effusions resulting from inflammatory processes in the pleura were
confounded with simple hydrothorax, which is not a variety of pleurisy.
Royer[217] and Laennec[218] divided hydrothorax into idiopathic and
symptomatic; Darwell[219] adopted in a great measure their views. They
did not draw the distinction between the passive transudation of serum,
constituting the condition known as hydrothorax, and exudations
resulting from idiopathic pleurisy. Before physical modes of exploring
the chest were used there was great uncertainty in the diagnosis of
collections of fluid in the pleural cavity.
[Footnote 217: _Dict. de Méd._, 1832.]
[Footnote 218: _Dis. of Chest_, Forbes's edition.]
[Footnote 219: _Cyc. Pract. Med._]
ETIOLOGY.--Dropsical effusion in the thorax is produced by the same
causes which give rise to collections of watery fluid in other serous
cavities and in the connective tissue, constituting general anasarca.
Primary among the causes is obstruction of the venous circulation in
the walls of the chest or in the lungs. Mitral disease, especially
insufficiency with dilatation, deranges the normal circulation in the
lung and its serous coverings, producing hyperæmia, oedema of the lung,
and finally serous effusions into the pleural sac. General dropsy
results. According to Fernet,[220] in dropsies resulting from mitral
disease oedema of the lungs and hydrothorax always precede all other
oedemas. Fraentzel,[221] on the contrary, states that it does not occur
until there is no longer any room for the transuded fluid in the deeper
portions of the subcutaneous tissues. Other diseases of the heart
produce hydrothorax. Whenever there is abnormally high venous pressure,
which invariably follows dilatation of the right side after
compensatory hypertrophy has reached its limit, and the heart literally
yields to the backed current of blood, we must expect dropsical
results. Intra-thoracic tumors, aneurisms, emphysema, and sclerosis of
the {571} lung cause hydrothorax by pressing upon the venous trunks and
upon the thoracic duct without producing general dropsy. Chronic
diseases, such as cancerous disease, chronic malaria, etc., produce
great exhaustion and give rise to general hydræmia. Especially is this
the case in chronic disease of the kidneys, such as the several
varieties of nephritis and amyloid degeneration, where there has been a
loss of albumen for a long time and the blood-serum has been rendered
poorer in solid constituents. Hydrothorax is not a disease, but a
symptom resulting from a variety of causes which produce physical
exosmosis of the serum of the blood.
[Footnote 220: _Nouveau Dict. Méd._, vol. xxviii.]
[Footnote 221: _Ziemssen's Cyc._, Amer. trans., vol. iv.]
PATHOLOGICAL ANATOMY.--Hydrothorax being merely dropsy of the thoracic
cavity, there is no lesion of the pleura. There is a collection varying
from 100 grammes to many liters of fluid in the cavity. It differs from
the effusion in subacute pleurisy in its small quantity of fibrin, in
having far less of albuminoid material, and no white blood-corpuscles.
The water collects almost always in both sides of the chest, more on
the side on which the patient lies in bed. In the recumbent position
the fluid gravitates posteriorly more than the effusions of pleurisy.
In the upright position it will follow Ellis's curved line more
regularly than in effusions resulting from pleurisy, for there are no
adhesion-bands interfering with its doing so. The fluid is limpid, of a
light-yellow or citron color. Its composition resembles that of the
plasma of the blood, but it contains more water and less of the
constituent elements. Alex. James[222] found that the amount of mineral
matter was the same in dropsical fluids in all parts of the body, and
that the organic albuminoid substances were larger in quantity in the
pleura than in any other cavity. The amount of organic substances
varied directly in accordance to the degree of pressure on the
different capillary vessels. The anatomical changes in the pleura and
the subpleural connective tissue are similar to those found in other
collections of dropsical fluid. They are swollen and thickened by
maceration with water. They become opalescent and less firm of texture.
The lungs retract as the fluid increases in quantity. As the filtrates
collect in both pleural sacs, the lungs do not forcibly collapse. The
patient would sink at once were this the case. The arch-tension of the
diaphragm is but rarely overcome, and consequently we must not expect
to find the liver and spleen pushed down, especially when there is
fluid in the peritoneal cavity. The position of the heart, unless there
is a marked difference in the collections of the two sides, is but
little altered, the retractive force of both lungs being impaired.
[Footnote 222: _Med. Times and Gazette_, Jan., 1880.]
