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NATIONAL LIBRARYJ)F MEDICINE
SURGEON GENERAL'S OFFICE
' LIBRARY.
Section
No. 113,
W. D.S. G.O.
no. <2.&L2:.f 2,
Presented to the
Statistical Division, Surgeon-General's
Library, United States Army
Washington, D. C.
The Prudential Insurance Co. of America
Newark, New Jersey
NLM051107336
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i^c vagus inhibition, gradual overfilling of
the ventricles, sudden exercise of augmentor power emptying ventricles with forci-
ble action allowing the heart to resume usual rhythm.
148
CARDIAC NEUROSES.
one or two ordinary but forcible contractions, and
then another series of delirious contractions in which first
and second sounds are altogether confused and the pulse
wave is a series of rapid percussion strokes of very great
variation in force. The sphygmogram shows the remarka-
ble variation in force of the radial pulse. This peculiar
rhythm is supposed to be due to independent ventricular
and auricular action. At times when the two coincide, the
slow beats occur.
Delirium cordis occurs frequently in mitral stenosis and
in dilated hearts of gouty origin, also in myocardial degen-
erations associated with chronic rheumatic arthritis. It
may occur merely as a temporary phenomenon or it may be
a permanent affair. It is startling at times, to feel the pulse
of a person who is well to all appearances and find
it tumbling around with such remarkable irregularity, yet
the subjective symptoms are unimportant though the subject
is usually aware of the irregularity in the pulse. Delirium
cordis sometimes appears during the paroxysm of bronchial
asthma. It may occur when digitalis acts unfavorably or is
not tolerated, and it is sometimes the herald of the approach
of asystolism. The treatment of delirium cordis includes
careful diet, antarthritics, general tonics, antacids and in
some cases cardiac stimulants.
The following case presented an interesting combination
of tremor cordis with delirium cordis.
Woman aged 50. Had always been in good health and
of remarkable powers of endurance. Had always been
much in public life and for the last three or four years her
public duties had been continuous and exacting. Had not
been well for a month and made considerable effort to keep
up with her work. For a week has had some irregularity of
the heart which was not particularly troublesome. Last
night had a sinking spell accompanied by dyspnoea and con-
siderable distress in the region of the heart. I saw her
towards morning about five hours after the attack began.
She was flushed though the surface of the body was cool and
the peripheral circulation was poor. There was moderate
dyspnoea which was increased by movement. Considerable
pain about praecordium with a painful consciousness of the
heart's action. There had been no loss of consciousness.
CARDIAC NEUROSES.
149
The neart was beating over 200 per minute and was so
irregular that it could not be counted wich the aid of a
stethoscope. The pulse was so weak at times that it could
hardly be felt. Tnere was gastric distress and flatulent dis-
tention of the abdomen.
Under treatment with digitalin and strychnia the pulse
improved and the rate came down to 160 per minute and
was not so irregular. About once in every 45 to 60 seconds
the irregularity would assume the form of a tremor cordis
lasting about eight or ten seconds when the usual pulse
would reappear for half a minute or more to be again inter-
rupted by tremor of the heart. The patient was not con-
scious of any difference in the heart's action during the per-
iod of tremor though the pulse at the wrist was merely a
tremulousness of the artery, if it could be felt at all.
There was increased force and area of cardiac pulsation
except during the tremor when little or no motion could be
felt. The heart was slightly dilated. There was no valvu-
lar lesion.
The patient gradually recovered so as to be about with
a fairly regular heart, and was lost sight of.
Gallop Rhythm. This is a peculiar rhythm of the heart
sounds which resembles the sounds produced by the hoofs
of a galloping horse. There are three sounds to each heart
action. In true gallop rhythm two of these sounds are dias-
tolic and the first diastolic sound is accentuated (Fraentzel).
Various descriptions have been given of the gallop rhythm,
Traube described a "sort of gallop rhythm," and Potain,
Johnston and Barie described it as a reduplication of the
first sound. Fraentzel's distinction as to the character of
the rhythm is morein conformity with its clinical manifes-
tations. He admits the doubtful nature of its development,
but assumes that it is due to weak heart action, reflux of
blood in the two arterial tracts at different times with a cor-
responding difference in the time of production of the second
sound in the two arterial tracts. There must be some other
causative element than weak heart, for gallop rhythm is not
common in hearts that are merely weak.
Gallop rhythm occurs in chronic nephritis (interstitial),
in some of the so-called idiopathic cardiopathies, in acute
and chronic anaemia, Addison's disease (Lagus, Fraentzel),
typhoid fever (second or third week, indicative of heart
150
CARDIAC NEUROSES.
failure), pneumonia (at or about the crisis, a sign of impending
collapse), typhus fever, diphtheria, acute rheumatism, acute
milliary tuberculosis etc. Though gallop rhythm appears
to be entirely independent of any demonstrable heart lesion,
it is nevertheless an evidence of weakness of the heart, and
in acute diseases, at least, is an indication for the exhibition
of heart stimulants.
In the following case gallop rhythm developed in a car-
diopathic patient suffering from influenza infection.
Woman aged 42. Chronic valvulitis (aortic regurgita-
tion and mitral stenosis) with good compensation. Influenza
with gastro intestinal manifestations eventuating in a ty-
phoid state. (Widal's test etc., excluded typhoid fever.)
The urine contained some granular casts. The total solids
about normal. Temperature from 97°F to 101.5QF. Pulse
iiregular, very weak at times. First two days pulse 160-180
per minute; fourth day fell to 38 per minule; varied from
40 to 58 for three days, then rose to 70 78, always irregular.
There were spells of restlessness with dilatation of per-
ipheral vessels followed by attacks of unconsciousness last-
ing from 2 to 10-12 hours. Gastric irritability and tympan-
itis were troublesome. On tenth day a well marked gallop
rhythm developed. The accentuation of the first diastolic
sound was well defined. The pulse at the time was 73 per
minute. An attack of unconsciousness on the twelfth day
was followed by death in six hours.
CHAPTER VII.
BRONCHITIS.
Inflammations of the bronchial tract have been classi-
fied from aetiological, pathological and topographical stand-
points by various observers. These distinctions, while
serving to individualize special types of the disease, are
more or less confusing. The simplest way is to restrict the
classification to those well marked clinical types which,
though they may at times exhibit unusual features, are still
sufficiently constant in their course to constitute definite
forms of bronchial inflammation.
Thus we find that bronchitis may be acute or chronic.
Acute bronchitis presents three distinct forms: acute
catarrhal (involving the larger tubes); bronchiolitis (capillary
bronchitis, suffocative catarrh), and fibrinous bronchitis
(croupous bronchitis, plastic bronchitis).
The unqualified term, acute bronchitis, applies to ca-
tarrhal inflammation involving only the larger and medium
sized tubes. [The term bronchiolitis is used as entirely dis-
tinct from broncho-pneumonia. The attempt to unify these
conditions clinically (Legendre, Rilliet, Roger and others)
is a mistake, although it is admitted that the morbid anatomy
of the two conditions is intimately associated. Nearly all
fatal cases of bronchiolitis have resulted in atelectasis or in
lobular consolidation. Autopsies, therefore, show the pres-
ence of these conditions, nevertheless, bronchiolitis is a dis-
tinct affection, and while the clinical divisions of Germain
S£e, of diffuse bronchitis of the finer tubes; bronchiolitis of
the intra-lobular branches; and broncho-alveolitis of the
alveolar bronchi, appear somewhat more subtle than the
possibilities of clinical diagnosis would warrant, we still be-
lieve in adhering to the principles of Laennec in recog-
nizing clinically a distinct affection of the bronchioles.]
Bronchitis is most common in infancy and in senile life,
152
BRONCHITIS.
because of minor degrees of individual resistance. Dentition
and abnormalities of the nasal and pharnygeal passages are
frequent factors in producing bronchial inflammation. Age,
sex, occupation, physical condition and habits influence the
occurrence of bronchitis so far as they induce added ex-
posure and lessened resistance to the influences which de-
termine bronchial inflammation. There is a marked feature
of heredity in some forms of recurrent asthmatic bronchitis
and in some cases of winter cough. Cachexia of gouty,
syphilitic, tubercular, alcoholic or nephritic origin predis-
pose to bronchitis. Spinal curvature and other deformities
of the chest predispose to bronchial inflammation.
^Etiology.—Acute bronchitis may result from the topical
effect of cold air on the skin or mucous membranes of the air
passages. This is difficult to reconcile with the clinical fact
that bronchial catarrh is more apt to result from a partial or
limited, than a general, exposure to cold. According to
Thomson, bronchitis seldom results from some irritant
property or ingredient of the inspired air acting on the
bronchial mucous membrane. Primary bronchitis occurs
with such contagions and infections as influenza, measles and
whooping-cough. Acute bronchitis may be secondary to
small-pox; also from general or cardiac weakness incident
to typhoid fever. Cachectic and septic conditions may give
rise to acute secondary bronchitis. Local irritations from
dust, gases or chemicals (iodine, bromine) may cause acute
bronchial catarrh.
Bronchiolitis is especially an affection of infancy and senile
life. It may be primary (one-third of the cases,—Roger) or
secondary, general or localized. All the causes of acute
bronchitis of the larger tubes may likewise cause bronchiolitis.
In a large proportion of cases it results in extension of the
former condition to the smaller tubes, especially in the in-
fectious diseases of childhood, although in many of these
cases it is primary. The influenza infections are especially
prone to induce bronchitis, which is frequently localized, par-
ticularly in the lower portions of the lungs. Measles and
whooping-cough are the most frequent causes of bronchiolitis
before the age of five years. Emphysematous conditions,
*
BRONCHITIS. 153
chest deformities, rachitis, spinal curvature and all con-
ditions which modify respiratory power, especially in young
and weak children, are contributory toward the occurrence
of bronchiolitis.
Fibrinous bronchitis is a rare affection. It occurs most
often in males (two to one—Fowler), and between the ages
of fifteen and forty-five, although it may occur at any age.
Occupations entailing exposure to cold and wet predispose
to its occurrence, and the associated conditions are pul-
monary tuberculosis, valvular disease, pneumonia, typhoid,
cutaneous diseases, pregnancy and the catamenia. These
conditions are, however, accidental, and the aetiology of
fibrinous bronchitis is not known.
Chronic bronchitis occurs most frequently in old age or in-
early life. It may be primary from exposure or from the in-
halation of irritating or poisonous air, especially when there
is some constitutional vice. Secondary chronic bronchitis
occurs most frequently as a result of acute attacks of bron.
chitis. Climatic conditions, senility, emphysema, alcohol-
ism, Bright's disease, gout, psoriasis and eczematoses. Mitral
lesions, pulmonary tuberculosis, the pressure from aneurisms
or mediastinal growths, bronchial stenosis or dilatation, are
some of the conditions which induce chronic bronchial in-
flammations.
Morbid anatomy.—In acute bronchitis there is hyper-
asmia of the inner fibrous coat which becomes swollen and in-
filtrated with lymph cells. The basement membrane be-
comes cedematous and irregular in appearance. The ciliated
columnar epithelium becomes detached in patches, and from
the deeper layer of flat cells various transitional forms of
cells are produce i and thrown off with quantities of leuco
cytes. All the structures of the bronchial wall become in-
volved and leucocytes infiltrate the muscular and fibrous
coats. The secretion of the mucous glands of the bronchi is
greatly increased, the epithelial and secreting elements of
the glands becoming desquamated. On post-mortem exam-
ination the bronchial lining may not appear much altered
owing to the action of the elastic fibres on the blood vessels.
In some cases it may be reddened in patches. The bronchi
¥
154 bronchitis.
may contain clear, yellowish or greenish mucus. Obstruction
of the tubes may produce distension of the alveoli. Pul-
monary congestion, oedema, or atelectasis may occur. Em-
physema of the surface or borders of the lungs develops.
The right heart is overtaxed and ultimately becomes dilated.
Bronchiolitis produces changes similar to acute bron-
chitis. Its greater gravity depends on the interference
with respiration from obstruction of a large number of the
smaller tubes, and from the weakened condition of the bron-
chial muscles, especially in children.
The lining of the tubes is markedly injected. The tubes
may be blocked with secretion and small beads of pus can be
expressed from the smaller tubes. Pulmonary emphysema,
atelectasis, oedema, and small, yellow areas of broncho-
pneumonia may be present. The bronchi may be more or
less irregularly dilated. The right heart may be dilated,
and venous obstruction is greater than in acute bronchitis.
Bronchiolitis is more often a general than a local affection.
Fibrinous bronchitis is entirely distinct from diphtheria
of the bronchi. Its exact pathological nature is not known.
Its dependence on any specific microbe has not been demon-
strated. The exudation may be limited to a few tubes or
may be scattered through numerous areas in both lungs.
The exudation forms a complete cast of the tubes affected,
but does not block the larger tubes, though the smaller
bronchi may be occluded with cylindrical, solid casts. The
expectorated casts vary in size from small pieces, or branches,
to complete casts of a bronchial tree from two to six or seven
inches long. Their minute subdivisions may end in a bulbous
extremity which may correspond to an infundibulum (Bier-
mer). The casts are white or gray in color, of firm con-
sistence, and may be flecked or stained with blood. The
larger branches have nodular prominences. A cross-section
of the larger casts shows a central lumen of more or less
size and a lamellar structure of the walls, which consist of
concentric laminae of fibrin enclosing in its meshes leuco-
cytes, mucous and epithelial cells. Charcot's crystals, pig-
ment cells, fat globules and blood corpuscles may also be
present. [Recently it has been claimed by Beschorner,
bronchitis.
155
Neelson and Grandy that -the exudation in fibrinous bron-
chitis consists of mucin and not of fibrin. Klebs and Ep-
pinger maintatn the fibrinous nature of the casts. In two
specimens recently obtained by me, a careful series of tests
made by Prof. Herzog, determined the casts to be of a
fibrinous nature.]
The trachea is seldom or never affected in this form of
bronchitis. After death the bronchial lining may be intact
and pale, or may be congested, or may be absent. The
bronchial wall may be inflamed. The lung may be emphy-
sematous or atelectatic.
Chronic bronchitis affects any portion of the bronchial
tract. It is usually limited to the larger and medium-sized
tubes. The bronchial membrane may be deeply injected
and of a purple or violet color. In the larger tubes longi-
tudinal layers may be formed by the elastic fibres of the in-
ner fibrous coat. The tubes are narrowed or dilated (bron-
chiectasis). The bronchial glands are enlarged and black in
color. Emphysema of the peripheral portions of the lungs
is usually present. Congestion and oedema of the base of
the lungs may occur and the heart may be hypertrophied or
dilated.
The ciliated epithelium disappears in places and is re-
placed by transitional cells. Dilatation of the blood vessels
and cellular infiltration cause great thickening of the inner
fibrous coat. Various stages of hypertrophy and atrophy
of the muscular coat will occur from the infiltration of the
bronchial wall or from dilatation of the tube. Peribron-
chitis is present to a greater or less extent, especially at
the periphery of the lung. The cartilages may be normal,
softened or calcified. The mucous glands are distended or
destroyed. The muscular coat of the small arteries is hy-
pertrophied and the capillary vessels dilated. Diverticula
of the mucous membrane may form through relaxation and
fissures in the middle coat. Induration of surrounding lung
tissue occurs. Ulceration of the bronchial lining is rare, but
may occur in tuberculosis and in very old people. Fistulous
communications may form. In tertiary syphilis, gummy
tumors and fibrous stenosis of the bronchi may occur.
156 BRONCHITIS
Foetid, putrid expectoration is generally associated with
bronchiectasis, though it may occur without it. The de-
composition of the secretion may cause no trouble or it may
cause gangrene of the lungs.
Clinical history.—The clinical history of acute bron-
chitis extends over a variable period lasting from a few days
to three or four weeks. Its duration depends largely on the
general resistance of the subject and on the condition of the
respiratory apparatus; pulmonary emphysema, induration,
pleuritic adhesions, etc., prolonging its cause considerably.
There may be a history of a common coryza, pharyngitis
and tracheitis preceding the bronchial symptoms, or the lat-
ter may come on suddenly without these premonitory con-
ditions, especially in children and old people, or where there
• has been previously successive attacks. A history em-
bracing any of the aetiological factors of the disease may be
obtained. An initial chilliness may occur, but rigors are
rare. The temperature is seldom above 101° F., and the
pulse is only slightly increased in rate. General malaise
and aching may be present. The special features are pain,
cough, expectoration and dyspnoea. The pain is an early
symptom and is usually a substernal soreness, or it may ex-
tend across the front of the chest, or, in localized bronchitis,
be located in any portion of the chest. The patient indicates
the seat of the pain with the flat of the hand and not with
the finger-tips, thus distinguishing it from the lancinating
pain of pleurisy.
The cough begins with the onset of the disease. It is
first dry and hacking and may be paroxysmal.* It is pain-
ful at first, and there is subsequent soreness about the sides
of the chest along the attachment of the diaphragm. With
the appearance of secretion the cough is not so painful, is
more connected and is performed with the deliberate intent of
promoting expectoration. The expectoration is at first
viscid and tenacious, but as secretion increases it becomes
frothy and may be streaked with blood. Later the sputum
*The most sensitive portion of the bronchial tract is at the bifurcation of the
bronchi (Nothnagel), though all portions are sufficiently sensitive to cause cough
except the smaller branches where accumulation of mucus may result only in
dyspnoea
BRONCHITIS.
157
becomes more watery or else more turbid and yellowish,
which indicates recovery. In the early stage the sputum
consists of clear fluid, ciliated and cylindrical epithelium
and mucous corpuscles; later of large numbers of pus cells,
epithelial cells, hyaline cells, granular matter, oil globules,
pigment granules and blood corpuscles.
Dyspnoea is usually not marked in a primary attack in
an adult. The breathing may be difficult, labored, but is not
much accelerated. In children, however, the respiratory
rate may be much increased. Moderate obstruction of the
tubes may produce much dyspnoea if previous attacks have
modified the functional ability of the lungs.
Bronchiolitis is a serious malady. Its mortality is vari-
ously given as from thirty to fifty per cent. In the majori-
ty of instances it is secondary to acute bronchitis of the
larger tubes or to the infectious diseases. It is peculiarly
an affection of infancy or old age. Whether it be primary
or secondary, its advent is announced by a rise in tempera-
ure of from two to three degrees. There may be a chill,
and in children convulsions may occur. There is frequent
paroxysmal cough and pain. In children there is drowsi-
ness, great dyspnoea, the nostrils are dilated, the respira-
tion is hurried, the face hot and flushed. The cough is
whistling or wheezing in character, the pulse is rapid and
the temperature 102-103Q F. The pulse gradually rises to
150-180 per minute, and the temperature to 104-105° F. in
the evening, although,as a rule, it is not as high as 104° un-
less pneumonia be present. The respiration may be from
sixty to ninety per minute. There is great restlessness and
signs of exhaustion. Delirium and coma may appear, fol-
lowed by death from asphyxia, preceded by blue lips, pale
or livid and cold face, thready pulse and cessation of cough.
The duration of bronchiolitis varies from one to three
weeks. Recovery occupies a longer time. Fibroid indura-
tion of the lungs extending to the pleura may result, Bron-
chial dilatation may occur in these indurated areas with sur-
rounding emphysema. There may be continued muco-puru-
lent expectoration. These cases may be mistaken for tu-
bercular disease.
158 BRONCHITIS.
The following history is from a case of bronchiolitis
complicating chronic bronchitis in an old person:
Mrs. S., aged 71. Has had chronic bronchitis for forty
years. Weight about 90 pounds. Bronchial tubes in right
lung dilated. Expectorates about a pint of mucus in 24
hours and has done so for years. Feb. 12th, '98, had some
pain in right chest, considerably more dyspnoea than usual.
Temperature rose to 103Q F. Pulse 130. Expansion dimin-
ished on right side. Respiratory sounds very feeble, per-
cussion pitch slightly raised, no consolidation, rales fine and
crepitating on same side. Very little air getting into lower
part of right lung Skin cold and surface somewhat cya-
nosed, expectoration diminished. Comatose part of the
time. Treatment: Five grains of ammon. muriate and half
teaspoonful of liq. am. acetat. every two hours; ^ grain of
strychnia every two hours; small doses of whisky occasion-
ally. Mouth wash of peroxide of hydrogen to cut viscid
sputa from throat. Recovery in three weeks.
Fibrinous Bronchitis presents a class of cases exhibiting
but one or two attacks (acute), and these may be separated
by years, but having had one attack there is a liability to
recurrence. In another class (chronic) there is a succession
of attacks, usually of a lesser grade of severity, the inter-
vals presenting an indifferent chain of bronchial symptoms
The clinical picture of the so-called acute form is repre
sented in the following histories:
Male, aged 40, married, beer-bottler by occupation, was
perfectly well until two years ago, when he caught cold
while working in a wet place. During last two years has
had repeated attacks of bronchitis. These attacks would
last a week or ten days and were characterized by a severe.
rasping cough. Expectoration was comparatively free and
there was no particular pain in the chest. About ten weeks
before his recent attack he began to cough and expectorate
large masses of tough, tenacious sputum, which was accom-
panied at times by some bloody expectoration. About four
weeks ago had high fever, great dyspnoea and distressing
cough. There was diminished expansion and dullness over
the lower two-thirds of the left lung as compared with the
right lung. This condition lasted three or four weeks dur-
ing which time he was confined to bed suffering from dysp-
noea, cough, and a temperature of above 102° F. Near the
end of the third week he expectorated considerable blood.
BRONCHITIS.
159
The temperature remained high and the dyspnoea and cough
distressing. Three days afterward he had a severe attack
of dyspnoea and cough. The temperature rose to 104° F.
After considerable effort he expectorated a large mass of
material consisting of a cast of the bronchi mixed with mu-
cus and some blood. The temperature became immediately
reduced and the dyspnoea relieved. Examination, a short
time after the cast was expelled, showed the air to be enter-
ing all parts of the left lung with comparative freedom.
The percussion note was almost normal and mucous rales
were to be heard all over both lungs. Improvement was
rapid.
The cast was gray with a tinge of brownish red. Total
length 10 cm. Two stems: the shortest about 1 cm. long
and about as thick as a lead pencil. The branches run out
to fine filaments with terminal dilatations. The larger tubes
have nodular prominences.
160 BRONCHITIS.
^ia-an^ 1 **
." A * M ^ V
^r %>* #
The following history with a specimen of the cast was
furnished me by Dr. R. Broughton, of Dwight, 111.
Woman, aged 34, weight 120 pounds. Mother of two
children. Anaemic. Has had several attacks of what was
supposed to be la grippe. On Nov. 21st, '97, complained of
headache, followed by a chill, then fever from 99 to 104° F.
for about a week. Very little expectoration, though she
had severe coughing spells. On Nov. 29th, after a severe
and exhausting coughing spell, she expectorated a well-
marked tube cast. Three other casts were expelled at in-
tervals of from threeto four days. Following the expulsion
BRONCHITIS. 161
of the cast the expectoration was frequent and bloody,
though not great in quantity. After the last cast was ex-
pelled the blood ceased. Death Dec. 9th. No autopsy.
In some of the "chronic" cases, small portions of casts
may be expectorated for days or weeks at a time. Pneumo-
nia is not an infrequent complication of the more severe
cases, and may be the cause of death. Fagge reports a
death by asphyxiation* from lodgement of a portion of a
cast at the tracheal bifurcation.
Chronic bronchitis is met with in its mildest form in the
winter cough of middle-aged or elderly people, which grad-
ually becomes a constant affair. It may occur as a result of
a succession of acute attacks and is marked by its proneness
to relapse. %
The cough gradually becomes continuous until the dis-
ease is marked by remissions rather than by intermissions
during its most favorable periods. The general bodily
strength and weight may be maintained for years against
this disease, but eventually becomes compromised, and
dyspnoea upon exertion becomes associated with asthmatic
breathing. Finally dyspnoea becomes permanent as a re-
sult of weakness of the right ventricle whose hypertrophy
has hitherto offset the resistance to the pulmonary circula
tion entailed by the changes in the pulmonary parenchyma.
The cough of chronic bronchitis exhibits great variety
in character, and in the quantity and quality of the expec-
toration. One variety is characterized by very viscid,
pearly, scanty expectoration (dry catarrh), with violent and
rapid paroxysms of coughing which may induce vomiting.
The mucus is dislodged and raised with difficulty and
emphysema is likely to develop in this form of bronchitis.
Gouty arthritis is likely to be associated with this form of
dry catarrh. Again, in gouty subjects with weak hearts,
we may have more sudden attacks resembling pulmonary
congestion and cardiac dyspnoea, with free expectoration.
In most cases of chronic bronchitis, two or three spells of
coughing during the day will be attended with quiet inter-
vals. In others, there is constant expectoration often de-
pending largely on cardiac weakness. In some cases, par-
162
BRONCHITIS.
ticularly in old people, the amount of expectoration may be
one or two pints in twenty-four hours (bronchorrhoea). It
may be liquid and frothy (bronchorrhoea serosa—Biermer)
or may be yellowish, or like the white of egg. Laennec de-
scribed a form of bronchorrhoea, under the title "Chronic
Idiopathic Pituitous Catarrh."
In the chronic bronchitis accompanying syphilitic les-
ions of the bronchi, the catarrh may be general, with second-
ary lesions, or localized, in the tertiary forms. Bronchial
stenosis or dilatation are usually responsible for the-profuse
foetid expectoration. Pain, emaciation and night sweats
may be present in these cases.
Foetid or putrid expectoration is usually associated with
bronchiectasis, stenosis, or with pulmonary gangrene, but
may be present without either of these conditions. The
breath may remain offensive after the expectoration has lost
its odor. Again, the fetor may come and go. Some of the
worst cases do not appear to be connected with any cause
in the tubes or lung tissue. Attacks of lobular pneumonia
are frequently a part of the clinical history of chronic bron-
chitis in both children and old people, and in the latter are
particularly to be feared.
Symptoms and diagnosis.—In acute bronchitis lateral
expansion is often deficient, and in children there may be
inspiratory recession of the interspaces and ribs at the sides
of the chest. The patient, during paroxysms of painful
cough, assumes an upright position, leaning straight for-
ward which is indicative of a bilateral source of the trouble
and distinguishes it from pleurisy. Palpation is negative
unless mucus in the larger tubes should produce a rhonchal
fremitus. The percussion note is unchanged or is hyper-
resonant from emphysematous conditions. Dullness at the
base suggests pulmonary congestion, oedema, or collapse.
Auscultation shows harsh, rough breathing, with some pro-
longation of the expiratory sound. Sibilant, wheezy respir-
ation is present during the dry stage. With the stage of
secretion there appears sonorous rhonchi in the larger tubes
large and small mucous rales in the medium sized tubes, and
sub-crepitant rales in the smaller tubes. These rales are
BRONCHITIS. 163
heard best during inspiration, but are also heard with ex-
piration. They maybe changed by coughing. The sibilant
rales are not apt to change on coughing as they are due to
narrowing of the smaller tubes. The fine, sub-crepitant
rales are heard just before the immediate end of the inspira-
tory act and differ from the crepitant rale of pneumonia by
being altered by coughing and are heard at times during
expiration. The pneumonic rale is heard at the end of in-
spiration, is not heard in expiration, is followed by a clear,
high pitched, expiratory sound and is not modified by cough-
ing or respiration. Pleuritic friction may resemble the rales
of bronchitis but occurs earlier in the inspiratory act than a
rale of the same size and character, and is not changed by
cough or respiration. Cardiac failure from mitral stenosis,
may give rise to a congestion of the lungs easily mistaken
for bronchitis, as the mitral murmur may disappear with the
advent of cardiac failure (Broadbent). The effect of
digitalis or perhaps of venesection, with the reappear-
ance of the murmur, will establish the nature of the
trouble.
Miliary tuberculosis has a higher temperature range
than acute bronchitis, and more prostration. Apical bron-
chitis must always be regarded as of probable tubercular
origin. Localized bronchitis in the lower part of the lungs
is a frequent result of influenza infections, the usual auscul-
tatory signs being confined to a small area, the upper por-
tions being clear.
Bronchiolitis changes the type of breathing, especially in
children. The upper portion of the chest scarcely moves
and is distended with residual air, while the lower ribs,
intercostal spaces and epigastrium show marked inspiratory
recession. The percussion note is unchanged in the lower
portions, or may be dull from collapse or oedema. In the
apices there is hyper-resonance.
Auscultation, early in the disease, shows good respira-
tory sounds in the upper chest, but feeble sounds below.
Later, when distention of the upper chest occurs, and in old
people with emphysema, the breath sounds will be generally
164 BRONCHITIS.
feeble. Any variety of rales may be present, but in the
lower portions of the lungs, especially posteriorly, we hear
the very fine, crackling rales characteristic of bronchiolitis.
They are not so finely crepitant as the pneumonic rale, nor
as bubbling as the oedematous rale. The distribution of the
rales determines the extent, generalization or localization of
the affection.
Bronchiolitis is distinguished from acute bronchitis by
higher temperature, greater difficulty in breathing, more
dyspnoea, poor circulation and the character of the rales;
from pneumonia, by absence of initial chill, of pain in the
side, of panting character of respiration, of pneumonic
sputum, of signs of consolidation. The temperature in
pneumonia is continuously higher than in bronchiolitis. Pul-
monary oedema is distinguished from bronchiolitis by its
associations, and location in the lowest part of the lungs
resulting from blood stasis. Miliary tuberculosis in children,
and acute pneumonic tuberculosis may resemble bronchiolitis.
The early apical signs in the former, and the higher and
more continued fever in the latter, as well as its location in
the upper lobes, will differentiate these conditions, at least
with the aid of the history, associations and sputum exami-
nation.
Fibrinous bronchitis is usually not recognized prior to the
expectoration of an exudate. After this has occurred signs
of bronchial catarrh in more or less limited areas may lead
to a provisional diagnosis, especially if followed by signs of
bronchial obstruction and pulmonary collapse of the same
region. Pneumonia might, however, give these same signs
and it is at times associated with fibrinous bronchitis. Con-
solidation would not disappear immediately on expectora-
tion of a cast, as may occur with collapsed lung from ob-
struction of the tubes. The temperature is unsafe as a
guide, as. during the acute symptoms, the temperature may
be as high in severe cases of fibrinous bronchitis as it would
be in pneumonia. ■
Chronic bronchitis is essentially different from pulmonary
phthisis, with which it is most easily confused, in its effect
upon the general condition of the subject. There is,in chronic
BRONCHITIS. 165
bronchitis, more or less distension of the upper portions of
the chest from emphysema. The clavicles are elevated, the
accessory muscles of inspiration are prominent in the neck,
as the vertical expansion of the chest is increased. The
supraclavicular depression is increased and in emphysema-
tous chests is filled, during coughing, with the distended
subclavian and innominate veins. The nose and ears ap-
pear thickened, the conjunctivae cedematous, the face turgid
or suffused. The skin is dry, loose and non-elastic, and the
veins are enlarged, tortuous and dark. All this is in distinct
contrast to the chronic consumptive. The signs elicited by
palpation and percussion depend on the relative amount of
emphysema, peribronchitis and induration of the lung tis-
sues which may have developed. Increased fremitus may
be felt in the dilated portions of the chest (upper portion),
provided the connective tissue is increased somewhat, and
the air pressure is marked. The percussion note is hyper
resonant but varying in character over the upper portion,
and may be hard and quite dull over the lower portions if
these are indurated, well-blocked with mucus, or are col-
lapsed, cedematous or congested. All varieties of dry and
moist rales are heard. The expiration is lengthened and
increased in pitch. The wavy respiration of bronchiectasis
may be heard at times after a coughing spell. Syphilitic
gummata, aneurisms and mediastinal growths may produce
symptoms easily confounded with chronic bronchitis.
