short time the seat of putrid transformations. False membranes undergo
alterations which produce fetid gases. The air, with its germs, its
humidity, and heat, the three grand factors in putrefaction, is thrown
in contact with substances of a putrescible composition. Marshall[111]
holds that sero-fibrinous effusions appear to have a greater tendency
to quick decomposition when air is admitted into the pleural sac than
the sero-purulent or purulent products. Pus, he considers, is more
stable and less inclined to rapid putrefaction than sero-albuminous
fluid. In quantity it varies from a very small number of grammes to
five or even six liters. By examining the fluid first drawn out we can
predict, by the number of leucocytes present, whether the pleurisy will
continue to be serous or will become purulent. If subjected to the
influence of ammonia, it will become thready, just as happens when pus
is suspended in water, if the fluid contains many of these
pus-elements. The purulent fluid may fill the whole or occupy but a
small part of the cavity, or again the interlobular spaces only may
contain the fluid, the cavity itself being empty. False membranes are
almost constantly present and adherent to the parietal or pulmonary
pleura; we find them also floating in the liquid. These false membranes
may be more or less voluminous. The flocculi, which may be as large as
an egg, undergo transformation when air is admitted, and become
horribly fetid. They may give rise to septicæmic symptoms. When we see
these enormous masses in the cavity, and are unable to get rid of them
by suction, we do not wonder that their presence should poison the
patient and the case become incurable. Pleurotomy is the only effective
mode of getting rid of these dangerous masses, with sometimes
gangrenous portions of pleural or lung-tissue. These false membranes
frequently form pouches and divisions for isolated quantities of fluid.
The false membranes are partly adherent and partly free, especially in
cases where there are pulmonary or thoracic fistula. These false
membranes differ in acute purulent pleurisies from those found in
pleurisies of long standing. They are but feebly adherent to the
pleura, and have a slight rose coloration. In old pleurisies the false
membranes are of greater density, sometimes from 6 to 8 mm. in
thickness. They are more adherent, and cannot be separated, and have a
grayish color. The physical state and position of the lung and
disposition of the adjoining structures are very similar to what they
are in serous effusions. In but few cases do the false membranes
envelop the whole of the lung. They pass over one part, and on to the
costal pleura. The pulmonary tissue is condensed, sometimes absolutely
impermeable to air, so that it will actually sink when dropped in
water, being in a state of atelectasis. In cases of shorter duration it
is found crepitant throughout its structure. Brouardet[112] called
attention to the inflammation in the under-pleural cellular tissue, as
well as in the interlobular connective tissue, forming interstitial
pneumonia, which determines condensation of this tissue and its
retraction after the manner of cicatrices, and afterward its
inextensibility. These explain the retraction of the thoracic walls and
the narrowing of the chest.
[Footnote 111: _Loc. cit._]
[Footnote 112: "Interstitielle Pneumonie," _Soc. Méd. des Hôp.
Bullétin_, 1872.]
{542} The most serious complication of this disease is the
pleuro-bronchial fistula[113] by which the fluid escapes through the
lung. The firm adhesions between the lungs and walls, forming enclosed
pockets, contribute in no small degree to the incurability of purulent
pleurisy. These pockets cannot be emptied thoroughly, nor can the
washings be made to penetrate them. The purulent secretion exercises a
destructive action over the tissues surrounding it, as well as upon the
viscera and walls of the chest: the soft parts become inflamed and
abscesses form; the intercostal muscles suffer atrophy and undergo
fatty degeneration, external openings occurring from ulceration. The
latter are found less frequently than pleuro-bronchial fistula. This
external perforation is habitually in front, in the upper intercostal
spaces, which, near the sternum, are very wide and not protected by
external intercostal muscles. The fifth intercostal is the most
frequent locality. There may be one or several openings. They may be
caused by the pus ulcerating through the parietal walls, or abscesses
may be produced in the walls and burst externally. Exceptionally, the
emptying of the liquid is by ulceration of the diaphragm into the
abdomen, causing fatal peritonitis. Some years since the author saw, in
consultation, a patient where the autopsy proved this condition. Rare
cases have been reported where the fluid escaped into the pericardium,
into the mediastinum, and into the opposite pleural cavity
(Fernet[114]). Bouveret[115] relates a number of cases in which the
discharge of pus took place through such unusual channels as the
oesophagus, the stomach, the intestines, and the pelvis of kidneys;
also where the pus perforated the posterior cul-de-sac of the pleura
and appeared in the posterior walls of the abdomen. In the last cases,
he states, it may point in the groin, the lumbar region, the buttocks,
or even in the thigh.
