that the line of flatness over the upper surface of a moderate effusion
is not horizontal when the patient is in the sitting or erect posture.
There has been considerable difference of opinion among the English[6]
and continental writers as to the exact disposition of the fluid: some
partially assent to Damoiseau's views; others, again, very materially
modify them. Wintrich,[7] who was one of the first among the Germans to
emphasize the percussion line of demarcation between a pleuritic
effusion and a contracted lung, says: "As the exudation gradually
increases, the level of the fluid does not present a line which is
horizontal or parallel to the ground, but one which descends toward the
ground at a more or less acute angle." Fraentzel says that the line is
never horizontal. Leichtenstein and Ferber[8] maintain that the line
depends upon the position of the patient early in the disease. Gee[9]
holds very much to this opinion. He states that the upper limit of the
surface of liquid, when it reaches as high as two inches above the
nipple, is horizontal. When lower than this, the dulness forms
irregular parabolic curves, which become smaller and smaller as they
descend. Austin Flint[10] says, in his more recent edition: "The upper
limit of the dulness or flatness, the position of the body being
vertical, is not in a continuous horizontal line extending over the
posterior, lateral, and anterior aspects of the chest." Flint,
Wintrich, and Fraentzel speak of the line being highest behind. Calvin
Ellis of Boston in two very suggestive papers[11] described a
curve-line made by the upper line of the effused fluid, which radically
differed from any one previously mentioned. "This curve begins, with
medium effusions, relatively low down on the back, passes outward from
the vertebral column, and soon turns upward and proceeds obliquely
across the back to the axillary region, where it reaches its highest
point. Thence it advances in a straight line, but with a slight
descent, to the sternum." Powell, however, does not find {489} that the
curve invariably commences at a lower level behind. G. M. Garland,[12]
in consequence of the resemblance of this curve to the italic letter
_S_, has named it, very appropriately, the letter _S_ curve. He adds
that, according to his experience, "this curve, as described first by
Ellis, may be traced, by proper percussion, in any case of free,
uncomplicated pleurisy when the patient's body is erect and the amount
of fluid present is not excessive. As any effusion increases in amount,
the curve of its distribution gradually rises and tends to flatten out,
so that it no longer presents its characteristic _S_ feature after it
reaches the second rib. At this point, when the fluid occupies nearly
the entire side, the curve comes quite near to the horizontal, but if
some of the fluid be withdrawn by aspiration or absorption the letter
_S_ curve will reappear and retreat downward in the inverse order of
its advance, until with entire absorption it becomes merged into the
normal boundary of the lung."[13] Garland quotes from two recent German
authorities--Heitler of Vienna and Rosenbach of Breslau--to the effect
that the line of flatness of the effusion extends lower on the back
than it does on the side, and that there is a triangle bounded by the
vertebral column, the upper curve from the bottom, and a line drawn
from the summit of the curve, where there is impaired resonance over
the lung from adhesions and oedema of the lung, but where there is no
fluid and no flatness. Garland had previously called attention to this
space, and had named it the dull triangle. He had warned all who sought
to trace the true line of pleuritic flatness to be careful not to
overlook this region. Heitler had likened it to a monk's hood cut
longitudinally through the centre and hanging apex down. Rosenbach made
this dull space, clearing up in exercise and deep breathing, as
distinctive between pleurisy and pneumonia. We must expect impaired
resonance on the posterior wall above the fluid, for the fibrinous
deposits from exudation collect there when the patient is in the
recumbent position. Garland[14] calls attention to the confused views
caused by confounding the two physical signs of dulness (or impaired
resonance) and flatness (absence of resonance), the latter only
indicating the presence of fluid. If the differential diagnosis between
the dulness on percussion over the dull triangle and the flatness over
the fluid be not carefully made by delicate, light percussion, the two
may easily be confounded and the fluid be thought to have arisen to a
much higher level than it has. In some cases, owing to greater
thickness in the walls and coverings of the chest and adhesions, it may
be more difficult to draw nice distinctions in percussion sounds. This
distinction can, however, be made if the percussion-stroke is used with
proper delicacy and lightness, and a comparison made between the two
signs, and not between them and vesicular resonance. If the percussion
be strong, the vibrations are communicated from the resonant lung above
the fluid, and deceive the examiner. The most effective manner of
percussing is at right angles to the general direction of the curve,
which is transverse across the chest. Thus examining, we have had ample
opportunities of confirming the statement of Ellis and Garland that the
curve line is never highest behind, even with the largest effusion.