Healed or quiescent cases of tuberculosis with emphysema
and bronchial catarrh may easily be mistaken, particularly
as these cases do not always exhibit bacilli in the sputum.
Tuberculosis may be engrafted on chronic bronchitis and
emphysema and not be recognized without examination of
the sputum.
On the other hand we occasionally find a few bacilli
in the sputum of chronic bronchitis merely as an acci-
dental matter; hence, a few bacilli in the sputum is not
always to be regarded as evidence of tuberculosis of the
lungs. When, however, the physical signs are more marked
in one or both apices, tuberculosis may be suspected whether
bacilli are found in the sputum or not.
166 BRONCHITIS.
Treatment.—The remedies for bronchitis are legion,
as the clinical index of any work on therapeutics will attest.
Many of these remedies, while of undoubted value, are as
certainly disagreeable and nauseating. A mixture of eight
or ten ingredients is as unscientific as it is objectionable
pharmaceutically. The simplest remedy is the best.
In acute bronchitis the natural course is towards recovery,
and a little well directed aid will usually be sufficient. In
the dry stage we wish to relieve pain, bronchial irritation,
and promote secretion. If the pain be severe and the pa-
tient distressed, hot poultices, sinapisms, turpentine lini-
ment or soap liniment with tincture of capsicum added may
be of service. Dry cupping may be useful at times. For
the soreness and irritation in the trachea and main bronchi,
nothing is better than an oil spray, using benzoinol (plain),
albolene etc. The patient can readily be taught to inha'e
these sprays. The oil, beside protecting the membrane
from the air, also induces secretion, which is the next object
to be attained. For this purpose, ipecac, antimony, or tar-
tar emetic are usually employed in doses not sufficient to
cause emesis. In robust patients, the quickest way to in-
duce secretion is to put one grain of tartar emetic in a cup
of water and give a teaspoonful every ten minutes until there
is slight nausea (Thomson). The syrup of ipecac may be
used in children for producing secretion, in five drop doses
every hour to a child two years old. Small doses of Dover's
powder (one grain) every hour can be used in adults. Small
doses of aconite frequently repeated are useful in children in
the early stage to lessen fever and circulatory excitement.
When secretion has begun and the cough is troublesome, as
it usually is by the time the case comes under observation,
the indications are to loosen the secretion so that it can be
removed with as little cough as possible, and to quiet the
irritability of the bronchial membrane, and lessen the cough.
For these purposes the following may be used;
R
Am. mur,, 3ii.
Codeine sulph., gr. v—vi.
Liq. am. acetat., §i.
m. Syr. tolu., q. s. ad Ini.
bronchitis 167
Syrup of yerba santa or glycyrrhiza may be used to
better cover the taste of the ammonia salt if advisable.
When there is the constant hacking cough of laryngeal
irritation, the following more sedative combination may be
used:
9
Am. raur., 3iss.
Morph. sulph., gr. iiss.
Fl. ext. cannabis ind., gtt xx.
M- Syr. tolu., q. s. ad liii.
When the acute symptoms are past, but the cough with
moderate secretion still persists, pills of terpin hydrate, or
syrup of hydriodic acid, or syrup of lactucarium may be of
service. At this stage, especially in old people, the follow-
ing is useful.
9
Sodii iodidi, 3iss.
Codeine sulph., gr. v.
Fl. ext. grindel. robust., 3vi.
M. Syr. tolu., q. s. ad liii.
This mixture is particularly effective in localized bron-
chitis. Opium should not be given to young children with
bronchitis, unless in very small doses of such a preparation
as the camphorated tincture. In localized bronchitis in chil-
dren the syrup of hydriodic acid is very useful. In children
with irritating cough and hoarseness, the following is of
benefit:
9
Am. raur,, gr. XLviii.
Tr. anemones pra tensis, 3i—ii.
Liq. am. acetat., 3vi.
m. Syr. tolu, q. s. ad liii.
In bronchiolitis we have a more serious condition to con-
front. In order to lessen the acute stage we may give acon-
ite in sufficient doses (one or two drops in liquor of the
acetate of ammonia every two hours). If any depression
results a little brandy will remove it. In children, in the
absence of lobular pneumonia, poultices are to be discounte-
168
bronchitis.
nanced, nor is opium admissable; it adds to the danger of
pulmonary collapse and pneumonia from mucous obstruction
of the weakened bronchial tubes. If the mucus is tena-
cious, a steam spray from lime water may give relief. Two
grains of muriate of ammonia, two or three drops of tincture
of bryonia, and fifteen drops of the liquor of the acetate of
ammonia, should be given every two hours. If the respira-
tion is above thirty-five per minute and difficult, five drops
of tincture of nux vomica should be given every two hours.
In adults, from ¥V to ^ of a grain of strychnia may be
used.
When dyspnoea is severe and mucous rales show that
mucus is obstructing the tubes, it is necessary to aid in ex-
pelling the secretion by causing vomiting. Ipecac, anti-
mony, and apomorphia tend to increase secretion and the
relief is not apt to be as permanent aswiien we use sulphate
of zinc and alum (five grains of each), or yellow sulphate of
mercury (two to five grains).
The chest should be covered by two or three layers of
flannel or a wadding jacket, In the latter stages, stimula-
ting applications to the chest, one or two drams of brandy
every hour, small and frequent drinks of hot milk, may all
be of service in general stimulation. The intimate associa-
tion of broncho-pneumonia with bronchiolitis, makes many
of the means used in the former condition of interest here,
but these will not now be considered.
In adults, stimulation with alcohol and strychnia is
necessary in the late stages of severe cases. The diet for
children should be milk with lime water. For adults milk
and seltzer water is best,
Fibrinous bronchitis is not particularly amenable to treat-
ment. During the attacks, the continuous inhalation of
vapor of creosote, guaiacol, or alkaline substances, may be
of use. Iodide of potassium in large doses is recommended
and should be tried. Intra-tracheal injections of glycerine
have been thought to aid separation of the casts. Olive oil
or liquid vaseline may also be used. In the recurrent forms,
change of climate may be tried though the results are very
uncertain.
BRONCHITIS. 169
Chronic bronchitis, of all bronchial inflammations, will
tax the resources of the physician most. The tendency to
relapse and the poor nutrition of the subjects of chronic
bronchitis, are the chief factors in the obstinate course of
the disease. Climatic treatment obviates, in a measure, the
probability of relapse. Some cases do well in a warm, moist
air, like the west Florida coast or the Bermudas. Others do
best in a warm, dry climate, such as is found in the south-
western states, or the ncrth-western states during summer.
In all instances sunshine is the main requirement.
The nutrition is to be improved by nourishing and easily
assimilated food and by tonic medicine. Iron is the chief
remedy of this kind. The iodide of iron is particularly ben-
eficial, though the tasteless tincture, citrate of iron and am-
monia, and Basham's mixture are all eligible. Strychnia
should be given to all elderly people with chronic bronchi-
tis, both as a respiratory and cardiac stimulant. In general
or localized chronic bronchitis in children the syrup of hy-
driodic acid is an efficient remedy. Cod-liver oil has long
done duty in chronic bronchitis. To those who can take it
it is a valuable remedy. The so-called alkaloids of cod-liver
oil (morrhuine, gaduine, etc.) appear to exert as much influ-
ence for good, on chronic bronchitis, as the oil itself, and
they are much more eligible for administration. A number
of histories might be cited proving this point. In a child
eight years old who suffered from bronchitis for five years,
and who had received all kinds of treatment including cod-
liver oil, which she was fond of, complete recovery occurred
in three months while under treatment with cod liver oil
alkaloids. The combinations of these substances with guai-
acol (liquid or carbonate) or creasote, is of good service.
These latter drugs are more beneficial in small doses than
in large ones, and should not be given in doses which dis-
turb the stomach in the slightest. Terebene is a valuable
remedy, although somewhat nauseating. It is best given in
emulsion made with acacia, in doses of ten to fifteen drops.
It is well adapted to cases with scanty, viscid secretion.
For the morning cough, Burney Yeo advises sodium
bicarbonate, gr. xv; sodium chloride, gr. v; spirits of chlo-
170 BRONCHITIS.
roform, m v, in anise water, taken with a little warm water
before rising. In old people a mixture containing iodide of
sodium or potassium (gr. v), tincture of belladonna (gtt, iii),
fluid extract of grindelia robusta or fluid extract of euphor-
bia pilulifera (gtt. xv-xx), and sufficient quantity of syrup
of tolu or syrup of yerba santa, will be found very useful.
Iodide of sodium and fluid extract of. grindelia robusta are
serviceable in localized bronchitis in adults.
One of the most efficacious means of treating various
forms of chronic inflammation of the upper bronchial tract
is by means of sprays. The vapor from a cup of boiling
water containing a teaspoonful of compound tincture of
benzoin is very soothing. Albolene or benzoinol may be
used as a vehicle for sprays. In dry catarrh a 2 per cent.
solution of menthol, camphor, oil of eucalyptus, chloride of
ammonium, wine of ipecac, etc., may be used. In dry asth-
matic bronchitis, lobelia, internally, is useful.
With bronchorrhoea we may use tar, turpentine, tere-
bene, copaiba, senega, terpin hydrate, or hydrastis cana-
densis. In foetid bronchitis, sprays or inhalations of aristol,
menthol or creosote may be used. In severe cases the creo-
sote vapor bath may be tried as recommended by Chaplin
{vide Bronchiectasis.)
In gouty bronchitis, much advantage will be found in
colchicum in connection with iodides. The various mineral
waters which are applicable to gouty conditions should be
used. Much good will result from an occasional mercurial
cholagogue followed by some aperient water. In syphi-
litic bronchitis iodides and mercury are, of course, the
chief remedies.
In the later stages of chronic bronchitis in old people,
when the right heart becomes dilated and dyspnoea is se-
vere, oxygen gas, large doses of strychnia hypodermati-
cally, and, under some conditions, venesection may be indi-
cated. When the expectoration is sticky and difficult to re-
move from the mouth and throat, these passages can be
kept clean and free from mucus by rinsing the mouth with
a little peroxide of hydrogen.
171
BRONCHIECTASIS.
Dilatation of the bronchi is comparatively rarely ob-
served clincally. Antomically it is not uncommon in its
association with tuberculosis and other morbid processes of
the lungs and pleura. In adults it is usually a secondary,
chronic affection. In children an acute form occurs, usual-
ly in association with secondary bronchitis in rickety child-
ren (Carr). Bronchiectasis is most common in males. It
occurs at any age but is most common during middle life-
^Etiology. — Bronchiectasis is always secondary to
some disease of the bronchi, lung or pleura. Chronic bron-
chitis, pulmonary cirrhosis, broncho-pneumonia, pulmonary
tuberculosis and chronic pleurisy are its most frequent as-
sociations. Changes in the bronchial wall and peribronchial
tissue, which weaken and destroy the elasticity of the bron-
chi, are the immediate factors in the production of the dila-
tation. These changes are most often induced by chronic
bronchitis, stenosis or. obstruction of the bronchi, pulmo-
nary collapse, pneumonia, emphysema£ cirrhosis of the
lung, and the various effects of chronic pleurisy.
Morbid anatomy.—The dilatation of the tubes may
be either cylindrical or saccular. The dilatations may be
connected by tubes of normal calibre—the moniliform dila-
tation of Cruveilhier. Cylindrical dilatation occurs most
often in the larger tubes. Usually there are constrictions
at various points. Saccular dilatation may involve large
sections of the lungs, the lung tissue having disappeared
and in its place are numerous sacks with an opening in the
bottom of each. A whole lobe may be thus affected ("turtle
lung"). The terminal bronchi are usually affected first and
the size of the dilatation is proportionately greater than in
the larger tubes (Biermer). The terminal extremities of
the tubes are closed or obliterated early in the disease. In
a large proportion of cases both lungs are affected. The
acute form in children involves many tubes. When dilata-
tion results from obstruction of a tube, collapse of lung tis-
sue, pleurisy, etc., it is limited to the area of lung involved.
The lower lobes are most often involved primarily, the apex
when secondary to tuberculosis
172
BRONCHIECTASIS.
The bronchial tubes exhibit the various evidences of
chronic inflammation of the mucosa. The walls and peri-
bronchial tissue are thickened. In the sacculated form the
walls may be thin. The tubes may be empty or may contain
purulent, foetid fluid of a gray or yellowish color, curdy or
inspissated; or, they may be filled with a clear, jelly-like
mucus without any particular odor. Various changes oc-
cur in the lungs and pleurae. Areas of gangrene occur
around dilated tubes. In the acute form in children the
chief changes are: Acute peribronchitis; the presence of
innumerable small cavities; small air containing vessels on
the surface of the lungs (Fowler.)
Clinical history.—Paroxysmal cough with the ex-
pectoration of quanties of purulent and offensive secretion,
more or less dyspnoea, some pain, occasional haemoptysis
and occasionally fever, are the usual features of the history.
The cough occurs in the morning or evening. As a rule
the intervals are comparatively free from cough and expec-
toration. The quantities expectorated at once, varies from
two to ten or twelve ounces, and from half a pint to two
quarts in twenty-four hours. If drainage is good, the cav-
ity will empty completely at a paroxysm of coughing.
Some cavities only drain when the patient is in certain po-
sitions. The odor of the sputum or breath may be very
offensive or it may not be noticeable.
The following case was one of saccular dilatation of the
lower branch of the left bronchus:
Young woman aged 22. Had a prolonged attack of
bronchitis when seventeen years old. Has had paroxysmal
cough ever since with considerable expectoration. For last
four years has had coughing spells in morning or evening
when she would expectorate a quantity of mucus. For last
two years these spells occur in the morning shortly after
rising. By getting in the knee-chest position with the left
shoulder as low as possible she is able to raise about six or
eight ounces of sputum in a few minutes, and is then free
from cough for the most of the day. The sputum is seldom
offensive. The expansion of the left side is slow and some-
what less than of the right. The fremitus is slightly in-
creased below the level of the third rib, percussion note
nearly normal, inspiration interrupted and wavy over a
bronchiectasis.
173
space extending from the third to the fifth ribs in the anter-
ior axillary line. Loud metallic rales are heard over the
same area.
Symptoms and diagnosis.—The physical signs ob-
tained in cases of bronchiectasis show every possible varia-
tion in accordance with the conditions with which it is asso-
ciated. The percussion note may be dull if the cavity is full;
if empty, the percussion note is raised, hollow or extra
resonant according as the fibrosis is marked or not.
Cracked-pot sound may be obtained in tubercular dilatations
of the upper lobe. In cylindrical dilatation the respiratory
sound will be tubular, blowing or hollow. Inspiration and
expiration may be wavy in character. In saccular dilatation
the breathing may be cavernous. There may be loud,
gurgling rales. At the end of inspiration a short puff or
blow may be heard, seemingly close to the ear (the "veiled
puff" of Skoda). The wavy, irregular character of the in-
spiration or expiration,and loud metallic crackles or gurgles
over a limited area, are the most characteristic evidences of
bronchiectasis. When a whole lung is full of small cavities
the percussion note may be tympanitic and the auscultatory
signs will be ill defined and low in pitch. Clubbing of the
fingers and toes may be marked.
The character of the sputum and the method of expec-
toration generally suffices to distinguish bronchiectasis
from emphysema. Pulmonary gangrene is generally sec-
ondary to acute pneumonia or to tuberculosis. Examina-
tion of the sputum is generally necessary to exclude tuber-
culosis, though the course of the two affections is different.
Tuberculosis may occur secondary to bronchiectasis. Lo-
calized empyema opening into the lung may be confused
with bronchiectasis, but its history, associated conditions
of the lung and pleura, and puncture, when that is possible,
will differentiate.
Bronchiectasis is rarely, if ever, recovered from. It
may end in gangrene, lobular pneumonia, fatal haemopty-
sis, or some cardiac or renal complication.
Treatment.—The indications are to maintain the gen-
eral strength and nutrition and to disinfect the bronchial
174 bronchiectasis.
tract. Superficially situated dilatations, especially of the
larger tubes may be disinfected by inhalations of aristol,
menthol, eucalyptus, creasote, guaiacol, tar or turpentine
sprays.
In a woman of 35, who had suffered from a bronchial
dilatation in the anterior middle portion of the right lung,
and who expectorated over a pint of mucus every twenty-
four hours, disinfection of the expectoration, which was
very offensive at times, was accomplished by the inhalation
of a spray of aristol (3 per cent.). This was used every
other day and made the trouble quite bearable.
More energetic treatment consists in the continuous in-
halation of coal-tar, creasote, guaiacol or cresoline vapor;
intratracheal injections; and hypodermic injections of ster-
ilized guaiacol or creasote. The vapor bath (Chaplin) is
giyen in a small room or compartment clear of furniture.
Commercial creasote is heated in a metal saucer over a
spirit lamp until clouds of vapor fill the room. The pa-
tient's clothes are protected by a cover, the eyes by goggles,
the nares by cotton plugs, and the hair, in women, by a bag.
The bath is given every other day at first, for fifteen or
twenty minutes, gradually increasing to an hour every day.
The bath produces violent coughing and profuse expectora-
tion and sometimes vomiting.
Intratracheal injections (Rosenberg) are made by inject-
ing a dram of the solution into the trachea by means of a
syringe, passing the nozzle of the syringe below the vocal
chords. Menthol (5-10 per cent.), guaiacol (2 percent.),
singly or combined, in oive oil, is recommended. By the
hypodermic method, thirty minims of twenty-five per cent.
solution of guaiacol or creasote in sterilized olive oil, may be
used but does not appear to have any advantage over the
inhalation methods of which the vapor bath is, according to
Fowler, decidedly efficacious.
Surgical treatment of a bronchiectatic cavitjr is seldom
possible, though in some instances may be advisable.
175
BRONCHIAL STENOSIS.
Geneial narrowing of the bronchial tubes resulting
from inflammatory swelling, catarrhal, croupous or diph-
theritic exudation is not included under this caption.
^Etiology.—Local bronchial stenosis arises from for-
eign bodies in the bronchi, cicatricial contraction of bron-
chial ulcers, sclerosis of the bronchial wall, malignant
growths, aneurisms, tumors of the lung or mediastinum or
hydatid tumors.
Morbid anatomy.—Foreign bodies are apt to lodge in
the right bronchus as that branch is more nearly in line with
the trachea in most individuals. Articles several inches in
length may, however, enter the left bronchus. Cicatricial
stenosis are almost invariably of syphilitic origin. Gum-
matous infiltrations of the mucosa break down, ulcerations
result and the subsequent scars and thickened sub-mucous
layer cause stenosis in one or several situations. In chronic
disseminated tuberculosis there maybe stenosis of the tubes
from thickening of the wall at points adjacent to a fibrous tu-
bercular nodule, and also from the cicatricial wall which
surrounds a cavity, involving also the entering bronchus
(Powell). A stenosis effected gradually, tends to the pro-
duction and retention of secretion behind the stenosis and
results in dilatation of the tube and fibrosis of the surround-
ing tissue.
A cavity may become closed and its contents become cre-
taceous or there may be intermittent discharge of its con-
tents under pressure of accumulated secretions. In rapidly
developed and complete stenosis there is collapse of the
area of lung tissue supplied.
Clinical history.—The history is variable. It is as-
tonishing what tolerance there is for foreign bodies in the
bronchi, provided they do not lodge at any of the specially
sensitive points.
A boy 15 years old, placed a blow pipe over a hat pin
which was loosely stuck in the floor. (The pin was steel,
about six or seven inches long and with a round ebony head.)
In attempting to suck the pin out of the floor he drew it
176
bronchial stenosis.
into his throat. He had a short coughing spell which soon
subsided. The pin had disappeared. During the next day
there was occasional coughing spells which were not severe.
Examination showed slow expansion of the left lung, partial
suppression of respiratory sounds in the same side wTith ex-
aggeration of the respiration on the right side. There were
no local signs of obstruction. Tracheotomy was performed
and the pin found in the left bronchus. It was broken in
the effort at extraction, the head and about three inches of
the shank being obtained. Three days afterward the re-
mainder of the pin was coughed up. No subsequent ill
effects.
Stenosis of the main bronchus will cause dyspnoea
and there is more or less cough and expectoration which
may be similar to that of bronchiectasis. The cough may
be spasmodic or laryngeal in type. There may be
pain if pulmonary collapse and dry pleurisy occurs.
Tumors, aneurisms and syphilis will modify the history.
Symptoms and diagnosis.— Partial stenosisgives rise
to diminished expansion of the affected side, recession of
the interspaces, costal margin, episternal and supraclavicu-
lar regions;diminished vocal fremitus,resonance and respir-
atory murmur. Rales and fremitus may be obtained over
the site of the obstruction, and interscapular stridor may be
heard. When the stenosis is of long standing or is com-
plete, signs of bronchiectasis, pulmonary fibrosis, consolida-
tion or collapse, with contraction of the side, will appear.
The unaffected lung shows a greater or less degree of com-
pensatory action with a corresponding intensification of the
physical signs.
When the examination leaves doubt as to the nature of
the obstruction, the probabilities favor aneurism, medias-
tinal growth, or cicatricial contraction from syphlitic gumma
(Fowler.) In stenosis from aneurism and malignant growths
the signs of these conditions develop early. Stenosis in
association with consolidation and profuse expectoration
may be mistaken for tuberculosis, empyema, or pneumonia.
The diagnosis is sometimes very difficult.
Treatment.—The treatment is largely symptomatic.
In syphilitic or aneurismal stenosis, iodide of potassium in
large doses should be used. Chloroform or oxygen may be
used for the paroxysmal dyspnoea caused by aneurism.
Powell recommends nitroglycerine for the same purpose.
Expectorants may give some relieve, though as a rule they
are of little use.
CHAPTER VIII.
ASTHMA.
For clinical convenience and from an aetiological basis,
several varieties of asthma have been recognized. It will
be found that these different forms of the disease represent
simply symptomatic variations of an affection which is neu-
rotic in nature, spasmodic in occurrence, and is character-
ized by a disturbed innervation of the bronchi which mani-
fests itself in spasm (Liebert) of the bronchial muscles and
is associated with spasm of the diaphragm and correlated
respiratory muscular apparatus, resulting in a special type
of dyspnoea.
Asthma may occur at any age. According to Salter's
statistics, thirty-one per cent, of the cases occurred during
the first decade of life. It is generally stated that asthma
is twice as frequent in males as in females, though if we in-
clude only the cases of typical spasmodic asthma, it is evi-
dent that it occurs as frequently in the one sex as in the
other.
The most individual clinical forms of asthma are the so-
called idiopathic or true spasmodic asthma, bronchial asthma,
dyspeptic, toxic, cardiac and hay asthma. These terms serve
only to specify certain aetiological factors which are associ-
ated with dyspnoea of asthmatic origin.
^Etiology.—Thirty-five per cent, of asthmatics give a
history of heredity, most often from the paternal side
(Thomson). Asthma is generally associated with a family
tendency to bronchitis or other pulmonary disorders or to
nervous affections. There may be a predisposition existing
through one generation only, or a distinct history of hered-
ity. Bronchitis (thirty-seven per cent.—Salter), fibroid tu-
berculosis, epilepsy and various nervous disorders are fre-
quently associated with asthma.
178
asthma.
The exciting causes of the asthmatic paroxysm may be
of central or peripheral origin. The central causes may be
emotional or neurasthenic or may be due to toxic irritations
from drug poisons, gout, diabetic or nephritic toxaemias {ure-
mic asthma)or to intestinal toxaemia (the so-called humoral form
of peptic asthma). Among the neurasthenic cases are those
induced by fright, worry, the excitement of important social
duties or the nocturnal cases which occur with darkness and
can be obviated by keeping a light in the sleeping-
room.
The asthmatic attacks which occur directly after the
ingestion of certain kinds of food and are accompanied by
gastric disturbance, are probabally of peripheral origin and
according to Salter are due to bronchial contraction produced
through reflex irritation of the pulmonary filaments of the
pneumogastric from irritation of the gastric terminations of
the same nerve. The most frequent seat of peripheral irri-
tation resulting in asthma is the bronchial tract. Climate,
locality, moisture, dust, etc., are factors which are closely
connected with bronchial susceptibility in the production of
an asthmatic attack, but even here, nervous conditions
seem, at times, to be potent in producing the prodromal
bronchial symtoms which precede the asthmatic attack, as
appeared in the following case:
Farmer, 39 years of age. Lived in a dry, heal thy part of
Iowa. For last ten years has suffered from asthma when-
ever he visited any of the large cities. The attacks are pre-
ceded by bronchia] symptoms. At home, on his own farm,
is never troubled. Last year he built a new house three-
quarters of a mile from his old residence but was unable to
occupy it because of severe asthmatic attacks which ap-
peared whenever he remained about the new house for a
day at a time. The attack would be preceded by cough,
wheezing and expectoration, beginning within two hours af-
ter he reached his house and resulting in a paroxysm of
asthma within eight or ten hours. When he returned to
his old residence the attack would cease within an hour or
two. The attack never appeared while the new house was
in process of construction but only when he attempted to
live there, and at the same time he could visit with im-
punity a new barn in process of building on his old
farm.
asthma. 179
Laughing, coughing, sneezing, forcible breathing etc.,
induce asthma by over-stimulating the bronchial muscles
(Wilson Fox). Gastro-intestinal irritations are next to bron-
chial disturbances as a cause for asthmatic attacks. Very
great variety and peculiarity is exhibited in relation to the
various articles of diet which induce the attacks. Intestinal
indigestion undoubtedly acts as a peripheral cause for
asthma but must also be classed among the causes of toxic
asthma. Constipation and flatulence may also induce at-
tacks of asthma. Nasal irritation acting through the sensory
branches of the fifth nerve is a frequent element in peri-
pheral irritations resulting in asthma. Nasal polypi, ex-
ostoses of the septum, turgescence of the cavernous tissue
covering the turbinates and a thickening of this tissue, are
given as a cause for asthma (Hack and others), and removal
of this tissue has been insisted on by many. Undoubtedly
many cases are due to nasal irritation and are relieved by
its removal, but that mere turgesence of the tissues will in-
duce asthma is not borne out by the clinical history of this
very common condition of the nasal membrane, or by its re-
moval in instance where it is the only nasal abnormality as-
sociated with asthmatic attacks.
Certain odors of animal or vegetable origin, dust, the
pollen of flowers, the odor of certain drugs, may all induce
asthma through the very erratic sensibility of some individ-
uals to the irritation produced by these various substances.
Unknown atmospheric conditions at certain seasons of the
year and in certain localities induce asthma {hay asthma).
Dental irritation in children may produce asthma. Uterine
irritation from polypi, irritation of the pneumogastric nerve
by neuroma or enlarged glands in the posterior mediastinum,
vertebral exostoses or disease of" the pneumogastric center
may bring about attacks of asthma. Cold to the surface of
the body, especially to the feet, may induce an attack, or it
may be associated with the disappearance of a cutaneous
eruption. Eczema, psoriasis and urticaria (Sir Andrew
Clark) are frequently associated with asthma, the latier
especially, as it is essentially a neurotic affection.
Morbid anatomy.—It is useless to review the various
180 asthma.
theories regarding the exact condition of which the parox-
ysm is the result. The nervous factor is generally recog-
nized,—some condition of the nervous system by which
stimuli, ordinarily of no moment, influence the vagus or
sympathetic nerves. Whether the motor branches of the
vagus are alone concerned (spasm of the bronchial muscles)
or whether hyperaemia of the bronchial mucous membrane
(Weber) from local vaso-motor paresis of sympathetic ori
gin is also a factor, is a disputed question. The occurrence
of both of these conditions most fully explains the various
types of the disease. Bronchial spasm (Williams and others)
is a main factor in the attacks, but some degree of spasm of
the diaphragm (Wintrich, Bamberger) and. possibly of the
inspiratory muscles (Jaccoud, See) is, in some instances,
necessary to explain the clinical manifestations.
There are no characteristic lesions of asthma. Various
changes in the bronchi and pulmonary tissue may occur,
and, in severe and prolonged cases, dilatation of the right
side of the heart will develop. The effect of the bronchial
obstruction is to cause increased inspiratory effort with still
greater difficulty in expiration; as a result there is gradual
increase in the amount of residual air in the lungs and over-
distention of the alveoli.
The amount of expectoration in asthmatic attacks is
very variable. In the bronchial type it may be abundant.
Generally, towards the end of the paroxysm, expectoration
is more or less free and consists of semi-transparent, gray-
ish mucus in pellets—"boiled tapioca" expectoration. Spiral
corkscrew threads of mucin (Curshman's spirals) and
pointed octahedral crystals (Charcot—Leyden crystals) are
found in the sputum. The latter are supposed to be a com-
bination of phosphoric acid with an organic base. While
spirals and crystals are not found as frequently in other
pulmonary affections as in asthma, they are in no way char-
acteristic of the latter affection.
Clinical history.—Very great variation is shown in
the history of the different types of asthma. When devel-
oped in childhood it may disappear in time. The longer
the duration and the more frequent the attacks, the greater
ASTHMA. 181
will be the degree of associated emphysema and the less
likely the probability of recovery. There may be a history
of various peculiar and interesting exciting causes or there
may be no exciting cause ascertainable. There is a wide
range of associated diseases and morbid states, or, there
may be absolutely no local or general condition discoverable
even in the most severe attacks of the true spasmodic form
of the disease.
The attacks may occur only at certain seasons of the
year. They may be weekly, monthly or yearly or be separ-
ated by several years. Periodicity is a marked feature of
nearly all forms of asthma. The spasmodic type is apt to
come on at night after a few hours sleep. There is apt to
be a feeling of somnolence or depression preceding the at-
tack, with or without bronchial symptoms. In bronchial
asthma there is every degree of combination of bronchial
and asthmatic symptoms. The dyspnoea may be more or
less continuous and the asthmatic feature merely an exacer-
bation when some exertion overtaxes the weakened heart
and distended lungs. Many of these cases, while termed
asthmatic, will hardly come under that designation. The
aetiological relations of asthma give many interesting points
in the clinical history of the various types of the disease
which are not necessary to recount.
Symptoms and diagnosis.—In the markedly spasi
modic forms of asthma the attacks may come on suddenly
and without warning, especially at night, though there are
generally some premonitory symptoms such as depression
or restlessness, wheezy breathing, abundant, pale, limpid
urine, constriction about the chest and some dry cough. The
subject may be wakened from sleep by difficult breathing
which soon becomes severe dyspnoea. He sits up, leans for-
ward, breathes slowly and laboriously. The face is slightly
congested or pale, there is profuse perspiration and an anxious^
careworn expression. The shoulders are rounded and ele-
vated and the hands grasp a chair or table in order to fix
the scapular and humeral attachments of the chest muscles.
The jugular veins are distended and the muscles of the neck
are prominent. The whole chest is lifted during inspiration
182
ASTHMA.
which is, nevertheless, short and inefficient. Expiration is
three or four times its usual length, but is more difficult and
inefficient than inspiration and the chest becomes more or
less fixed in a condition of inspiratory distention. There is
no pause after expiration, inspiration beginning immediately,
suddenly and forcibly. The respiratory rate may not be in-
creased; the pulse is rapid and feeble and may disappear
during inspiration (pulsus paradoxus);the temperature is nor-
mal or depressed; and the patient, while in the severest dis-
tress, is not alarmed. Persistent itching of the chin, ster-
num, or between the scapulae may be present during the
earlier part of the paroxysm (Salter).