SYMPTOMS.--The general accumulation of watery fluid is not attended by
any pronounced symptom until it has reached the point of interfering
mechanically with the normal play of the lungs. At first dyspnoea is
only perceptible on increased physical exercise. When the quantity is
excessive, the individual suffers when perfectly quiet. The patient,
until the fluid is excessive, lies on his back as the most comfortable
position, but as the quantity increases he is often obliged to sit up
in bed.
The dyspnoea is ordinarily much more oppressive than in pleuritic
effusions, because both lungs are compressed. There is no rise of
temperature, no pain in the side, no tenderness on pressure, no
acceleration of the pulse, and but rarely any cough, as there is in
pleurisy. The dyspnoea often becomes very painful, and may even produce
orthopnoea, being accompanied by short and frequent acts of breathing.
Where there are very large amounts of fluid the mechanical interference
with the breathing is so great that cold sweats, cyanosis, and asphyxia
follow, the pulse becoming smaller and more feeble until the patient
dies.
The physical signs are, in general, the same as those of pleuritic
effusions, especially the subacute form, with some slight variation.
Inspection {572} and mensuration do not aid us as in pleurisy, for in
hydrothorax the accumulation of fluid is bilateral instead of
unilateral. The tension is not sufficient to dilate the walls of the
chest. Palpation shows absence of vocal resonance, but not invariably,
for we are unable to compare the two sides. We must remember that we
have oedema of the walls of the chest, which would partially prevent
the thoracic vibrations from being felt. Percussion flatness is not as
absolute as it is in pleurisy, unless the fluid is in excessive
quantity, for the tension of the fluid is feebler and the lung contains
more air. The lung is never completely compressed, as in pleurisy,
there being no fibrinous bands to constrict it. The percussion
vibrations, unless very lightly made, are communicated to the lung; and
so there is dulness instead of flatness. The absence of fibrinous bands
permits the fluid to change its position with the varying postures of
the patient. This rarely occurs in pleuritic effusions after the first
few days. Finally, Skodaic tympanic resonance at the apex is but seldom
met with in simple hydrothorax.
Auscultation.--The presence of fluid between the lung and parietes
prevents us from hearing the vesicular murmur. The distant bronchial
respiration is rarely heard in hydrothorax, as it is in pleurisy,
because the lungs are not completely deprived of air, and when present
is less intense. Ægophony is frequently heard over the upper limit of
the fluid, the whispering voice being transmitted through the fluid.
Owing to pulmonary oedema there are subcrepitant râles, but never
pleuritical friction sounds.
DIAGNOSIS.--Ordinarily, the diagnosis ought to be made without
difficulty. The only disease with which there can be any danger of
confounding it is subacute pleurisy. The principal points of
differential diagnosis have been enumerated above. In subacute pleurisy
(latent pleurisy) we have, in less intensity, the ordinary pleuritic
symptoms. The pleuritic friction murmur is present, and a fluid
containing the products of inflammation. Very exceptionally is subacute
pleurisy double, whereas hydrothorax is almost invariably so.
The history of the case enables us to arrive at an accurate diagnosis.
The withdrawal of a small quantity of fluid with a fine perforated
needle, and its chemical and microscopical examination, will complete
the diagnosis in doubtful cases.
Oedema of the lung can scarcely be confounded with hydrothorax. The
absence of the physical evidences of water in the cavity, and the
crackling sound heard in auscultation, are distinctive of oedema.
PROGNOSIS.--The prognosis is always serious, but it depends upon the
nature of the disease producing the dropsy. If this can be removed, the
collection of water may disappear. But, unfortunately, the circulatory
diseases which produce it are generally chronic and incurable. The
fluid can, by general treatment and mechanical means, be reduced, and
the life of the patient prolonged and made comparatively comfortable.
Sooner or later a large number of cases must succumb.
TREATMENT.--The treatment should first be directed to the primary
disease causing the dropsy. If heart disease be the promoting cause, we
must, by means of digitalis, endeavor to promote compensating
hypertrophy, and by arsenic and iron improve the quality of the blood.