Wintrich and his German followers hold a different view. In moderate
effusions it is highest in the axilla, from which point it turns
downward posteriorly to touch the vertebral column at the interscapular
region. In front it extends downward toward the sternum. R. Douglass
Powell[15] reports cases with drawings, showing that in typical cases
the fluid does not take a water-level, "but a curve, having its
convexity upward in the lateral region." When the effusion becomes
excessive and fills the whole cavity, there is flatness on percussion
everywhere. As the fluid subsides, however, from absorption or from
mechanical removal, the distribution again resumes, to a greater or
less degree, its previous shape. {490} In moderate effusions there is,
ordinarily, the dull triangle posteriorly, and Skodaic resonance under
the clavicle in front in the anterior triangle. On the left side the
lower limit of the effusion can be recognized by the flatness being in
the shape of the arch of the diaphragm. In cases complicated by
adhesions or by pathological changes in the lung itself the curve is
changed, and in some the Ellis curve is straighter than in others.
Adhesions form sometimes early in the disease. They mechanically
interfere with the usual distribution of the fluid, as do catarrhal,
tubercular, or pneumonic consolidations, and, indeed, emphysematous
conditions. All these physical alterations of structure modify the
elastic force of the lungs. According to Mohr's statistics, adhesions
were wanting in 47 per cent. of the cases analyzed by himself.
Garland's experiment of injecting glue and plaster of Paris, and
subsequently cocoa-butter, into the pleura of living and dead dogs, and
by moulds testing the curves formed, showed that if the dogs were
suspended by the head the curve of flatness on percussion was very
similar to the Ellis curve. On removing the casts after they had
solidified, he found they closely corresponded to the shape and
position indicated by the physical signs elicited before opening the
chest.
[Footnote 5: _Archives générale de Méd._, 1843.]
[Footnote 6: See Hyde Salter, _Lancet_, 1865; Powell, _Trans. Roy. Med.
and Chir. Soc._, vol. lix.; W. N. Stone, _Lancet_, 1877; Le Gros
Clarke, _Roy. Soc. Med. and Chir._, 1872.]
[Footnote 7: Quoted by Garland, _N.Y. Med. Journal_, 1879.]
[Footnote 8: _Ibid._]
[Footnote 9: _Auscultation and Percussion_, 1877.]
[Footnote 10: _Practice of Medicine_, 1880, p. 130.]
[Footnote 11: _Boston Med. and Surg. Journ._, 1874 and 1876.]
[Footnote 12: _Pneumono-Dynamics_, New York, 1878.]
[Footnote 13: _N.Y. Med. Journal_, Nov., 1879.]
[Footnote 14: _Pneumono-Dynamics_.]
[Footnote 15: _Med. Times and Gazette_, Oct., 1882.]
Ellis's observations, and those of Garland with his experiments, have
given us the most accurate views as regards the form of the curved line
of flatness.
