and unexpected deaths in cases of fibro-serous pleurisies. Not only has
this resulted in cases where the fluid was excessive in quantity, but
also in cases where the amount was moderate. Wilson Fox (_Brit. Med.
Journ._, Dec., 1877) gathered from medical literature between 50 and 60
sudden deaths from effusions of all kinds. Syncope has been the usually
assigned cause of death. Négrié[45] collected 12 cases of unexpected
deaths from pleurisy, and there were but 2 of them where syncope could
be assigned as the cause of the fatal termination. Of the remaining 10
cases, 3 were caused by what is invariably a grave complication,
pericarditis, and 7 by clots formed in the heart or pulmonary artery.
In the cases where pericarditis existed the deaths occurred as early as
the eleventh or twelfth day. In the other cases death occurred as late
as from the twentieth to the forty-fifth day. Woillez[46] reports 2
cases where death was produced by supervening congestion of healthy
lung.
[Footnote 45: _Thèse de Paris_, 1864.]
[Footnote 46: _Loc. cit._]
COMPLICATIONS AND SEQUELÆ.--The inflammation may extend by contiguity
to the lung-parenchyma, pneumonia supervening after a few days, or it
may appear to come on simultaneously. It is, however, a rare
complication. Lacaze[47] reported one case, and that followed
thoracentesis; Lugrol reported a similar case.
[Footnote 47: _Loc. cit._]
Pneumonia does not appear to commence after the effusion has reached
the point of compressing the lung. The inflammations frequently are
peribronchitic and broncho-pneumonic. The mediastinum may become
involved. Fraentzel states that it can never be clearly proved that
simple croupous pneumonia exists as a complication of primary pleuritis
on the side affected; on the sound side it occurs occasionally. Laennec
taught that the compression by the fluid always tended to prevent the
occurrence of pneumonia. Anstie's opinion was that when the lung is
compressed to carnification it is incapable of inflammation. The most
formidable way in which pneumonia may complicate pleurisy is where,
considerable effusion existing in one pleura, inflammation attacks the
opposite lung. It may be doubted whether this ever occurs in truly
primary pleurisies: kidney disease, specific fevers, pyæmia, etc.
nearly always precede it. Hyperæmia or congestion of the opposite lung,
without its amounting to pneumonia, does occur, and is a very grave
complication. The same may be said of double pleurisy and peritonitis
as resulting from blood-poisoning. It rarely happens in primary acute
pleurisy that both pleuræ become involved. When such is the case,
however, it is generally tubercular in its nature, and necessarily a
very grave if not a fatal complication. Walshe reports having seen 4
cases of idiopathic bilateral pleurisy in persons thoroughly healthy
and perfectly free from constitutional taint of {513} any kind. In all
the pericardium was involved, and in 1 the peritoneum. They were all
fatal. Acute pericarditis from extension of the inflammatory process is
a frequently-occurring complication. When the inflammation extends to
the pericardium, the effusion is of the same character as that of the
pleurisy, whether it be sero-fibrinous, purulent, or hemorrhagic. It is
a complication of great gravity and is sometimes the cause of a fatal
termination of the pleurisy. We have never met with endocarditis as a
complication, but Fraentzel speaks of having seen it in acute pleurisy
in children. Before complete carnification occurs oedema of the lungs
may be produced on the diseased side or in the healthy lung. This
pulmonary oedema, when it attacks the sound side, is acute, being
produced by rapid pulmonary congestion, which causes free, albuminoid,
and frothy expectoration, often ending in asphyxia. The serum and
albumen of the blood by transudation pass into the bronchi and the
alveoli, and fill them more rapidly than they can be expectorated: the
subject dies by suffocation. Auscultation reveals fine vesicular râles,
characteristic of oedema of the lungs, closely resembling the fine
crepitation of pneumonia. Traube has named this oedema pneumonia
serosa. Engorgement it certainly is, but it can scarcely be designated
a pneumonia. It closely resembles the oedema we meet with after
thoracentesis, which has been named by Hérard expectoration
albumineuse.
Bronchial catarrhs, when complicating pleurisies, cause dyspnoea, add
much to the discomfort, and protract the duration of the disease.