[Footnote 113: See section on Pneumothorax.]
[Footnote 114: _Loc. cit._]
[Footnote 115: _Journal de Méd._, Dec. 16, 1882; _N.Y. Med. Rec._,
March, 1883.]
SYMPTOMS.--In a large number of cases of purulent pleurisy the general
symptoms do not differ materially from those of fibro-serous
pleurisies. Sometimes, however, they do. This is according to whether
they are acute purulent or chronic purulent pleurisies.
In acute purulent pleurisy the disease commences in the same way as the
ordinary acute fibro-serous pleurisy. Indeed, the first effusion is
ordinarily serous in appearance, and afterward it becomes purulent. We
have the initial chilliness more or less marked, accompanied by the
characteristic pain in the side and dry cough, the fever keeping up,
even as high as 103° to 104° F.; and soon the signs of an effusion
supervene. In a few days, ordinarily, in acute fibro-serous pleurisies,
the febrile exacerbation disappears. Graves[116] states that the extent
of a pleurisy is not augmented after twenty-four hours. In acute
purulent pleurisy the fever persists in spite of treatment; the
effusion increases, sometimes less rapidly than in the serous variety,
but in a continuous manner. If thoracentesis is performed about the
eighth or tenth day, we notice that the fluid is opaline and contains a
large quantity of pus. After this the fluid is reproduced, and as it
forms the fever continues; the skin is hot and dry, the appetite
impaired, and sweats appear during the night. In examining carefully
the thoracic walls we find oedema of the diseased side. Later on there
will probably be oedema of the lower extremities.
[Footnote 116: _Clin. Méd._, edited by Neligan.]
Chronic purulent pleurisy is marked by symptoms somewhat different. It
commences in a similar manner to that of acute pleurisy, with fever,
but in a few days the fever disappears. In the evenings there may be
some febrile action with slight chills. It is remarkable that
frequently vast collections of purulent fluid do not give rise to
chills. The fluid augments progressively, but sometimes very slowly,
and often it appears to remain stationary for a long time. This
condition continues sometimes for many months. The {543} patients are
pale and feeble, although they may get up and walk until the quantity
is increased to such an extent as to impair their breathing capacity.
Then the forces of the body by degrees diminish, and the appetite is
impaired to a serious extent. The face becomes pale and the lips
discolored. From time to time diarrhoea supervenes and oedema of the
chest-walls is noticed, and general anasarca comes on without albumen
in the urine. If nature does not open an orifice through the parietes
of the chest or through the bronchi for the discharge, the patients
finally succumb in the last degree of wasting with profuse sweats and
fetid colliquative diarrhoea.
PHYSICAL SIGNS.--These, with some modifications, are very similar to
those of ordinary sero-fibrinous pleurisy. We have the same dilatation
of the chest, but it is more frequently localized. The oedema of the
thoracic walls is almost characteristic of the presence of pus in the
pleural cavity. We may, however, meet with it in fibro-serous pleurisy
and in cachectic subjects on the side of decubitus. Then, again, there
are cases of purulent pleurisy where it does not occur. It must be
looked for with care, especially at the lateral portion beneath the
armpit.
Mensuration and percussion afford especial evidences of purulent
pleurisy, and frequently they discover encysted points.
The tubular quality of respiratory sounds is more pronounced, as are
also the amphoric characters at the apex, caused by long-continued
pressure of the compressed lung around the large bronchi. Ægophony is
less frequently heard, the bronchophony is distant and less distinct,
and vocal fremitus is more completely abolished. The non-transmission
to the ear of the whispered voice through the walls of the chest
(Bacelli's sound) in purulent pleurisy is a sign of considerable
significance in tracing the transformation from serous fluid into pus.
We must, however, bear in mind that when the sero-fibrinous effusion
contains fibrinous flocculi, it has the same effect as a purulent fluid
in interfering with the passage of the voice. (See article ACUTE
PLEURISY.)