Nearly all modern authorities, including Peter, Gerhardt, and Paul
Niemeyer, admit that fluids in the pleural sac assume more or less
irregular curves, and not a hydrostatic, horizontal level. Whatever may
be the nature and consistence of the effusion, fibro-serous,
sero-purulent, or purulent, it does not behave in its distribution as
if it were in an open vessel. But few writers, however, have troubled
themselves to ascertain the causes of this apparently abnormal
condition. They appear to have completely overlooked the facts that had
been discovered in regard to the mechanics of the chest in connection
with respiration and the circulation. Physiology had shown, especially
by Marry's researches, the negative force of the lungs in aspirating
the blood from the large venous trunks into the right side of the
heart, and thus assisting the whole venous circulation. John
Hutchinson[16] drew attention to the antagonism existing between the
expansion of the chest by muscular action and that of the lungs and the
chest-walls. Hyde Salter[17] showed that at the commencement of
inspiration thoracic elasticity was favorable to inspiration, but as it
advanced it became an expiratory force with lung-tension against
further expansion. R. Douglass Powell[18] drew further attention to
these facts in connection with respiration and its modification by
disease. Le Gros Clarke[19] showed that atmospheric pressure over the
abdomen kept the diaphragm in a condition of arched passive tension. He
claimed that this negative force resisted the elasticity of the lung,
and was the means of retaining the supplemental air in the lung and
limiting the encroachment of abdominal organs.
[Footnote 16: _Trans. Med. and Clin. Soc._, 1846.]
[Footnote 17: _Lancet_, Aug., 1865.]
[Footnote 18: _Trans. Clin. Soc._, 1870.]
[Footnote 19: _Trans. Roy. Soc._, 1872.]
Douglass Powell in March, 1876,[20] in an elaborate and very suggestive
paper on "Some Effects of Lung Elasticity," gives the practical bearing
of these physiological facts in clinical medicine, as indicating a
better insight as to the true mechanism and relative value in diagnosis
of some signs of chest diseases, especially as to the importance of
thoracic resilience as a force in respiration.
[Footnote 20: _Trans. Roy. Med. and Clin. Soc._, vol. lix.]
W. H. Stone early in 1877[21] reported his experiments on sheep as to
the amount of negative pressure exerted by the lungs, and concluded
that it was equal to four to five inches of water. He moreover showed
that even when the effusion was considerable in the pleural cavity, the
lung still had contractile force sufficient to support two inches of
water, so that to evacuate the {491} fluid it was necessary to use
external suction sufficient to overcome this lung-traction. In
December, 1877, G. M. Garland[22] gave to the public the results of his
observations and experiments in regard to the form of the curve of
distribution assumed by the pleural fluid, and its causes. He
demonstrated that "the lung, by virtue of the strength of its
contractility, takes the effusion along with it in its retraction, and
that thereby assumes a pneumono-dynamic instead of a hydrostatic
level," and that the Ellis curve was the true line of the upper level
of the fluid in free, uncomplicated pleuritic effusion. Thus the
physical cause of this condition was the retractile force of the lung
lifting up the fluid. This is aided by the elastic resistance of
thoracic walls and the negative pressure exercised by the effused
liquid. The normal line on right side of demarcation between lung and
liver is the letter _S_ curve drawn out, the summit being high and the
anterior branch correspondingly depressed. The modifications of this
normal line in pleuritic effusions represent the effect of the negative
pressure of the fluid. The decline in the Ellis curve toward the
sternum shows that the elastic energy of the anterior part of the lung
is feeble compared with that in the axillary region. "The layer of
fluid is of less thickness above than at the base of the lung against
the diaphragm. The upper surface takes its shape from the lung, which
lifts it up by its retractility, and the effusion by its weight exerts
a negative pressure upon the lung. The mass of the fluid is held when
in moderate quantity in the supplemental space between the lower border
of the lung and the diaphragm" (Garland). The atmospheric pressure from
the interior of the lungs and from the exterior of the chest-wall keeps
the costal and parietal surfaces of pleura together. Skoda, Powell,
Stone, Homolle, and Quincke have shown the retractile energy of the
lung, but the credit of drawing especial public attention to it, and of
afterward elucidating the subject in its practical application to the
study of pleurisy and in putting the whole subject upon a scientific
basis, is unquestionably due to G. M. Garland of Boston.
[Footnote 21: _London Lancet_.]
[Footnote 22: _Pneumono-Dynamics_, Boston, 1878.]