Barth[48] speaks of dilatation of bronchi as a complication of
pleurisy. Woillez[49] calls attention to a complication which has been
generally overlooked by the authorities--a persistent pain which some
patients suffer in the side of the chest a long time after the disease
has been cured. The most dangerous complications are syncope, formation
of clots, venous emboli, and exaggerated distension of the thoracic
walls by the effusion.
[Footnote 48: _Mém. de la Soc. Méd. d'Obs._, Paris, 1856.]
[Footnote 49: Article "Pleurisy," _Mal. Aigu. Resp._, 1872.]
Sequelæ.--The connection of pleurisies, especially chronic, with
subsequent tuberculosis, is very generally admitted. Bartholow says:
"The importance of pleuritis as a cause of phthisis is hardly
sufficiently recognized in inducing tubercular deposit, and by adhesion
limiting the movements of the organs, and thus inducing diseases."
Anstie says: "It is now well established not merely that pleurisy often
occurs in phthisical lung disease, but that pleurisy itself is capable
of setting up true tuberculosis even in previously healthy persons.
This is specially apt to occur where purulent effusion has been allowed
to remain too long in the pleura, or where paracentesis has been
performed repeatedly for empyema, the wound being closed in the
interval." Modern authors thus consider that a productive field is
offered for the bacillus tuberculosis.
Flint states that "in an analysis of 47 cases, in 3 the subsequent
development of phthisis was probable, although not demonstrated, and in
1 case only the occurrence of this disease as a sequel was certain." Of
53 cases reported by Blakiston, not one became phthisical during
several years after recovery from the pleurisy. Flint says the effect
of chronic pleurisy with effusion in a person already phthisical is to
arrest or retard for a time the progress of phthisis. We have mentioned
the retraction of the chest-walls with deformity of shoulders and
spine, and the permanent dislocation of the heart and larger
blood-vessels, as serious results, as also the orifices produced by the
bursting of the empyemas outwardly. These may all in time, with
judicious care and treatment, be very materially lessened, and even
cured. Empyema sometimes causes destruction of the periosteum of the
ribs and subsequent necrosis. It is questionable whether there are any
cases of pleurisy which do not leave more or less extensive adhesions
{514} between the two pleural surfaces. In many cases they do not, it
is true, seem to injure seriously the general health, yet they must
impair the full functions of the lungs. How frequently this is the case
is shown at autopsies of persons dying of other diseases, where we find
extensive adhesions when we had no reason during life to suspect that
such would be the case. Adhesive bands may interfere with the expansion
of the lungs and cause chronic bronchial catarrhs, ending in death.
Caseous pneumonias are among the sequelæ of pleurisy. When the false
membranes are thick and numerous, the lung remains impervious to air
and useless. This condition sometimes produces bronchiectasis. While it
is true that the lungs, when the effusion is not great enough to
actually compress them, sometimes retain their expansibility for three,
six, or even eight months, yet there are cases where they do not expand
after being bound down for months, and then we have depression of the
walls of the chest. Woillez met with 6 such cases.
DIAGNOSIS AND PROGNOSIS.--The diagnosis of the several varieties of
pleurisy ought easily to be made by the due appreciation of the general
symptoms and physical signs we have enumerated. Cases occur where the
differential diagnosis is not free from difficulties, even to the most
careful of observers. Pleurisies on the left side are more easily
diagnosed than those on the right side. Most of the signs are much more
frequently observed on the left than on the opposite side: some of them
are rarely met with except on the left. Before the discovery of the
science of auscultation and percussion pleurisy and pneumonia were
frequently confounded. By their aid the two diseases may ordinarily be
diagnosed with precision. In both there are chilliness, fever, cough,
and dyspnoea. At the initiation of acute pleurisies, we expect for
several days more or less of chilliness, but in pneumonia one, or at
most two, decided rigors. The temperature in primary pleurisy rarely
goes beyond 100° F. in the first twenty-four hours, whereas in croupous
pneumonia, in the same length of time, it not unfrequently rises to
103° F. or 104° F. In consequence of this high temperature in pneumonia
the skin becomes hot and dry, with frequently a bright spot on the
cheek corresponding to the side of the diseased lung. This is not the
case in pleurisies, where, on the contrary, we have a pale, anxious
expression of face. The comparatively mild fever of pleurisy is
continuous. We have not, as in pneumonia, the marked changes, often of
two or three degrees, between the morning and evening temperatures, nor
have we critical days (between the fifth and eleventh) where the fever
breaks with rapid defervescence.