DIFFERENTIAL DIAGNOSIS can be but indifferently reached by considering
the points mentioned. An exploratory puncture enables us to decide with
certainty as to the nature of the fluid. Without this the diagnosis is
often very difficult. In acute purulent pleurisy the diagnosis is most
difficult, especially at an early period, because the general symptoms
and the local signs resemble closely those of ordinary pleurisy. When,
however, the disease is further advanced, and we have the earthy aspect
of countenance with oedema of the thoracic walls, we can be nearly
positive in our opinion. Moutard-Martin[117] speaks of this localized
oedema at the level of the fluid as a certain indication of the
purulent character of the fluid. But this oedema, as he admits, does
not always exist. It is wanting in many cases, and it may be found in
cases of sero-fibrinous effusion where the patient has been lying on
the side, and in other cases of advanced cachectic disease. Formerly,
there were many more errors of diagnosis, which were only discovered at
autopsies, but now, thanks to aspiratory punctures, the diagnosis is
much more accurate, and indicates to us the rational treatment. In both
varieties of purulent pleurisy there is a tendency to discharge by
making orifices through the walls of the chest or through the lung.
This is nature's mode of spontaneous cure. The most common is the
pleuro-bronchial fistula, and the period of the disease at which this
accident may occur is very variable. Woillez[118] cites a case where it
occurred as early as the twenty-eighth day; ordinarily it occurs at a
much later period, sometimes as late as the eightieth day. It comes on
early in purulent pleurisy. In infants the perforations take place as
early as in fifteen or twenty days, and are favorable to the cure in
one-half of the cases. Saussier in 29 {544} perforations of this kind
counted 15 cures. The symptoms of this accident are easy of
recognition. They vary according as the pleuritic effusion is diffused
through the whole pleural cavity or is limited, encysted, or
interlobular. In the first variety, where we have the physical
evidences of the presence of pus, suddenly, during a paroxysm of
coughing, the pus is forced up through the bronchi, and the patient in
a very short time expectorates a considerable quantity, varying from a
few grammes to a liter or more. The quantity thus thrown off depends
upon the diameter of the fistula. It may be excessive, as in a case
recently observed by the author where suffocation was produced, causing
syncope, asphyxia, and death, the flow being so rapid as to fill up the
bronchi to such an extent that the patient could not get rid of it. In
many cases the pus is brought up more gradually, with successive coughs
or with changes of position. Frequently vomiting is produced by the
flow from the vomica. After the first instantaneous evacuation of pus
(ordinarily continuous, sometimes intermitting) purulent expectoration
takes place. The patient may pass hours without any discharge, when
suddenly a severe cough brings up a quantity of pus, and again may
spend days without further expectoration. Pleuro-bronchial fistulæ may
have a valvular character, so that air may or may not be admitted into
the pleural sac as the pus is discharged. With or without the formation
of pneumothorax there is a tendency to cause putridity of pus. In cases
of children, who swallow their expectoration, it often produces a very
troublesome diarrhoea. The course of the disease and its prognosis are
necessarily altered according to conditions met with. When the air does
not penetrate, we observe that the diseased side becomes depressed and
the swelling, previously noticed, disappears. The flatness on
percussion diminishes or disappears entirely. On auscultation we have
coarse râles, sometimes just inside the fistulous orifices, sometimes
at a considerable distance. The general symptoms, as well as the
physical signs, improve, and the case advances slowly toward cure.
Ordinarily, the pus expectorated from the pleura, when free from
contact with the air, is odorless, but it is rarely as unpleasant as in
bronchial dilatations, unless it is long retained in the cavity, when
putrefaction ensues. When the air enters from the bronchi, it
frequently acquires a disgusting odor. If the air enters the pleura and
takes the place of the pus, the chest remains enlarged. Indeed, it
sometimes increases in size to such an extent as to cause suffocation
unless the pus and gas are withdrawn. The valve made by the false
membrane allowing the air to enter the cavity, but not to escape from
it, causes the fluid to accumulate rapidly, and we have pneumothorax to
a very painful degree. The diaphragm is pushed down, and, if the
disease is on the right side, the liver is forced down, and descends to
a level with the umbilicus.
[Footnote 117: _Purulent Pleurisy_, 1872.]