ETIOLOGY OF FIBRO-SEROUS PLEURISY.--The etiology of acute primary
pleurisy is frequently obscure. It may be hæmatic in origin, or it may
be secondary, arising from pathological causes or antecedent disease.
It is difficult to state with certainty whether it occurs in perfectly
healthy persons, because there may be occult pathological conditions
which cannot be appreciated. However, individuals are attacked with
acute pleurisy who to all appearance, both to themselves and to those
around them, are healthy. Authors differ very widely as to the disease
being ever caused in healthy persons by exposure to cold. The older
writers bring many proofs that such is the case. Ziemssen states that
he could not trace the disease to exposure to cold in a single instance
in 54 cases. Anstie holds the same view. Loomis states that in all
instances where it (pleuritis) has followed upon exposure he has been
able to find some predisposing cause. It is undeniable that pleuritis
very frequently indicates the existence of some constitutional
cachexia. Vital statistics show that it is more frequent in winter and
spring than at other seasons. The vicissitudes of the weather, of
temperature, and other atmospheric conditions have unquestionably a
marked influence on the prevalence of the disease. Drafts of air
passing over the chest or over other parts of the body, particularly
when the subject is surrounded in-doors with a warmer atmosphere, wet
clothing, intensely cold or a raw, damp atmosphere inhaled by persons
coming out of a comparatively high temperature, especially if they are
improperly protected by clothing, appear to be direct causes of primary
pleuritis. If individuals thus exposed are debilitated by fasting, by
such medicines as mercury, iodine, iodide of potassium, by
over-exertion, by free perspiration, or by previous disease, they will
be still more liable to contract the disease. Overheated apartments,
especially at night during the {492} sleeping hours, frequently are the
direct cause of acute pleurisies or of croupal pneumonias. These cases
are of such frequency that we are obliged to differ from the high
authorities who consider the pleura as free from acute idiopathic
inflammations as is the peritoneum.
There are numerous predisposing causes which, when examined, are found
to lessen the power of resistance of the organism. Senility is an
important one; so is childhood. Formerly it was supposed that pleurisy
rarely attacked children. This view was prevalent because the disease
often escaped detection. Of all chest diseases in children, mistakes in
diagnosis are most frequently made with pleuritis.
We might suppose that this disease would be frequently met with in
children, because they are oftentimes ill protected against the
vicissitudes of the weather; besides, their feebleness predisposes them
to feel keenly such shocks to their powers of endurance. The disease
may occur at any age, and is more common under two years than was
formerly supposed (Eustace Smith). Empyema is the form most frequently
found in children, the effusion soon becoming purulent in them.
Ziemssen tabulates the ages of 54 children whom he treated for primary
pleuritis: first year of life, 3; second, 1; third, 7; fourth, 4; the
remaining 39 between the ages of five and sixteen years.
Pleurisies are more frequent in males than in females, in the
proportion of 5 to 3, owing to the greater exposure of the former to
the exciting causes, and notwithstanding their stronger organisms.
Among the predisposing causes we must not fail to give due importance
to the malhygienic conditions which so powerfully impair the forces of
the body. Prominent among these are sedentary occupations, imperfect
alimentation, city lives, overwork of mind and body, deficient
sunlight, overcrowded houses, and dampness of soil. These and many
others interfere with the formative forces and lessen the power of
resistance to exciting causes of pleurisy.
Traumatic pleurisies are caused by injuries or other mechanical causes.
Injuries to the walls of the chest, contusions, burns, scalds, and
lacerations which are superficial, frequently give rise to primary
traumatic pleurisies. If the ribs are fractured, or blood, air, or pus
gets into the pleural cavity, we have what has been termed secondary
traumatic pleurisies.
Secondary Pleurisies.--The exciting causes of secondary pleurisies are
numerous. They are pathological, and more readily appreciated than the
causes of primary pleurisies. Owing to the anatomical connection
between the lungs and the pleura, diseases, acute and chronic, of the
former frequently give rise to pleurisies.