Pleurisy is a more prolonged disease, and is not self-limited. The
cough of pleurisy is short and quick, with no expectoration, unless it
is thin, frothy mucus. In pneumonia the cough is longer, and is
accompanied by a tenacious expectoration, more or less free, and
generally (not always) tinged with blood. The rusty-colored sputa is
almost characteristic of pneumonia. At first there is a marked
difference in the dyspnoea in the two diseases. In pleurisy it is
superficial, because the lungs are not freely expanded in consequence
of the accompanying pain. In pneumonia it is deeper and the oppression
is greater. The struggle for breath in the first stage of pneumonia is
frequently alarming to witness. The relative frequency of pulse and
respiration is more modified in pneumonia. The stitch-like, cutting
pain in pleurisy is characteristic and very circumscribed, whereas in
pneumonia, unless the pleura is involved, there is little or nothing
beyond a dull soreness. We have in pleurisy the restrained movement of
the side affected, and corresponding increase of movement of the
healthy side. Not so in pneumonia. At the beginning of croupous
pneumonia we generally have the crepitant râle heard in inspiration,
but not observed in pleurisy. The friction sound, if present, heard in
inspiration and expiration, is equally characteristic of pleurisy. If,
as sometimes happens, we do not hear either {515} the crepitant râle or
the friction sound, we must be cautious in our diagnosis until we have
the more definite symptoms of the next stage.
Later on in the clinical course of the diseases, in their second
stage--consolidation in pneumonia and effusion in pleurisy--the
physical signs enable us to make the differential diagnosis. We expect
dulness in both diseases, but it is more absolute in pleuritic
effusions, and to the finger, as a pleximeter, the resistance is
greater. In pneumonia there is very seldom complete dulness over the
whole side of the chest, for there are frequently lobules not
consolidated, or spots where the solid deposit has been partially
absorbed. Moreover, the area of dulness is not bounded by that peculiar
curved line, with its concavity at the base behind, facing the
vertebra, gradually becoming convex as it turns upward and forward
toward the axilla, again descending toward the sternum, as is the case
in pleuritic effusions. Changes of position of the patient may cause
the fluid, when in large quantity, in pleurisy, unless prevented by
fibrinous adhesions of the two surfaces, to gravitate to a greater or
less degree, and thus alter the points where we have flatness on
percussion. The enlargement of the thorax, the bulging of the
intercostal spaces, the marked displacement of the organs, and the
frequently complete obliteration of the semi-lunar space, are
characteristic of excessive pleuritic effusions. The displacement of
the neighboring organs, especially of the heart, is a very valuable
diagnostic sign of pleurisy.
There are, however, other conditions besides the presence of fluid,
such as new growths and pneumothorax, which, by increasing the contents
of the chest, may produce the same result. We may also meet with cases
of congenital malposition of heart or instances where infantile
disease, or constrained position, necessitated by occupation, have
caused malformation of the contents of the chest.
The most characteristic percussion sign of effusion in pleurisy is the
semi-tympanitic (Skodaic) or amphoric resonance high up in front. In
rare cases it is found in pneumonia, but it is most pronounced over the
consolidated lung, whereas in pleurisy it is above the level of the
fluid. The vesicular murmur is not heard below the level of the fluid,
unless very feebly at its upper surface, nor indeed is the passage of
the tidal column of air up and down the bronchial tubes. In pneumonia
bronchial respiration and increased resonance of voice rapidly
supervene; whereas in pleurisy the voice is obliterated. In pneumonia
we find the characteristic loud, high-pitched, brazen bronchial
respiration over the whole of the consolidated portion. When a tubular
quality is given to the inspiratory murmur in pleurisy, it is a
diffused, distant, and low-pitched sound from the compressed lung.
There is a marked contrast between the increased vocal fremitus of
pneumonia and its entire absence in pleurisy. In pneumonia there is
strong bronchophony with a jarring thrill to the ear, but there is not
the displacement of the adjacent organs, the increased volume of the
affected side, nor the widening and bulging of the intercostal spaces,
with sometimes fluctuations, perceived on auscultatory percussion, as
in pleurisy.