If Bright's disease be the cause, the skimmed-milk diet, with iron and
manganese, must be given with remedies which lessen the hydræmic
condition of the blood. Digitalis, diuretics, jaborandi, and drastic
purgatives give decided results. Of all purgatives, elaterium in
decided doses (¼ grain), guarded by conium or hyoscyamus, causes most
relief by producing free watery stools. Mechanical means must be
resorted to without hesitation. It is best first to remove the fluid
from the lower extremities by the insertion of Southey's capillary
canula with caoutchouc tubing attached. Large quantities of water may
{573} thus be drawn off without local irritation, erysipelatous in its
nature, being produced. Thoracentesis by aspiration averts death very
often, and gives the greatest possible relief when the effusion is
large enough to produce dyspnoea. In a case under the author's care
life was prolonged many months and large quantities of fluid were
removed. Altogether, there were twenty-two operations and 1563½ ounces
of water removed. As often as every week one or other side had to be
emptied, the quantity removed each time varying from 49 ounces to 112
ounces. For two months previous to death filtrates collected in the
abdominal cavity also, and had to be frequently withdrawn.
Pneumothorax.
DEFINITION.--A collection of atmospheric air or of gas in the pleural
cavity. Pneumothorax ([Greek: pneuma] and [Greek: thôrax]).
In ancient times gaseous collections were frequently noticed in serous
cavities, especially on opening the chest for empyema and at
post-mortem examinations. The presence of air resulting from laceration
of the lungs by fractured ribs was known and designated as emphysema
thoracis. Air in the pleura was considered as an accidental
complication which occurred with empyema or as formed after death.
Morgagni and others mentioned the presence of gas as formed in the
pleural cavity. Itard[223] was the first to speak of it as a disease
and to name it pneumothorax. Owing to the imperfect knowledge of
pathology at that period, he attributed the production of the air to
the decay of the lung from chronic suppuration, and to the
decomposition of the long-retained pus. Laennec was the first to give
an accurate anatomical and clinical account of the disease.
[Footnote 223: _Thèse de Paris_, 1803.]
HISTORY.--Pure pneumothorax--that is, pneumothorax caused by the
presence of air alone in the pleura--is but rarely met with, except for
a short time, when it has been introduced from without by traumatic
injuries. The irritating effects of gas, unless it comes in small
quantities through the ribs from wounds in the chest-walls, are very
frequently followed in a short time by the production of a quantity of
serosity or of pus. If air is introduced into the pleural cavity from
perforation of the lung, there is also liquid matter from the lungs of
such a character as at once to provoke inflammatory action. Such a
condition is then denominated hydro-pneumothorax or pyo-pneumothorax.
The latter was, in fact, recognized by Hippocrates by the sign of
succussion, though not so designated.
ETIOLOGY.--Laennec divided pneumothorax into three distinct varieties:
1st, essential pneumothorax, resulting from the spontaneous formation
of gas in the pleural cavity; 2d, pneumothorax from putrid
decomposition of liquids effused into the pleura; 3d, pneumothorax by
perforation, due to rupture into the pleura or to an accidental opening
by which atmospheric air or gas from the lungs is introduced into the
pleural cavity. This division, having Laennec's high authority, was for
a long time generally received. It has now been established that the
pleuræ cannot secrete air.
Proust[224] collected 25 cases of so-called spontaneous pneumothorax,
and showed that they could all be otherwise satisfactorily explained.
In some cases errors of diagnosis had been made by mistaking tympanitic
sonority at the anterior-superior portion of the chest, or the
existence of the amphoric breathing found in pleurisy, for
pneumothorax. Some were cases of pneumonia in which tympanitic
percussion resonance deceived observers. Then, again, there was found,
among the cases cited, pneumothorax resulting from rupture of a
tubercular cavity or of a hydatid. In tubercular cases Proust found
that the orifices made were so small--no larger, as Gairdner of {574}
Edinburgh had stated, than a pin's point--that they could not be
detected, or that they had cicatrized before the post-mortem
examination, or perhaps closed by adhesive false membranes. Other
investigations by Ewald[225] and Jaccoud[226] have confirmed Proust's
views that essential pneumothorax does not occur. Researches in
pathological physiology disprove the possibility of a serous membrane
producing a secretion of gas or of its passing from the blood through
the capillary walls. We therefore conclude that pneumothorax from
secretion of air within the pleura is contrary to physiological facts
generally accepted, and is disproved by pathological investigations.
[Footnote 224: _Ibid._, 1862.]
[Footnote 225: Quoted by Fraentzel, _Ziemssen_, vol. iv.]
[Footnote 226: _Gaz. hébd._, 2^{ème} serie, 1864.]
The second variety in Laennec's division--namely, where the gas results
from decomposition of fluid in the pleural cavity--has been supported
by such high authorities as Hughes Bennett, Townsend, Wunderlich, and
Jaccoud. Yet it is difficult to understand how it could occur. The
contact of air appears to be necessary for the decomposition of serum
and pus in the pleural cavity. While shut up in a cavity coated with
neo-membrane, a fluid may certainly remain undecomposed for a long
time, and undergo decomposition as soon as taken out of the cavity.