Among acute affections of the lungs, the several forms of pneumonia are
the most frequent causes of pleurisies. Fraentzel states that we always
find fibroid pneumonia associated with pleurisy as pleuro-pneumonia,
even when the inflammation of the lung-tissue itself does not reach the
pulmonary pleura. There is an intimate connection also between caseous
pneumonia and pleurisy. This is sometimes quite circumscribed, and
leads to adhesion of the pleural layers at the affected spot; sometimes
it is diffused over a great part of the pleura, and it is then not
infrequently associated with a considerable outpouring of different
kinds of effusions. Catarrhal pneumonia rarely occurs without secondary
pleuritis (Fraentzel). Pleurisies may also be caused by violent
bronchial catarrhs or by hemorrhagic infarctions.
There are cases where, from the presence of tubercles under the
parietal pleura, inflammatory action is set up and pleuritis ensues.
Vomicæ bursting into the pleural cavity or tubercular perforation in
pulmonary phthisis gives rise to pleurisies. Inflammation of the liver,
cellular abscesses, and pericarditis may cause secondary pleurisies.
Diffuse peritonitis is often complicated with pleurisy, the
inflammatory process extending from the {493} peritoneum to the pleura,
through the diaphragm, by means of the serous canaliculi. This
frequently occurs in puerperal peritonitis, and is almost invariably
fatal (Fraentzel). The author had a case of fatal peritonitis in a man
sixty-five years of age, which originated from an empyema. There was no
rupture nor perforation of the diaphragm, so that the inflammatory
process must have extended from the pleura to the peritoneum by means
of these canals. Malignant diseases of the mammæ, oesophagus, lungs,
and hydatids produce secondary pleurisies. Eruptive fevers, especially
scarlatina, variola, typhoid fevers, are among the most frequent
pathological causes of secondary pleurisies. It is doubtful whether
their germs pass through the circulation or through the lymph-canals,
and produce local inflammation of the same nature as their own, or
whether they render the pleura more sensitive to shocks of various
kinds. Rheumatism, gout, and nephritic diseases are frequently followed
by pleurisies. As we have rheumatic endocarditis and pericarditis, in
like manner there are rheumatic and uræmic pleurisies. Alcoholism and
pyæmia, septicæmia and the puerperal state, especially during the first
month after parturition, are powerful predisposing causes of
pleurisies, as are also any morbid conditions of the skin, kidneys, or
intestinal canal which interfere with their eliminating or depurating
functions. This includes all forms of blood-poisoning. Hutchinson says
that children suffering from congenital syphilis are especially liable
to serous inflammations, and that pleurisy is in them a not uncommon
cause of death. Niemeyer denounces the impropriety of giving the name
of secondary pleurisy to all cases of pleurisy occurring in subjects
with broken-down constitutions or weakened by other diseases. We often
meet with such cases when Bright's disease exists. Niemeyer holds that
it is not dependent upon renal disease, but upon the increased
predisposition for all kinds of inflammatory disease. A trifling cause
will sometimes excite a pleurisy when the resistance of the organism is
materially lessened by previous disease.
SYMPTOMATOLOGY.--Rational Symptoms.--These vary according to the
severity of the disease. Ordinarily, attacks of acute pleurisy come on
suddenly, and it rarely happens that there is any appreciable feeling
of malaise. Usually the first symptom is an acute pain in the side,
which alarms the patient. The significance of this severe stitch is
generally appreciated, as the subject at once calls attention to his
sufferings. The pain is sharp, cutting, stabbing, that causes him to
hold his breath as long as possible. When he is forced to breathe, it
is by the action of the superficial intercostal muscles. He endeavors
to fix his diaphragm and hold it rigid in order to prevent the surfaces
from coming in contact and thus increasing his agony. This causes him,
necessarily, to breathe frequently in order to get sufficient air. The
greater the intensity of the pain, the more frequent and shorter are
the respiratory acts. The dyspnoea and the effort to lessen the pain
give the patient an expression of great suffering. Usually, the pain is
felt over a circumscribed spot under the nipple of the affected side.
