side, usually its most prominent symptom. In the sense in which
Hippocrates used the word [Greek: pleuritis], it meant all kinds of
pain in the side, especially such as are of a violent character.
Pleurisy was mentioned by Celsus, and was still better defined by
Galen. Æctæus, however, was the first to describe it with precision and
to speak of its treatment. These ancient authors viewed the disease as
seated in the layer of the pleura lining the ribs or external parietes
of the chest. More modern writers contended that the disease was more
frequently in the expansion of the pleura over the lungs and other
parts. Boerhaave and Van Swieten contended for the separate and
distinct affection of the pleura. Sydenham, Hoffman, and Morgagni
believed that the pleura and the substance of the lung were generally
both implicated. Pinel was the first to definitely establish the
difference between pleurisy and pneumonia from the anatomical lesions.
Laennec laid the foundation of our present knowledge. He was followed
by Andral, Chomel, Louis, and Cruveilhier in Paris, and by Forbes and
Williams of London and Stokes of Dublin. They demonstrated, by the
physical signs and general symptoms during life and by the post-mortem
lesions, that inflammation may commence in and be limited to the pleura
in some cases, and in others that it may extend to and involve the
lungs. Again, they showed that in some instances the lung may be
inflamed without involving the pleura generally, yet that in the large
proportion of cases the disease may originate in one organ and extend
in a greater or less degree to the other, thus implicating both of
them. Previous to Laennec the incomplete anatomical knowledge of the
nature of the serous membrane, the pleura, as a capsule of the lungs,
and the thoracic organs and walls, as well as the theoretical views of
the nature of inflammation as a morbid process, led to erroneous views.
Their diagnoses were made from general symptoms only. Pleurisy was
considered the more common disease. Avenbrugger, Corvisart, and
Laennec, by their discoveries of the accurate physical modes of
exploration of chest diseases, gave far more reliable data for
differential diagnosis. Now we have, in addition to the general
symptoms, the modern refinements in auscultation and percussion, the
delicate measurements of Woillez's cyrtometer, Ransome's stethometer,
and Pravaz's and Alex. Wood's hypodermic exploring-needles to enable us
to attain great accuracy in the diagnosis.
CLASSIFICATION.--Pleurisy is one of the most common diseases of the
{484} respiratory apparatus. Though apparently simple, careful study
shows it to be extremely complex. It occurs in very different forms and
in a great many modifications, according to the producing causes and
the numerous lesions which follow its course. We might classify the
forms of pleurisy, according to their causes, as primary or secondary,
tubercular, traumatic, etc.; or we could designate them according to
their anatomical lesions, as dry pleurisy, pleurisy with effusion,
general or parietal pleurisy, encysted, multilocular, purulent,
hemorrhagic, etc. A methodical classification of all these forms is
difficult if we attempt to base it upon the prominent characteristics
or the lesions. We prefer a classification which enables us to study
separately the clinical varieties which are most frequently met with,
and therefore the most important. The symptomatology shows that the
inflammatory process in pleurisy is of different degrees of intensity.
We propose for our study to divide them into two main groups, according
to the nature of the exudation:
Fibro-serous pleurisy, Acute,
Chronic.
Purulent pleurisy, Acute,
Chronic.
They may be local or general. When they result from disease of
neighboring parts, they are generally local. Each of these groups
comprehends primary and secondary varieties.
In the first, we have an exudation resembling the plasma of the blood.
The effusion is not serous, for the fluid is spontaneously coagulable,
whereas serum is not. It is not properly termed fibrinous, for it
contains more albumen than fibrin. Fibro-serous is the most accurate
term by which to designate it. The watery portion gravitates to the
lowest part of the cavity, while the plastic deposit is thrown out over
the two surfaces of the pleura. In the most acute forms the general
symptoms, especially the pain and fever, are well marked. The exudation
is at first largely fibrinous, but it is afterward more fluid in its
character. In milder cases, the latent variety of the older authors,
frequently designated as the subacute form, the subjective symptoms are
so slight that the individual is not aware of his condition until the
exudation, which is largely sero-fibrinous, mechanically interferes
with his respiration. When first recognized these cases are really
often chronic. They frequently remain sero-fibrinous in their character
for a long time. Sometimes they become sero-purulent (the intermediary
variety), and later purulent. Purulent pleurisies (empyema) are those
where pus is the product of the inflammatory action. They may be acute
(empyema d'emblée) or the result of transformation of acute or chronic
fibro-serous pleurisies.