The thorax is much distended; the ordinary clothing
may not meet around the chest by two inches. The dia-
phragm is lowered as much as possible, the supra-clavicular
fossae recede during inspiration and there is absence of the
usual areas of cardiac and hepatic dullness with epigastric
pulsation. The percussion note is hyper-resonant, vocal
fremitus is absent, the vesicular murmur is feeble or absent,
or is covered by high-pitched sibilant rales and sonorous
rhonchi which are very changeable as to location. If bron-
chitis be present the rales may be more or less liquid or
crackling in character. The long, wheezing expiration and
the accompanying dry rales are positive proof of bronchial
spasm. Every possible gradation as to severity and dura-
tion of attack is met with in the true spasmodic form of
asthma, as well as various degrees of bronchial symptoms
which remain after the attack in the bronchitic form. Af-
ter an attack of purely spasmodic asthma has subsided there
may not be a single abnormal sign about the patient's chest.
In severe cases cyanosis may be marked and capillary re-
tinal haemorrhages may occur (Walsh). The urine is abund-
ant, pale and of low specific gravity and the solids are di-
minished (Ringer).
The dyspnoea of asthma is distinguished from that of
laryngeal or tracheal stenosis by its expiratory, instead of
inspiratory, nature and by wheezing instead of stridor.
Laryngeal dyspnoea is accompanied by increased movements
of the larynx and by diminution in the size of the chest and
ASTHMA. 183
elevation of the diaphragm. In cardiac asthma there is
rapid, panting or sighing breathing and the expiratory act
is. not prolonged. In aneurismal dyspnoea there is tracheal
tugging, localized dullness, pulsation, and brassy cough as
concomitant signs, with, perhaps, signs of pressure on the
bronchus,—diminished breathing in the left upper lobe,
aphonia from vocal paralysis.
Treatment.^-Asthma rivals bronchitis in the number
of medicaments employed for its relief. This is owing to
the neurotic nature of the disease and the consequent vary-
ing aetiological factors. These factors must be carefully
studied in the individual case and the treatment directed ac-
cordingly. The patient's knowledge and observation of his
own case is often most useful in directing the treatment.
Relief of the paroxysm in no wise influences the contin-
uance of the disease. The remedies used for the relief of
the paroxysm are all neurotics which have only temporary
symtomatic effects and if the disease is to be cured it must
be done through the administration of constitutional remedies
such as iodides, arsenic, iron, strychnia, quinia, cod liver oil,
etc. These remedies are to be persisted in for long periods
and are much aided by controlling the attacks in the mean-
time by the neurotics. Iodide of sodium, strychnia and
fluid extract of euphorbia pilulifera is a combination whose
prolonged administration has given me much satisfaction,
especially in the bronchitic form of asthma.
Climate is an important factor in the treatment of the
asthmatic. Here each case is a law unto itself, very strik-
ing peculiarities being observed in relation to climate. Gen-
erally speaking, a moderately elevated, dry climate is best,
particularly in the pine or fir regions. It is generally stated
that the smoky, gas-laden air of large towns is agreeable
to asthmatics. This may be true of the purely spasmodic
form of asthma, but in my experience is not so of the bron-
chitic form in which such cities as Pittsburg, in spite of its
comparatively favorable latitude, elevation and location in
the petroleum belt, is entirely unsatisfactory as a residence
for asthmatics with branchial symptoms. Chicago is to a
like extent objectionable because of the rapid and radical
184
ASTHMA.
changes in temperature and moisture. Northern New York
Wisconsin, Michigan, Minnesota, Idaho, Wyoming, etc.,
are particularly favorable localities for the asthmatic.
In the spasmodic form due to susceptibility to atmospheric
conditions incident to certain seasons of the year, and in hay
asthma, asojourn at the seaside is often beneficial. Many of
these cases, especially of hay asthma, are entirely free from
attacks while at Mackinac Island, a locality that, while en-
tirely surrounded by water, has a particularly dry, exhilar-
ating atmosphere. Cases of asthma which have developed
marked emphysema must not be sent to a high altitude be-
cause of the resulting strain on the right side of the heart.
In preventing attacks of asthma each case must be
treated symptomatically. Peptic asthma involves the treat-
ment of every variety of dyspepsia. In addition to dieting,
the administration of twenty grains of strontium bromide
and ten grains of sub-carbonate of bismuth, three or four
times daily, is of great benefit. Flatulence, constipation,
uterine irritation and nasal irritation must be relieved. In
the cases exhibiting great nasal sensibility to odors, gases,
temperature etc., with hyperaemia or turgescence of the tur-
binate coverings, it is best to treat them persistently with
soothing, cleansing and disinfecting sprays or steam inhal-
ations. In the absence of abnormal bony or soft tissue
growths or septum deviations, operations for the removal of
tissue or cauterizations are not advisable. The ultimate re-
sults are not nearly as good as many rhinologists have in-
ferred from the immediate effects of such treatment. For
nocturnal attacks of spasmodic asthma, thirty grains of
potassium bromide and a dram of Hoffman's anodyne, at bed
time, will often prevent attacks (Thomson). Iodide of so-
dium or potassium and arsenic are the most useful prophy-
latic drugs. Tincture of lobelia and fluid extract of stra-
monium are useful adjuvants. The iodides should be gradu-
ally increased until a fairly large daily dose is given with-
out producing physiological effects. Hot coffee, a liberal
drink of whisky, the fumes of burning nitre paper (blotting
paper soaked in a solution of nitrate of potash,gr. xxx ad Si)
or tobacco will at times ward off an attack of asthma. Sker
ASTHMA.
185
ret recommends 5 to 10 grains of citrate of caffein at bed time
for the prevention of morning attacks, and five grains every
four hours during attack in bronchial asthma. The vapor
of turpentine or ammonia, or painting the pharyngeal wall
with a solution of ammonia (Ducros, Trousseau) or swabb-
ing the nasal passages with a solution of cocaine, may abort
attacks in cases of nasal and pharyngeal irritation.
In bronchial asthma, besides the palliative treatment,
the following is useful:
n
Natrii iodidi, 3ii-iii
Tr. nucis vom., 3iv
Tr. belladonna;. 3i-ii
Spts. eth. sulp. co., fiss
m. Elix. q. p. ad §vi
Sig. 3ii every 6 hours.
For the relief of the paroxysm of asthma we rely al-
most entirely on the neurotics and stimulants. Belladonna,
hyoscyamus, stramonium, duboisia, the nitrites (amyl, ni-
troglycerine, sodium), iodide of ethyl, opium and ether are
the most serviceable. Much relief is obtained from the
fumes of the numerous asthmatic cures, all of which contain
more or less of the first four drugs enumerated.* The fol-
lowing is a good formula for a powder for aslhma:
Belladonnae f°l->]
Stramonii fol., i z-
Lobelise fol., j
Silphii lacin., fol., J
M. Potasii nitratis §ss.
Fiat pulv.
Thomson recommends full doses of tincture of bella-
donna or an injection of atropine at the nape of the neck to
arrest the asthmatic paroxysm. Nitroglycerine and chlor-
oform are useful for an attack but the latter is more or less
*Candles designed for the administration of stramonium by inhalation (candelaa
stramonii) are made of 150 parts of pulverized stramonium leaves, 70 of potassium
nitrate, and three of balsam of Peru. Stramonium cigarettes (cigarettae stramonii
contain one gramme each of stramonium leaves. Compound stramonium ciga-
rettes (cigarettae stramonii com positaB) contain one gramme each of a mixture of 3
grammes of stramonium leaves and 1 gramme each of the leave* of belladonna a'nd
tussilago farfara.
186 PULMONARY EMPHYSEMA.
dangerous. A few drops of pyridine inhaled from a hand-
kerchief or butter plate is often efficacious.
The most efficient remedy for an attack of spasmodic
asthma is a hypodermic injection of morphine (£ gr.). The
combination with atropine is advisable. There is little dan-
ger of drug habit and the best relief is obtained in the
purely spasmodic cases. Morphia should not be given in
cases of bronchial inflammation with dyspnoea and only in
small doses, if at all, to cases of bronchitic asthma with
pronounced bronchial symptoms.
The general management of the asthmatic involves
much symptomatic treatment not necessary to detail here,
but the more closely the individual case is studied the better
will be the results.
PULMONARY EMPHYSEMA,
In pulmonary emphysema there is dilatation of the alve-
oli of the lungs and atrophy of the alveolar walls. Two
forms are usually described; a vesicular, and an interlobular
or interstitial form. The latter is entirely distinct from the
former to which reference is always made by the unqualified
term emphysema.
There are four clinical varieties of emphysema, which,
while not constituting distinct forms of the disease, are yet
sufficiently well marked to merit clinical division. They are
general emphysema (volumen pulmonum auctum, chronic hy-
pertrophic emphysema, large lunged emphysema,—Jenner),
senile emphysema (small lunged emphysema, atrophic emphy-
sema, senile atrophy of the lungs), localized emphysema (com-
pensatory emphysema) and acute emphysema (dilatation of
the lungs). Pathologically the last variety is not a form
of emphysema, as there is no atrophy of the alveolar walls
but simply acute dilation of the alveoli which may or may
not be recovered from.
Emphysema may occur at any age, but is most common
during adult life. It is more frequent in men because of
greater exposure to predisposing conditions.
^Etiology.—The distention of the air spaces is the
primary change and precedes the atrophy of the alveolar
walls. In the atrophic form it is possible that this order
PULMONARY EMPHYSEMA. 187
may be reversed. Exclusive of compensatory emphysema
it is probable that failure of nutrition (Jackson, Waters) is
a frequent element predisposing to the development of em-
physema.
The increased air tension which dilates the spaces is
brought about by increased expiratory force (Mendelssohn,
Jenner) which first dilates those portions of the lungs which
are in contact with the most yielding portion of the chest
walls, i. e., the apices, anterior border of the upper lobes
and the margins of the base of the lungs. The inspiratory
theory (Laennec, Gairdner,Rindfleisch) is not now accepted
as the general cause of emphysema, though in the produc-
tion of localized emphysema the inspiratory cause is un-
doubtedly an important factor.
Bronchial obstruction, cough and muscular effort are
the most important factors in producing emphysema. Occu-
pations involving straining, lifting, playing on wind instru-
ments tend to produce the disease. Chronic bronchitis,
asthma, whooping-cough, laryngeal, tracheal and bronchial
stenoses cause general emphysema. Localized emphysema
may result from any disease of the lungs or pleurae which
limits the action of a portion or the whole of a lung. Com-
pensatory emphysema of an entire lobe or lung may thus de-
velop or localized emphysema may develop in the lobules
adjacent to areas of pulmonary atelectasis, infarctions or
consolidation.
In those cases where emphysema is not accompanied by
or precedes the development of, those mechanical causes
already enumerated, the cause rests in nutritive changes in
the lung texture which destroys the elasticity of the lung
and renders it unable to withstand the ordinary air pressure
incident to the process of respiration.
Interlobular emphysema occurs from wounds of the
lung, rupture of the alveoli from overstrain, as in coughing,
in connection with laryngeal diphtheria especially after tra-
cheotomy, or in advanced cases of general emphysema from
the rupture of air sacs.
Morid anatomy.—The distention of the air passages
begins in the inter-alveolar spaces (Rindfleisch). This in-
188 PULMONARY EMPHYSEMA.
crease is at the expense of the alveoli opening into the in-
fundibular cavities in relation to which the alveoli are nor-
mally about one third smaller. The dilatation maybe primar-
ily in the alveoli. The pressure diminishes the blood sup-
ply to the alveolar walls and their epithelium undergoes
fatty degeneration. The septa between the alveoli become
partially or completely destroyed and the walls between adja-
cent infundibular, or alveolar spaces give way, the spaces
coalesce and form round cavities of varying size which may
be traversed by remnants of vessels or wall. There may be
more or less connective tissue development, especially in
connection with cases of chronic bronchitis.
These processes involve considerable destruction of the
pulmonary capillary circulation. According to Rindfleisch
communication is established between the pulmonary and
the bronchial veins which relieves the tension in the pulmon-
ary artery but does not aerate the blood. The over dis-
tended lungs lose their elasticity and the inspiratory trac-
tion force exerted on the circulation is lost. This, together
with the obliteration of the capillary vessels, increases the
pressure in the venous system and the right heart suffers.
Pressure in the vessels of the bronchial wall causes conges-
tion of the bronchial membrane. The bronchi may be di-
lated, particularly in localized emphysema, or they may be
obliterated or run as fibrous cords across the emphysematous
sacs. The bronchial walls are usually thickened, though in
atrophic emphysema they may be thinned.
The lungs are maintained in the position of ordinary in-
spiration. The diaphragm is lowered and the heart dis-
placed downward and becomes more nearly horizontal. The
hypertrophy of the heart is, in time, followed by dilatation,
tricuspid regurgitation, dilatation of the right auricle and
the usual congestions of the liver, stomach, kidneys, brain,
and oedema of the tissues.
When interlobular emphysema occurs alter trach-
eotomy, the air passes behind the deep cervical
fascia into the chest. From the mediastinum it may pass
along the tissue around the bronchi and blood vessels and
appear on the surface of the lung as small beads or bubbles
PULMONARY EMPHYSEMA. 189
of air beneath the visceral pleura. Interlobular emphysema
from any cause shows itself as small air bubbles in the in-
terstitial tissue of the lung and in rows beneatn the pleura.
Pneumothorax and pulmonary collapse are the most fre-
quent associated lesions of interlobular emphysema. There
may also be general subcutaneous emphysema of the neck,
face and arms or trunk.
In general emphysema when the chest is opened the
lungs do not collapse. The margins are in contact with the
sternum and the apices fill the suprascapular spaces. The
auricular process of the left upper lobe occupies the prae-
cordial space, the diaphragm is depressed, the lung tissue is
soft, of a grayish color,somewhat pigmented, non-crepitant
and may pit on pressure. The surface may have a frothy
appearance or large rounded blebs may occupy the margins
of the upper lobes, or the bases. These air sacs may be
pedunculated. The lung tissue is dry and bloodless except
at the base where it may be cedematous or congested if bron-
chitis or weak heart have been present. Pleural adhesions
are not so frequent as in other diseases of the lungs. Ather-
oma of the pulmonary artery is frequently present.
In senile emphysema the lungs are small and collapse
readily and are deeply pigmented. The vesicles are fused
from atrophy of the septa. The margins may be much di-
lated and large air sacs may be present. The bronchi are
dilated and their walls thin, membranes congested and they
may contain puriform fluid. Collapse and oedema of the
posterior portions of the lower lobes are frequent. The
chest is rigid and small and the lower ribs oblique and in
contact with each other. Senile emphysema is associated
with general atrophy and wasting of the bodily tis-
sues.
Local emphysema is secondary to some disease of the
lungs, bronchi or pleurae,areas of arrested pulmonary tuber-
culosis, cavities, bronchial dilatations, atelectasis or fibroid
areas in the lung or pleuritic adhesions and indurations.
The apices and the posterior and upper portions of the lower
lobes are frequent locations for this form of emphysema.
Local areas of fibroid or collapsed lung may be surrounded
190
PULMONARY EMPHYSEMA.
by, or imbedded in, emphysematous tissue. Large air cavi-
ties are usually absent in compensatory emphysema.
The so-called acute vesicular emphysema is simply anover-
distention of the alveoli. It may result from acute bronchi-
tis, violent inspiratory efforts, partial stenosis of the trachea
or bronchi by collapse of the lung increasing the strain on
the remaining portion, asphyxia from any cause. While it
occurs most often when the above causes are fatal, it also
occurs in non-fatal cases and may be recovered from.
Clinical history.—The history of emphysema is in
nowise characteristic. The insidious advent of the disease
accustoms the subject to the altered conditions of respira-
tion and there is little complaint until the condition becomes
severe. The history mainly refers to the symptoms caused
by the associated affections, particularly the bronchitis,
and it is quite common to have patients who are markedly
dyspnoeic remark that if the cough were better they would
get along all right with the breathing. The dyspnoea is
always present, is likely to be paroxysmal and is increased
by exertion or interference with the action of the diaphragm
by flatulence. In children the history may point to an attack
of whooping-cough as the origin of the dyspnoea. In ad-
vanced cases orthopncea is present and the patient may not
be able to lie down. Cyanosis may be more marked than the
degree of dyspnoea would lead us to expect. Haemoptysis
may occur and may be severe though usually unimportant.
Cough and expectoration are related to the accompanying
bronchitis and are particularly troublesome in cold wet
weather. The appetite is poor, digestion bad and the o-en
eral nutrition much below par.
Senile emphysema is associated with a history of gen-
eral senile atrophy. The ability for exercise is limited and
the respiratory necessities consequently less. Dyspnoea is
therefore not marked. Paroxysmal dyspnoea is uncommon
though the associated bronchial inflammations may be at-
tended with shortness of breath. Local and acute emphy-
sema have only such history as is associated with the condi-
tions which cause them. With a history of severe disease of
one lung or pleura with loss of functional ability we may
PULMONARY EMPHYSEMA.
191
have a general emphysema of the opposite lung which is
essentially compensatory in nature and yet may ultimately
differ in no way from the ordinary morbid developments in
the large lunged variety of emphysema.
Sudden and urgent dyspnoea following tracheotomy,
with or without symptoms of pneumothorax, or severe
dyspnoea after violent attacks of coughing or in advanced
stages of general emphysema, may indicate the development
of the interlobular form of emphysema.
Symptoms and diagnosis.—The symptoms of emphy-
sema are generally modified by those of the associated le-
sions of the chest. The dyspnoea, cough, cyanosis, general
appearance of the patient and the conformation of the chest
are characteristic in the well developed forms of the disease.
The general symptomatology of the so-called hypertro-
phic form of the disease is well illustrated in the following
history of an out-door clinic case:
M. D., wood turner, aged 49. Always healthy until five
years ago when he had a severe attack of bronchitis during
the winter. The following winter had another attack of
bronchitis and since then has suffered from more or less
dyspnoea and cough with frothy expectoration. He is usually
worse during the winter months. Has never had any bloody
expectoration. At present suffers from dyspnoea which, at
times, is paroxysmal and distressing and is always worse on
exertion. Cough is more or less troublesome and is attended
with scanty, viscid expectoration. Has no pain but there is
a sense of constriction about the lower portion of the chest.
The pulse is small, weak and at times irregular. Tempera-
ture normal, appetite poor, digestion bad, sleeps fairly well.
The patient is slightly cyanosed. The cervical veins
are distended but there is no jugular pulsation beyond that
conveyed from the carotid artery. The facial lines are dis-
tinct and his face has a careworn expression. The alae nasi
are widened, the lips thick, the eyes prominent and the con-
junctivae injected. The finger ends are clubbed. The abdo-
men is prominent, the liver and spleen lower than normal
and somewhat enlarged from congestion. Thore is no oedema
or ascites.
His chest is enlarged in all its diameters, paricularly in
the antero-posterior. It is rounded (barrel shaped) in form
with the shoulders elevated and the scapulae rotated some-
192
pulmonary emphysema.
what on their axes, the posterior borders and lower angles
standing well out from the chest wall. The whole chest
looks shorter though the vertical diameter is increased by
downward displacement of the diaphragm, and the oblique
diameter by the more horizontal position of the ribs and the
widening of their interspaces. The clavicles are well for-
ward and the inspiratory muscles of the neck are prominent
and tense. The junction of the maubrium with the body of
the sternum (angulus Ludovici) is prominent and the lower
portion of the sternum slightly depressed. The costal angles
are widened. The suprascapular depressions are effaced,
the upper intercostal spaces are even with the ribs but the
lower spaces are depressed and there is inspiratory reces-
sion of these spaces below the fourth interspace; when he
coughs the spaces bulge slightly. The respiratory excur
sion of the chest is limited and the expiration is much pro-
longed. The heart impulse is absent from the usual situa-
tion and there is systolic epigastric impulse. A few dilated
veins are present along the anterior and lateral portions of
the chest corresponding to the attachments of the diaphagm.
On palpation we find the fremitus barely perceptible
over the upper chest. Below the level of the fifth rib in the
axillary line the fremitus is increased on both sides. The
cardiac impulse is not felt in its usual situation. The per-
cussion note ishyper-resonant,low in pitch, empty in quality
and of great intensity even over, the areas of increased frem-
itus and is not appreciably modified by inspiration or ex-
piration. The resonance extends in the mammillary line to
the eighth rib on the left and to the sixth rib on the right.
Behind it extends to the eleventh rib. The respiratory mur-
mur is feeble and suppressed over the upper portion of the
chest, below the fourth rib it is somewhat harsh. The expir-
ation is about three times as long as the inspiration and over
the areas of increased fremitus it is slightly higher pitched.
Laterally and in front, crackling rales are heard below the
fourth ribs. Behind, at the bases, the rales are finer. The
heart sounds are weak and distant; the first sound, having
lost its muscular tone, is short and indistinct. The second
sound, over the pulmonic area, is markedly accentuated.
In senile emphysema dyspnoea is usually not severe ex-
cept during exertion, bronchial and asthmatic symptoms are
not very pronounced. The subjects are emaciated. Venous
congestions, cyanosis, clubbing of the fingers, displacement
of the heart and diaphragm are absent. The barrel shape
of the chest is not marked, though the lateral diameters are
PULMONARY EMPHYSEMA. 193
diminished. The ribs are oblique and the interspaces are
wide above, while below they are very narrow. Inspiration
is shallow and there is inspiratory recession of the inter-
spaces. The percussion note is low in pitch but clear in
tone and empty in quality. The respiratory sounds are
feeble and the expiration but moderately prolonged. There
may be rales at the base of the lungs.
In localized emphysema the signs are modified by the
conditions which cause it. These conditions generally re.
suit in more or less condensation of local areas of lung tissue
largely from interstitial increase of tissue. These areas,
surrounded by emphysematous tissue, will give marked in-
crease in fremitus with a low. pitched percussion note of
empty quality. This apparent anomaly in physical signs is
due to the more dense tissue being surrounded with alveoli
in which the air tension is greatly increased.
When signs of local emphysema are present in an apex
of the lungs they may be due to compensatory emphysema
developing as a result of the changes incident to a healed or
quiescent local tuberculosis.
Enlargement of a portion or the whole of a lung as a re-
sult of extensive disease or contraction of the opposite lung
may, according to Fowler, be regarded as a true hypertro-
phy,—if the functional activity be increased (puerile breath-
ing), or as emphysematous if the activity be decreased
(feeble breathing with prolonged expiration).
Acute vesicular emphysema is characterized by the signs
of marked distention of the chest with air, urgent dyspnoea,
perhaps cyanosis and such additional signs as may attend
the cause of the attack.
The symptoms of interlobular emphysema are dimin-
ished respiratory sounds in connection with urgent dyspnoea.
Signs of pneumothorax and collapse of the lung, or perhaps
of general subcutaneous emphysema, may be present.
The diagnosis of emphysema is usually not difficult. In
pneumothorax the affected side is enlarged, the spaces ob-
literated, movement is restricted or absent and is exagger-
ated on the opposite side. The percussion note is more
amphoric or tympanitic in quality and the breath sounds
194
PULMONARY EMPHYSEMA.
more indistinct than in vesicular emphysema. It may often
be difficult to estimate the exact status of cases of combined
emphysema, bronchitis and failure of the right ventricle,
but treatment will often aid us in this respect. Aneurisms
of the transverse portion of the arch of the aorta may pre-
sent bronchial and dyspnceic symptoms, but the presence of
local dullness or the absence of hyper-resonance together
with the brassy cough and tracheal stridor, will aid differ-
entiation.
Treatment.—Emphysema, when atrophy of the septa
has occurred, is not a curative affection. The future of the
case must be judged by the condition of the heart and gen-
eral nutrition. Most of the patients are under treatment for
some of the associated affections, for, to the emphysematous
state itself, they become largely indifferent because of its
gradual development and progress.
The direct treatment of the emphysematous condition
by means of compressed air baths (Williams) or by the in-
spiration of compressed air and expiration into rarefied air
(Waldenburg), while productive of increased comfort and
some benefit to the patients, is not directly curative and in-
volves the application of troublesome methods of mechanical
treatment. Emphysematous subjects should seek such
localities as furnish atmospheric conditions and air pressure
suitable to their impaired respiratory power. Many cases
do well at the sea level though the changes in temperature
in winter and the dampness may aggravate their condition.
The tendency towards bronchitis and asthmatic dyspnoea
renders a warm, dry climate the most advantgeous. The
altitude must be decided by the condition of the right heart
and the respiratory capacity. As failure of the right heart
is the chief thing to guard against, a permanent residence at
a considerable altitude is dangerous.
Tne general nutrition of the patient must be increased
by diet and tonics. Iron, arsenic and strychnia are the best
tonics. Iodide of potasfium in from five to ten grain doses
is very useful. Iodide of sodium may be used in place of
the potassium salt. A useful combination is the fol-
lowing:
PULMONARY collapse.
195
3
Ferri arsen., gr. i.
Ext. nucis vom., gr. £.
Peps, purse gr. i.
m Ext. cascara sag., • gr. |.
The various remedies already detailed for use in bron-
chitis and asthma are to be used when these conditions are
associated with emphysema and as these are the complaints
with which patients come for relief, such remedies consti-
tute a large part of the therapeutic measures called for in
emphysema. The functions of the liver and bowels must be
watched. Occasional doses of mercurials are of great ser-
vice at times. When congestions and oedema appear, digi-
talis is to be used as in other conditions attended with ataxia
of the heart. Strychnia in large doses is very useful in these
cases.
With paroxysmal attacks of dyspnoea morphia should
be used with caution if there is much bronchitis present.
With marked cyanosis from an overtaxed right ventricle
venesection may be indicated.
PULMONARY COLLAPSE.
Collapse of the lung may be congenital (atelectasis) or
acquired. The term atelectasis was formerly reserved for
cases of partial or complete failure to expand the lungs at
birth, while collapse referred to the airless condition of
lung tissue which had exercised function. The two terms
are largely used synonomously at present but we shall use
the unqualified term collapse as referring to the acquired
variety. Undoubtedly, in some instances of the congenital
form, the term atelectasis is etymologically more correct.
^Etiology.—Congenital collapse occurs from obstruc-
tion of the bronchi by mucus, meconium or the pressure of
enlarged bronchial glands. Enlargement of the abdomen
may cause collapse by interfering with the action of the
diaphragm, or collapse may occur from congenital disease,
muscular weakness,or from mechanical injury during labor.
Collapse of the lung occurs from bronchial obstruction, from
bronchitis or broncho-pneumonia, especially in connection
with whooping cough or measles, from diphtheria of the
196 PULMONARY COLLAPSE.
bronchi or trachea, fibrinous bronchitis, bronchiolitis, cedema
of the lungs, thoracic aneurism, mediastinal tumors, bron-
chial stenosis, bronchiectasis (from mucus obstruction), pul-
monary embolism, thrombosis and infarction. The various
diseases and morbid growths of the nasal, pharyngeal or
laryngeal passages may, if sufficiently severe or prolonged,
cause collapse of the lung. Pressure on the lung from
pleural effusions or on the diaphragm from abdominal dis-
tention may cause collapse. An opening into the pleural
cavity is always followed by more or less collapse of the
lung. Pneumothorax and pyopneumothorax are followed
by collapse more or less complete. Great weakness or
paralysis of the inspiratory muscles or of the diaphragm,
such as occurs in severe or prolonged fevers or in weak and
badly nourished,rachitic children, may cause collapse of the
lower portion of the lungs. Weakness of the intercostal
muscles, with partial collapse of the lower portion of the
lungs during the first year of life, produces contraction of
the lower portion of the chest with "pigeon breast," and
other deformities of the costo-sternal articulations.
The generally accepted view as to the mechanism of the
production of collapse of the lung is that it is due to absorp-
tion of air from portions of lung tissue whose bronchi are
obstructed by secretion or other causes. The absorption
occurs through the agency of the blood vessels, alveolar
walls and,the elasticity of the lung tissue (Lichtheim). In
collapse occurring without bronchial obstruction, it is sup-
posed to be due to paralysis of the inspiratory muscles
(Fagge, Pearson—Irvine).
Morrid anatomy.—Areas of collapse are usually more
marked in the surface of the lung than in the deeper parts.
The margins of the lower lobes along the vertebrae, the mid-
dle lobe of the right lung and the peripheral portions of the
upper left lobe, are the usual sites for collapse. The col-
lapsed areas present as irregular, depressed, bluish-red or
violet colored masses which are smooth and resistant, do
not crepitate, and which sink in water. Serum may be ex-
pressed from the tissue, which is usually somewhat con
gested. If the collapse has not existed very long the area
PULMONARY COLLAPSE.
197
may be dilated by insufflation, when it will be red in color
and crepitant. Numerous small areas or large tracts may
be affected according to the extent of the cause. Incom-
plete collapse of a lung,as from pleural effusion,the organ is
heavy, airless, of a bluish-gray color and less shiny than the
lobulated variety.
A collapsed portion of lung may regain its normal con-
dition, may become cedematous and congested (splenization),
or, in compression collapse, when comparatively large areas
are involved, the air is gradually expelled or absorbed and
the tissue becomes dry, tough and flesh-like (carnification).
When the collapse is permanent the alveoli are compressed
and obliterated. Interstitial tissue developments occur.
The small bronchi may dilate and contain pus. Atrophic
changes may occur and a local mass of indurated tissue may
remain.
Extensive congenital collapse may cause sufficient ob-
struction of the pulmonary circulation to prevent the closure
of the foramen ovale and the ductus arteriosus and cause
dilatation and hypertrophy of the right heart.
Clinical history. —In congenital collapse there may
be a history of sleepiness and inability to nurse, feebleness
and arrested growth, coldness, lividity; cyanosis, asphyxia
or convulsions may be present if some congenital lesion of
the circulation complicates the case. The history of col-
lapse of the lung is the history of its aetiological fact-
ors.
Symptoms aind diagnosis.—In congenital collapse the
child is feeble, cries weakly, the temperature is sub-normal,
the breathing slow and feeble. There is inspiratory reces-
sion of the interspaces and the lateral regions of the chest.
The lower chest is contracted and the sternum prominent.
The breath sounds are feeble all over the chest and,perhaps,
absent at the base except when the child cries or coughs.
Fine rales may be heard at the base. If much cyanosis is
present the child will probably not live many days.
Collapse of the lung may be attended by sudden and
severe dyspnoea, rapid and feeble pulse, cyanosis and un-
consciousness, or, if the area be small, no particular symp-
198
PULMONARY collapse.
toms may be present. Inspiratory retraction of a portion of
the chest wall, dullness on percussion or a hard, tympanitic
note if emphysematous patches have developed; feeble re-
spiratory sounds; tubular or bronchial breathing; fine rales
heard only after a deep inspiration where breath sounds are
absent, (partial collapse), are the principal signs of collapse
of the lung. These will be associated with the various
physical evidences of the pleural and pulmonary causes of
collapse.
Collapse from pleural effusion may be mistaken for
pneumonia. There may be tubular breathing but it is more
distant, the vocal sounds and fremitus are Jess marked or
absent, as are the fever and sputa of pneumonia. The per
cussion note is more flat, and position may alter the level of
the flatness. In miliary tuberculosis the previous history
of cough,fever, loss of flesh,and the family history, will aid
in differentiating.
Treatment.—In atelectasis in the new-born the fauces
must be cleared of mucus. Breathing may be established
by placing the child in a hot bath and splashing it with cold
water, or switching it with a wet, cold towel. Artificial res-
piration, insufflation of the air passages, irritation of the
fauces, stimulating liniments, etc., may be used. The child
should be kept warm under all circumstances. If the incu-
bators now in use in maternity hospitals are not to be had,
the child should be well wrapped in cotton-wool when not in
the warm bath.