Recent researches in regard to putrid fermentations appear to confirm
the view that the presence of air is absolutely necessary to produce
that effect.
We believe, therefore, that perforation, with rupture of the visceral
or parietal layer of the serous membrane, causing the introduction of
air into the pleural cavity, is the invariable cause of pneumothorax
and of hydro-pneumothorax. The causes of the rupture are in the lung,
in the pleura, or in the adjoining organs. They may be traumatic or
non-traumatic: the latter may be perfectly designated pathological
causes, because the pneumothorax is always secondary, following upon a
pre-existing pathological condition.
Traumatic pneumothorax may take place in consequence of an injury to
the thoracic walls, of an exterior injury, or of a penetrating wound.
The parts may be so bruised that pleural necrosis gives rise to sloughs
and resulting openings. Fracture of ribs may tear the lungs, and allow
air to enter the connective tissue and produce local emphysema. Violent
contusions, as in a case recently observed by the author, produce
laceration of the lung without the rib or costal pleura being injured.
Non-traumatic or Pathological Causes.--Laennec taught that pulmonary
tuberculosis was the most frequent cause of pneumothorax; and further
observation has demonstrated the correctness of this view. Walshe
states that such is the case in 90 per cent. of the cases of
perforation of the lung. In 131 observations reported by Saussier,[227]
81 were from pulmonary phthisis, principally from caseous pneumonia.
Fraentzel[228] says, from his own observation, that 90 out of 96 cases
of pneumothorax are produced by vomicæ on the surface of the lungs in
the course of caseous pneumonia. Grisolle states that nine-tenths of
the cases result from rupture of a lung-cavity. Fuller[229] reports 22
cases, in 18 of which the disease was produced by tubercular
ulceration. Chambers,[230] at St. George's Hospital, reports that 21
out of 23 were tubercular. Fernet[231] states that pneumothorax results
in nine-tenths of the cases from some of the forms of pulmonary
phthisis.
[Footnote 227: _Thèse de Paris_, 1841.]
[Footnote 228: _Ziem. Cyc._, vol. iv.]
[Footnote 229: _Dis. of the Chest_, p. 226.]
[Footnote 230: _Dec. Pathologicum_, cap. v. sec. v.]
[Footnote 231: _Nouveau Dict._, vol. xxviii.]
Ordinarily, pneumothorax is unilateral; only exceptionally is it met
with on both sides. In tubercular cases it is twice as common on the
left side as on the right (Condrin[232]). In the total of 146 cases
reported by Louis, Walshe, and Powell, 94 were on the left side;
whereas when it is consecutive to a pleuritic effusion it is almost
always on the right side--17 out of 18 (Saussier[233]).
[Footnote 232: _Thèse de Paris_, 1882.]
[Footnote 233: _Ibid._, 1841.]
{575} In tubercular cases perforation of the lung may occur at any
period of the disease; the most frequent time, however, is that of the
softening or while excavations are being formed, where adhesions have
not yet protected the two sides by binding them together with
neo-membranes. It may come from a small cavity. Andral met with cases
where only a few tubercles existed. Townsend reported a case where one
tubercle burst immediately under the pleura. The superior lobe of the
lung is where the perforation generally occurs, because it is there
that the tubercular lesion ordinarily commences and is most advanced
(Louis). It is least frequent in chronic fibroid phthisis and most
often met with in acute pneumonic phthisis. Douglass Powell[234]
reports cases where sinuses extended from cavities, and finally burst
into the pleura. Sometimes the rupture occurs at the base of the
superior lobe, about the third or fourth rib; it may happen, however,
at any point of the lung; it has even occurred at the base of the lung
lying on the diaphragm (Houghton[235]).
[Footnote 234: _Med. Times and Gaz._, Jan. and Feb., 1869.]
[Footnote 235: _Cyc. Pract. Med._, vol. iii.]
Saussier[236] shows by the following table the relative frequency of
the principal causes of pneumothorax in 131 cases:
Pneumothorax with phthisis . . . . . 81
" " empyema . . . . . 29
" " gangrene . . . . . 7
" " pulmonary emphysema 5
" " apoplexy . . . . . 3
" " hepatic fistula . 2
" " hydatids . . . . . 1
" " hæmothorax . . . . 1
[Footnote 236: _Thèse de Paris_, 1841.]