[Footnote 118: _Traité Clin. des Mal. Aigues des Organes Resp._, 1872.]
The collection of gas and fluid may be in such excess as to produce a
concavity of the upper surface of the liver, while the organ is forced
down into the abdomen. E. Moutard-Martin[119] explains this extreme
condition by the fact that the fistulous orifice being at the superior
portion of the lung, the air having equalized the interior pressure
with the exterior pressure, the liquid obeys the laws of gravity, and
depresses the diaphragm. The fluid thus does not reach the level of the
pulmonary fistula. Under these circumstances the expectoration may
cease altogether unless the patient, by change of position, allows it
to flow outward through the orifice.
[Footnote 119: _Loc. cit._]
The physical signs of this condition of pyo-pneumothorax are very
marked and characteristic. Above the level of the fluid there is
ordinarily a great exaggeration of resonance on percussion, especially
at first. At the end of a few days, however, this resonance is
sometimes materially modified, and we have obscurity of the percussion
vibrations. Percussion, by itself, may lead {545} us into error of
diagnosis which the other modes of physical exploration will correct.
On auscultation we hear the amphoric murmur, which is sometimes of
great intensity, and at others so feeble and distant as to require
great attention on the part of the auscultator. These varieties of the
amphoric respiratory sound appear to depend more upon the position of
the pleuro-bronchial fistula, and upon the greater or less free
circulation of air through the fistula, than upon the extent of the
cavity (E. Moutard-Martin). This sound and the amphoric voice are the
two principal auscultatory phenomena. There is also the vibrating
metallic tinkling produced always in expiration. Although the physical
cause may exist, this latter is by no means a constant sign. It may
disappear for hours, and even days together, and then be heard for a
short time. Sometimes it is only heard when the patient coughs suddenly
and violently. When heard it is a very valuable indication of the
presence of a pleuro-bronchial fistula. Auscultatory percussion gives
us a still more valuable diagnostic phenomenon--the metallic amphoric
reverberation--especially if we percuss with a metallic percussor over
a metallic pleximeter. The Hippocratian splashing caused by succussion
is a more characteristic sign of pyo-pneumothorax than any other we
have mentioned. Other signs may fail, and often this is the only sign
present. Almost all the symptoms and signs that have been considered
characteristic of the presence of pus may coexist with a perfectly
limpid sero-fibrinous effusion. We may even have in serous effusions a
high, fluctuating temperature, profuse sweats, and quick pulse lasting
several weeks. On the other hand, purulent effusions may be associated
with symptoms of so mild a character as to lull suspicion. Previous to
the application of exploratory punctures for purposes of accurate
diagnosis, purulent pleurisies were confounded with the milder disease
until so far advanced as to be too late for effective treatment. Now we
can without risk discover purulent pleurisies at their very
commencement, and before they reach the point of great danger to the
subject we can relieve them by thoracentesis, and afterward pursue the
treatment for a radical cure.
Limited, circumscribed pleurisies, such as are found at the base of the
surface of the diaphragm and in the interlobular fissures, as well as
those involving the pleural cavity itself, may empty their contents
through the bronchi. As we have shown, the diagnosis of these forms is
often very obscure and difficult. The fine capillary exploring-needle
is a safe, and often a reliable, means of diagnosis. It may happen that
we can only guess at the nature of the disease until, after a
protracted cough, there is ejected by the mouth a quantity of pus, and
the diagnosis is made clear. We may perhaps discover a point of
flatness at the base or about the centre of the lung, but often this
flatness is very incomplete, because the collection of pus does not
always reach the thoracic wall. It may, indeed, be separated from it by
healthy lung-texture. Auscultation may discover coarse râles or even
gurgling with cavernous respiration. The voice sometimes has the
character of pectoriloquy, at other times of bronchophony: the cavity
is rarely large enough or the walls sufficiently firm to give the
amphoric tone. Under these circumstances there is neither metallic
tinkling nor Hippocratian succussion. The diagnosis of bronchial
fistulas caused by encysted pleurisies may be confounded with
tubercular cavities or with dilated bronchi. The exact position,
however, of the lesion, the rapid manner of the first purulent
expectoration, and the nature of the pus expectorated, will enable us
always to arrive at an accurate diagnosis. We must remember that in
bronchial dilatation the disease is developed by degrees, and the