Pulmonary collapse from bronchial obstruction and pul-
monary inflammation is to be treated with the remedies ap-
plicable to such causes. It is sufficient to mention the pos-
sible danger of opium in bronchitis or bronchiolitis in adding
to the possibility of collapse from mucus obstruction, and
also to the advantage of emetics, in the same conditions, in
preventing collapse by the removal of secretion, though they
must be given with judgment.
In collapse from paralysis of the muscles of inspiration
and of the diaphragm, artificial respiration may be of con-
siderable benefit. In collapse secondary to indurations of
lung tissue, thickening of the visceral pleura, pleural adhe-
sions and effusions; pulmonary gymnastics, deep breathing,
compressed air inhalations, residence at a moderately high-
altitude, are some of the means of promoting lung expan-
sion and developing compensation, if not actual restoration
of function in the collapsed lung.
CHAPTER IX.
PULMONARY CONGESTION.
The bronchial circulation is subject to the same modifi-
cations as occur in other portions of the general circula-
tion. The mechanism of circulatory changes in the pulmon-
ary vessels has, however, caused much discussion. It is gen-
erally conceded that the pulmonary vessels are influenced
by the vaso-motor nervous system and that congestion of
these vessels may result from vasomotor disturbances. Ob
struction to the passage of blood through the left side of
the heart, obstruction to the general circulation, and degen-
eration of the blood may induce congestion of the pulmon-
ary circulation.
Congestion of-the lungs may be acute (active) or chronic
(passive.) The so-called compensatory hypercemia is a form
of active congestion. Varieties of chronic congestion are
brown induration and hypostatic congestion or splenization.
^Etiology.—Active congestion occurs in the first stage
of pneumonia and in all inflammatory affections of the lungs;
in rapid heart action from violent exertion or excitement;
from vaso-motor paresis; from drinking large quantities of
alcohol; from sudden change in air pressure in croup,
laryngitis or whooping-cough ;from the rarefied air of high
altitudes or from the sudden removal of large pleural ef-
fusions. Active congestion also occurs in connection with
infarctions of the lungs, capillary embolism of the pulmon-
ary arteries, acute dilatation of the heart, acute myocardi-
tis in connection with acute diseases and in rapidly devel-
oped cardiac failure in chronic cardiopathies.
Chronic congestion results most frequently from the ob-
struction incident to chronic heart lesions, particularly mi-
tral disease. It occurs in typhus fever, typhoid fever or
measles (splenization), or in any disease marked with severe
blood changes. In bed-ridden subjects, from any chronic
disease, congestion may develop in the lowest portion of the
200 PULMONARY CONGESTION.
lungs (hypostatic congestion). In mitral disease the conges-
tion is especially liable to assume the characteristics of
brown induration.
Morbid anatomy.—In acute congestion the pulmonary
capillaries are prominent, the alveolar epithelium becomes
swollen and granular and may proliferate. Red blood cor-
puscles may be found free in the alveoli. The lung tissue
is red and contains an excess of blood. Red, frothy fluid
flows from the cut section. (Edema may be present. Ac-
cording to Fowler the color of the tissue depends on the de-
gree of aeration of the blood at the time of death.
In chronic congestion the lungs are heavier than normal,
are of a dark-red, bluish or black color. The congestion
begins in the lower lobes first. Dark blood flows from the
cut surface of the lung. (Edema and extravasation may oc-
cur in the interstitial tissue. The alveoli contain swollen
and granular cells and fibrin and leucocytes may be found
(Cornil and Ranvier). In hypostatic congestion or spleniza-
tion there is interstitial oedema and scattered red or yellow
foci due to blood extravasation or to broncho-pneumonia.
The tissue is homogeneous, firmer, contains little air and
there is alveolar collapse. When the tissue is airless and
tough it looks like muscle tissue and is sometimes called
"carnified lung." At times the tissue is friable, there is col-
lapse, oedema and mechanical hyperaemia, constituting a con-
dition called "hypostatic pneumonia."
In brown induration the lungs may be smaller in size if
emphysema is not present. They are firmer and do not col-
lapse. Pleural thickening, adhesions and pigmentation
may be present. The lung tissue is irregularly pigmented,
dry, and contains less air than normal. Brownish, serous
fluid may present from the cut surface (Vircbow's "brown
oedema"). There is elongation and dilatation of the pulmon-
ary capillaries. The epithelial cells lining the alveoli are
swollen, filled with dark brown pigment and are attached to
the walls or are free in the alveolar cavity. Red corpuscles
may be present in the intra-alveolar exudation. The lymph
spaces of the alveolar walls contain pigment, which is also
present in the interlobular peribronchial and perivascular
PULMONARY CONGESTION.
201
tissues which are thickened. There is congestion and
oedema of the bronchial lining with dilatation of its vessels.
Haemorrhagic infarction may be present in the lung tissue.
The lung is brownish, red or mottled with brown or black
specks or streaks and is more dense and thicker than nor-
mal lung tissue.
Clinical history.—The history of pulmonary conges-
tion is covered by that of its aetiological factors. Dyspnoea,
cough and blood-stained, watery expectoration may be prom-
inent. In acute congestion there is sudden, urgent dyspnoea
with a sense of constriction about the chest, but no pain. In
chronic congestion more or less dyspnoea will be present but
is not complained of as the patient becomes somewhat accus-
tomed to it. The temperature may be elevated.
Symptoms and diagnosis.—Increased frequency of
respiration with dyspnoea and blood-stained expectoration
combined with harsh respiratory sounds and fine crackling
rales, especially in the lower portion of the lungs are the
chief symptoms of acute congestion. Chronic congestion
may show feeble respiratory sounds, harsh respiration with
prolonged expiration and fine bubbling or crackling rales
from oedema.
The aetiological associations will indicate the nature of
the congestion. Pulmonary embolism and infarction are
characterized by rapid, panting breathing and the expiration
is not prolonged. After the urgent symptoms of the onset
of acute congestion have passed off the breathing is not
panting. In asthma, the prolonged expiration and the char-
acteristic rales will differentiate. Pneumonia is excluded
by the absence of the chill, temperature, characteristic ex-
pectoration and by the presence of its more definite physi-
cal signs.
Treatment.—In acute congestion developing suddenly
with urgent symptoms, such as cyanosis and lividity, relief
must be obtained as the right heart will fail. Dry cupping
over the entire chest or venesection (eight or ten ounces)is de-
manded. Steam inhalations, turpentine stupes to the chest,
aromatic spirits of ammonia, ether, digitalis, and heat to the
extremities may be used. Large doses of digitalis are use-
202
pulmonary cedema.
ful in active congestion from alcohol, and alcoholic stimula-
tion may be advisable in acute congestion from sudden car-
diac failure in acute fevers and myocardial disease. The
bowels should be kept freely open with saline purgatives.
In chronic congestion the treatment will vary with the
nature of its cause, and need not be repeated here.
PULMONARY (EDEMA.
Pulmonary oedema is a secondary affection which is us-
ually combined with more or less congestion of the lung of
which it may be the result. An "acute" form of pulmonary
cedema occurs in which its secondary nature may not be de-
termined.*
^Etiology.—(Edema of the lung occurs in connection
with pneumonia, bronchitis, emphysema, nephritis, the var-
ious diseases of the heart, scorbutus, purpura, anaemia and
heart weakness in infectious fevers. Obstruction in one
part of the pulmonary circulation may cause oedema in an-
other portion. In cases of general dropsy pleural ad-
hesions on one side of the chest may cause oedema of the
corresponding lung while there may be hydrothorax of the
opposite side. Encysted pleurisies may cause local oedema
in the adjacent lung tissue.
Morbid anatomy.—Pulmonary cedema is characterized
by serous exudation in the alveoli and interstitial lung tis-
sue. Pale, frothy, fluid flows from the cut surface of the
lung or is easily expressed; it is blood-stained if congestion
be present. The lung tissue does not collapse, is pale or
tinged with red, has a gelatinous appearance, pits on pres-
sure, is heavy and may be friable.
Collapse of the lung, pneumonic conditions and various
degrees of congestion may be present. CEdema occurs most
often in the lowest portions of the lungs. The pleural sur-
faces are moist and the cavities of the pleurae may contain
some fluid.
Clinical history.—Rapid breathing, dyspnoea, more
or less cough with watery,frothy expectoration are the prin-
* Acute oedema with non-febrile onset and rusty,watery expectoration was styled
pneumonia serosa by Traube.
PULMONARY CEDEMA.
203
cipal features of the history. The dyspnoea may be sudden
and severe. The temperature will be normal unless eleva-
ted from some associated cause.
Symptoms and diagnosis.—The pulse is increased in
frequency, is feeble, and irregularity may mark the severe
cases. Cyanosis, lividity, distension of the cervical vessels
and extreme dyspnoea marks failure of the right heart.
When cedema is associated with acute congestion the lungs
may be over-distended.
In most cases inspection and palpation are negative,
The percussion note will be partially dull over the lower por-
tions of the lungs. In chronic heart disease, oedema is apt to
be most marked in the left side at the lowest portion of the
lung. The breathing is harsh, feeble or suppressed in the
lowest portions. Towards the end of inspiration, and possi-
bly with the commencement of expiration, fine crackling
rales are heard resembling somewhat a crepitant rale.
Larger, moist, and occasionally dry rales are heard.
The crepitating rales of cedema are more liquid in char-
acter and not so closely bunched, as to time, as those of
pneumonia. Their occurrence on both sides in the most
dependent part of the lungs, together with their associa-
tions, the watery expectoration, the absence of chill,
temperature etc., will differentiate oedema from pneumonia.
In bronchitis there is fever, tenacious, mucous expectoration,
the dullness in the lower lung is not marked, the rales are
not so fine and are more widely scattered than in oedema.
The persistently rapid breathing of pulmonary infarction
and the localized physical signs are sufficient to distinguish
it from oedema. In asthma and hydrothorax, the physical
signs of. these affections will be sufficient to prevent confu-
sion.
The following case may be regarded as one of acute
pnlmonary cedema:
Man, aged 41 years, a baker by trade. Has a slight,
aortic stenosis, with perfect compensation, which causes no
disturbance. In Febuary, '95 had a severe attack of influ-
enza with some bronchial symptoms. During this attack
the temperature was not above 101° F. On the fourth day of
204
pulmonary cedema.
the influenza the temperature rose to 102.5Q F., there was some
pain in the chest and considerable dyspnoea. The next day
the expectoration, which had been mucoid and rather heavy
and tenacious, became more liquid, then watery and frothy
with very slight blood stains. There was considerable
dyspnoea and cough. The greatest quantity of expectora-
tion was, as near as could be estimated, over two quarts in
twenty-four hours. The watery expectoration lasted three
days and diminished gradually. Recovery ensued.
It could not be determined, in this case, that the condi-
tion of the heart had anything to do with the production of
the pulmonary oedema.
Treatment.—The treatment of pulmonary oedema is
largely that of the diseases with which it is associated.
When cedema occurs with diseases of the kidneys, elimina-
tion by the kidneys, skin and bowels must be pushed. Dry
cupping over the chest and lumbar regions may be used. In
acute fevers the occurence of cedema is an indication for
general and cardiac stimulation. Calomel and salines are
useful as purgatives. [Lemoine recommeds a decoction of
the inner bark of the elder (Sambucus niger) for oedema and
ascites due to subacute nephritis. MacGregor reports
good results from strophanthus in oedema pulmonum.]
Strychnia and digitalis are the most useful stimulants in
most cases. When oedema of the lungs develops in connec-
tion with diseases of the heart, more energetic use of these
remedies is demanded. The occurrence of cedema at the
base of the lungs during acute febrile disease generally in-
dicates failure of the right ventricle and is an indication for
large doses of strychnia which should be given hypodermi-
cally (tjV to TV gr. every two to four hours as necessary).
Strychnia is here a temporary stimulant and should be
pushed. In chronic cardiac disease cedema is not so amen-
able to strychnia and we depend more on smaller doses
combined with digitalis.
205
PULMONARY INFARCTION.
Infarction of the lung {pulmonary apoplexy, embolic pneu
monitis—Jurgensen) is a circumscribed form of pulmonary
haemorrhage. Some writers describe, under the head of
diffuse pulmonary infarction, haemorrhage into the lung sub-
stance from rupture of aneurisms, vascular erosions from
cancer, abscess, gangrene, traumatism, or very large infarc-
tions. The true haemorrhagic infarction such as occurs from
aseptic embolism of the pulmonary artery, is the form un-
der consideration.
^Etiology.—Infarction of the lung occurs most fre-
quently in cases of mitral stenosis or regurgitation where
long continued and marked increase in pressure causes rup-
ture of small pulmonary veins or capillaries (according to
Ganurtz these infarcts are due to the rupture of newly
formed vessels.) Embolism and thrombosis of the pulmon-
ary vessels cause infarction of the lungs.
Considerable difference of opinion has been expressed as
to the effect of embolism and thrombosis on the organ in which
they produce infarction. The frequent presence of thrombi
in the right heart, the presence of an embolus in the largest
artery entering the infarction and the resemblance of these
infarctions to those of the spleen and kidneys which are
known to result from embolism, are facts in favor of the
embolic origin of pulmonary infarctions; atheroma of the
pulmonary artery, thrombosis of the main artery entering
the infarction (without embolus) and the formation of infarc-
tion during great slowing of the blood current, are facts in
favor of thrombosis. On the other hand, all these causes
may present without infarction,as infarction may occur with-
out any of these factors. Again, the experimental produc-
tion of embolism in animals does not result in infarction.
Embolism does not always cause infarction as the circu-
lation may be restored through the bronchial arteries or by
anastomosis in the capillaries of adjoining lobules (Vir-
chow, Kiittner). It is evident from these considerations
that infarction of the lung may arise from either of these
206 PULMONARY INFARCTION.
conditions and that no one is absolutely necessary to its
production.*
All the causes of embolism and thrombosis, therefore,
may cause infarction. Thus we may have pulmonary infarc-
tion from detachment of a thrombus in a systemic vein in
phlebitis, of a cardiac thrombus in asystolism of the right
heart, of a thrombus in the main trunk of the pulmonary
artery. Vegetative endocarditis of the right heart, and,
possibly, of the left heart also, may give rise to embolic in-
farction of the lung. Fat embolism, air embolism, new
growths and phleboliths are possible, though rare, causes
of embolic infarction. Phthisis, vegetative and ulcerative en-
docarditis, scurvy, purpura haemorrhagica, gangrene of the
lungs, cholera, yellow fever, typhoid fever, tyhus fever and
acute yellow atrophy may be accompanied by infarction of
the lungs.
Morbid anatomy.—Infarctions of the lungs occur in
the lower lobes and in the outer and lower portions of the
upper lobes. They are conical in form, somewhat irregular
in outline and in some instances globular in shape (interior
of the lung.) They vary in diameter from a fraction of an
inch to that of an entire lobe. The apex of the wedge-
shaped mass is at the point of obstruction in the artery with
the base outward, projecting, possibly, above the level of
the pleura. They are dark-red in color, firm, with well de-
fined margins and may be multiple and confluent. They re-
semble tumors and lobular pneumonia but are distinguished
by their color, shape, position and associations and from
pneumonia also, by their well defined limits.
In infarction the bronchioles, alveoli and pulmonary
capillaries are filled with red blood corpuscles. Catarrhal
*Conheim and Virchow state that a plug does not necessarily exist in all cases,
but Conheim says that when emboli block a terminal artery hemorrhagic infarction
always results. The manner in which blood enters the obstructed area has long
been in dispute. It is generally conceded that there is reflux of blood through the
veins or capillaries. Litten claims that the reflux of blood is through the vessel.,
of the capsule of the organ. Hamilton maintains that embolism has nothing to do
with the production of infarction, that it is caused by rupture of the capillaries
and that the wedge shape of the infarction is due to the shape of the terminal
bronchus and its air vessicles to which area the blood is confined. Kokitansky be-
lieved that embolism always existed in haemorrhagic pulmonary infarction.
PULMONARY INFARCTION.
207
cells are present in the alveoli and there may be traces of
fibrin. The adjacent pleura presents extravasations or
fibrinous exudation. Old areas of infarction show pigmented
areas of coarse, fibrous lung tissue. Neighboring bronchi
may be dilated. Dissection of the artery involved almost in-
variably shows thrombosis with, probably, an embolus
(Fowler). In small infarctions the blood may be expector-
ated and the circulation reestablished.
Clinical history.—Infarction does not occur in rap-
idly fatal cases of embolism as two or three days are re-
quired for the formation of an infarction. There may be a
history of over-exertion or excitement, expectoration of
small blood clots, uneasiness or constriction about the chest
increase in the dyspnoea or syncope (cardiac cases), cere.
bral symptoms or pain if pleurisy be present. If the cause
is a septic embolus there may be chills, hectic fever,diarrhoea,
and prostration.
Symptoms and diagnosis.—Infarction may be pre-
ceded by irregular intermittent heart action in cardiac cases.
The temperature may be 101-102° F. or may not be above
100° F. If the infarction is sufficiently large there may be in-
creased fremitus, localized dullness, bronchial breathing,
or localized friction sound and tenderness on forcible per-
cussion over the same area (Head). Sub-crepitant and crep-
itant rales may be heard. (Edema and emphysema may mask
the physical signs. In septic processes the sputum may be
dark from mixture with blood or the contents of an abscess
cavity may be expectorated. Perforations of the pleura,
pneumothorax and pleurisy may occur.
The expectoration of scanty, dark masses of blood is the
most characteristic symptom. Extreme dyspnoea of sudden
advent, rapid breathing, great pain, agony and fear of death
marks the occurrence of extensive embolism of the pulmon-
ary artery rather than infarction. The sputa of echinococci
and of cancer of the lung resembles that of infarctions but
their longer duration and associated signs with microscopic
examination of the sputum will differentiate.
In the following case infarction of the lung occurred in
connection with acute endocarditis and pericarditis:
208
pulmonary infarction.
Girl aged ten years. Acute rheumatism followed by
dry pericarditis and endocarditis with mitral localization
and extensive regurgitation. Both sides of the heart were
much dilated, liver enlarged, pulse rapid and irregular, con-
siderable dyspnoea, temperature 99.5° F. During the third
week of illness the dyspnoea became suddenly worse, with
some pain in the left side of the chest. The temperature
rose to 102° F., pulse more rapid,some cough but no expec-
toration.
Examination of the chest showed a spot, in the anterior
axillary line about the level of the fourth rib on the left side,
which presented dullness, bronchial breathing and a local-
ized friction sound. These signs presented over an area
about an inch and a half square. Subcrepitant rales were
subsequently heard in this area and all local signs disap-
peared in about a week. The child subsequently died from
dilatation of the right heart.
Treatment.—The treatment of infarction of the lung
is largely expectant. Absolute rest is imperative. In
cardiac cases stimulants and digitalis are necessary. Strych-
nia is the best stimulant. Codeine or small doses of mor-
phine are useful for the dyspnoea (Gerhardt recommends
musk and alcohol for the heart and morphine for the dysp-
noea.) In collapse, stimulation to the extremities by hot ap-
plications and dry cups over the chest may be used; with
great dyspnoea and cyanosis, wet cups or venesection may be
demanded. In septic infarctions, stimulants, tonics and
supporting treatment are indicated. Infarction of the lungs
occurs so seldom apart from other more common affections,
that our therapeutic measures are usually directed toward
the latter and beyond symptomatic means for the patient's
relief. Infarction demands little attention.
209
HAEMOPTYSIS.
The term haBmoptysis indicates the expectoration of
pure blood and does not include the rusty sputum of pneu-
monia, the slightly-stained expectoration of combined oedema
and congestion of the lung or the slightly-streaked expector-
ation which may occur in acute bronchitis.
The consideration of haemoptysis as a distinct affection
has no pathological, justification. However, its occurrence
in cases presenting no other subjective or objective evidence
of disease and the clinical necessity for regarding it, for the
time being at least, as the only apparent affection, together
with the established precedent, must be our excuse for us-
ing the term haemoptysis in this connection. Bleeding
from the nasal or pharyngeal passages,mouth orgums(spuri-
ous haemoptysis) in persons with diseases of these passages,
anaemia or haemorrhagic diathesis,is not included under this
heading.
^Etiology.—Diseases and growths in the larynx or tra-
chea may cause haemoptysis. Its most frequent cause is
active or passive hyperaamia of the bronchial mucous mem-
brane with or without weakness or degeneration of its ves-
sels. Ulceration of the bronchial membrane or rupture of
an aneurism into the bronchi may rarely cause haemoptysis.
It is an early symptom in tuberculosis with or without
bronchial symptoms. Some authorities regard the develop-
ment of tuberculosis as certain when haemoptysis occurs
without any other ascertainable cause. This is too radical
a view, as, in many instances, the bleeding is but an evi-
dence of the weakness of the capillary vessels and loss of
tone which constitutes the predisposition to, but does not
necessitate, the development of tuberculosis.*
Any inflammatory disease of the bronchi or lung may be
attended with haemoptysis. Tumors of the lung, hydatids
bronchiectasis, actinomycosis, pleurisy, abscess of the
liver, traumatism of the chest, lesions of the mitral valve,
pulmonary embolism or thrombosis, degeneration of the
pulmonary artery in emphysema or senile life, vaso-motor
"Rlndfleisch savs that when haemoptysis is followed by tuberculosis,the haemor
rhage is due to vas'cular tubercular infiltration.
210 HAEMOPTYSIS.
affections, the rupture of aneurisms of the aorta or of
branches of the pulmonary artery, tubercular disease of the
pulmonary artery, scurvy, purpura, haemophilia, leucocy-
thaemia, pernicious anaemia and the malignant type of infec-
tious diseases may be attended with haemoptysis.
It is generally conceded that haemoptysis may occur
vicariously with menstruation (vicarious haemoptysis) though
some authors consider it doubtful in the absence of disease
of the lungs. I have seen two cases in'which haemoptysis
occurred every four to six weeks in young women between
fourteen and seventeen years of age in whom menstruation
was not regularly established and who afterward developed
into perfectly healthy women without any evidence of pul-
monary disease. In these cases local conditions of blood
pressure, from vasomotor disturbances, are undoubtedly
concerned in the production of the vicarious haemorrhage.
Morbid anatomy.—After fatal haemoptysis the bron-
chial membrane will be dark-red, swollen and ecchymotic.
Thick,cylindrical blood casts may be found in the bronchi of
the same lung, or opposite lung if the patient has been ly-
ing on that side. The aspiration of blood into other portions
of the lung causes pinkish patches in the lobules. If the
haemoptysis occurred sometime before the examination no
trace of the bleeding may be found. Small nodules much
resembling infarctions may result from aspiration of blood
into air cells. In tubercular haemoptysis tubercular
changes may be found in-the walls of the vessels. In ad-
vanced tuberculosis an aneurism may break into a cavity
causing gradual leakage through the clot, or there may be
immediately fatal haemorrhage. The rupture of the vessel
may be caused by tubercular ulceration of the vessel wall.
Clinical history.—The following histories illustrate
the most frequent types of haemoptysis. The first case is
one of bronchial haemorrhage from loss of tone in the bron-
chial capillary vessels:
Lawyer aged 38. Height 5 ft 10 inches; weight 148
pounds. In 1891 had a slight haemorrhage accompanying an
attack of bronchitis of moderate severity; spat up a small
quantity of blood on two occasions. There were slight
HAEMOPTYSIS.
211
streaks of blood in the sputa for two days afterward. In '93
had another slight attack of bronchitis with the expectora-
tion of a small quantity of blood. In'96 had an attack of
laryngitis with some bronchial irritation and cough. Dur-
ing this attack he spat up clear blood on three different oc-
casions. Examination at this time showed nothing except
slight harshness of the inspiration over the trachea and main
bronchi. The temperature was 99 F. for three days but sub-
sided without treatment. Examination of the lungs in
March '98 showed nothing abnormal. There had been no
recurrence of the haemoptysis,and only once of the bronchial
trouble. No tubercle bacilli were found, at any time, in the
sputum. He has gained in weight and strength and consid-
ers himself perfectly well.
The following case is one of haemoptysis in mitral re-
gurgitation with temporary dilatation of the right heart:
Man aged 58, seen in consultation. Had an old mitral
regurgitation with fair compensation but had overtaxed his
heart causing dilatation of the right side. He was a large,
fleshy man and when seen by me was lying in bed suffering
from dyspnoea and was somewhat cyanotic. As he could
not turn in bed he had caused newspapers to be fastened to
the wall on either side of him and would turn his head either
way and expectorate clear blood on these papers with force
and precision. The total quantity of blood was considerable
and the haemoptysis lasted several days. The lower extrem
ities were covered with petechias. He subsequently recov-
ered and was about in apparently good health when last
heard from.
The following case is one of haemoptysis in tubercular
lobular pneumonia. These cases present a distinct clinical
type in which haemoptysis is an early and at times persist-
ent symptom. It appears conjointly with the rise in tem-
perature and continues while the blood pressure is high. It
is due to the severe collateral congestion attending the lob-
ular inflammation which latter is generally tubercular in
nature:
Young man aged 24 years, clerk by occupation. Height
5 ft. 8 inches: weight 136 pounds, healthy appearance. Pre-
vious general health good with the exception of two attacks
of slight haemoptysis in connection with slight bronchial in-
flammation.
In March '89 had an attack of haemoptysis. Would spit
212
HAEMOPTYSIS.
up a teaspoonful of clear blood several times in an hour.
Temperature 102.5 F., pulse 120 per minute and of high ten-
sion. Examination showed bronchitis and lobular pneumonia
of the upper lobe of the right lung. The acute symptoms
lasted six days during which time the bleeding continued in
spite of all kinds of astringent remedies, ergot internally and
ergotin hypodermically. These remedies were stopped and
the blood tension lowered, through aeonite and the con-
tinued loss of blood, when the r.aemoptysis ceased. The
lung did not clear up after the acute stage of the dis-
ease had passed. Acute tuberculosis developed. Death in
six months. No tubercle bacilli were found until after the
attack of lobular pneumonia.
Other similar cases could be cited in which successive
attacks of lobular pneumonia occurred with haemoptysis,
eventuating in tuberculosis and in which bacilli could not be
found during or subsequent to the first attack of pneumonia.
In the following case fatal haemoptysis occurred in a
subject of pulmonary tuberculosis with a large cavity in the
upper right lung. There was probably some connection be-
tween the occurrence of the haemorrhage and circulatory ex-
citement incident to sexual effort:
Man aged 35 years. Tuberculosis of right lung, cavity
in right upper lobe. Had lost much flesh but was able to at-
tend to business. Sept. 15th, '87 retired to bed feeling as
usual. Shortly afterward had a sudden haemorrhage,
brought up a large quantity of blood, went into collapse and
was dead when I reached him fifteen minutes later.
It is probable that the haemorrhage in this case resulted
through tubercular ulceration of a vessel or the rupture of
an aneurism into the cavriy in the lung. There was free
bronchial communication with the cavity.
Symptoms and diagnosis.—The quantity of blood ex-
pectorated varies from a mere streak or clot to one or two
pints. It is alkaline in reaction, bright red in color or of a
venous hue if the quantity be great. It is more or less
frothy and may be mixed with sputum. The statement of
the patients and friends in regard to the quantity of blood
expectorated should be received with caution as a half tea-
cupful, in their eyes, usually means about two teaspoonsful
by actual observation.
haemoptysis. 213
When the blood has remained in the lung it is black or
brown and may form moulds of the tubes and such clots or
pieces may be expectorated for several days after a haemor-
rhage. The haemorrhage is usually sudden, unannounced
and most often not connected with violent exertion. The
subject is made aware of it by the presence in the throat of
a salty substance with or without cough. With severe cases
there is pallor, faintness and collapse. The pulse is rapid,
the temperature normal or sub-normal, except in pneumonic
cases when it will be elevated. In all cases the temperature
may be elevated after the bleeding has ceased. The men-
tal effect on the patient produces great restlessness and
anxiety.
The physical signs are usually negative. The patient
should not be disturbed for examination, and percussion
should not be be practiced as it affords no information and
disturbs the patient. Auscultation may show localized signs
of liquid in the bronchial tract or harsh breathing confined
to a certain area, but most often is entirely negative.
In the diagnosis spurious forms of haemoptysis should
be excluded. Examination of the larynx should be made to
exclude affections of that organ. Haematemesis is accom-
panied by vomiting and gastric symptoms, the blood is dark,
grumous and mixed with food. (The blood in haemoptysis
may be swallowed and give rise to haematemesis and melaena.)
In many cases it is difficult to tell just what haemoptysis
may indicate and it is well to give a cautious opinion even
though local signs of tuberculosis are not clear and bacilli are
are absent from the sputum, as, in a large number of cases,*
when blood is freely expectorated, tuberculosis has already
commenced.
Treatment.—In the milder forms of haemoptysis the
treatment is confined to general methods in regard to the
patient:s common condition, with such special medication as
the condition of the bronchial tract may demand. In the
more severe forms such as occur with lobular pneumonia or
*According to Sir Andrew Clark,recurrent haemoptysis may occur in asthmatic
subjects without any sign of serious disease of the lung developing either at the
time or subsequently. Newman reports cases of haemoptysis without pulmonary
lesions being found post mortem.
214
Haemoptysis.
in the early periods of tubercular infection, absolute rest in
bed is the first requisite. The nervous excitement of the
patient must be calmed as much as possible by assuring him
of the absence of immediate danger. If cough is troublesome
it should be quieted by sucking small pieces of ice or by
small doses of morphine. Hot drinks and extensive cold
applications should not be allowed. If the haemorrhage is
profuse moderate doses of morphine should be given hypoder-
mically (f i gr). If the blood is not fully expectorated, but
tends to accumulate in the lungs, morphine should not be
given. The bowels should be freely moved with salines as
this tends to reduce the blood pressure. Nitro-glycerin
should not be given because of its stimulant action on the
heart.
The use of the time-honored astringents is of little or
no value in these cases, but, like salt, of which the patient's
friends will probably insist on his partaking in spoonful
doses, if they serve to reassure the patient and modify the
pernicious activity of his friends, there can be no harm in
their administration. Ergot is probably more harmful than
beneficial in these cases. The blood tension is usually high,
and if so the bleeding will probably continue until it is low-
ered through the effect of drugs or the loss of blood. Ergot
maintains the vascular tension and its beneficial action,
through contraction of the particular vessels involved, is
decidedly problematical. The use of aconite in sufficient
doses to lower the blood pressure is much more rational and
effective. Two-drop doses of tincture of aconite root, with
ten grains of sodium bromide, may be given every hour or
two until the blood pressure is relieved and the patient
quieted. The action of aconite should be carefully watched.
In haemoptysis accompanying cardiac disease strych-
nia and digitalis should be given. The necessity of reliev-
ing the stagnation of blood in the lungs is much more ur«
gent than is the danger of a moderate increase in the blood
pressure, in fact the former effect can only be produced
through the latter means. In some cases when the right
heart is over-filled, venesection may be indicated, indeed,
in the severe form of haemorrhage accompanying lobular
pneumonia with high blood pressure, venesection is the
quickest way to relieve the tension and stop the bleeding.
Dry cupping may be of service in some cases.
The diet should be light and easily assimilated. Milk,
meat-essences etc., are best. The after treatment involves
hygienic and climatic measures as well as general tonic med-
ication. Alcohol and tobacco should be prohibited.
CHAPTER X.
PNEUMONIA.
Pneumonia (lobar, croupous, fibrinous) is an acute in-
flammation of the lungs of infectious origin. It has special
aetiological, pathological and clinical features which distin-
guish it from other acute inflammations of the lungs. These
characteristics are so distinctive that it is advisable to re-
strict the unqualified term pneumonia to the affection under
consideration.