By this division we shall be able to take into consideration the
fundamental causes of all the forms of pleurisy. Starting from the
simple primary form, we shall be able to study special varieties of
secondary pleurisies, such as tubercular and rheumatic.
Next, we shall examine separately the hemorrhagic variety as distinct
from hæmothorax. The localized forms, such as the interlobular,
diaphragmatic, and mediastinal, will be studied as varieties caused by
their development in different localities.
The simplest plan to elucidate the whole subject of pleurisy is to
analyze carefully, in the first place, the unquestionably acute
disease, primary pleurisy, and afterward to connect with it the study
of the several forms and varieties. Acute primary pleurisy has a
sero-fibrinous exudation, and is the most common form of the disease.
In it are best defined the usual characteristics of this inflammation.
We consider this the principal type of this class, and with it shall
study the development and character common to all the varieties of
inflammation of the serous membrane of the thoracic cavity.
PATHOLOGICAL ANATOMY OF FIBRO-SEROUS PLEURISY.--The anatomical {485}
changes in all forms of pleurisy begin by hyperæmia of the vessels of
the serous membrane and of the subserous connective tissue. This is
followed by an exudation of a liquid, a pseudo-membranous deposit. In
acute primary cases this is first noticed on the costal pleura. The
pleura itself shows, by puffiness and oedema with red points and small
ecchymosed spots, that the inflammatory process has affected it. In a
few hours, in acute cases, there is found a thin deposit of fibrinous
lymph of a reddish-yellow tinge, with more ecchymosed spots, resulting
from the rupture of fine capillary vessels. The pleura is somewhat
thickened and loses its transparency, and is studded with very fine
granulations. Under the microscope it is shown that the epithelial
cells are swollen, that their number has been largely increased by
proliferation, and that they have been detached in great quantities.
The granulations are scattered over the pleural surfaces, and separate
the pleura from the fibrinous deposit. The connective tissue is loaded
with liquid, in which are found in increased quantity leucocytes which
have migrated through the walls of the blood-vessels.
Over the surface of the pleura there is a tissue of granulations
composed of embryonic cells, which are derived from the proliferation
of the elements of the connective tissue. In this tissue of new
formation we find new blood-vessels coming from those belonging to the
subserous tissue, which advances through small points, even to the free
surface of the granulations. These vessels are very thin and brittle.
They sometimes rupture and cause ecchymoses of the pleura and of the
false fibrinous membranes--sometimes effusions of blood, which,
becoming mixed with the serum in the pleural cavity, cause hemorrhagic
pleurisies. This new tissue is susceptible of organization, and of
transformation progressively into a tissue analogous to that of a
cicatrix. Under the plastic exudation we find abundance of embryonic
cells, which become elongated and spindle-shaped in the formation of
new connective tissue. This is at first tender, but may become dense
and fine over circumscribed points, so as to produce bands which
enclose and touch the effusion. This is the origin of the organized
neo-membranes which are found on the surface of the pleura. It is,
moreover, this tissue of granulations which constitutes the bands which
unite the parietal to the visceral pleura, the adhesions being produced
by the contact and the union of vegetations or neo-membranes developed
on the two opposed layers of the pleura. The membranes form the
filamentous thin bands which draw obliquely together portions of the
pleural sac. These lesions are very often slight and rudimentary in
simple acute pleurisy, but are found well developed in purulent
pleurisy, especially when it is chronic. These are hyperplastic
parenchymatous lesions of the pleura. Acute inflammation of the pleura
gives rise to two distinct forms of exudation--the plastic, deposited
on the free surface of the serous layers or formed in flakes in the
fluid; and the serous, which falls into the dependent portions of the
cavity. The plastic may exceptionally exist alone. Their formation
together is the rule. Anstie questions whether the serous effusion ever
occurs without the fibrinous. The plastic exudation takes the form of
granulations more or less prominent, constituting a bed of very
irregular rough points. So long as the period of inflammation
continues, new plastic deposits are formed over the old ones. They thus
increase in thickness. The neo-membranes which play such an important
rôle in the natural history of pleurisies increase very rapidly. Little
by little, they are transformed into firm, very resisting tissues. They
may become fibrous, cartilaginous, or even calcareous in their
structure. These false membranes develop more freely at first when the
opposing surfaces are kept apart by the effused liquids. The rubbing of
the two pleuræ together seems to impede the process of organization.