Sometimes it is experienced as low as the sixth or seventh intercostal
space, but rarely posteriorly below or under the scapula or in the
axilla. In children the seat of pain is not always in the chest. Their
lower intercostal nerves are often affected, and the sensation being
referred to the ends of these nerves where they ramify on the abdominal
wall, the pain is often seated in the abdomen. Such being the case in
children, care must be taken not to confound pleurisies in them with
epigastric or hypochondriac irritations. In adults, the pain is rarely
located in the abdomen when it is caused by pleuritis in the lower
portion of the pleural surface or in that part covering the diaphragm.
In children there is also much tenderness on pressure. In what has been
termed subacute or latent pleurisy the stitch may be entirely absent.
Valleix found pain in 40 cases out of 46. Sometimes it is absent {494}
in ordinary breathing, but is brought on by sneezing or violent
coughing or strong percussion. In severe cases, the effusion coming on
rapidly, the pain may subside by the second day. If the effusion comes
on slowly, the pain may keep up for six or eight days. The continuance
of the pain always shows that the inflammatory process in the pleura is
continuing, although the pulse and the temperature may be normal. The
renewal of the sensation of pain after the pleurisy has passed away
justifies us in the conclusion that there is a return of the
inflammation. When the pain is agonizing, with signs of collapse, it is
indicative of a secondary pleuritis arising in the course of a chronic
caseous pneumonia. Tubercular and purulent exudations are distinguished
from the sero-fibrinous by the longer duration and the greater
intensity of the pain--two circumstances which afford a reliable basis
for the diagnosis of such cases. The severe pain in pleuritis is
probably caused by the inflammation extending to the sheaths of the
nerves and to the nerve-texture itself (neuritis), as well as by
inflammation of the pleura itself.
Severe attacks of acute exudative pleurisy may commence with a severe
initiatory chill, followed by high fever, but ordinarily there are in
pleurisy slight rigors, initial in their character. Some authors
question whether they are not caused by the limited points of pneumonia
connected with the pleuritis. If the rigors occur at regular intervals
for days, we have reason to suspect tubercular trouble or empyema. The
temperature does not run any regular course in pleurisy, nor does it
bear any fixed relation to the pulse and the respiration. It usually
varies from 100° to 102° F. In violent, acute cases it may reach 105°
F.
Careful observations with the thermometer give us important indications
by which to diagnose the nature of the pleurisies. In those of a
tubercular nature the temperature continues high, from 100° to 104° F.,
for weeks. When the effusion becomes purulent the temperature becomes
like that of hectic fever--in the morning normal, and in the evening
rising to 102°, or even 103½° or 104° F. Sometimes the temperature is
one or two degrees higher on the diseased side than it is on the
healthy side.
As in other inflammations, the pulse in this disease varies
considerably. The researches of H. Newell Martin show that there is
ordinarily a constant ratio between the pulse-rate and the temperature.
If the temperature be high (over 102° F.), we must expect the pulse to
be as frequent as 115 or even 120 per minute. In mild cases, where the
temperature does not go beyond 99.5° or 100° F., the pulse will not
exceed 90 to 96. In slight cases, where the fibrinous exudation is very
limited, the pulse may not exceed 80. In tubercular and purulent
pleurisies the pulse may vary between 100 and 120. When there is a
relapse the pulse advances as the temperature rises. Anstie has called
attention to the quality of the pulse, which follows a uniform course
on the whole, regard being had to the general vital condition of the
patient. In the first stage of acute pains, with more or less tendency
to shivering, the pulse, as tested with the sphygmograph, presents the
algid form--_i.e._ the pulse-waves are very small and nearly devoid of
secondary markings. As soon, however, as flushing of the face occurs,
and a general sense of burning heat of the skin, the pulse passes to
the true pyrexial type; the waves become large and dicrotic. The
sphygmograph uniformly shows that the large and somewhat bounding pulse
is always less resistant than that of health.