Empyema ranks second as a producing cause of pneumothorax. Ordinarily,
by direct necrosis of the parietal pleura, an orifice is made through
which the pus is evacuated through the bronchi, and air in inspiration
enters the pleural cavity by the bronchial fistula. Pyothorax is
converted into pyo-pneumothorax. The valvular opening may, however, be
closed by inspiration so that air cannot enter, or adhesions may limit
a portion of the pleura, and then we have a circumscribed pneumothorax.
Empyema, by producing ulceration of the thoracic walls and pointing
exteriorly (emphysema necessitatis), leaves fistulæ through which air
enters the pleural cavity.
Gangrene of the lung by sloughs allows air to penetrate. Bronchiectasic
cavities sometimes become the seat of putrefactive changes and
ulcerations through the lungs into the pleura. Infective emboli being
arrested in the smaller peripheral branches of pulmonary arteries, air
enters the cavity; it is thus that pneumothorax arises in various kinds
of surgical diseases when infective emboli pass into the circulation
(Fraentzel). Flint[237] reports a well-marked case of pneumothorax,
lasting less than one month, where there was every reason to suppose
that it had been caused by rupture from interstitial emphysema. W. T.
Gardner had previously reported a similar case. Saussier found
emphysema was a cause in only 5 out of 131 cases. Fraentzel speaks of
emphysema as rarely being a cause. Perforation of the oesophagus,
ulcerative, cancerous, or traumatic from the use of bougies, produces
pneumothorax. Suppurating bronchial glands--a case of which was met
with by the author--bursting into the cavity produce pneumothorax.
Hydatids of the lungs, abscesses of the abdomen, sometimes coming even
from the cæcum and from the liver, burst into the pleural cavity and
introduce air. Echinococcus cysts of the liver are occasionally emptied
into the pleural cavity.
[Footnote 237: _Practice of Medicine_, ed. 1881; _Series of Amer. Clin.
Lectures_, article "Pneumothorax," 1875.]
{576} Pneumothorax is more than four times as frequent in men as in
women. One-third of the whole number of cases occurs in persons between
the ages of twenty and thirty years; one-tenth between the ages of ten
and twenty; one-twelfth between thirty and forty (Saussier[238]).
Although pneumothorax has a number of exciting causes, yet they are all
comparatively rare except pulmonary tuberculosis and purulent pleurisy.
[Footnote 238: _Thèse de Paris_, 1841.]
PATHOLOGICAL ANATOMY.--In traumatic pneumothorax and simple cases, such
as from the bursting of emphysematous alveoli, the presence of air is
the only pathological product. If the pleura and adjoining organs are
not diseased, the rupture or tearing cicatrizes rapidly, and the air
disappears in a few days by absorption. If a quantity of air be
admitted, the pneumothorax may last for months; yet if the pleura is
healthy, the air itself will not produce local changes. If blood or
morbid products flow in with the air, then inflammatory changes occur,
and we have deleterious products effused. Demarquay and Leconte[239]
demonstrated the innocuousness of introducing air into healthy pleural
sacs of dogs, having injected it repeatedly into the same dogs without
any unpleasant result. These observers analyzed the air after it had
remained in the chest, and confirm Davy's[240] researches as to the
changes in its condition. The oxygen diminished gradually, and finally
disappeared, while carbonic acid replaced it to nearly the same amount.
This air from the pleura approximated in composition to the air of
expiration. When blood and bronchial secretions with pus are thrown
into the pleura, they promptly produce more serious results, especially
intense suppurative pleurisy. Duncan[241] found in a case of
pyo-pneumothorax a fetid gas to contain 26 parts of sulphuretted
hydrogen and carbonic acid and 74 parts of nitrogen. Secondarily,
lesions are produced--hydro-pneumothorax and pyo-pneumothorax. In other
cases, the pleura having been previously the seat of chronic disease
with purulent effusion, this latter undergoes fetid changes and
septicæmia results. Under these circumstances the pathological changes
are similar to those we have described as found in empyema. We find
like increase of tissue-formation, of pus, and of the development of
the gases, sulphuretted hydrogen and sulphydrate of ammonia, which give
rise to a horrible fetidity. The quantity of air varies very much, as
does the amount of fluid: there may be a small quantity of air and much
fluid, or the reverse.
[Footnote 239: _Gaz. Méd._, 1864.]
[Footnote 240: _Phil. Trans._, 1823.]