patients do not expectorate suddenly a notable quantity of pus;
tubercular caverns are ordinarily at the summit. The mode of
expectoration is different, and the matter expectorated does not
present the same purulent and homogeneous characters. {546} The general
health is very different where encysted pleurisies exist from what it
is in patients suffering from tubercular cavities. In the former case
it is comparatively good; there are no profuse night-sweats, diarrhoea,
etc. Perforation through the thoracic walls may take place at a period
more or less remote from the commencement of the disease. The first
indication of this result is, ordinarily, a pain over a limited point
of one or two of the intercostal spaces, followed, in a few days or a
week, by a raised sensitive point on the surface, without change of
color of the covering skin. This may remain a long time in an unchanged
condition, but generally it increases gradually until it becomes soft
and fluctuating, reducible by pressure, but increased in size by
efforts to cough or by forcible expectorations. The skin over the
raised point becomes thin with a purplish tinge; suddenly, from some
effort to cough or unusual exertion requiring suspension of breath, it
bursts and gives exit to a quantity of pus far out of proportion to the
size of the small tumor. Sometimes there are several such points in the
same subject, appearing simultaneously or consecutively, especially if
the discharge is not free through the first one. Ordinarily, there is
but one which appears on the anterior portion of the chest about the
fifth intercostal space or in the intra-mamillary line. These orifices
sometimes close and then reopen. Of 18 cases of empyema necessitatis
collected by John Marshall,[120] 1 occurred in the sixth intercostal
space and 17 in the fifth, and 6 of his own cases in the fifth, beneath
the nipple. This is, as he states, the weak point of the chest,
relatively unprotected by the adjacent muscles. The internal
intercostal muscle, the weakest portion of the great pectoral, and the
thin fascia, are the only coverings at that point. There is valid
reason why special bulging and spontaneous perforation should occur
there. The spot also corresponds nearly with the middle of the pleural
cavity when distended. The fifth intercostal space is wider than those
below, and its limiting ribs, held to the sternum, give firmness to its
borders--conditions which help the thinness of the walls in determining
the place of perforation. In children perforation often takes place in
the very wide second intercostal space. The perforation, although it
may contract in size, persists and remains a fistulous canal,
permitting air to enter and to escape. The fluid rarely becomes fetid
unless there is a pleuro-bronchitic fistula or air is otherwise freely
admitted. Sometimes when the orifice is oblique, the air does not enter
at all. When the purulent effusion escapes through the thoracic walls,
the patient experiences at once manifest relief. The respiration
becomes better, the fever decreases, the sweats disappear, the appetite
improves, and the general condition is decidedly ameliorated. This
improvement persists as long as there is free discharge, but if from
any cause it ceases, we have a return of serious symptoms. If no air
enters, percussion and auscultation show the gradual disappearance of
the evidences of disease; but if air enters we have the signs of
pyo-pneumothorax, amphoric breathing, metallic and succussion sounds.
The diagnosis of parietal openings is comparatively easy: the quantity
of pus, its odor, with the physical signs, show its nature. With care
this form of pleural opening is distinguishable from a fistula made by
caries of the ribs or by vertebral abscesses, and not communicating
with the pleura. The existence of a thoracic fistula does not prevent
the formation of pleuro-pulmonary fistula, and reciprocally a parietal
fistula can be found where the other has been previously formed. The
abscesses following purulent pleurisies and empyema have been long
recognized. Hippocrates mentioned them as contributing to a favorable
prognosis in empyema.
[Footnote 120: _London Lancet_, March, 1882.]
Pulsating empyema is where the lesion is situated in the neighborhood
of the heart or of the aorta, which transmit their impulse. They are
also sometimes called pulsating tumors, rising and falling with
alternate movements of {547} inspiration and expiration (Stokes,
Graves, and Aran). These cases strongly simulate aneurisms. According
to Fraentzel, the fluid is always purulent. In 1 case reported by him,
and in 2 cases seen by Traube, pericarditis with effusion was present.
Douglass Powell mentions two well-marked cases of pulsation in the left
supra-mammary region where the diagnosis between effusion and aneurism
was very difficult, but where paracentesis removed a large quantity of
fluid and the signs of pulsation ceased. In these cases there was
present neither pus nor pericarditis.