According to Wagner, the lymphatics are dilated and contain a liquid
poor in corpuscles. The newly-organized and vascular {486} tissues
often become the starting-points of fresh inflammatory processes and of
new products.
Exudations are of two kinds--liquid and pseudo-membranous. When the
inflammation extends over a limited surface, the fibro-plastic
exudation may be the only one; in which case the disease soon
terminates with local adhesions. This is dry pleurisy, which is rarely
primary in its origin. Ordinarily, the principal lesion of acute
pleurisy consists in a sero-fibrinous effusion which collects in the
cavity of the pleura; almost always the liquid effusion exists in
decided quantity. In it there are suspended fibrinous flocculi, and on
the surface of the pleura are found false membranes. The nature of the
effused liquids has been thoroughly studied, ample opportunities having
been furnished since thoracentesis has been so extensively used. The
quantity of liquid is very variable, from a few grammes up to several
liters. The terms small, moderate, and abundant are used to designate
the quantity--one-half of a liter is considered a small quantity;
moderate, one to one and a half liters; abundant effusion, two to two
and a half liters; very abundant, when the effusion goes beyond three
liters. The liquid is transparent and of yellowish-amber color. It is
darker when the fluid has been some time in the chest, and resembles
that of bouillon. Sometimes it has a rose tint when the liquid contains
a sufficient quantity of red globules, or it may be somewhat opaque
when it encloses a large proportion of leucocytes.
The presence of a few red globules does not constitute a hemorrhagic
pleurisy, nor does the presence of a small quantity of leucocytes make
a purulent pleurisy. It is only when they are very abundant that they
severally give those characters to the effused fluid. Dieulafoy
states,[1] after frequent examinations of aspirated serous fluid of
acute pleurisy, simple and frank, that it contains the smallest
quantity, from 500 to 600 red globules to the cubic millimeter, while
the white globules were from fifteen to twenty times more numerous. In
some instances he counted 1500, 2000, and even 3000, red globules to
the cubic millimeter without the coloration of the liquid being
sensibly modified. He adds that the liquid from the pleura has not a
perceptible rose tint unless it contains from 5000 to 6000 red globules
to the cubic millimeter. He concludes that there is no tendency to
transformation into purulent pleurisy unless the number of red globules
reaches 4000 or 5000 to the cubic millimeter. Rindfleisch (ed. 1869,
Leipzig) states also that upon their number and that of the
proliferated epithelial cells, with the floating flocculi, depends the
convertibility of the serous into purulent effusions.
[Footnote 1: _De la Thoracentèse par Aspiration dans la Pleurisie
aigue_, p. 42, Paris, 1878.]
Chemical Character of Effused Fluid.--Mehu[2] gives the composition of
the fluid as closely resembling that of the serum of the blood. He
found in it the same elements--water, albumen, fibrinogenous matter,
salts, red globules, and leucocytes. The proportion of these principal
constituents of the blood was greatly modified in the pleuritic liquid.
The quantity of water was always increased. On the other hand, the
quantity of substances in solution was greatly diminished. The
exudation was really blood-plasma, more or less diluted, in which the
relative proportion of the constituent elements varied according to the
intensity of the inflammation. It has the same alkaline reaction, and
it is spontaneously coagulable, owing to the presence of the fibrin
which is in solution in the serum, the proportion of fibrin making it
coagulate more or less rapidly. Mehu found the quantity of fibrin to
vary from 09.073 to 19.276 to the kilogramme. The same mineral
substances were found, but in less quantity, than in plasma of blood.
The intensity of the inflammation causes alterations in the composition
of the exudations. The more acute the inflammation, the greater is the
quantity of albumen and of fibrinogen. The fibrinogenous matter
contained in the {487} exudation is coagulated only by contact with the
air. One portion of it becomes concrete in the interior of the body in
the form of fibrinous flocculi, which float in the fluid, and in the
false membranes, which are deposited in successive layers on the
surface of the inflamed pleuræ. This coagulation takes place in a
manner analogous to that of the coagulation of the fibrin in a drop of
blood. These false membranes are almost always found in acute
pleurisies, but their development is very variable. Sometimes they are
very thin, friable, and readily disappear; again, when the inflammation
is intense, they last a long time and cover thickly both pleuræ.
