjects,
the prognosis is very grave. Should the pus be sufficient in quantity
to embarrass respiration, it can be drawn off cautiously by aspiration.
The open method of drainage and free incisions should not be used, for
experience has shown that they injure instead of benefiting the
patients.
[Footnote 215: _Mal. des Enfants_.]
[Footnote 216: _Ziemssen's Cyc._, vol. iv.]
Hydrothorax.
From [Greek: hydôr], water, and [Greek: thôrax], the chest.
DEFINITION.--Dropsy of the chest. The accumulated fluid in the pleural
cavity which resembles the serum of the blood is not the product of
inflammation, but is caused by mechanical obstruction to the
circulation or by blood-poisoning. Hydrothorax is never idiopathic, but
invariably secondary, resulting from disease, not of the pleura, but of
the circulatory system or of the blood itself.