Although both diseases are ordinarily unilateral, yet we more
frequently meet with double pneumonia than with double pleurisy. It
must be borne in mind that we may discover the coexistence of pneumonia
and pleurisy. When this does occur special care must be taken in the
diagnosis. In cases of pleurisy on the left side, sometimes the impulse
of the heart forces the two surfaces of the pleura together, and causes
us to hear a pleural, cardiac friction sound. It has the rhythm of the
heart, and is heard when respiratory movements have been suspended.
This sound is limited to the left border of the heart. Care is needed
to prevent the error of diagnosing pericarditis.
The diagnosis of pleurisy from hydrothorax, or passive transudation of
fluid into the cavity of the pleura from mechanical causes or
blood-poisoning, depends upon the recognition of the fact that
ordinarily the latter is not {516} ushered in by fever--that it is
bilateral, and is frequently accompanied with dropsy in other parts of
the body. Transudations being slowly developed, the lung gradually
contracts, and the presence of the fluid is tolerated for a
considerable time; indeed, it is not until it is excessive that it
compresses the lung. Thus, dyspnoea is not ordinarily produced until
the accumulation is very great.
Sometimes the diagnosis between pleurisy and intercostal myalgia, or
pleurodynia, is confused and uncertain. The pain may be as intense and
the respiration as jerky where there is no pleurisy, if there is great
soreness of the muscles between the ribs. The pain is, moreover,
accompanied by more or less rise of temperature. Oftentimes the
respiration is as painful as in pleurisy, for the individual
instinctively refrains from causing the muscles to contract. Usually
there is greater tenderness on pressure over the walls of the chest,
less fever, and the area of pain is larger in this form of muscular
rheumatism. The friction sound, if present, makes the diagnosis clear.
We sometimes remain in doubt for twenty-four hours.
Intercostal neuralgia less closely resembles pleurisy. It occurs
without fever, generally in anæmic subjects or in those debilitated by
chronic general diseases, especially uterine. The tenderness is limited
to several points along the course of a nerve, at the exit of the nerve
from the spinal cord, in the axillary region, and near the sternum.
Pericardial effusions and aneurisms can ordinarily be readily diagnosed
from pleurisies. Their positions in the cavity are so well defined, and
the accompanying physical signs are so characteristic, that they ought
not to be confounded with pleuritic effusions.
Solid tumors and cysts occupying a considerable portion of the pleura
or bulging into it from the mediastinum may deceive us into thinking
that there is an effusion. They displace organs, press upon the lungs,
or intervene between the lung-texture and the walls of the chest, thus
preventing us from hearing the entrance and exit of air and the
vibrations of the voice. Not containing air, we have flatness on
percussion. Being solid conductors, we have with them increased vocal
fremitus, whereas in pleuritic effusions it is not perceived.
Ordinarily, tumors are found at the superior or central portion of the
chest, and cause an irregular bulging of the walls instead of the
general enlargement caused by liquid effusions. Before the discovery of
the present modes of physical diagnosis intra-thoracic growths,
especially cancerous ones, were frequently confounded with pleurisies
by even the most careful observers. Now such errors are only
occasionally committed. The history of the case, the general symptoms,
absence of fever, etc. will assist us in making the differential
diagnosis. A careful examination by physical exploration will give us
valuable aids. The bulging produced by malignant growths is not so
marked nor is it so uniform. The dulness on percussion is not so
pronounced. It does not vary from changes of position of patient. The
displacement of heart and other organs is not so marked. Hunt[50] calls
attention to the considerable blood-stained expectoration from cancer.
He calls it currant-jelly expectoration. We must look also for the
characteristic signs of cancerous cachexia and enlargement of glands in
the axilla and in the supra-clavicular fossa. The exploring
aspirator-needle will generally enable us to arrive at an accurate
diagnosis, with the assistance of a microscope to examine the fluid or
solid matter withdrawn. The fluid thus obtained from cancer is
generally blood-stained.
[Footnote 50: _Loc. cit._]
Inflammations of the pleuræ are sometimes caused by the presence of
intra-thoracic tumors. Abscesses of the liver and echinococci cysts may
ascend, and, pushing the diaphragm before them, occupy the pleural
sacs, and thus simulate pleuritic effusions.