Pneumonia may be primary or secondary. In its pri-
mary form it is most common in the temperate zone and is
usually sporadic or endemic. It may occur in an epidemic
form (Sturges and Coupland), especially when accompany-
ing or following epidemics of influenza. Pneumonia is more
common in winter and spring, and the monthly variations of
its incidence follow those of scarlet fever and diphtheria
(Folsom). Men are more often affected than women (2^ to 1).
While no period of life is exempt, pneumonia is less fre-
quent in infancy than in adult life, being most common from
the second to the fifth decades of life. The time-honored
idea that pneumonia was a disease of robust constitutions
only, was due to the fact that this type of individuals ex-
hibit mainly the sthenic form of the disease and not the
atypical forms from mixed infections or secondary inflam-
mations.
Apparently, the death rate from pneumonia has in-
creased since 1852, though to some extent this is due to the
better classification of atypical cases, especially those which
simulate typhoid fever.
^Etiology.—Pneumonia is due to infection of the lung
with microorganisms. To regard the local conditions
simply as the characteristic expression of a general disease
is no more rational than to attempt to explain the symptoms
and clinical course of the disease by the altered mechanical
216
PNEUMONIA.
relations of the heart and lungs without reference to the
toxic conditions which arise during its course. The exact
relations of the subsidiary aetiological factors of pneumonia,
in lessening the resistance of the individual or in producing
a favorable culture field for the growth of organisms, are
questions which are yet largely undetermined.
The extent to which direct infection or contagion is
possible in pneumonia, is a matter of discussion. While it is
evidently not actively contagious in the sense that small-
pox is, still, numerous reports indicate the possibility of di-
rect transmission of the infection, especially when the sub-
ject has been exposed to predisposing causes.
The names of Klebs. Sternberg, Friedlander, Frankel
and Klein are most intimately associated with the bacteriol-
ogy of pneumonia. The work of these observers, together
with that of Talamon, Weichselbaum and others, has dem-
onstrated that pneumonia is accompanied by the presence
and development of microorganisms in the inflamed lung
tissue but that neither the pneumococcus of Frankel (Micro-
coccusPneumoniaeCrouposae,Diplococcus Pneumoniae, Micro-
coccus Pasteuri,—Sternberg), Friedlander's Bacillus (Bacil-
lus Pneumoniae) or Klein's Baccillus (Bacillus Pneumoniae)
are invariably present in pneumonia.
Frankel's pneumococcus is most frequently met with
and appears to be most pathogenic of pneumonia. It may
be present in the secretions of the mouth, nose and bron-
chial tract of healthy individuals. These various organisms,
together with the streptococcus pyogenes, staphylococcus
pyogenes aureus or albus and other organisms, may be pres-
ent collectively or separately in pneumonia. Again, any or
all of these organisms may be impossible of demonstration.
Various lesions independent of pneumonia may be caused by
the pneumococcus.*
Exposure to cold, mechanical injury or chemical injury
of the lung does not directly produce pneumonia.
*According to Pearce the pneumococcus is invariably present in lobar pneu-
monia and its complications. Its presence in pure culture in the majority of cases
indicates its aetiological relations. General infection, in fatal cases, is quite fre-
quent and therefore of considerable importance both from a bacteriological and a
clinical point of view.
PNEUMONIA.
217
Climatic conditions have much to do with the preva-
lence of pneumonia. From November to March is the pe-
riod when pneumonia is most apt to occur. The sudden
changes of temperature, and the great degree of atmos-
pheric moisture common to this period, are particularly
favorable to the development of pneumonia. The low tem-
perature and dry, penetrating winds of high altitudes may
favor the occurrence of pneumonia. Duerck has shown that
in persons dead from other diseases than pneumonia,' the
lungs may contain bacteria similar to those found in pneu-
monia, especially the diplococcus pneumoniae; that injec-
tions of bacteria into the trachea of animals was not fol-
lowed by pneumonia unless irritating substances were also
injected, which latter, on exposure to cold alone, also
caused pneumonia. Eshner thinks the harmful effect of
cold depends on the resulting hyperaemia of the lungs. The
fact that the pneumococcus can lose its virulence and then
revert to its original type, biological characteristics and
virulence (Kruse and Panisi, Eyre and Washbourn) may ex-
plain some features which seem irreconcilable with the bac-
terial origin of pneumonia.
Overwork, bodily injury, mental exhaustion, poor food,
alcoholism, etc., may predispose to the development of
pneumonia. Bright's disease, typhus fever, typhoid fever,
erysipelas, rheumatism and influenza are the diseases most
frequently predisposing to secondary pneumonia. During
the last few years influenza has been especially prominent
as a factor in the causation of pneumonias which have been
marked by the atypical nature of their course and the mixed
character of their infections.
Pneumonia is apt to recur in persons who have once
been affected with it.
Morbid anatomy.—Pneumonia occurs more often in
one lung than in both, the right lung being most often af-
fected (2 to 1). In the majority of cases the disease begins
in the lower portion of the lower lobes and spreads so as to
involve'a portion, the whole, or even more than a single
lobe. It may, however, begin at any point and involve any
218
PNEUMONIA.
amount of tissue. It is frequently confined exactly to the lim-
its of a single lobe. The middle lobe of the right lung is
seldom affected except in association with other portions of
the same lung. In children the apices are affected more fre-
quently than in adults, the left lung being also more often in-
volved.
The pleura over the inflamed area is usually involved
and inflammation of the pericardium, bronchial glands, med-
iastinal tissue,peritoneum and meninges are frequent accom-
paniments.
The inflammatory process in pneumonia consists of three
stages: the stage of engorgement; the stage of red hepa-
tization and the stage of gray hepatization.
Engorgement. In this stage the lung is exceedingly vas-
cular and there are the ordinary changes in the vessels
characteristic of inflammation. The lung is dark red and
its specific gravity and absolute weight are increased; its
elasticity is lessened, it is less crepitant and more friable
than normal and pits on pressure. Sticky, frothy, reddish
fluid exudes on section.
Red Hepatization. In this stage there is exudation of
liquor sanguinis and migration of blood cells into the lung
tissue. Extravasations of blood may occur from the rup-
ture of small vessels. The exudation coagulates in the air
cells and terminal bronchioles forming a semi-transparent
coagulum entangling leucocytes and red corpuscles in its
meshes. The fibrin filaments are most numerous in cases
due to the diplococcus pneumoniae (Wichselbaum). Mononu-
cleated leucocytes are as numerous as multinucleated, and
pneumococci may be present in both.
The lung is increased in size and may show the impres-
sion of the ribs. It is heavier than in the first stage, solid,
sinks in water and cannot be inflated. The pleura covering
the inflamed area is opaque and covered with lymph. The
prominent, firm, dark area of inflamed lung can be recog-
nized before section is made. The lung tissue does not
crepitate, is friable and tears with a granular fracture. The
coagulations project from the alveoli and bronchi and can
PNEUMONIA. 219
be lifted or pulled out. There is irregular hyperaemia of
the adjacent tissue but no lobular involvement. Beyond
swelling and granulation, the alveolar epithelium sustains
little change as, also, do the walls aside from containing a
few leucocytes. The color of the lung is dark reddish-
brown, grayish or marbled.
Gray Hepatization. In this stage the leucocytes fill the
alveoli and infiltrate the alveolar walls whose epithelial
cells have become more swollen and granular. The tissue
has a uniform appearance having lost the granulations of
the first stage. Disintegration of the fibrin, decolorization
of the red cells and fatty degeneration of the white cells oc-
cur, with, in advanced cases, partial destruction of the al-
veolar walls.
The weight, density and friability of the lung is in-
creased; its tissue is soft and pulpy. A puriform liquid ex-
udes from the cut surface and the color becomes irregularly
gray or yellowish white owing to fatty degeneration of the
cells and to post mortem expression of blood (Rindfleisch).
Advanced stages of gray hepatization have been termed
"purulent infiltration" and "suppuration" of the lung.
These stages of the morbid process in pneumonia pro-
gress irregularly in different portions of the lung and may
advance rapidly or slowly. The bronchi of the affected
area are more or less inflamed and contain a blood-stained
mucus or a dark, watery exudation if the lung is cedema-
tous.
The blood of a pneumonic patient, when drawn, coagu-
lates slowly. The red corpuscles having settled, the clot
has a "buffy coat." This condition (hyperinosis) is not char-
acteristic of pneumonia. A greater or less degree of leu-
cocytosis (Piorry) is usually present. According to Cabot,
leucocytosis is present early and continues throughout the
febrile period; it diminishes just before or at the crisis and
disappears gradually after the fall of temperature; if infec-
tion is slight and reaction vigorous, leucocytosis is slight;
if infection is marked and reaction also, leucocytosis is con-
siderable; if infection is marked and reaction is slight, leu-
cocytosis is absent. In other words, leucocytosis may be
220
PNEUMONIA.
regarded as evidence that the system is putting forth an
effective struggle against the infection.
Pneumococci may be found in the blood. Their pres-
ence there gives, according to Kohn, an unfavorable prog-
nosis as there may be a "pneumococcus sepsis" as a cause
of death.
The morbid process in the lung in pneumonia may ter-
minate in resolution, abscess, gangrene, or cirrhosis of the
lung.
Resolution is effected through degeneration and absorp-
tion of the inflammatory products. It is doubtful if re-
covery ever ensues from advanced stages of gray hepatiza-
tion. According to Weismayer the presence of streptococci
should lead us to expect delayed resolution.
Abscess is a rare result of pneumonia. Pye-Smith con-
siders it extremely rare, and undoubtedly it is, as a direct
result of fibrinous pneumonia, but as a secondary result
either of circumscribed gangrene or of delayed resolution
from associated pleurisy or empyema,particularly in connec-
tion with mixed infections, abscess is occasionally found as
a result of pneumonia.
Gangrene is very rare and occurs in debilitated subjects
from coagulation of blood in the pulmonary or bronchial
vessels, extensive extravasations of blood or from septic
conditions of the inflammatory products.
Cirrhosis. In delayed resolution in pneumonia the al-
veolar walls may become involved in a new growth of fibro-
nucleated tissue which may very rarely develop into a
fibroid induration or interstitial pneumonia of varying ex-
tent (Addison's "marbled induration"). As a result of
croupous pneumonia, however, this termination is very
rare.
Clinical history.—While in some instances the de-
velopment of pneumonia may be preceeded by irregular
pains, anorexia, and general malaise, and, in cases of mixed
infection, the development may be slow and indefinite, in
the majority of cases of typical pneumonia the onset is
sudden, preceeded only by headache or a nervous chilliness
or shivering. Sudden pyrexia followed by sudden and se-
PNEUMONIA.
221
vere rigor in adults, or vomiting or convulsions in children,
marks the incidence of the disease. When the chill has
passed the patient is prostrated and the headache may con-
tinue. The skin is hot and dry, the pulse quick, the tem-
perature reaches from 103° to 104° F. within a few hours.
Pain in the affected side may be very acute and may be the
chief source of distress. It is increased by breathing,
coughing or movement. There is short, irritating, hacking
cough usually most troublesome in apical pneumonias and
in children. The breathing is rapid, panting in character
and shallow if there is much pain. A marked feature of the
clinical history is the change in the pulse-respiration rate,
the normal ratio of 4 1 being altered to 3-1 or 2-1, so that a
pulse rate of 90 may accompany a breath rate of 40. There
is slignt morning remission and evening exacerbation of
temperature. The urine is scanty, dark, of high specific
gravity; the urea and uric acid are increased, the chlorides
diminished and it may contain albumen, blood and fibrinous
casts.
The sputum is at first frothy and scanty but soon be-
comes viscid and tenacious. It sticks to the mouth or lips
and adheres to the sputum cup. It usually assumes a char-
acteristic rusty-brown color but may be thin and of a dark
brown hue (prune-juice expectoration). The sputum con-
tains blood corpuscles, epithelial cells, mucoid cells, granu-
lar cells, oil globules and sometimes casts of the finer
bronchi.*
The face, especially the cheeks, is flushed and of a
dusky-red or purplish color. In some cases dyspnoea and
cyanosis may be marked, though the latter may be present
without the former.
In typical cases, for a period of from five to ten days,
there is little change in the patient's condition beyond cessa-
tion of pain and headache, lower tension of the pulse, less
•Chemically, the sputum is marked, during the febrile period, by the absence of
alkaline phosphates, excess of potash over soda, excess of sulphuric acid (Bam-
berger),26 pericent. of fixed salts as compared with 18 per cent.in normal mucus—the
greatest increase being in the sodium chloride. During resolution these charac-
teristics disappear.—Fowler.
2 22
PNEUMONIA.
flush in the cheeks, disturbed sleep with irregular delirium,
brown and dry tongue with dry and fissured lips, more or
less tenacious sputum and in some cases a small collection of
herpes labialis or facialis. At any time from the third to
the tenth day, but usually from the fifth to the eighth day,
there occurs the "crisis."*
The first sign of the crisis may be a great change in the
general aspect of the patient, a transition from great an-
xiety, restlessness or delirium to calmness and assurance of
recovery such as occurs so suddenly in no other disease.
The patient sleeps; the skin becomes moist or there may be
profuse perspiration; the temperature falls to 98° or 97°
and the pulse to 60 or less; dyspnoea and delirium disappear.
The temperature rises on the following day to 99.5C or 100c
and then falls to normal or slightly below for the first days
of a convalescence which usually occupies from two to three
weeks,
This typical clinical course is subject to very great va-
riations in the various clinical types of identical infections,
infections of different nature, mixed infections and from
complications.
Among the most dangerous of the irregular forms of
pneumonia in which special forms of infection cannot be
demonstrated are the secondary pneumonias which compli-
cate typhoid fever, typhus, relapsing fever, small-pox, ery-
sipelas, septicaemia and sometimes diphtheria or scarlatina,
nephritis, diabetes, alcoholism, cardiac disease and those
which occur after surgical operations. In many of these
instances the pneumonia can be demonstrated as of a septic
type, but often this cannot be done. These pneumonias are
marked by absence of rigor, gradual and irregular rise in
temperature, absence of pain though pleurisy may be ob-
served on physical examination, absence of expectoration
and of the characteristic condition of the urine. They are
essentially latent in type, convalescence is protracted and
the mortality rate is high.
*The crisis occurs most frequently on the seventh day from the initial rigor (24
percent.), on the fifth day in 15-16 per cent., sixth or eighth days in 12 per cent.,
ninth day in 10 per cent., and in all cases between the fifth and ninth days in 72
per cent.—Fowler.
PNEUMONIA.
223
Primary pneumonia may also show great variation in
its clinical course in the character of the onset which may
be marked by great restlessness or delirium especially in
debilitated or alcoholic subjects or in apical pneumonia es-
pecially in children. The expectoration may be muco-puru-
lent, greenish or bloody (haemorrhagic pneumonia) especially
in old people.
The crisis may occur with slight fall of temperature
which rises again to its previous height and defervescence
may occur by lysis or there may be no critical period.
The temperature may rise gradually or suddenly and
then vary from 101° to 103°, defervescence being by lysis.
Great variation is shown in the temperature charts of irreg-
ular cases. In some degree the temperature shows the
vital resistance of the individual.
Gastro-intestinal symptoms may be marked. Vomiting
at the onset is common in children. Diarrhoea may be
troublesome at the outset or at the crisis,especially in septic
pneumonia.
Among' the types of pneumonia which present charac-
teristic departure from the ordinary course of the disease is
latent pneumonia which occurs in debilitated subjects and in
the aged. The clinical course of this type and the physical
signs are so indefinite that a diagnosis is often deferred
until post mortem. Migratory pneumonia is a form of the
disease in which there is successive invasion of other por-
tions of the lungs co-iucidently with resolution in the por-
tions primarily affected, each invasion being marked by the
usual clinical features of the disease. Epidemic pneumonia
is met with apart from the influenza pneumonias (Fox,
Whitelegge, Sturges and Coupland). Particular epidemics
are characterized by special clinical features as a rule.
Bilious pneumonia is a type which is said to be associated
with pneumonia of the right lung and not to affect the course
or prognosis of the disease (Pye-Smith). My own exper-
ience in this regard is directly contrary to this opinion.
According to Banti the icterus is due to accidental haemo-
lytic action of the diplococcus and is therefore haemogenic.
The clinical course of the following case would agree
224
PNEUMONIA.
with the haemogenic theory of the origin of the icterus.
Man aged 56 years. Height 5 feet, 8 inches, weight 215
pounds. Manufacturer. Had syphilis twenty years pre-
vious to present illness. Subsequent health good. Present
illness of five days duration, began with slight chill. The
temperature reached 102° on the second day but never ex-
ceeded that point. No pain, little cough, no expectoration,
moderate delirium. Examination showed complete consoli-
dation of lower lobe of right lung. The bowels were loose,
three to four small, thin, dark but not offensive passages
daily. On third day of illness developed jaundice which
gradually became quite marked and of a brownish yellow
hue. The pulse was above 110 and feeble. Delirium and
stupor continued. Pulse became more rapid. Jaundice
persisted. Death on seventh day.
Various other types of pneumonia are described, such
as typhoid, recurrent, pythogenic, cerebral, intermittent,
ephemeral, alcoholic, senile, etc., but they have no features
not common to irregular forms of any of the regular types
of the disease.
Among the irregular forms of pneumonia which are due
to a different form of infection and in which the pneumo-
coccus has a subsidiary part or is absent altogether, is the
influenza pneumonias and septic pneumonia. Since the ad-
vent of influenza in epidemic form, many cases of pneumonia
have followed an irregular course marked principally by er-
ratic clinical course and indefinite physical signs. The fol-
lowing case may be classed as one of influenza pneumonia:
Young woman aged 24 years. Previous health good.
March 29th, 1896 was taken ill with fever and slight cough.
No chill. Temperature 101°. No pain, tongue slightly
coated, no flush on cheeks, no physical signs. On the 22nd,
slight dullness over lower lobe of left lung. On the 24th
the dullness was marked and faint bronchial breathing
could be heard. The limits of the inflamed area could not
be determined. The sputum was scanty, mixed with air and
never rusty. It contained numerous organisms which cor-
responded morphologically to the characteristics of the in-
fluenza bacillus. No pneumococci were found.
The course of the disease was protracted. The temper-
ature remained about 101° until the 3rd of April when it be-
gan to decline, but did not reach normal until the 10th of
April. The physical signs began to clear as the tempera-
PNEUMONIA.
225
ture declined but the breathing was diminished for some
time after the temperature had subsided.
Septic pneumonia may occur in connection with puer-
peral or surgical sepsis or pyaamic conditions from any
cause. In some cases its origin is difficult to determine.
The following case was probably due to infection through
the intestinal tract:
Professional man, aged 45 years. Height 6 feet, 1 inch;
weight 210 pounds. Athletic, vigorous constitution. Had
been overworking for two years. Was taken sick on Tues- -
day. I saw him first on Sunday. The temperature had
ranged from 101° to 103°. Pulse 110 to 120. Moderate
diarrhoea, slight delirium. There was no pain in the chest,
no cough or expectoration. Headache was constant.
At the base of the right lung there was slight dullness
and harsh breathing. The abdomen was slightly tympani-
tic and tender. Widal'stest and the Diazo reaction were neg-
ative. By Tuesday the temperature was 104°, pulse 120 and
the signs of consolidation in the right lower lobe were con-
clusive. There was moderate leucocytosis. The sputum
was scanty, frothy and contained a very few pneumococci, a
number of staphylococci and a few influenza bacilli(?).
There was no special change in the patient's condition for
six days, the temperature varying from 101° to 104° and
the pulse from 110 to 120, the delirium continuing as did the
slight cough, expectoration and irregular diarrhoea. At
the end of six days the temperature began to decline and
after switching between 99Q and 102° for five or six days
reached the normal and improvement was then slow but
steady. The illness was followed by marked mental and
physical exhaustion from which recovery was gradual.
The mixed infections whose organisms are associated
with the pneumococcus either from the beginning of the at-
tack or during the course of the disease, cause marked ir-
regularity in the clinical history of pneumonia, as is exhib-
ited in the following case:
Miss S, aged 22 years. -School-teacher. Taken sick
November the 15th with a typical attack of pneumonia. The
temperature ranged,for the first six days, from 102.5Q in the
morning, to 103.4° in the evening. The patient was very
restless. On the seventh day the temperature was 101.8°
and 10.2° and the patient seemed better though there was no
perspiration. The pulse was five or six beats faster and
the respiration about the same (45). Examination at this
226
PNEUMONIA.
time showed commencing resolution in the left lung which
had been involved. The right lung was clear. Eighth day,
temperature 103°; ninth day, 103.6° and 104.2°. Examina-
tion showed that resolution was progressing in the left lung
and that there was no evidence of pleural involvement. Un
derneath the spinal border of the right scapula there was a
patch of lobular pneumonia which was not there on the
seventh day. Examination of the sputum at this time
showed pneumococci in abundance, a great many staphylo-
cocci and a few streptococci. On the 13th day the patient
commenced to perspire, the temperature was 101.2° and
100.6°, and on the 14th day 98.8° and 97.8°. The respira-
tion and pulse were unusually rapid at this period, being 46
and 100 respectively. A slow but steady convalescence
ensued.
The complications which are most likely to modify the
clinical course of pneumonia are pleural effusion, empyema,
pericarditis, endocarditis, myocarditis, meningitis, paroti-
tis, bronchitis, emphysema, valvular lesions, nephritis and,
according to Bristowe, colitis.
Pleurisy is considered as part of the history of pneu-
monia by some observers and though some degree of pleu-
ral inflammation is usually present it is not invariably so and
for clinical purposes pleurisy may be regarded, when it can
be recognized, as a complication. Pleurisy with effusion is
present in about 25 per cent.of the fatal cases. Pneumococ-
ci are generally found in the exudation. The pleurisy may
come on at the time of hepatization (para-pneumonic.—
Lemoine) and the exudation is then apt to be serous. In
children and young people the pleurisy is apt to be purulent
and come on at, or immediately after, the crisis. [In a re-
cent case of apical pleuro-pneumonia in a child, the acute
pleurisy apparently subsided, but after the crisis the tem-
perature immediately returned to 102° and empyema devel-
oped.]
Pericarditis is a grave complication (one-half cases fatal.
—Huss) It may occur when any portion of either lung is
affected. Pneumococci are found in the exudation. The
crisis of the pneumonia is incomplete and the febrile period
prolonged. Ulcerative endocarditis may complicate pneu-
monia (11 per cent, of fata cases.—Osier) and pneumococci
PNEUMONIA.
227
are found in the vegetations. Acute and chronic endocar-
ditis frequently complicate pneumonia, the latter in 17 per
cent, of fatal cases and occurring most often in connection
with pneumonia of the right lung. Myocarditis may be
expected in connection with all severe cases of pericardi-
tis or endocarditis associated with pneumonia, but it also oc-
curs independently, from toxaemia, and is evidenced by
oedema of the lung. The latter condition is present in fifty
per cent, of the fatal cases of pneumonia. Bronchitis and
empyema are frequent complications. The former may
be especially dangerous.
Parotitis occurs at or after the period of crisis, usually
in elderly people. Suppuration is the rule and gangrene
may follow. Meningitis is a rare but usually fatal compli-
cation of pneumonia. Other complications are met with
which modify the clinical history chiefly in regard to the
period of convalescence.
Death from pneumonia rarely occurs before the fourth
day of the disease. The period of greatest danger is from
the fifth to the ninth day. When the crisis is delayed or
the temperature drops a degree or two and then returns to
its former height, search should be made .for some disturb-
ing element. Exclusive of infants, the death rate steadily
increases as age advances. Hospital mortality is greater
than that of private practice. As to children, opinions dif-
fer. Females show a greater mortality than males (in 33.
606 cases; males 19.4 per cent., females 28.7 per cent.—
Wells). Various statements are made regarding the gener-
al mortality of pneumonia. If statistics prove anything
they show that pneumonia is a fatal disease. [The statis-
tics of Dr. E. F. Wells— Jour. Am. Med. Ass'n, June 9, '92,—
233,780 cases of pneumonia collected from various sources
show a mortality of 18.1 per cent. Recent figures furnished
me by Dr. Wells bring the total number of cases up to date
to 366,544, with a mortality of 17.6 per cent.]
According to Osier the mortality statistics are -uniform
and, apart from complications, death is due to toxaemia or
mechanical interference with the heart or respiration. In
sudden death the action of the specific toxins on the heart
228 PNEUMONIA.
center is more important than the effect of fever on the
heart.
Symptoms and diagnosis.—A few hours after the
onset of pneumonia the patient presents a somewhat char-
acteristic appearance. He lies on his back if the disease is
central or basic, or on the side if there is pleurisy and much
pain. His expression, in the former instance, may be rath-
er dull and apathetic, while in the latter case it will be anx-
ious and he will be restless. The skin is hot and burning,
the face flushed and the cheeks, over the malar prominences,
will be red or purplish. The alae nasi dilate with respira-
tion which is short, quick and panting in character. The
full, strong pulse, high temperature and short, hacking
cough complete a picture of serious illness which the physi-
cal examination, at this time, fails to corroborate. In no
other disease will a person be so ill and yet, apparently,
have so little the matter with him, as in the first stage of
pneumonia, except, perhaps, some types of influenza. Al-
butt says that a "sure diagnosis can be made from the as-
pect of the patient, the pain, the sputum, the urine and the
fever, without the aid of percussion and auscultation.''
Nevertheless physical examination remains the only method
of ascertaining the exact nature, location and extent of the
disease.
Within a period, which varies with the type of the dis-
ease, of from a few hours to the second day after the onset,
we can detect evidence of the morbid process in the lung.
Inspection, palpation and percussion are usually negative
though there may be slight restriction of motion, and per-
haps slight dullness On auscultation over the inflamed
area the respiratory murmur is suppressed as compared'
with other portions of the lung. It may be slightly harsh
and later becomes broncho-vesicular in character. Just
before or coincidently with these indefinite signs we may
be fortunate in hearing the diagnostic sign of the first stage—
the crepitant rale ("le signe pathognomonique du premier
degre' de la peripneumonie."—Laennec). This sign lasts but
a short time and is frequently not heard at all. The indi-
viduality of the crepitant rale has been denied by some ob-
PNEUMONIA.
229
servers, it being identified with pleuritic sounds by them
It is, however, entirely distinct from pleuritic friction.
Crepitant rales take place immediately at the end of the
audible inspiratory sound and occur as a bunch of very
fine crepitations occupying but a second of time and pro-
ducing on the ear an impression of numerous, individual but
simultaneous sounds, similar to the impressions made on the
eye by the numerous but individually distinct lights of a
Roman candle at the immediate time of explosion.* When
heard a few times this rale is readily recognized and is sim-
ulated only by the rale of oedema, from which it is distin-
guished by its later occurrence and the more liquid quality
and scattered occurrence of the rales of oedema.
By the third or fourth day the signs of consolidation be-
come well marked. Motion is much decreased. Fremitus
may be increased, or absent if there is much tissue involved
and little air in the lobe. Percussion gives a dull, high-
pitched note. On auscultation the vesicular sound is en-
tirely lost and the breathing is bronchial in character—soft,
high-pitched and blowing in quality and distant from the
ear. If, however, a large portion of a lung is involved and
the tubes are filled with mucus, bronchial breathing may be
entirely absent. Bronchial breathing is plainest during ex-
piration, and in central pneumonias may, perhaps, be heard
only during that portion of the respiratory act.
Bronchophony is well marked in this stage and in some
cases modified pectoriloquy may be heard. The breathing
in the uninvolved portion of the lung is exaggerated. These
physical signs, together with the high temperature, charac-
teristic pulse and other symptoms, continue until the crisis
is reached. When this has occurred if we examine the lung
*Thc physical explanation of the crepitant rale is ever in dispute. It is gen-
erally taught that it is due to the separation, by the air, of the walls of the terminal
bronchial passages or the alveoli. This is objected to by those who hold that the
air enters those pussages only by diffusion. They claim that the crepitant rale is a
moist, bubbling rale. It would appear that the time of occurrence of the crepitant
rale and the absence of a moist quality is not consistent with the latter theory, for,
if the air interchanges in the smaller passages by diffusion alone the air cannot
produce a rale at this particular time. Moreover we would call attention to the
possibility of introducing oils directly into the alveoli by the inspired air (Thomas
Jour. Am. Med.Ass'n.—May 28, l^flsi.
230
PNEUMONIA.
we find the local conditions unchanged and it appears sur-
prising that such a remarkable change should occur in the
general condition of the patient and the local condition in
the lung remain apparently unchanged. The phenomenon
of the crisis in relation to the local condition of the lung is
an effective argument in behalf of the toxic origin of the
general symptoms of pneumonia
About, or shortly after, the crisis, examination of the
lung will show moist crackling rales (rales redux) at the
periphery of the portion first consolidated. More air is
heard entering the affected lung, the rales spread all over
the affected area and resolution is well under way. Dullness
will disappear within a few days unless pleural exudation or
interstitial pneumonia maintain the percussion pitch. Many
modifications in the physical signs may occur.' The clear-
ness with which they present will depend on the absence of
pleural exudation and adhesions and on patency of the tubes
leading to the consolidated area. When the tubes are con-
solidated, no signs beyond dullness and loss of motion may
be obtained.
The most unfavorable symptoms in pneumonia are a
rapid, weak pulse, especially if the second pulmonic sound
becomes gradually more short, snappy and intense; an ir-
regular or intermittent pulse; cyanosis and rapid breathing,
though cyanosis does not always depend on the mechanical
obstruction in the lesser circulation but bears some relation
to the toxaemia. Tympanitis, hiccough, subsultus tendin-
um, delirium, and hyperpyrexia are unfavorable symptoms.
Apical pneumonia and double pneumonia of the bases are
most likely to show unfavorable departures from the usual
course of the disease.
Among those conditions whose physical signs simulate
pneumonia, is pleural effusion, which is identified by the
greater loss of motion, greater compensatory motion, apex
displacement, loss of fremitus, flat percussion note with
curved upper line of dullness, better marked sub clavicular
Skodiac resonance, absence of vocal sounds over fluid, or at
least a modified form of pectoriloquy or egophony, espec-
ially in children. (Tubular breathing may be heard on the
PNEUMONIA.
231
left side at the lower angle of the scapala when the lung is
much compressed by the fluid.) The affected side is usually
increased in size in pleursy with effusion.
Aggregated areas of tubercular consolidation may simu-
late pneumonia, but its course and the sputum examination
will decide. Large infarctions with pleural effusion may
resemble pneumonic consolidation. The erect position of
the patient, the severe and sudden dyspnoea, and probably
the presence of chronic heart lesion will aid the di-
agnosis.
The asthenic, septic form of pneumonia may be mistaken
for typhoid fever. Widal's test, and the presence of leucocy-
tosis in pneumonia, will help differentiate if the physical
signs are not conclusive before these tests are reliable.
Meningitis in children simulates pneumonia before the
development of physical signs in the latter disease. In
meningitis the cry, the attitude, retraction of the head and
abdomen, the cerebral type of vomiting, intolerance of light
and the simultaneous occurrence of headache and delirium,
will distinguish it from pneumonia.
(Edematous crepitation may be mistaken for pneumonic
crepitation. The former is more widely disseminated, softer
and more liquid in-quality and is not followed by signs of
complete consolidation.