Occasionally they envelop the effusion and produce veritable cysts and
localized pleurisies. Their color is opaline or semi-transparent when
recently formed, but opaque when old. Their consistence varies
according to the duration of the disease. At first they are soft,
impregnated with fluid, easy to tear or break; later on they become
resistant and almost dry. The microscope shows these false membranes to
be formed of crossed fibrillæ, with intervals containing white
blood-corpuscles, with voluminous, swollen epithelial cells of serous
membrane, proliferated and detached.
[Footnote 2: _Arch. général de Méd._, 1872.]
When the pleural inflammation subsides, the exudation is destined to
disappear. Usually the cure is produced by the reabsorption of the
effused products. The liquid part of the exudation, the serosity, is
absorbed by the lymphatics, which are found frequently dilated, and
some of them are filled with fibrinous coagulations and the leucocytes.
The solid parts, the false membranes, concrete fibrin, and cells
disappear with more difficulty. They undergo granulo-fatty
metamorphosis, and are then taken up by the lymphatics.
These fibrinous false membranes are not, as was formerly supposed,
susceptible of organization. It is only the neo-membranes, formed by
the proliferation of the elements of the pleura, which are organized or
organizable. It is these that form bridles or ligaments which attach
the lung to the thoracic wall, and are susceptible of transformation
into cartilage or even into bone. In chronic cases these new membranes
bind the lung down, impair its expansive powers, and inflict great
damage upon the respiratory force.
Care must be taken to distinguish between the neo-membranes and the
plastic and liquid exudations. These last contain transitory-formed
elements entangled in the fibrinous layers. They are principally
lymph-corpuscles, containing solitary nuclei, together with a few
epithelial cells, almost always in process of disintegration, and
isolated blood-corpuscles (Fraentzel).
Distribution of Fluid.--The situation and form in which the effusions
are found in the pleural cavity furnish important data for study as
applicable especially to diagnosis. At the commencement of the disease
the effused plastic products form a thin covering to the pleural
surface--a slight cushion interposed between the lung and the thoracic
wall. Later, the fluid products gravitate by their weight to the lowest
portion of the cavity of the pleura; then, as they increase in
quantity, they gradually rise or are drawn to the superior portion of
the thorax. Once formed, these effusions are but slightly movable and
but little displaced by the varying positions of the patient, unless
the quantity be very great and no adhesions or bands have been made. If
the effusions be of viscid consistence, or if false membranes exist,
they are mechanically prevented from moving. The serous transudations
of hydrothorax always occupy the most dependent portion of the cavity,
but observation shows how frequently the pleuritic effusions are
immovable, being maintained and suspended between the diaphragm and the
lungs, and imprisoned in the situation where they form by the false
membranes.
Previous to 1843 the authorities universally taught that the effused
fluids in the pleural cavity obeyed, as they would in an open vessel or
in a vacuum, the law of gravity. They never appeared to question but
that the fluid {488} would necessarily assume its hydrostatic level,
and consequently that it would reach a horizontal line in all parts of
the chest. The distribution and the form which the effusions take were
first studied by Damoiseau.[3] Fernet and D'Heilly[4] maintain that
Damoiseau perfectly established the form and disposition which the
effusions take in pleurisy. To study them well we must bear in mind,
they say, three facts: the irregularly conical form of the pleural
cavity; the effect of gravity; and the habitual position of the patient
when lying down. Damoiseau and these authors utterly ignored the
retractile force of the lung, as well as that of the diaphragm, and the
resiliency of the thoracic walls, as effecting the position of the
fluids in the pleural sac. If we observe that the patient at the
commencement lies ordinarily on his back, the thorax being raised and
more or less inclined to the horizontal position, we easily appreciate
that the effusion ought to accumulate, at first, behind, in the most
dependent portion of the costo-vertebral gutter, below the inferior
angle of the scapula; then, as it increases in quantity, it rises and
obliquely strikes the conoidal cavity, which encloses it, and makes on
its surface curves resembling those of an oblique conic section
(Damoiseau). As Damoiseau described the pleuritic line of flatness as a
parabola, it was highest in the axillary region, where it first
appears; thence, as its summit rises, its branches advance downward and
outward to the sternum and the vertebral column.
[Footnote 3: _Thèse de Paris_, 1845.]
[Footnote 4: _Nouveau Dict. de Méd. et Chir._, Paris, tome xxviii.,
1880.]