{517} Pulmonary atelectasis, caseous inflammation of the tissue of the
lung, aneurisms of the large thoracic blood-vessels, may, without care,
be mistaken for pleurisies. It is very important to ascertain the
nature of the fluid effused into the pleural cavity, whether or not it
is serous, sero-fibrinous, purulent, or hemorrhagic. Generally this can
be done by careful study of the accompanying general symptoms and the
clinical history of the case. If there are repeated irregular rigors
from the beginning, followed by high fever and free perspirations,
there is every reason to fear that the fluid is purulent. If symptoms
of blood-poisoning develop, we are still more confident that there is
pus. Its hemorrhagic character may be inferred when great pallor,
weakness, and lowered temperature suddenly appear during an acute
attack.
Bacelli's physical sign known as pectoriloquie aphonique, or the
passage through the effused fluid of the whispered voice, has
considerable significance as a means of testing the nature and
character of the fluid. His conclusion was that, when heard, it showed
the fluid was fibro-serous; when not heard, it revealed to us that the
effusion was purulent or sero-purulent. Laennec had noticed that in
voiceless consumptives the whispers would sometimes resound as if the
patient shouted in the ear of the auscultator. R. Douglass Powell
reported[51] 10 cases bearing upon the value of this sign. In 6 of
these, in which the fluid was clear, 5 yielded the sign, the sixth did
not. In 2 acute cases, when the effusion was purulent, the sign was
heard. He adds that he has heard the sign to perfection in fetid
sero-purulent effusion. Mercadie[52] claims that when pectoriloquie
aphonique is heard in purulent effusions it is only at the uppermost
part of the fluid near its limit, where it has become very thin from
the weightier portion, the flocculi, and the leucocytes falling to the
dependent portion of the sac. Care must be taken in listening for this
sign. The patient must be ordered to speak each syllable slowly and in
a whisper, distinctly counting up to twenty or thirty. If it be present
we ought to be able to perceive that the syllables sound, to the ear,
clearly articulated along the height of the effusion. The sound is
caused by the transmission of the whisper without any buzzing and
without continuous murmur. The maximum of intensity of this sound is
heard along the vertebral gutters and along the posterior base of the
pleural cavity. It becomes feeble in its distinctive character as we
approach the axillary region and also immediately under the angle of
the scapula. The theoretical objection has been made to this sign that
its production is contrary to well-known physical laws of the
conduction of sound-waves. It is said because the sound originates in
the air it must be indifferently conducted by fluid; moreover, that its
transmission ought to be in proportion to the density of the fluid,
whereas this sound is best conducted by a thin fluid. Walshe's
explanation of the greatly-increased sound-conducting power of a
consolidated lung in croupous pneumonia was that it was owing to its
homogeneity of structure. Bacelli avails himself of this principle to
account for our hearing through a fibro-serous fluid the whispered
sonorous waves, and our not hearing them when the fluid was
sero-purulent or purulent. In the latter case the fluid is excessively
heterogeneous, containing leucocytes in abundance, besides layers of
membranes, flocculi, and blood-discs. The sound-waves are lost as they
pass through these media of different density. We have found it to be a
physical sign of value in the differential diagnosis of the nature of
the fluid, yet its presence is not pathognomonic of serous effusions.
In thin fluids it is generally heard, and ordinarily it is not found in
purulent pleurisies. If well marked, it indicates a fibro-serous
effusion. Its absence does not necessarily show purulent pleurisy. Its
greatest value is as indicating the purulent transformation of a
fibro-serous effusion.
[Footnote 51: _Trans. Int. Med. Cong._, 1881, vol. ii.]
[Footnote 52: _Thèse de Paris_, 1876.]
Thanks to modern investigations, we have in the very fine needle of the
{518} aspirator, or that of the hypodermic syringe, a delicate and sure
means of accurate diagnosis, not only as to the nature of the fluids,
but as to that of tumors and growths which may be confounded with them.
We would not use for exploration a trocar and canula. We consider it
best to employ a short needle in aspiration, for fear that a delicate
hypodermic needle might break. Flint states that he has known several
instances of this accident. Aspiration can be performed with perfect
safety, and, indeed, without any fears of unpleasant results even if we
perforate an aneurism. The orifice made is so small that the tissues
close the moment the needle is withdrawn after making the exploratory
puncture. If care be taken to cleanse the instrument and to use
Listerism that no deleterious germ be introduced, the operation is
harmless. (See Purulent Pleurisy.)
Blunders in diagnosis, however, will rarely occur if an examination is
conducted with great accuracy, and if we follow the course of the
disease with care.