Treatment.—In view of the mortality rate of pneumo-
nia its treatment becomes a most important matter. As an
infectious disorder of self-limited course it is evident that
the natural tendency is toward recovery which would occur
in all cases if we could avoid certain contingencies. This
fact is only emphasized by the low mortality rate, under
widely different methods of treatment, obtained in certain
series of cases by different observers. That these contin-
gencies do not depend on the extent or stage of the pulmo-
nary lesion is shown by the rapidity of the post-critical
change in the general condition of the patient and the fact
that the mortality rate shows no direct relationship to the
degree of pulmonary involvement. Aside from the compli-
cations due to identical or associated infections we must
consider then, that the phenomena of the disease, aside from
232
PNEUMONIA.
the local condition of the lung, as well as most of its dan-
gers, are due to toxaemia.
The phenomenon of the crisis is generally admitted to
be due to the development, during the course of the disease,
of an anti-toxin, and experimental work has lately been di-
rected towards the production of an artificial serum contain-
ing these anti-toxic properties. The Klemperers, Bonome,
Emmerich and others have proved the possibility of protec-
tion from pneumococcus infection in aninals by the use of
immunized serum. Washbourn has succeeded in producing a
standardized serum from which he reports good results, De
Renzi and others report favorable results from similar
serums. While the outlook is favorable for the production
of a serum with which we may mitigate the severity of the
disease, if, indeed, we may not cut short its course, the
matter of serum therapy in pneumonia is entirely in
an experimental stage at present. In the meantime we
must adhere to a more or less expectant plan of treatment
into which routine, dogmatic methods of cold baths, hot
baths, ice coils and heroic dosing of any sort must not be
allowed to overshadow individual indications. Our main
efforts should be to lessen the effect of the toxins on the
heart and nervous system and to keep up elimination.
The diet of the pneumonic patient should be light and
easily assimilated. Milk is best but soups,broths or any of
the concentrated foods may be used. The forced feeding of
large quantities of food is very objectionable as it is apt to
result in digestive disturbances which interfere with the
action of the diaphragm. In an adult, not over two quarts
of milk should be allowed in twenty-four hours. The food
should be given about every four hours
The patient's chest should be covered with a wadding
jacket cut in two sections and pinned over and under the
arms.
During the first stage of the disease we must allay the
general nervous and vascular excitement. Aconite and ver-
atrum viride are the best remedies for this purpose. I pre-
fer the former as being safer and fully as efficient as the
latter. Ten grains of sodium bromide, one half drop of
PNEUMONIA. 233
tincture of aconite root and twenty drops of liquor of the
acetate of ammonia or of sweet spirits of nitrous ether,
every two hours, makes a useful combination for this stage.
If much pain is present there is no objection to a hypoder-
mic of morphine or the addition of one-half agrain of codeine
to the above mixture. If the skin is dry and burning and
there is headache, three grains of phenacetine with two
grains of sulphate of quinia (in capsules) every three or four
hours will relieve these conditions as well as modify the
temperature if it is high. If there is severe pleurisy pain,
especially in the apical pleuro-pneumonias of children, a
hot poultice will give much relief. There are objections, of
course, to their unskillful application, but these do not apply
when a little care is taken.
It is well to begin the treatment of a case with moderate
calomel.purgation. The bowels should not be allowed to
become constipated at any stage, especially if the patient is
on a milk diet, as the dry feces may become impacted in the
rectum and have to be dug out. Teaspoonful doses of Hus-
band's magnesia will be useful for a laxative during the
progress of the case.
The cough and expectoration may be made easier by
giving from five to seven grains of muriate of ammonia, one-
sixth of a grain of codeine and twenty drops of liquor of
the acetate of ammonia in syrup of tolu every two or three
hours. It is well to continue this throughout the disease
and to combine with it five grains of potassium acetate to
promote elimination by the kidneys, the codeine being left
out if necessary. Plenty of water should be allowed the
patient between the hours of feeding. Tepid sponge baths
should be given twice daily. The patient's mouth should
be rinsed frequently with equal parts of peroxide of hydrogen
and water.
The temperature need cause no alarm unless it keeps
persistently in the neighborhood of 105° F., which is seldom
the case if the capsules mentioned above are used. If it does
we may resort to cold baths, cold applications, or ice coils
as is deemed best. The heart should be carefully
watched. The strain is on the right ventricle and can be
234 PNEUMONIA.
best judged by the force of the second pulmonic sound.
When this becomes louder, more snappy and high-pitched,
the right side of the heart needs support. This aid is best
given by strychnia. It is good policy to begin the adminis-
tration of strychnia early, giving 7V of a grain three or
four times in twenty-four hours. When the right heart
shows strain the strychnia should be pushed, giving ^ of
a grain every two to four hours by hypodermic. In desper-
ate cases ^3 of a grain may be given every two hours.
One young man,seen in consultation, took,.from the sixth to
the ninth day, TV of a grain of strychnia every two hours
night and day, and during a portion of this time TV every
hour for six doses. One to two ounces of whisky was also
given every two hours for a portion 6f the time. He re-
covered.
Digitalis may be used conjointly with the strychnia, in
which case digitalin is preferable, using about ^ of a
grain every four to six hours. As a rule I have not em-
ployed digitalis except in cases of pneumonia associated
with chronic cardiopathies. If, after the fourth or fifth
day, the pulse tends to become faster and the patient rest-
less or delirious, whisky in ounce doses should be given
with the strychnia every two to four hours until the crisis
is reached. I find, however, that I have used whisky very
seldom. At the time of crisis if the temperature falls below
98° F., and the pulse is weak and there is profuse perspir-
ation, a couple of ounces of whisky in hot water, dry fric-
tion of the body and a hot, dry blanket will aid matters
materially.
Venesection is seldom employed at present. There are
times, however, when it is useful. In the first stage of
sthenic cases with a full, high-tension pulse and great rest-
lessness, the abstraction of a few ounces of blood will give
great relief. Again, in the later stage, when there is much
lung tissue involved and the mechanical strain on the right
heart is great, venesection may be much safer and quicker
than to attempt to drain the blood into the peripheral vessels
by the vaso dilators, especially as these drugs are de-
cidedly dangerous at this stage of the disease.
PNEUMONIA. 235
Oxygen gas is of great utility Lin pneumonia, both in
those cases where dyspnoea and cyanosis seems to depend
largely on the reduction:]of breathing space, and in those
where prostration is so great that the labor of breathing is
telling on the vitality of the patient. While I cannot say
that I have known oxygen.to be the direct means of saving
life, I am sure it has prolonged life in a number of instances
and in others has done much towards tiding the patient over
the dangerous period. Nitro-glycerine is a remedy which,
if used at all, should be restricted to the first stage. In the
advanced stages, especially if the heart is weak and toxaemia
is well marked, nitroglycerine is a dangerous remedy
to use.
Among the special forms of treatment devised for
pneumonia.hydrotherapy has always been prominent. Cold
in the form of cold baths, applications, affusions, ice pack
or ice coil is variously recommended. Baruch advises
tubbing in children, with the water at 95° F., reducing ac-
cording to circumstances; for adults, the cold compress on
front or back of chest with the water at 60° F.; if there is
delirium, precede by cold affusions. Ice packs and coils are
recommended by many and undoubtedly are attended with
benefit in many instances. In children, however, they are
more difficult to apply than are warm applications. Hayem
thinks that cold baths are more powerful for good in child-
ren than in adults. Bozolo says that baths are well borne; do
not produce collapse; lower the temperature for a consider-
able time, and give the lowest mortality rate of any form of
treatment: they should be given every three hours. Hot
baths have teen recommended by some but have not been
much employed.
Large doses of digitalis as a routine treatment have been
actively advocated by Petresco, who gives from 90 to 100 or
140 grains of the powdered drug daily. His reports are favor-
able both as to its action on the temperature and on the mor-
tality of the disease. Barth advises a maximum daily dose
of 45 grains of the powdered leaf in infusion. Maragliano
recently claims to have established beyond doubt the spe-
cific action of digitalis on the pneumococcus. A small amount
236 PNEUMONIA.
will kill the cocci in cultures and will also neutralize the
toxicity of pneumonia toxins in injections. Patients
are able to take larger doses of digtalis because of its effect
in neutralizing toxins. If this be correct it may help to ex-
plain the seemingly inexplicable statements of Petresco.
Creasote internally (Casati) and by inhalation (Robinson),
formate of soda (Rochon) and many other remedies have
been specially advocated in the treatment of pneumonia, but
no specific value has become attached to them.
In delayed resolution of pneumonia we may adopt the
conclusions of Stengel: that in cases showing a tendency to
delay, as manifested by dullness and persistent broncho-
vesicular respiration; systematic breathing exercises, pul-
monary gymnastics, etc., are important; where marked
dullness persists, counter-irritation, tonics and stimulants
are indicated; the production of aseptic abcesses are of
doubtful utility and often impracticable.
In the various types of pneumonia the treatment must
be varied to meet the indications. We must remember,
however, that the symptoms, regular and ^irregular, are
mainly toxic in nature; that cerebral symptoms are more
likely to occur in cases showing marked toxaemia, come
early and have no relation to the amount of lung tissue in-
volved.
The complications of pneumonia may modify the man-
agement of the disease as they may become, temporarily,
the chief issue. They are to be managed as individual
affections with due regard to their connection with the
pneumonic condition.
CHAPTER XI
LOBULAR PNEUMONIA.
Lobular pneumonia (broncho- pnenmonia, catarrhal pneu-
monia) is an inflammation of the lung tissue occurring,
as a rule, secondary to inflammation of the bronchi. For-
merly it was regarded as due to direct extension of catarrhal
inflammation from the tubes to the alveoli, but the presence
of various septic organisms in lobular inflammation of the
lungs has modified this view more in accordance with the
clinical facts. Undoubtedly, in very young people, the so-
called simple form of lobular pneumonia occurs from direct
extension of a catarrhal inflammation of the bronchi. On
the other hand we find isolated areas of lobular inflammation
occurring in portions of the lungs where there has been no
previous bronchitis and which can only be explained by the
infection, by aspiration or otherwise, of the lobules in-
volved.
^Etiology.—Mixed infection is rather the rule than
the exception in lobular pneumonia. The various organ-
isms which have been identified with this form of pneu-
monia are the streptococcus pyogenes, the pneumococcus
of Friedlander, the staphylococcus, the colon bacillus, the
micrococcus lanceolatus and the tubercle bacillus. These
organisms may present singly or in any combination in lob-
ular pneumonia. [In Pearce's analysis of forty-six cases,
the most frequent single infection was by the streptococcus,
and the most frequently combined organisms were the
streptococcus, staphylococcus pyogenes aureus and pneu-
mococcus.]
Recognizing an anatomical and clinical distinction
between bronchiolitis and lobular pneumonia, it is appar-
ent, in view of modern bacteriological knowledge, that di-
rect infection or irritation of the lobules, through the aspir-
ation into them of organisms, or secretion, or both, is fre-
238
LOBULAR PNEUMONIA.
quently the cause of lobular pneumonia, and that the latter
occurs entirely independently of contiguous bronchial in-
flammation.
While lobular pneumonia is most frequent in infancy
and old age, it may occur at any time of life in weak and de-
bilitated subjects. Any influence which weakens individ-
ual resistance predisposes toward the development of this
form of pneumonia. The various causes of bronchitis, irri-
tation of the respiratory tract by the inhalation of gases,
dust, particles of carbon or metals, the aspiration of food,
saliva, blood or discharges of various kinds into the lungs,
infection by the organism of actinomycosis, the bacillus of
glanders or the specific infections of measles, whooping-
cough, diphtheria or variola may cause lobular pneumonia.
Bronchitis and tuberculosis are the diseases of the lungs
which most frequently cause lobular pneumonia. Tubercu-
lar lobular pneumonia is a marked feature of the clinical
history of acute pulmonary tuberculosis. Pulmonary in-
farction, abscess, gangrene, collapse, and traumatism may
cause lobular pneumonia. Pulmonary collapse, which
sometimes seems to precede the inflammation, probably acts
as a cause of the latter by modifying the circulation and re-
sistance of the alveolar tissues, thus favoring infection.
The exanthemata, the infectious fevers, rickets, dysentery,
and extensive burns of the skin (Wilks) may be accompanied
by lobular pneumonia.
Morbid anatomy.—Lobular pneumonia is more fre-
quently bilateral than any other form of pneumonia. It
occurs in any portion of the lungs, though, with the excep-
tion of tuberculous pneumonia, it is most often found in the
lower portions. It may occur as scattered areas of lobular
consolidation (disseminated pneumonia), or the aggregation
of numerous areas of consolidation may resemble, clinically
and anatomically, the croupous variety of pneumonia. Iso-
lated patches involving but two or three lobules may occur.
The lesions of lobular pneumonia and its associated
conditions present a great variety of anatomical changes.
Bronchitis is most always present, but in some cases of tu-
bercular or other infection by aspiration, previous bronchial
LOBULAR PNEUMONIA.
239
inflammation of that particular area will not be found.
More or less congestion, oedema and emphysema will be
present. Large or small areas of collapse may be present,
particularly at the base or along the free borders of the
lower lobes of the lungs.
Areas of the lobular pneumonia are conical in shape
with their base outward like collapsed lobules. The base
of the pneumonic patch, if at the surface, is raised, never
depressed. The mass is less pliable and more nodular than
that of collapse and its pleural surface is more apt to be
covered with lymph. Pneumonic patches may be distinct
or ill defined. They vary in size from a pea to a hazelnut.
On section they are dark red or greyish with yellowish cen-
ter; soft, friable, smooth or slightly granular. The patches
may be discrete or form racemose groups. When aggre-
gated in large areas the surface of the cut lung is not as
uniform as in croupous pneumonia, greater variety of stage
being exhibited. Fusion <3f lobules, irregular peripheral
distribution and slight or absent pleural exudate distinguish
lobular from lobar inflammation. Fused patches of lobular
inflammation may be paler, drier and firmer than usual and
resemble gray hepatization.
In the early stages of lobular inflammation the alveoli
contain fluid, red corpuscles and leucocytes; the alveolar
epithelium is swollen and graular. The alveoli become
filled with a mass of cells consisting mainly of leucocytes,
in the acute form, and of epithelium in the more chronic
variety. In septic cases haemorrhagic exudation, suppura-
tion, or sloughing and gangrene may occur. The walls of
the finer bronchi are infiltrated with small round cells and
their lining proliferates. Peribronchial infiltration is usu-
ally present.
Resolution through fatty metamorphosis, expectoration
and absorption, is the usual termination, though this pro-
cess is slower than in croupous pneumonia and may occupy
a sufficient length of time to induce thickening of the alve-
olar and bronchial walls and dilatation of the finer bronchi.
In chronic cases, fibrosis and bronchial changes may be
marked. In tubercular cases caseation, encapsulation or
240 LOBULAR PNEUMONIA.
necrosis results. Enlargement of the bronchial glands,
emphysema, collapse, carnification and hypostatic pneu-
monia are frequent accompaniments of lobular pnemonia,
Clinical history.—There is no disease of the lungs
which presents so varied a clinical course as does lobular
pneumonia. Occuring at the extremes of life and in associa-
tion with various infectious disorders; favored by toxic and
septic conditons and lowered vitality, it exhibits a complex-
ity of physical signs and clinical symptoms closely inter-
woven with those of the affection of which it is a more or
less intimate component part.
The onset of lobular pneumonia is not so sudden as that
of croupous pneumonia, nor is its advent marked by a chill.
In association with the infectious diseases of children, the
advent of the pneumonia may be marked by convulsions,
delirium or vomiting; more often it is announced by a more
or less sudden rise in temperature, dyspnoea and cough.
In old people the advent may be* very insidious and marked
only by great prostration and slight rise in temperature and
respiratory rate; cough may be entirely absent.
The temperature range is irregular. In children it may
be of high as 104°—105°. Marked remissions and exacerba-
tions occur. In old people the temperature may not go
above 101°. Defervescence is by lysis, a critical period not
being observed. The breathing is rapid, shallow, and var-
ies from forty to ninety per minute, being most rapid in
children. The pulse is rapid, small and feeble, and varies
from one hundred and ten to one hundred and eighty.
The cough is short, hacking, dry and may be painful. Ex-
pectoration is scanty, slightly viscid and may be absent in
children or old people, and in the latter there may be no
cough. Dyspnoea, cyanosis and orthopncea may be
present.
Lobular pneumonia is a marked feature of the clinical
history of acute pulmonary tuberculosis in which its re-
curring attacks mark the progress of this fatal disease.
Again, the inception of the tuberculous process may be
characterized by a lobular pneumonia. Haemoptysis is a
frequent symptom of these attacks of tubercular lobular
LOBULAR PNEUMONIA.
241
pneumonia, as in the following case recently referred for
opinion:
Mrs. T. aged 23. Good health until three months ago
when she developed a slight cough. Three weeks ago the
cough became worse, there was fever, loss of appetite and
strength. Two weeks ago began to spit up blood and has
continued to expectorate bloody mucus and at times clear
blood. Pulse, 110; temperature, 101°. Examination
showed a well marked lobular pneumonia involving the
upper third of the superior lobe of the right lung.
Lobular pneumonia may occur in connection with bron-
chitis and in the absence of bronchiolitis, probably through
the aspiration of secretion into the lobules. The following
instances illustrate this:
Man aged 38. Tinner by trade. Has a slight attack of
bronchitis which has existed about a week. Two days be-
fore presenting himself he felt worse; his cough was drier,
breathing somewhat shorter and he felt feverish. His
temperature, at the time of examination, was 101°; pulse,
100. Auscultation showed harsh breathing with a few mu-
cous rales in the upper part of the right lung. In the ante-
rior axillary line at the level of the sixth rib on the left side
there was an area about the size of a silver dollar which
showed bronchial breathing with few fine crackling rales at
the periphery. The respiration between this point and that
of the bronchitis in the upper lobe was normal.
Examination, a week later, showed resolution to be
well advanced in the small pneumonic area, while there was
another area, about two inches in diameter, at the lower
angle of the left scapula, which showed dullness and bron-
chial breathing. This area cleared up in about a week and
the patient was discharged.
Boy aged 9 years. Has been troubled more or less for
two years with an asthmatic form of bronchitis. Three
days before presenting himself at the clinic he became
worse; his cough became dry and irritating, his breathing
rapid and short, there was fever and thirst and he com-
plained of some pain beneath the left shoulder blade. At
the time of examination his temperature was 101.5°; pulse,
110. There were a few moist, and occasional sonorous
rales throughout both lungs. In the lower posterior por-
tion of the left lung there was a well defined area of consol-
idation about an inch and one-half in diameter, surrounded
242 LOBULAR PNEUMONIA.
by fine sub-crepitant rales. Over this area the breathing
was distinctly bronchial in character.
One week later the boy returned feeling much better.
His temperature was normal, pulse, 80. Auscultation of
the inflamed area showed harsh breathing with mucous
rales.
The duration of lobular pneumonia is indefinite. It
may last from a week to three or four weeks. If only a
few aggregated lobules are involved resolution may be ex-
pected in a week or ten days. If there is successive invasion
of'segregated areas, the course of the disease may be much
prolonged. This is most likely to occur in the tubercular
pneumonias of acute phthisis.
Lobular pneumonia is most fatal in children before the
age of five years, and when secondary to measles and whoop-
ing-cough, and in old people in connection with bronchitis.
Symptoms and diagnosis.—The symptoms of lobular
pneumonia are varied and irregular. When the disease oc-
curs in connection with measles, whooping-cough or with
bronchiolitis, it is ushered in by fever, rapid pulse and
breathing, possibly some dyspnoea; the cough changes, be-
coming dry, hacking and annoying, with scanty, more viscid
expectoration.
In children, especially in connection with bronchiolitis,
the rhythm of the breathing is changed; the respiratory
pause being before, instead of after, expiration. There is
rapid, forcible inspiration, a pause, explosive expiration
immediately followed by inspiration. Short pauses in re-
spiration may occur or the breathing may assume the
Cheyne-Stokes type. When much bronchitis is present
or a considerable number of lobules are involved, the
breathing will be difficult and dyspnoea will be present.
The alas nasi show respiratory dilation, the accessory
muscles of respiration act strongly. If bronchial obstruc-
tion is marked, the forcible action of the diaphragm
causes inspiratory depression of the epigastrium. General
cyanosis and lividity are unfavorable signs.
The dyspnoea does not correspond to the physical signs,
as a deep-seated lesion may show marked dyspnoea and but
LOBULAR PNEUMONIA. 243
few physical signs, while a more diffuse affair with high
temperature may be accompanied by little dyspnoea (North-
rup.) The dyspnoea may accord with the degree of ob-
struction from bronchitis. When bronchiolitis is severe,
dyspnoea, cyanosis and lividity are more pronounced, the
respiratory tract becomes less irritable, cough ceases and
the patient seems better, but as the right heart begins to
dilate there is increased cyanosis and lividity, cold ex-
tremities, inability to cough, diminished frequency of
breathing, rapid, feeble pulse, dilated pupils, insensible
corneae and death by asphyxiation.
In old people the symptoms may be very indefinite.
The fever may be slight, cough absent, breathing not very
rapid, and dyspnoea absent if bronchitis is not severe, and
only a careful physical examination will indicate the nature
of the trouble.
When lobular pneumonia occurs secondary to bronchitis
we may be able to trace the extension of the bronchial in-
flammation inwards by the appearance of small mucous,
sub crepitant and fine crepitating rales,or, the first evidence
may be that of consolidation in a hitherto uninvolved area
of lung. The crepitant rale is definative of pneumonia and
seldom heard in lobular pneumonia. Harsh breathing or
broncho-vesicular breathing with a variety of moist rales
are the usual signs of the early stages. When consolidation
has occurred we may get bronchial breathing and bron-
chophony if the area is large enough or if the associated
bronchitis does not obscure these signs. A small, superficial
area of consolidation without much or any bronchitis, will
give distinct signs of consolidation, while a much larger
but more deeply seated area accompanied by bronchitis
which obstructs the tubes, will furnish very indefinite signs.*
Percussion dullness depends on the same factors as the
breath sounds, but is not so reliable, as the pitch of the note
is more effectively modified by intervening areas of normal
lung tissue. It is only when isolated areas of superficial
*Xorthrup warns against mistaking the tubular quality of the breathing heard
between the scapula? in dyspnceic children, for bronchial breathing. This mistake
is not likely to occur if more attention is given to the pitch of the expiratory
sound than to the quality of the respiratory sounds.
244 LOBULAR PNEUMONIA.
inflammation, or large areas from aggregation of inflamed
lobules, occur,that percussion will give reliable information.
In children when numerous areas of collapse are added to
lobular inflammation, and in old people when carnification
of the lung, hypostatic pneumonia, lobular pneumonia and
collapse are inextricably mingled in the base of the lungs,
the physical signs are decidedly indefinite, there being
simply lost motion, partial dullness and suppressed respira-
tory sounds.
When, through the aggregation of numerous inflamed
lobules, considerable areas of consolidation occur, the
disease may resemble croupous pneumonia. The secondary
nature, slower development, the absence of chill, lower and
more irregular temperature, more rapid pulse, slower res-
piration, the involvement of only a portion of a lobe, its
bilateral occurrence and the presence of disseminated
areas of consolidation in other portions of the lung,
together with the demonstration of streptococcus, staphylo-
coccus, or a mixed infection, will differentiate.
Bronchiolitis with extensive collapse of the lung, in
children, is to be distinguished from pneumonia chiefly by
the development of rapid breathing, dyspnoea and cyanosis
before or without a corresponding elevation of temperature.
The physical signs may be practically identical. However,
this condition is, as a rule,but a precursor of pneumonia, and
the distinction is, therefore, not important. In infants, the
differentiation between pleurisy and pleuropneumonia may
be impossible except by the use of exploratory puncture.
In older children a considerable degree of pleurisy is more
apt to be associated with croupous than with lobular pneu-
monia. Enteric fever and meningitis may closely simulate
lobular pneumonia.
Acute disseminated tuberculosis of the lungs may be, in
the beginning, impossible of differentiation from lobular
pneumonia except through the presence of the bacillus
tuberculosis. A lobular pneumonia constitutes the essential
anatomical lesion of this form of phthisis and the nature of
the disease is determined by demonstrating the nature of
the infection.
LOBULAR PNEUMONIA. 245
The most unfavorable symptoms of lobular pneumonia
are rapid, feeble or irregular pulse, sudden fall in tempera-
ture, cessation of cough, slowing of respiration with
changes in its rhythm, the appearance of stupor, delirium,
cyanosis or lividity.
Treatment.—The management of lobular pneumonia
is largely symptomatic. It is not apparent that specific
treatment can be of benefit, unless, through the agency of
some serum, such as anti-streptococcus serum, we can
avoid the irregular terminations which are likely to occur
in inflammations depending on severe infections with
pyogenic organisms.
In lobular^meumonia in children the patient should be
placed in a well-ventilated room. If the cough is loose and
the child perspires, the air should be fresh and dry. If the
cough is tight, the expectoration viscid and scanty and the
skin dry and hot, a tent may be arranged around the bed
and the air be kept charged with steam by some sort of va-
porizing apparatus. The diet should be milk or some of
the prepared milk or beef foods. Lime-water should be
added to the milk and the food should be given in small
quantities every three hours. Unless pain prevents, the
position of the child should be frequently changed so as to
favor deeper inspiration, especially when bronchiolitis is
present.
Stimulant expectorants must be given. Muriate or car-
bonate of ammonia, senega, etc. Two grains of chloride of
ammonia, one-fourth of a drop of tincture of aconite root,
fifteen drops of the liquor of the acetate of ammonium may
be given every two hours to a child two years old. [Dr.
Burney Yeo recommends benzoate of soda internally, and a
warm, alkaline spray containing bicarbonate of soda, gly-
cerine and carbolic acid.] When the cough is troublesome
it must be controlled with small doses of paregoric, Dov-
er's powder or codeine. Care must be exercised in the ad-
ministration of these sedatives, especially when bronchio-
litis is present, as they may add to the danger of paralysis
and obstruction of the bronchial tubes and consequent col-
lapse of the lung. When cyanosis is present, especially in
246 LOBULAR PNEUMONIA.
old people, oxygen is of great service and may be adminis-
tered more continuously and effectively when warmed by
passing it through a spiral metal coil placed an warm water
(Fowler).
In children, the chest should be protected with a cotton-
batting jacket. When pleurisy is present a poultice is
most useful in relieving pain and nervous dyspnoea, It
should be applied so as not to obstruct respiration, should
be covered with dry, warm flannel and not be allowed to be-
come cold. If expectoration is scanty and mucus obstructs
the tubes, an occasional dose of one grain of powdered ipe-
cac may relieve this condition, or„ if the obstruction threat-
ens asphyxiation, larger doses (five to fiftefn grains; five
grains for a child one year old) to produce vomiting, may
be necessary, In asphyxiation from associated collapse of
the lung, inflation of the lungs has been recommended.
The abdomen is tightly wrapped with a bandage, the nose
closed with the operator's fingers and his mouth applied to
that of the child. This method is of doubtful utility. If
the pulse and respiration become very rapid, strychnia must
be given in stimulant doses and preferably by the hypoder-
mic method. In children, from one one-hundredth to one-fif-
tieth of a grain may be used every two to four hours; in
adults from one-thirtieth to one-twentieth of a grain at
similar intervals. Many cases may be tided over the dan-
gerous period by the energetic but careful use of strychnia.
Various hydrotherapeutic measures are recommended
for the relief of high temperature and dyspnoea in lobular
pneumonia. Undoubtedly these measures are the most val-
uable at our command for this purpose, when properly mod-
ified to suit the circumstances of the individual case. Jur-
gensen recommends a twenty minute bath at a tempeiature
of 77g to 80Q P., combined with cold sponging of the chest;
the bath to be repeated whenever threatening symptoms re-
appear or the temperature reaches 103° P. Wilson Fox ad-
vises a cold bath (from one to three minutes) at a tempera-
ture of 65° to 70° F., with cold applications to the chest.
Pye-Smith advises tepid sponging and tepid baths. Fow-
ler advises, for high temperature, dyspnoea and cyanosis,
LOBULAR PNEUMONIA. 247
hot baths (104° to 110° F.) with cold affusions (60Q to 65° F.)
over the chest and back. Whatever degree of cold we em-
ploy, the best evidence of its efficiency is diminished fre-
quency of pulse and respiration. No absolute rule can be
laid down based on the temperature. Children bear high
temperature well, and a temperature of 103° cannot be held
as abstract evidence of the necessity of a cold bath. It is
rather the combination of high temperature, pulse and res-
piration, which indicate the employment of hydrotherapeu-
tics. My own experience is very favorable to cool sponging
frequently repeated, or bathing, for from five to fifteen
minutes, at a temperature of 98° to 100Q F. The child can
then be wrapped in a wet towel and a blanket and allowed
to rest for from fifteen minutes to an hour when it should
be gently rubbed and wrapped in a dry blanket. Northrup
recommends a convenient method, of placing the nude child
in a hammock made of a towel and lowering it into the bath
tub, bathing its face meanwhile with the same water as is
used for the general bath. This method avoids much hand-
ling of the child and is convenient, In old people, baths, if
used at all, should be confined to sponging, as the exhaus-
tion incident to the administration of baths is greater than
in children.
When the circulation shows evidence of failure, digi-
talis and alcohol may be indicated temporarily, though
these remedies will be less often necessary if strychnia is
given early enough and in sufficient doses.
In the management of the convalescing period we must
use general and special calisthenic exercise, deep breath-
ing exercises, climatic treatment, nutritious diet, tonic med-
ication, as cod liver oil, guaiacol, iron and quinine, iodide
of iron, syrup of hydriodic acid, mineral acids, in short, ev-
ery medicinal or hygienic means which will increase the pa-
tient's strength and respiratory capacity and lessen the dag-
ger of secondary processes in the lungs.
248
PULMONARY FIBROSIS.
Fibrosis of the lung (chronic pneumonia, interstitial
pneumonia, cirrhosis of the lung) is the result of a produc-
tive inflammation produced by influences of moderate sever-
ity but of protracted course. It is characterized by grad-
ual increase in the connective tissue of the lung and results
in induration of the pulmonary tissue and obliteration of
the alveoli of the lung.
It is evident that there is no disease of the lungs with
which fibrosis, in some degree or extent, may not be associ-
ated; while in some instances, as in tuberculosis, it consti-
tutes a conservative process of nature, and a necessity to
to the limitation of the infective process. We are not sur-
prised, therefore, to find the aetiological nomenclature of
fibrosis of the lungs resulting in the description of several
special forms of the disease which, while they may have
certain more or less distinctive clinical features, have yet
no generic or pathological individuality and which are not
entitled to be described as special forms of pulmonary dis-
ease. Such varieties of fibrosis as pneumoconiosis, syphi-
litic sclerosis of the lung, etc., will therefore be considered
as types of the progressive induration characteristic of
fibrosis of the lungs.
The essential features of fibrosis of the lungs is the in-
crease of the tissues of the walls of the alveoli and of the
interalveolar, interlobular and sub-pleural tissues. Topo-
graphically, any one of these tissues may be chiefly affected,
though as a rule they are all more or less involved.
^Etiology.—Fibrosis of the lungs occurs secondarily
to some disease of the alveolar or bronchial wall or pleura.
Its most common cause is the chronic disseminated form of
{Tulmonary tuberculosis. Lobular pneumonia, especially
in early life, is frequently the cause of fibrosis starting as a
thickening of the alveolar walls. Bronchiectasis, pulmon-
ary collapse, bronchial obstruction from pressure of an
aneurism, and new growths in the lung, pleura or oesopha-
gus may induce fibrosis of the lung. In cases of protracted
resolution of croupous pneumonia there may be a slight in-
PULMONARY FIBROSIS. 249
duration of the alveolar walls which in rare instances may
cause extensive fibrosis of the lung.
The following case of diffuse fibrosis was probably sec-
ondary to pneumonia:
Woman aged 42 Married. Always been healthy with
the exception of an attack of pneumonia nine years ago from
which recovery was slow. For the last two years has had
cough with gradually increasing dyspnoea on exertion. Spits
up a little white, glairy mucus, particularly in the morning.
Temperature 98.5C; pulse 98. Has lost some flesh. Has no
pain and appetite and digestion are fair. Examination
shows marked contraction of the left side of the chest with
great restriction of motion on that side. There is compen-
satory enlargement of the right side of the chest. The
heart apex is displaced upward and to the left. The finger
ends are not clubbed. Vocal fremitus is marked all over
the left side and the percussion note is high-pitched and
has a woody, hard tone slightly tympantic in quality under-
neath the left clavicle. Very little air enters the left lung
and the respiratory murmur is high in pitch and of a tubu-
lar quality with prolonged expiration in the upper por-
tion of the lung. No rales are heard except an occasional
mucous click. There is exaggerated or puerile breathing
in the right lung. No tubercle bacilli can be found in the
sputum.
In this case the length of time the disease has probably
existed; the absence of fever, night sweats, emaciation,
destructive processes in the lung and of bacilli would seem
to refer the cause back to the previous attack of pneumonia.
A special form of pneumonia is described (subacute in-
durative pneumonia.—Kidd, primary parenchymatous pneu-
monia.—Buhl, Heitler) in which fibrosis of the lung is a
chief lesion.
Syphilitic gummatous growths in the lung may be asso-
ciated with interstitial fibrosis having a tendency to extend
along the vessels or tubes. There is also a diffuse form of
fibrosis occurring in children with congenital syphilis.
This form is rare and not much is known about it.
The inhalation of solid, irritating particles of dust, met-
als, etc., is a frequent cause of fibrosis of the lungs. Nu-
merous designations have been given fibrosis from this cause.
When due to particles of carbon it has been known as anthraco-
250 PULMONARY FIBROSIS.
sis; siliceous particles, as chaliosis or silicosis: of metallic
particles, as siderosis; of cotton particles, as byssinosis, etc.
Pneumoconiosis is the term usually employed for this variety
of fibrosis, though such names as coal miner's phthisis, pot-
ter's phthisis, knife grinder's phthisis, etc., are sometimes
used. Any dusty occupation may give rise to pneumoconi-
osis.*
The intimate association of fibrosis and tubercular
changes in the lungs has occasioned much doubt as to the
occurrence of non-tubercular pneumoconiosis, and as the lat-
ter disease is liable to show secondary tubercular infection,
it may be very difficult to determine the nature of the pri-
mary changes. It is, however, considered, by the majority
of observers, that tubercular infection is not necessary
to the development of pneumoconiosis.
"Corrigan's pneumonia" (interstitial) which was claimed
to develop without apparent cause, Sir Andrew Clark's
"fibroid phthisis," and Harris' "secondary" interstitial pneu-
monia are all conditions of the same inherent nature, vary-
ing^ perhaps, in their aetiological factors but all manifes-
ting the general tissue change of fibrosis of the lungs.
With empyema or in connection with long standing ef-
fusions in the pleurae we may have fibrosis of the lungs de-
velop either as dense bands of thickened interlobular con-
nective tissue or as a more general fibrosis.
Morbid anatomy. —The morbid anatomical features of
the lung in cirrhosis are necessarily varied in degree and
extent. It is not necessary to review here the degrees of
fibrosis that may be associated with the various pulmonary
lesions.
In general and well advanced fibrosis of the lung the
organ is diminished in size. The tissue is dense, °firm,
♦Claisse and Josue conclude that the lesions of pneumoconiosis are not due to
direct action of dust but to infectious processes which are superadded; verv small
dust particles may migrate through the pulmonary tissues without causing dis-
turbance; large particles produce, by traumatism, a soil upon which inhaled or-
ganisms develop; morbid conditions influence pneumoconiosis only when they
are of long duration; lesions of the lymph nodes increase pneumoconiosis by im-
pairing the circulation and the elimination of dust particles by the lymphatics;
pneumogastric lesions favor pneumoconiosis by destroying the resistance of the
upper air tracts and by producing vaso-motor troubles.
pulmonary fibrosis.
251
smooth and may be, in spots, almost cartilaginous in con-
sistency, It may be deeply and irregularly pigmented.
The alveolar structure may be entirely in places. The
bronchi are irregularly dilated and may contain irritating
secretions which, when not removed by expectoration may
give rise to secondary inflammation, ulceration or excava-
tion; caseous changes are absent in non-tubercular cases.
The pleurals thickened and may be adherent.
When secondary to croupous pneumonia these changes
begin in the walls of the alveoli and ultimately involve the
interlobular tissue. According to Green and Goodhead the
intra-alveolar products of a croupous pneumonia have been
known to become vascularized and develop into fibroid
tissue. In lobular pneumonia and pneumoconiosis the
changes begin in the alveolar walls but the peribronchial
and interlobular tissues are more actively concerned in the
process.
When secondary to pleurisy the tissue growth of fibro-
sis extends from the thickened pleura along the interlobu-
lar lymph vessels and spreads to the peribronchial tissues.
The lung may be thus encapsulated or traversed by numer-
ous bands of dense fibrous tissue.
In collapse of the lung there are haemorrhagic and pig-
mentary changes, fibrosis of the alveolar walls, destruction
of the epithelium and fusion of the alveolar surfaces.
Clinical history.—The clinical history of fibrosis of
the lungs is necessarily varied. The minor degrees of fibro-
sis have no history apart; from that of the lesions with
which they may be associated and which they modify.
When fibrosis is secondary to croupous, lobular pneu-
monia or chronic pleurisy there is a history of protracted
and incomplete recovery from these conditions. There is
cough with frothy, mucopurulent or nummular expectora-
tion. Haemoptysis may occur even in non-tubercular cases.
More or less dyspnoea will be present. Fever may not be
present and will not be high unless sepsis from excavation
or bronchial dilatations should occur. The course of the dis-
ease is protracted and the later stages marked by cardiac
failure.
252
PULMONARY fibrosis.
In pneumoconiosis there is a history of dusty occupa-
tion, of a bronchitis which had no definite time of onset and
which is troublesome in the morning and on changing from
a,warm to a cool atmosphere. The expectoration is not
free and consists of glairy mucus which may be pigmented.
Recurrent exacerbations of the bronchial catarrh occur.
Dyspnoea gradually becomes troublesome. Asthmatic
symptoms may be prominent. Loss of strength and flesh
occur and the patient seeks quietude in a warm atmosphere.
In syphilitic fibrosis the clinical history will differ but
little from that of other forms. The cough is the earliest
and most prominent symptom. Expectoration, fever, etc.,
have the same causal relations as in other varieties of fibro-
sis.
The pleurogenic form of fibrosis is illustrated in the
history of the following case:
Boy aged 12 years. Good family history. When seven
years old had an attack of illness, probably some form of
acute pneumonia, which was followed by an empyema. The
pleural fluid was aspirated several times and finally an im-
perfect drainage was instituted. The discharge from the
pleura stopped after several months. He now suffers
slightly from cough and considerably from dyspnoea on exer-
tion. On examination we find much retraction of tie left
side below the fourth rib. The heart is displaced backward
and upward, the stomach toward the right and downward
and there is an evident degree of scoliosis. The upper part
of the left lung is dilated and there is inspiratory retraction
of the left side over the affected area and no air can be heard
passing in or out of this portion of the lung.
Symptoms and diagnosis.—Aside from the indefinite
subjective symptoms the signs of fibrosis are mainly physi-
cal. The affected side will show restricted motion in part
or in whole and may be considerably smaller than the oppo-
site side. If the fibrotic changes are restricted to the lower
portion of the lung, marked contraction of this portion may
be shown with compensatory enlargement of the upper por-
tion. There may be decided displacement of the heart up-
wards, backwards, or to the right if the right side is af-
fected. In extensive fibrosis marked clubbing of the finger
ends may be present.
pulmonary fibrosis.
The vocal fremitus is usually increased over the affected
area though it may be absent over the lower portion of the
lung if the latter is very hard. The percussion note is high-
pitched and of a dull wooden, or amphoric character if there
are bronchial dilatations or cavities. Increased vocal reson-
ance, broncho-vesicular breathing, bronchophony or pector-
iloquy with high-pitched, prolonged expiratory sound and
possibly bronchial or cavernous breathing may be heard if
there is complete consolidation or cavities. Various sized
mucous rales, gurgles, or mucous clicks may be heard.
The physical signs, as well as the subjective symptoms,
are modified by the degree of emphysema and bronchial dil-
atation which may have developed.
In dust phthisis the discoloration of the sputum or the
presence of foreign substances in the expectorated matter
may indicate the nature of the disease.
The following case of pneumoconiosis presents the
usual history:
Man 47 years old. Bohemian, married. Good family
history. Wood turner by trade. Has been employed for
years in a mill at very dusty work. Has coughed for sever-
al years, more in winter than in summer. Lately has been
free from cough only when in a warm atmosphere. Expec-
toration has become more abundant, thicker and recently
decidedly fetid. For the last four months has been cough-
ing up a quantity of foul smelling mucus in the morning.
He is decidedly dyspnceic and at times slightly cyanosed on
exertion. His finger ends are markedly clubbed. Temper-
ature 99.5°; pulse 100.
Examination shows retraction of the lower part of both
sides of the chest, particularly of the left side. Lateral ex-
pansion is almost entirely lost. There is increased fremitus,
vocal resonance and high-pitched percussion note all over
both lungs. The percussion note, over the region of the
fourth left rib just inside the mammillary line, is hollow in
character and there are gurgles, pectoriloquy and cavernous
breathing in the same region. Numerous rales and breath-
ing of a tubular quality are heard throughout the lower two-
thirds of both lungs. No bacilli in the sputum.
These cases are likely to develop tuberculosis during
their course and after this has occurred a correct diagnosis
may be difficult.
254
PULMONARY fibrosis.
Besides the congenital syphilitic fibrosis of children
there may occur various degrees of fibrosis and secondary
conditions resulting from acquired syphilis. These condi-
tions may or may not be associated with gummata, or ulcer-
ative lesions of the respiratory mucosa, and constitute the
so-called cases of syphilitic phthisis.
The following case is probably one of syphilitic fibrosis
of the lungs though the diagnosis rests on the absence of
bacilli from-the sputum, the subject being alive:
Man aged 39 years. Waiter by occupation. Family
history good. Had a hard chancre eighteen years ago which
was followed by sore throat and a skin eruption. Never
had pleurisy or pneumonia. For the last five years has had
a cough which is worse in winter and which has been espec-
ially troublesome for the last year. Expectoration which
was formerly scanty and frothy has lately been muco puru-
lent and at times somewhat offensive. Has lost flesh and
strength and there are occasional pains through the chest.
Examination shows loss of motion of the lower portion
of both lungs with signs of marked induration of the left
lung below the fourth rib and of the posterior and lateral
portions of the right lung below the sixth rib. No bacilli
have been found in his sputum. He has improved consider-
ably, in a general way, on iodide of potassium and biniodide
of mercury.
The diagnosis of localized fibrosis of the lung is not
difficult and rests on the character of the physical signs.
In the diffuse varieties the main question is whether they
are, or are not, tubercular. This question Is determined,
principally, by the presence or absence of tubercle bacilli.
Non tubercular fibrosis is usually unilateral and begins in
the lower lobes in contrast with the characteristic apical in-
vasion of the tubercular form. Rare cases of primary basic
tuberculosis of fibrotic nature may occur and be difficult of
diagnosis but here we must remember the probability of
tuberculosis occurring in connection with fibrosis which was
primarily non-tubercular.
Pleural effusion which has not fully absorbed and which
has prevented expansion of the lung may closely simulate
fibrosis. There may be a greater degree of retraction than
the same extent of fibrosis would occasion, while the voice
PULMONARY FIBROSIS. 255
and breath sounds will be diminished rather than increased.
When bronchiectasis is added to this condition the diagnos-
tic difficulties are increased.
Pulmonary fibrosis with bronchiectasis may be very dif-
ficult to distinguish from an empyema or hepatic abscess
which has perforated the lung. The diagnosis may rest on
the result of an exploratory puncture.
Malignant growths in the lung or mediastinum may
simulate fibrosis. The latter is favored by long duration,
compensatory enlargement of the opposite lung, frothy,
mucopurulent or fetid (if there is bronchiectasis) expectora-
tion and considerable cardiac displacement. Pressure signs,
dullness extending across the median line, persistent pain
in the chest and red-colored, gelatinous expectoration are
indicative of malignant growths.
Treatment.—In the localized fibrosis resulting from
pleurisy, lobular pneumonia, bronchiectasis, etc., deep
breathing, pulmonary calisthenics, general hygiene, tonics
and perhaps climatic treatment, are the means available.
In diffuse fibrosis we must employ iron, strychnia, cod-liver
oil and all the measures indicated in chronic lung disease
whether the case is tubercular or not. In very chronic
cases strychnine is valuable as a stimulant to the right ven-
tricle which sooner or later will fail to keep up the lesser
circulation.
Climatic treatment is very important in these cases as
they run the risk of repeated attacks of bronchitis as wrell
as the more serious danger of tubercular infection in non-
tubercular cases if they remain in moist,changeable climates.
Warm, dry air with sunshine, is what they need. The alti-
tude should not be too high,—not over twelve or fifteen
hundred feet if the fibrosis is at all extensive. The selec-
tion of a proper climate may be difficult and must rest with
the patient as the physician can only give general directions
suitable to the individual case. In a recent case of fibrosis
of the lower part of the right lung secondary to pleurisy,
the patient, a physician, had tried many localities without
finding one which seemed adapted to his case. He required
2 56
PULMONARY FIBROSIS.
warmth, dryness and a moderate altitude. These conditions
can only be obtained by varying the place of residence at
different seasons.
In syphilitic cases the iodides and mercury should be
given. In advanced cases it may be well to omit the mer-
cury and give iron, strychnia and cod-liver oil with the
iodide of potassium. Tubercular fibrosis in a syphilitic sub-
ject should be treated mainly as a case of tuberculosis, con-
tinued mercurial courses being inadmissible. Syrup of the
iodide of iron is a useful remedy in these cases.
In cases of fibrosis of the lung associated with well de-
veloped bronchiectasis accompanied by offensive expectora-
tion the treatment should be such as has been advised for
bronchial dilatation—intratracheal injections of guaiacol,
creosote vapor baths, etc. Surgical interference, for the
drainage of bronchiectatic cavities resulting from fibrosis, is
of doubtful utility especially in syphilitic cases. In tuber-
cular fibrosis the treatment is that of chronic tuberjular dis-
ease of the lung and is considered under that subject.
CHAPTER XII
PULMONARY ABSCESS.
Pulmonary abscess is a more or less circumscribed col-
lection of pus within the lung. The term abscess of the
lung is frequently applied to collections of pus within the
chest which have little pathological resemblance to ordi-
nary abscess. These collections may be single or multiple.
While pulmonary abscess is almost always the result of some
other disease of the lung, we are justified in considering it
a distinct clinical affection because of its individual features.
Etiology.—Single abscess of the lung occurs in con-
nection with pneumonia, from softening and necrosis of an
area of consolidated lung tissue and is favored by constitu-
tional vices and alcoholism; also, from injuries, as fractures
of the ribs, or'penetrating wounds of the lung. Multiple
abscesses of the lungs are usually pyaemic in nature and oc-
cur from the softening of infarctions of the lung, from septic
embolism of the lung and from septic broncho-pneumonia.
Pulmonary abscess may occur in tuberculosis of the
lung, from the rapid breaking down of a large caseous area;
in bronchiectasis with destruction of the bronchial walls and
contiguous structures, or possibly without such changes; in
connection with non-tubercular cavities resulting from local
destruction of blood supply; from suppuration of an hydatid
cyst of the lungs; from extension to the lung of suppurative
inflammation of the pleura, bronchial glands, mediastinum,
sub diaphragmatic space, liver, and, in rare instances, of the
spleen and pancreas. Malignant disease of the oesophagus
may cause abscess of the lung tissue. Circumscribed gan-
grene may end in abscess. The most frequent cases of
abscess of the lung are those secondary to pneumonia,
pyaemic infection of the lung, and to empyema.
Morbid anatomy.—Tie m^.-bid anatomical conditions
25h pulmonary abscess.
with which abscess may be associated are very varied, but
these conditions do not belong to pulmonary abscess.
Abscess following pneumonia occurs most often in the
middle or upper lung. Multiple pyaemic abscesses occur in
any portion of the lungs but may be confined to the base or
lower portions. They are of small size, from that of a split
pea to that of a chestnut, and, when at the surface of the
lung, are covered by small areas of pleural inflammation.
These embolic abscesses are surrounded by a zone of hyper-
aemia and are apt to be near the surface of the lung with
their bases just beneath the visceral pleura.
In cirsumscribed gangrene the necrosed tissue may be
expelled through a bronchus and granulation tissue may
form in the walls of the cavity and generate pus. These
cavities may close by granulation and cicatrization.
The expectorated matter from a pulmonary abscess con-
sists of pus of a yellow or yellowish-green color containing
elastic fibers and particles of lung tissue. There is,usually,
little or no odor at first. Many kinds of organisms are pres-
ent, the most frequent being pneumococci and streptococci.
The discharge from an encysted empyema, suppurating
bronchial gland, etc., which breaks into a bronchus, will not
contain elastic fibers except at the immediate time of rupture
Clinical history.—The clinical history of pulmonary
abscess is necessarily varied. The principal symptoms—
pain, cough, dyspnoea and fever—are common to various'
disorders with which abscess may be associated or of which
it may be the result, and the latter may be well advanced
before it is possible to individualize any of these symptoms
as indicative of abscess of the lung.
Multiple embolic abscesses of the lung may give no his-
tory apart from that of a pyaemic state, with, possibly, a
small amount of fetid expectoration. The occurrence of
embolic abscess may be marked by sudden, sharp pain in
the chest.
The history of sudden and profuse expectoration of pus,
with or without pain, may be the first reliable indication of
an abscess of the lung.
When abscess of the lung occurs from pneumonia the
pulmonary abscess.
259
fever maintains, or returns to, a high degree and subse-
quently shows a fluctuation indicative of sepsis and is ac-
companied by sweating and, perhaps, rigors. Dyspnoea
may be troublesome but exhibits no features specially indic-
ative of abscess, and the same may be said of the cough and
pain.
The course of pulmonary abscess depends on the nature
of its cause. It may be prolonged; death may occur from
sepsis or from septic lobular pneumonia due to infection by
material from the abscess cavity. Single abscesses follow-
ing pneumonia may heal by cicatrization after the discharge
of the contents of the cavity. This termination, while rare,
I have known to occur in more than one instance, as in the
following case:
Boy aged 18 years. Previous health good. Had a
moderately severe attack of pneumonia of the right lung.
After the crisis the temperature rose to 102.5° F. and showed
a daily fluctuation from 99° F. to 102.5° F. with daily
sweating.
Examination, six days after the crisis, showed an area
in the right mammary region which exhibited dullness, sup-
pressed respiratory sounds, increased fremitus, and rales
surrounding this area. There was considerable pain in the
right side of the chest. Four days later a considerable
quantity of pus was expectorated which contained some
elastic fibers. The patient was very weak and exhausted
and continued to expectorate quantities of pus daily which
became offensive. The odor was controlled by inhalations
of an oil solution of menthol, aristol and eucalyptus. The
temperature ranged from 99° F. to 101° F. The pain gradu-
ally disappeared. Pectoriloquy and amphoric voice and
breathing were obtained over the area where signs of con-
solidation had been present.
The patient gradually improved under tonic treatment
and nutritious diet, and three months later was, apparently,
well; the cough and expectoration having ceased. At this
time the signs of a cavity could not be obtained, there being
simply increased fremitus, partial dullness and breathing
of a high-pitch and of tubular quality over the area involved.
Symptoms and diagnosis.—Pain in the chest, cough,
fever, dyspnoea and the expectoration of a quantity of pus
containing elastic fibers are the symptoms of abscess of the
260 PULMONARY ABSCESS.
lung, in most instances these symptoms are character-
ized by their indefiniteness. Sudden pain in the chest fol-
lowed by cough, dyspnoea and septic temperature indicates
embolic abscess, especially in connection with septic condi-
tions in which emboli are liable to occur. Continued py-
rexia after pneumonia, especially if of a sep+ic type, cough
and rapid respiration are suggestive of abscess.
The physical signs are not always conclusive but when
taken in connection with the subjective symptoms a diag-
nosis can usually be reached.
Before discharge of the contents of the cavity has oc
curred there will be localized dullness, diminished breath
sounds, and, perhaps, increased fremitus. If there are sev-
eral areas of softening there will be crackling rales around
these areas. At this stage the absence of displacement of
the apex beat of the heart, and the presence of fremitus are
important in the exclusion of pleural effusion.
When a cavity has formed there may be a tympanitic
quality to the percussion note if the cavity is near the sur-
face of the lung, or the note may be high-pitched and me-
tallic in quality. Perhaps cracked-pot resonance may be
obtained. If the cavity has free communication with a bron-
chus the percussion note may be higher with the patient's
mouth open than with it closed (Wintrich's change of pitch),
or, if the cavity be of greater diameter in one direction than
another and contain fluid, the percussion pitch will vary in the
upright and recumbent positions(Gerhardt's change in pitch).
Again, the rise in percussion pitch with the mouth open
may b? obtained only when the patient is recumbent (Win-
trich's interrupted change in pitch).
The voice sounds may be amphoric in quality and pector-
iloquy may be obtained. Careful study of the loud and
whispered voice sounds -is of great value. The breathing
may be cavernous in character and, perhaps, amphoric in
quality. Gurgles and metallic tinkling may be heard.
Bronchiectasis and circumscribed gangrene are the
affections within the lung most likely to simulate abscess.
In the former the sputum will not contain elastic fibers, and
pyrexia may be absent, or, at least, not marked or of a sep-
PULMONARY ABSCESS.
261
tic type. The history is different from that of abscess.
In gangrene the course is more rapid, there is greater
prostration and constitutional disturbance, the expectoration
is fetid and extremely offensive and contains broken down
lung tissue.
In hydatid cysts of the lung the general symptoms are
milder than those of abscess. The percussion note, in the
center of the affected area,has a more absolute flatness.. The
characteristic hooklets in the expectorated matter are decis-
ive when obtained.
Abscess of the liver, sub-phrenic abscess, mediastinal
abscess, encysted empyema, etc., breaking into the lung,
may usually be diagnosed through the history and physical
signs present prior to the involvement of the lung. Pus,
from these sources, discharged through the bronchi,will not
contain fibers of pulmonary tissue except, perhaps, at the
immediate time of rupture.
Abscess and empyema are alike most frequent after
pneumonia, and if the latter be encysted, as is likely in a
pneumococcus infection, it may readily be mistaken for
abscess, especially if it discharges into a bronchus. The
constitutional disturbance attending abscess is more severe
than with empyema, also, the fever, rigors, sweating, pain
and cough are more severe. Empyema shows more change
in the contour of the affected side and more limitation of
motion. Loss of fremitus, less abrupt transition from flat-
ness to partial resonance, greater interference with conduc-
tion of voice and respiratory sounds also characterize em-
pyema. When an empyema discharges through a bronchus
the signs may resemble those of a cavity in the lung so
closely as to make the distinction between them impossible
by the physical signs alone.
The following case illustrates this:
Little girl aged 6 years. Had an indefinite illness last-
ing three months with a history of irregular fever. At time
of examination had a temperature range of from 99° F. to
102.5° F. There were signs of effusion in the left pleura.
Drainage was advised but was delayed for some time. A
small amount of pus was discharged through an opening be
tween the fourth and fifth ribs. A few weeks after this th
262
PULMONARY ABSCESS.
child br gan to spit up pus and the temperature range was
from 1C0° F.to 105° F. 'There were now signs of a cavity
under the center of the left scapula. The lower left lung
was much retracted. The physical signs were identical with
those of a cavity in the lung substance. Examination of the
discharge showed at first pneumococci and streptococci; later
a few tubercle bacilli.
Treatment.—The medical treatment of abscess of the
lung consists in nourishing food and the liberal use of such
tonics as iron, quinine and strychnia; the employment of
such antiseptic inhalations as have been recommended in
bronchiectasis, if the cavity has emptied and the discharge
is fetid. Pyaemic abscesses are usually beyond treatment,
medical or surgical.
In single abscess following pneumonia, if the discharge
is free and septic symptoms not alarming, it is well to post-
pone 'surgical interference in order to see if the cavity will
not close by cicatrization. In deciding the advisability of
operation the points to be considered are the general con-
dition of the patient, the nature of the primary disease, the
location of the cavity, whether it is multiple or single ab-
scess, the possibility of free drainage and the condition of
the pleural tissues. Cases of pulmonary collapse, circum-
scribed gangrene and abscess resulting from septic accumu-
lations in the bronchi from the pressure of tumors, aneu-
risms, injuries to the throat, etc., are not surgical cases and
these conditions should always be excluded.
After having located the diseased area as nearly as pos-
sible, the presence of pus must be determined by exploratory
puncture. These punctures may be repeated several times
if necessary to locate the cavity. It is not always easy to
locate a cavity with the exploring needle, as the location is
apt to be higher in the lung than the signs indicate. The
exploration may be made without anaesthesia, though in
many cases this is impossible. Chloroform is the best an-
aesthetic for this purpose and the anaesthesia must not be
profound. If pus is obtained the needle is left in place as a
guide, and exsection of one or more ribs is proceeded with.
As it is difficult to tell how much room is needed, it is well
PULMONRY ABSCESS. 263
to make a vertical incision instead of the oblique one often
used in operating for empyema.
As it is often impossible to tell with certainty that
pleural adhesions are present it is well to proceed, up to
the point of incising the pleura, as if they were absent.
Godlee recommends stitching the pleural surfaces together,
including a space from one and a half to two inches in diam-
eter, with six or eight stitches. The pleura is now incised
and if air draws through into the pleural cavity, more
stitches are introduced. This method has several ad-
vantages over a primary operation for producing pleural ad-
hesions. If the abscess is near the surface of the lung a
pair of sharp pointed forceps are introduced along side of
the needle, the latter is withdrawn and the opening enlarged
with the finger. Even in deep-seated abscesses it is proba-
ble that this method of entering the lung is preferable to the
use of the actual cautery. Haemorrhage may be controlled
by plugging. The drainage tube should be fixed to the
chest wall with plaster, as it is more likely to become dis-
placed than in empyema. The wound of the soft tissues
should be treated with chloride of zinc (40 grains to the
ounce) and packed, around the tube, with gauze wet in the
same solution and covered with iodoform (Godlee).
Irrigation of the cavity should not be practiced. Anti-
septic powders may be introduced, but they do little good.
A few layers of gauze covered by oakum or wood wool is a
convenient dressing when the discharge is abundant and
offensive. Frequent change of dressings is necessary. The
tube should be removed frequently and cleaned. It should
not. however, be removed for the first two days or it may be
difficult to reintroduce it. The tube should remain until ex-
pectoration has ceased and the discharge through the wound
has diminished to a teaspoonful or so daily.
PULMONARY GANGRENE.
Gangrene of the lungs is a condition of necrosis and de-
composition of lung tissue. It is almost always secondary
to inflammatory conditions of the lung. Laennec's divisiou
of circumscribed, and diffuse gangrene, is still adopted as
264 PULMONARY GANGRENE
most convenient, though in the so-called circumscribed va
riety its peripheral limitations cannot always be defined.
Pulmonary gangrene is not frequent, as the post-mortem
statistics of various hospitals show its presence in from only
one-half to three-fourths of one per cent, of the cases of
pulmonary disease.
^Etiology.—The microorganisms which induce gan-
grene may reach the lungs through the bronchi, blood ves
sels, or by extension from some adjacent organ. Various
organisms are found in the necrotic lung tissue. The
staphylococcus pyogenes aureus is supposed to be the pri-
mary cause of the necrosis (Bonome). Special microbes
have been described, and such organisms as leptothrix,
aspergilli, sarcinae, etc., are frequently found. It is likely
that several saprophytic organisms may be involved in the
production of gangrene.
Gangrene of the lungs occurs in connection with pneu-
monia, and while rare its occurrence is favored by lack of
nutrition, alcoholism, diabetes, nephritis and senility. In-
fluenza pneumonia may be followed by gangrene. The in-
fluence of mixed infections in pneumonia upon the occur-
rence of gangrene is not fully understood. Lobular pneu-
monia, secondary to the infectious diseases, may rarely
terminate in multiple foci of gangrene.
Pulmonary gangrene may supervene upon septic in-
flammation occurring in connection with chronic pneumonia.
Bronchiectasis may cause gangrene by the retention of sep-
tic products in the bronchi, or through the occurrence of
septic lobular pneumonia of adjacent lung tissue or even of
the opposite lung through inhalation of septic material.
Loss of sensibility or paralysis of the larynx allowing
of the passage of food, secretions, etc., into the bronchi
may, particularly in the insane, be a factor in producing
gangrene of the lungs. Regurgitated matter from the
stomach may also be drawn into the lungs. Gangrene of
the lungs may occur secondary to cancrum oris, epithelioma
of the mouth, tongue or oesophagus, diphtheria, etc. Sup-
purating bronchial glands may, by establishing communi-
on tcfn between the oesophagus and bronchi, cause gangrene.
PULMONARY GANGRENE, 265
Tumors or aneurisms in the mediastinum or lungs may
cause gangrene by obstructing the bronchi and causing dila-
tation of the tubes, retention of secretions and septic pneu-
monia and gangrene. Pressure of tumors upon the vessels
or nerves of the lungs has been considered a cause of gan-
grene. Pulmonary tuberculosis rarely results in gangrene.
Septic emboli in the lung may cause gangrene. They
may occur from thrombosis of the lateral sinus, thrombi
in the uterine veins in puerperal fever, or from the veins
surrounding foci of suppuration. Typhoid fever, ery-
sipelas and many other conditions may cause embolic gan-
grene of the lungs.
Abscess of the liver, fecal abscess, sub-diaphragmatic
abscess, cancer or gangrene of the oesophagus may cause
gangrene of the lungs by extension. Wounds and injuries
of the lungs with extensive extravasation of blood may be
followed by gangrene with or without pneumonia. Poison-
ing by foul air may result in gangrene of the lungs.
Morbid anatomy.—If the gangrenous area is near the
surface of the lung the pleura will be inflamed and covered
with lymph. The gangrenous area may be small or may in-
volve the greater part of a lobe. Embolic gangrene maybe
wedge-shaped.
In circumscribed gangrene the necrotic area is sur-
rounded by a zone of inflammation by which nature at-
tempts to limit the extension of the process. The gan-
grenous area may be black, gray or greenish and the ne-
crotic tissue may have been partially expectorated. The
contents of the cavity will be fetid, of a pulpy or semi liquid
consistence, and may consist largely of blood. The walls of
the cavity may be ragged, or may consist of granulation tis-
sue. Well developed induration may surround the cavity in
cases which have lasted some time. The bronchi and ves-
sels of the affected area may remain as shreds in the necrosed
mass, or may have been destroyed. The neighboring bronchi
are inflamed and contain fetid material.
In circumscribed gangrene there may be one or more foci.
The lower lobe is more often affected than the upper lobe,
and the peripheral portion of the lung is more involved than
266 PULMONARY GANGRENE.
the centre. The lung tissue surrounding the gangrenous
area is congested or consolidated, and surrounding this is an
area of well marked oedema.
When the gangrenous area extends rapidly, severe
haemorrhage may occur from rupture of vessels. Perfora-
tion of the pleura may uccur. Abscess of the brain is some-
times associated with circumscribed gangrene of the lungs.
The bronchitis which accompanies gangrene and which re-
sults from the irritation of decomposing material in the
bronchi may be very severe.
Diffuse gangrene has no limiting zone of inflammation.
The affected area usually has a fetid odor, is gray or black
in color, of a doughy or pulpy consistence, or may be a semi-
fluid mass in a ragged cavity. The pleura may be necrotic
and empyema or pyopneumothorax may be present.
Diffuse gangrene, while rare, is sometimes met with in
connection with pneumonia, and rarely after obliteration of
a large pulmonary artery though the infection resulting
from this cause does not often sphacelate. The larger por-
tion of a lobe may be involved.
Clinical history.—There may be no history indica-
tive of gangrene of the lungs. In the insane or in diabetic
subjects and in embolic gangrene even the odor of the
sputum and breath may be absent.
The very great variety of aetiological factors for gan-
grene of the lungs lead us to expect a marked want of uni-
formity in its clinical history. There may be a history of
chills with irregular fever and great prostration. Pain may
be present if the pleura is involved. Haemoptysis may be
an early symptom and may rarely be profuse and fatal.
Dyspnoea may be severe in cases showing great prostration.
Cough may or may not be troublesome. Fetid breath
usually precedes expectoration. The expectoration is yel-
low, brown or black; purulent or bloody; alkaline at first,
but later acid. It forms three layers on standing: an upper
of grayish froth; a middle, watery and clear; and a lower
layer containing shreds of lung tissue and, possibly, elastic
fibers.
In rare instances large fragments of lung tissue may be
PULMONARY GANGRENE. 267
coughed up. According to Osier elastic tissue is almost in-
variably present in the sputum. The fetor of the sputum is
more marked than in fetid bronchitis or pulmonary abscess.
It is particularly offensive when there is free communica-
tion between gangrenous cavities and the bronchi.
When gangrene follows pneumonia there may be early
prostration, small, feeble, irregular pulse, septic fever and
fetid expectoration. In some cases of gangrene after pneu-
monia, with great prostration, cough and expectoration
may be absent.
Symptoms and diagnosis.—Fever, cough, pain, dys-
pnoea, great prostration, fetid breath with expectoration
presenting the characteristics of gangrenous sputum are
the chief symptoms of gangrene of the lungs. The physi-
cal signs are often more inconclusive than the general
symptoms.
Signs of consolidation followed by evidence of the for-
mation of a cavity, especially after pneumonia, and with the
characteristic sputum and breath will enable us to diagnose
circumscribed gangrene. In children there maybe only the
signs of broncho-pneumonia.
In diffuse gangrene there will be evidence of more or
less complete consolidation of the lung. The voice and re-
spiratory signs of consolidation are modified or wanting as
the bronchi of the affected area are more or less occluded.
The diagnosis rests mainly on the history, prostration,
fever and characteristic sputum and breath. The sputum
should be examined microscopically for lung tissue,
Bronchiectasis, putrid bronchitis, pulmonary abscess
with fetor, rupture of an empyema into the lung, and local
necrosis of a phthisical cavity may resemble pulmonary
gangrene. In all lung cavities, other than gangrenous,
presenting fetor, the appearance of the fetor is subsequent
to the signs of a cavity, while in gangrene the fetid expec-
toration precedes the signs of a cavity. In empyema there
will be a history of pleurisy prior to the expectoration of a
quantity of pus, possibly fetid; but gangrenous odor will
usually be wanting and lung tissue will be absent from the
expectoration unless at the immediate time of rupture.
-,)M PULMONARY GANGRENE-
Treatment.—The treatment of pulmonary gangrene is
chiefly supporting, with absolute rest in bed. If there is
much pain or cough small doses of morphia may be given,
but care should be taken not to depress the patient.
Quinine, strychnia, whisky and milk with concentrated,
nourishing food are the chief necessities. Disinfection of
the air passages may be accomplished by the methods recom-
mended for bronchiectasis. If the creasote bath cannot be
tolerated, inhalations of vapor of carbolic acid (f per cent.)
may be used. Carbolic acid is also recommended for inter-
nal use in doses of from four to twelve grains daily. An in-
haler may be used for vaporizing the air passages, satura-
ting the sponge with a solution of creasote, menthol, aristol,
eucalyptus, etc., using from ten to fifteen per cent, of any
combination desired.
The subcutaneous injection of guaiacol in sterilized oil,
in daily doses of fifteen grains or more, is highly recom-
mended by Weil. Several observers have reported good re-
sults from these injections. Injections of antiseptic sub-
stances directly into the affected area of lung has been ad-
vised but is of doubtful utility. Traube advises the internal
administration of the acetate of lead; recoveries have been
reported under this treatment.
When gangrenous- cavities are circumscribed and acces-
sible, drainage is to be considered.
CHAPTER XIII
PULMONARY TUBERCULOSIS.
Pulmonary tuberculosis (consumption, phthisis) is an in-
fectious disease of the lungs caused by the bacillus tu-
berculosis. It is the most widespread and prevalent disease
affecting the human family. Existing from the earliest times
and recognized by Hippocrates it has continued its ravages
through centuries and still maintains its position as the
most fatal malady of mankind.
One-seventh of all deaths from disease are said to be due
to some form of tuberculosis. The U. S. Census Report for
1*90 gives 102,1** deaths from consumption. Vaughn esti-
mates, from the Census Report, that one person out of every
sixty of the population is affected with tuberculosis.
Statistical evidence is in favor of the decrease of tuber-
culosis, and some local statistics show marked diminution of
the disease. According to Russell there was a decrease of
44 per cent.in the death-rate from tuberculosis in the city of
Glasgow from 1H60 to 1H94. In Massachusetts there is re-
ported a decline of 20.2 per cent, per 10,000 in the death-rate
from pulmonary tuberculosis between lK"Jo and 1*95. Biggs,
commenting on the prevention of tuberculosis by the New
York Department of Health, says, "The death-rate in NewT
York from tuberculosis shows an almost regular and rather
rapid decrease from year to year". Pollock says, "We have
witnessed the immense decrease of deaths from phthisis and
a decided lengthening of its duration. Fewer die of it, and
are slow to die when affected.*'.
The modern conception of the nature of tuberculosis, the
result of the discoveries of Koch, is a striking endorsement
of the doctrines of Laennec who maintained the unity o
tuberculous processes; also of Villemin who in 1*65 demon-
strated the infective nature of tuberculosis by inoculation
experiments.
270 PULMONARY TUBERCULOSIS.
^Etiology.—We will not consider here the morpho-
logical characteristics of the tubercle bacillus nor the con-
ditions governing its culture and existence. In the vast ma-
jority of instances its presence in the lungs is the result of
post natal infection. This infection occurs through the air
passages or through the blood vessels, and, in rare instances.
by extension from the bronchial lymphatics. Infection may
occur in several ways.
Hereditary transmission. The possibility of inherited tu-
berculosis has long been a matter of dispute between those
who believe in its direct inheritance (Cohnheim,Baumgarten)
and those who believe only in the inheritance of constitu-
tional predisposing factors. Sims Woodhead says. "From
the public health point of view the tubercle bacillus must be
looked upon as the fons et origo mali, and all statistics that
have recently been collected go to prove that the tubercle
bacillus does its work,as a rule, in the post natal period. Al-
though there may be a few eases of congenital tuberculosis,
all statistics point to the fact that tuberculosis is contracted
after birth". According to Ransome heredity may act
through direct, active infection before birth; through hered-
itary transmission of latent germs: and through the trans-
mission of a susceptible constitution, but heredity has much
less to do with consumption than is popularly supposed.
Direct transmission must occur through the sperm, the ovum
or through the blood by the medium of the placenta. Al-
though bacilli have been found in the semen (Jani, AVeigert)
experimental results (Gartner) and clinical evidence are a-
gainst this method of transmission. Osier considers the fact
that the bacillus will not attack the nuclear material of which
the spermatozoon is made as good negative evidence on this
line. Baumgarten has detected bacilli in the ovary of the
rabbit artificially fecundated with tuberculous semen. The
possibility of infection by the ovum cannot be denied in view
of the above experimental facts.
The most frequent method of congenital transmission
is through the blood current by way of the placenta. This
was suggested by Cohnheim and developed by Baumgarten,
who believes the bacillus is introduced through the placenta
PULMONARY TUBERCULOSIS. 271
and umbilical vein ("placental infection"), or by the vum it-
self (' 'germinative or congenital infection"). Buggs has found
bacilli in the uterine wTallatthe site of the placental insertion,
in the blood of the umbilical vein, and in the vessels of the
infant's liver. Against Virchow's objection that the bacilli,
in germinative infection, would interfere with the develop-
ment of the ovum, Baumgarten brings his theory of the
latency of tuberculosis. While the possibility of the latency
of tuberculosis is borne out by the experiments of Mafucci
with avian tuberculosis, the acceptance of Baumgarten's ap-
plication of his theory in explanation of atavism in tuber-
culosis is hardly to bo expected.
Both clinical evidence- -as shown by the presence of tuber-
culosisin27.8 per cent, in 2,576 autopsies on children who died
who died during the first year of life (Botz), and by the fre-
quent occurrence of localized tuberculosis in children, and
experimental results are in favor of the occurrence of con-
genital tuberculosis. On the other hand, inoculations made
from the tissues of foetuses from tuberculous mothers are
usually negative, and the percentage of cases of congenital
tuberculosis is very small. Ogle's statistics show that be-
tween the second and tenth years of life there is a great de-
cline in the mortality from tuberculosis, and that between
the tenth and twentieth years of life the liability of females
to tuberculosis is fifty per cent, greater than males. These
facts do not conform with Baumgarten's theory of latent
tuberculosis. These matters refer particularly to the gen-
eral infection of tuberculosis and we will not pursue them
further.
The manifestations of parental heredity have been va-
riously estimated at from ten to sixty-six per cent. The fre-
quency of its manifestation is the principal source of the gen-
eral belief in the heredity of tuberculosis. The belief that
fathers transmit the disease most often to sons, and, per contra,
mothers to daughters, is not borne out by statistics. It is
generally stated that females are the subjects of hereditary
tuberculosis more often than males, and that heredity is most
often from the maternal side.
Infection by inhalation. The inhalation of dust contain-
272 PULMONARY TUBERCULOSIS.
ing bacilli is probably the most frequent method of infection.
Fltigge thinks that infection is not produced by dried spu-
tum or dust containing bacilli, but by finely divided particles
of sputum floating in the atmosphere.
The greater frequency of tuberculosis in towns and cities
and in the most condensed districts of these places indicate
the greater facilities for infection which attend the massing
of many individuals within restricted limits. Bacilli have
been found in the dust of street-cars and various public places.
Nutall estimates that a patient with moderately advanced
tuberculosis expectorates from one and a half to four billions of
bacilli in twenty-four hours. If this be any where near the
truth the effect of the free exercise of the great American
prerogative of frequent and indiscriminate expectoration can
be readily surmised. Cornet's inoculation experiments
with dust from hospital wards, asylums, prisons etc., show
a degree of infectiousness more or less proportionate to the
constancy of occupancy by tuberculous cases, and of inverse
relation to the degree of cleanliness etc. Medical wards were
six times as infective as surgical wards. Again, bacilli were
not found in dust from two wards occupied by tuberculous
cases. Pollock, judging from the results in the Brompton
Hospital for Consumptives, does not favor the idea that hos-
pital infection is frequent.*
The fact that the vast majority of cases of tuberculosis
are of the respiratory system; the great prevalence of the
disease in institutions where inmates are confined to close
quarters and a limited amount of fresh air; and the direct re-
lation between the incidence of the disease and the degree
of intimacy of association with tuberculous subjects or infect-
ed dwellings or places, all emphasize the possibilities of in-
fection by inhalation.
Infection by inoculation. The experiments of Villemin,
Cohnheim, and Salmonson have proved the possibility of
this mode of infection. Inoculation may occur through the
skin by washing soiled linen, scratches from a broken spit-
*Hance found the dust from various public places infective. Joccond Dumont
pallier think contagion in hospitals unlikely, Pean thinks it likely. Terrier, Dehove
think hospital contagion extremely likely to occur,
PULMONARY TUBERCULOSIS.
273
toon, infected earrings, infected hypodermic syringe, in mak-
ing post mortem examinations on tuberculous subjects, and
in performing circumcision. Baumgarten says that inocu-
lation of the superficial layers of the skin is impossible, sub-
cutaneous inoculation being necessary to insure infection.
Inoculation by the alimentary canal may occur through kiss-
ing consumptives, by the use of infected tableware, and by
contact with coughed up particles of sputum. Direct inocu-
lation through the generative passages, while possible, must
be extremely rare. Gerlach, Ballinger and others have shown
the infective quality of milk from tuberculous cattle. [Hay
found bacilli in 51 out of 351 separate samples of cows' milk,
and in 4 out of 204 mixed samples.] Ernst has shown that
milk may be infective even in the absence of tuberculous
mammitis in the animal from which it is obtained. Accord-
ing to Bang butter made from the milk of tuberculous cows
may be infective. Osier thinks the frequency of mesenteric
tuberculosis in children may be explained by the infective
qualities of milk.
Experiments show the possibility of infection in animals
by the use of the flesh of tuberculous subjects. This mode of
infection is extremely rare in human tuberculosis but presents
possibilities which should be guarded against. The Royal
Commission upon Tuberculosis states, "We must believe that
any person who takes tuberculous matter into his body in
curs some risk of acquiring tuberculous disease."
Inoculation, on the whole, plays an unimportant part
in the mode of infection of human tuberculosis.
Predisposing causes to infection. The geographical dis
tribution of pulmonary tuberculosis shows that while prac-
tically absent in certain arctic regions, deserts, and at great
altitudes, yet in no habitable part of the earth does there
exist complete immunity.
Climate. The climatic conditions favoring infection are
moisture and heat. The bad effect of wet sub-soil was shown
by Bowditch in 1862, who said "A residence on or near damp
soil is one of the primal causes of consumption in Massachu.
setts". Buchanan's investigations corroborate this view in
regard to the effect of wetness of soil. While hot climates
274
PULMONARY TUBERCULOSIS.
seem to favor an active course for tuberculosis, we may ac
cept Hirsch's statement that "The mean level of the temper-
ature has no significance for the frequency or variety of
phthisis in any locality". Low altitudes, moisture, rapid
and extensive changes in temperature, and cloudiness are
the climatic features which favor pulmonary tuberculosis.
Race. No race is exempt. Aboriginal people develop
susceptibility when removed from their usual conditions of
existence. Thus the Negro in Africa is not as susceptible
as in America though this race exhibits unusual susceptibil-
ty under all conditions. Susceptibility in the American
Indian has increased since the conditions governing his
early history have changed. Statistics show that a relative
immunity exists among the Jews.
Sex. Apart from difference at certain ages there is
practically no variation between the sexes as to liability to
infection, the mean annual mortality for a period of thirty
years being 2*1.4 for males, and 2428 for females (Kidd).
Ogle's statistics show that for the first fewT years of life the
mortality for the twTo sexes is alike; between five and thirty-
five the female mortality greatly exceeds the male; after
this period the male mortality exceeds the female. This
applies to pulmonary tuberculosis and not to general tuber-
culosis. The influence of pregnancy on infection has been
much discussed. Pollock states that the periods of puberty,
of gestation, of parturition and lactation are dangerous to
individuals predisposed to tuberculosis. This is true with
possibly the exception of pregnancy in certain individuals
in whom the latter state stimulates nutrition to an extent
which antagonizes all pulmonary diseases.
Age. No age is exempt. Hippocrates states the recog-
nized fact that pulmonary tuberculosis is most frequent from
the eighteenth to the thirty-fifth year. [18*1__1890 of
397,559 total deaths, 118,59* were from consumption, at ages
between 25 and 35 years.— Ransome.] Landousy has demon-
strated the tuberculous nature of several cases of broncho-
pneumonia in children under two years of age.
Occupation and environment. Occupations involving the
breathing of impure, overheated, or dusty air predispose
PULMONARY TUBERCULOSIS. 275
to infection. Sedentary or indoor work, bad ventilation and
drainage, the overcrowding of employees in close quarters
etc., are factors of environment. Flick's investigations in
Philadelphia, and Ransome's in Manchester, England, have
demonstrated that infection clings to certain dwellings once
they have become infected by tuberculous residents.
Individual predisposition. The modern understanding of
the infectious nature of tuberculosis has tended to modi-
fy the ancient theory of predisposition—a theory dating
from the time of Hippocrates and Galen and postulated on
presence of a special predisposition to tuberculosis. It is
argued by many that individual predisposition consists
merely in an inherited general constitutional liability to all
depressing influences, i. e., the predisposing factors of tu-
berculosis. This argument does not materially affect the
position of those who hold to the doctrine of predisposition.
Statistics undoubtedly show family tendency to tuber-
culosis, and, moreover, show that the mother's influence is
greater than the father's as regards both sexes; and that
the disease appears at an earlier age when there is family
tendency, particularly in females. Could Baumgarten's
theory of latent tuberculosis be established in all its phases
the matter of predisposition would assume a new position.
General and local diseases. Measles, whooping-cough,
influenza, variola, diabetes, insanity, syphilis, and, in some
degree, all depressing diseases predispose to tuberculosis.
Bronchitis, pneumonia (rarely), pleurisy, chronic heart dis-
ease particularly stenosis of the pulmonic valves, are pre-
disposing factors to tuberculosis of the lungs.
The opinion that a large proportion of pleurisies are
tuberculous is supported by post-mortem evidence and by
the subsequent history of these cases. Rokitansky taught
an antagonism between tuberculosis of the lungs and physi-
cal changes in the heart resulting in obstruction to the
pulmonary circulation. This has been denied by many, but
is supported by several observers of great clinical experi-
ence. Louis believed in the antagonism between mitral
disease and tuberculosis, and J. E. Graham states that mi-
tral stenosis antagonizes tuberculosis of the lungs. Ott
276 PULMONARY TUBERCULOSIS.
believes that left-sided disease of the heart is antagonistic
to pulmonary tuberculosis. The fact that mitral disease is
■ occasionally associated with tuberculosis of the lung does
not invalidate these views. My own experience is decided-
ly in accord with these observers as I have never seen tuber-
culosis of the lung develop in a person the subject of disease
of the left side of the heart wluch particularly affected the
pulmonary circulation.
The following case is of interest in this connection:
Woman aged 24. Married. A few weeks after child-
birth she developed an acute, lobular, tubercular pneumonia
of the right lung. After three weeks of severe illness there
were two weeks of improvement when another attack of
pneumonia developed, followed by signs of a cavity in the
right lung. Shortly afterward she developed an acute
rheumatism with signs of an acute endocarditis with mitral
localization. After the appearance of the mitral lesion
(regurgitant) there was much improvement in the lung
symptoms and the patient was soon up and about, and after
several months adopted a change of climate. While re-
covery was impossible in this case the advancement of the
disease was undoubtedly checked by the occurrence of the
mitral lesion.
It is claimed that traumatism is a factor in producing
tuberculosis. Surgeons, generally, recognize the effect of
traumatism in disseminating local tuberculosis. Mendels-
sohn has recorded cases where contusions of the chest have
been followed by pulmonary tuberculosis.
Morbid anatomy.—Histologically a tuberculous nodule
is a non-vascular structure consisting of a central substance
made up of one or more multinucleated giant cells, or of a
granular substance surrounded by giant cells. These cells
may be connected by a network of anastomotic processes;
outside of the central structure there is usually found large
epithelioid cells with large nuclei and granular protoplasm.
These cells lie in the network formed by the processes
from the giant cells; surrounding these structures is a more
or less indefinite zone of lymphoid cells contained in a homo-
geneous, or fibrillated reticulum which is best marked in
slowly developed lesions.
The changes which occur in a tuberculous nodule are
PULMONARY TUBERCULOSIS. 277
caseation and fibrosis. Whether the change assumes one
form or the other depends on the mode and extent of the
infection, and on the resisting power of the individual.
This defensive action of the body against the action of the
bacilli is supposed to depend in part on phagocytosis (Met-
schnikoff), and partly on an antitoxic action of the serum
and blood plasma which is derived from the leucocytes
either by a process of excretion or by their destruction.
In caseation the cells in the center of the nodule become
swollen, fused, and lose their structure (coagulation necro-
sis.—Cohnheim) becoming opaque and homogeneous (gray
tubercle); fatty degeneration occurs and the nodule becomes
cheesy and of soft consistence and yellow color (yellow
tubercle), particularly in large and diffused lesions. Ca-
seous lesions may soften and form a cavity or they may be-
come calcified by the deposit of lime salts and be expector-
ated or encapsulated.
Fibrosis occurs when coagulation necrosis is limited and
the zone of lymphoid tissue is transformed into dense con-
tracting tissue. This change postulates resisting power of
the tissues and is Nature's method of limiting the lesion. It
occurs in infections of limited severity and extent especially
when occurring through the vessels.
The type of the lesion in the lung will depend on the
mode of infection. If this is through the vessels, coming
from a caseous focus in some other organ or tissue (Buhl) or
in the lung itself or as part of a general tuberculosis, there
results a more or less extensive eruption of disseminated
miliary nodules from embolic arrest in the alveolar walls.
These nodules are most numerous at or near the apex of the
lung. The lung tissue between the nodules may be normal,
congested or cedematous, or may present areas of consolida-
tion. In some cases there is a tendency to necrosis and
softening of the nodules if the case is not too rapidly fatal;
in others there is a tendency to fibroid induration of the al-
veolar walls and surrounding tissues. Fusion of the nod-
ules, in the earlier stages before the softening of "yellow"
tubercle appears may give the tissue a gray, gelatinous ap-
pearance (Laennec's gray infiltration).
278 PULMONARY TUBERCULOSIS.
If the infection occurs through the air passages lodg-
ment is found in the terminal bronchioles or the alveoli, and
there results peri-bronchitis and broncho-pneumonia. The
structural changes are, chiefly: epithelial accumulation
within the alveoli; fibrinous exudation and leucocytes in the
alveoli; cellular infiltration and thickening of the alveolar
walls and terminal bronchi; increase in the interlobular con-
nective tissue. These changes are variously associated and
the preponderance of one or the other will depend on the
type and stage of the lesion. The alveolar accumulation of
epithelial cells is similar to that of ordinary lobular pneu-
monia and is a characteristic lesion of the majority of cases
of acute tuberculosis of the lungs, and of the acute phases
of the so-called fibro-caseous variety.
Fibrinous exudation and leucocytes within the alveoli
are found in some of the most acute forms of the disease—
the lobar type of pneumonic tuberculosis. The consolida-
tion resembles that of croupous pneumonia but there is more
or less epithelial proliferation. These intra-alveolar changes
give the tissue a reddish or grayish-yellowT color. It is
friable and soft with a more or less lobulated periphery.
the breaking down of the tissue may form cavities of vari-
ous sizes with the soft, irregular walls.
Infiltration and thickening of the alveolar walls and
bronchioles is a constant and characteristic lesion of all
cases of pulmonary tuberculosis. It replaces and gradually
obliterates both the alveoli and the pulmonary capillaries,
which latter effect is probably largely responsible for the
tendency to retrograde metamorphosis exhibited by fibro-
caseous tuberculosis of which this lesion is particularly
characteristic.
Increase in the interlobular connective tissue is a fea-
ture of the chronic forms of tuberculosis. There is a great-
er tendency to fibroid development than in the inter-alveolar
tissue, less tendency to degeneration, and blood supply is
generally maintained. Extensive induration of the lung
may result from this process in chronic tuberculosis. Cavi-
ties, when present, have dense, fibrous walls.
More or less bronchial catarrh is associated with these
PULMONARY TUBERCULOSIS.
279
changes. The bronchial wall is infiltrated with cells and
ulceration may be present. The peri-bronchial tissue may
show cell infiltration. Large cavities may be traversed by
fibrous bands formed from bronchi, or arterial chords which
are generally closed by thrombosis and obliterating changes
before ulceration of the wall results in haemorrhage. Aneu-
rism of the vessel may occur, however, before these
changes take place, and be followed by fatal haemor-
rhage.
Bronchial stenosis, dilatation, ulceration; pulmonary
emphysema, collapse, oedema, gangrene; pleural adhesions,
thickening; miliary tuberculosis of the pleura or pericardium'
pneumothorax, pyopneumothorax, and tubercular enlarge-
ment of the bronchial glands in children (Loomis, Ballinger)
are the principal associated chest lesions. Lesions of other
organs are frequent.
The lung lesions occur in endless variety and degrees.
and we will not attempt to recount them. Miliary nodules
are frequently found in the lung having been distributed by
the circulation from a focus of inspiratory origin and pneu-
monic nature. More frequently the secondary foci are due
to transmission of infective material by aspiration aided by
gravitation from one part of the lung to another.
The characteristic apical invasion of tuberculosis which
is common to all varieties of the disease is generally ex-
plained on the ground of lessened functional activity. This
localization is most commonly an inch or twTo belowr the im-
mediate apex and nearer the posterior surface than the an-
terior. A less common location is just below the outer third
of the clavicle in the outer portion of the upper lobe. Fowler
shows that tuberculous lesions of the lung progress, as a
rule, by distinct routes and almost always from above down-
ward. From the primary foci in the apex, extension is
downward in the anterior portion of the lobe just within the
margin. The middle lobe of the right lung is usually affect
ed secondarily to the upper right lobe, and late in the dis
ease. It frequently escapes altogether.
The lower lobe of the lung previously affected becomes
involved early, usually before necrosis of the upper lobe
280
PULMONARY TUBERCULOSIS.
has occurred and before the opposite apex is affected. The
site of the lesion in the lower lobe is a spot midway between
the border of the scapula and the spinous processes of the
vertebrae and opposite the fifth dorsal spine. Fowler con-
siders the involvement of this area early in the disease as
characteristic of the chronic varieties of tuberculosis and of
immense clinical importance. Extension from this area is
backward and along the line of the interlobular septum.
Extension toward the base is usually by scattered areas.
Basic lesions occurring in the absence of apical lesion are
either non-tubercular, or the tubercle is secondary. Inva-
sion of the opposite apex, to that primarily affected, may
be early, but usually not till after the invasion of the lower
lobe of the lung primarily affected. The lesion is symmetri-
cal with that of the primary lesion, but occasionally may affect
the upper lobe close to the septum and opposite the axillary
region. Occasionally the lesion crosses from the upper lobe
of one lung to the upper portion of the opposite lower lobe.
Cavities result from necrosis and ulceration of a tuber-
culous area, usually from the result of these processes upon
the bronchi of the affected area which become dilated from
retained secretion. The center of a caseous area may ulcer-
ate and form a cavity without involving the bronchi. Three
forms of cavities are found: The recent ulcerative cavity
of acute cases, with soft necrotic walls without limiting
membrane,—these cavities may rupture into the pleural
cavity and cause pneumothorax: Cavities with well defined
walls of limiting membrane which secretes pus and which
gradually undergoes slow necrosis with increasing size of
the cavity,—these cavities may be crossed by trabeculae of
arterial and bronchial cords, and are found in the chronic
varieties of tuberculosis: Stationary cavities, quite small,
with smooth lining membrane surrounded by dense, fibrous
tissuet—they may communicate with the bronchi {cicatrices
fistuleuses. —Laennec).
Clinical history.—No one infection of the human or-
ganism exhibits such a varied clinical history and course as
tuberculosis, and espcially so in regard to its pulmonary
manifestations of which many classifications embodying
PULMONARY TUBERCULOSIS.
281
much variety of nomenclature have been made. It is un-
necessary to discuss these classifications.
Basing our distinction partly on the mode of infection
and partly on the gross character of the pathological
changes, we recognize four more or less distinct types of
pulmonary tuberculosis, i. e., miliary tuberculosis, fibroid
tuberculosis, acute pneumonic tuberculosis, and chronic
pneumonic tuberculosis. The frequent combination of
these types of the disease gives pathological and clinical
justification for the various classifications which have been
alluded to, but for the sake of brevity and clearness the
above division has advantages.
Miliary tuberculosis of the lungs occurs as a feature of
general tuberculosis, or an eruption of miliary tubercles
may occur as a current or terminal event in other forms of
pulmonary tuberculosis. A caseous focus may discharge
into a branch of the pulmonary vein (Weigert). In some
cases, as in those which follow measles, whooping-cough
typhoid fever, etc., no source of infection can be discovered.
Miliary tuberculosis is more common in children than
in adults, and is rare after fifty, though it may occur at any
age. The lungs are large, hyperasmic and full of discrete
tubercles of recent formation about the size of a pin's head
and gray in color or semitransparent. When miliary tubercu-
losis is secondary to chronic lesion ofthe lung the tubercles
are less clearly defined, are grouped together, show casea-
tion, and are most plentiful in proximity to the original le-
sion. The primary lesion may assume a broncho-pneumonic
type.
There is a history of sudden onset with general
malaise, loss of appetite, headache and fever. Haemop-
tysis may mark the onset or there may be marked bronchi-
tis with muco-purulent or rusty sputum. Dyspnoea is se-
vere and out of proportion to the physical signs. Cyanosis
is a distinctive feature because of its severity. It is most
marked in the lips and finger tips. The cheeks are flushed,
cough troublesome, pulse rapid and feeble, and the respira-
tion may be from forty to eighty per minute. The temper-
ature ranges from 100Q to 103.5° F. and according to Fowler
282
PULMONARY TUBERCULOSIS.
presents a continuous and an inverse type. In the former it
rises gradually and continues high with slight morning re-
missions; in the latter the maximum temperature is in the
morning instead of the evening.
A typhoid state may develop towards the end of the
case. Acute miliary tuberculosis is generally fatal in from
two to three weeks though it may last for three or four
months.
Fibroid tuberculosis is a chronic miliary tuberculosis oc-
curring most often as a primary affection of the lungs in
persons of good resisting power and without predisposition.
In these persons a moderately severe or extensive infection
through either the vessels or air passages may result in
miliary tubercle with a tendency to fibroid transformation
rather than caseation and softening.
It occurs most often in men and in those wdiose dusty oc-
cupations favor sclerosis of the lung tissue. Apical invasion
is the rule as in other forms of tuberculosis though second-
ary lesion may occur in any portion of the lung. The le-
sions occur as isolated nodules which are indurated, pig-
mented and feel like shot in the lung tissue; or are grouped
as nodules or areas of induration. Fibroid miliary tubercu-
losis of the lung may occur in connection with intestinal and
mesenteric tuberculosis, and there is also, as a rule, miliary
tuberculosis of the pleural and pericardial surfaces, as in the
following case:
Woman aged 57. Family history good, previous health
fair. Sick several months with irregular diarrhoea. Had
lost flesh rapidly. Temperature 99.5° F., pulse 100. Lungs
showed general induration most marked in the apices. No
bronchitis, cough or expectoration. The abdomen was fiat
and irregular, deeply seated nodules could be felt. The
diarrhoea could not be controlled for more than a day at a
time. She became greatly emaciated and died three months
after coming under observation.
Post mortem examination showed intestinal and mesen-
teric tuberculosis, miliary tuberculosis of the pleural and
pericardial surfaces and general disseminated miliary tuber-
culosis of both lungs with well-marked fibrosis.
The history is one of gradual onset, with some cough
PULMONARY TUBERCULOSIS.
283
and gradual loss of flesh and strength, extending over a
period of several years, or, with a history of this kind last-
ing for a year or two there may be entire absence of all
subjective symptoms, the process having been arrested.
Again, a portion of the lung—usually the apex—may be
markedly changed, with no history of illness other than
gradual loss of strength.
More or less cough is present though it may be absent.
Fever is usually slight (one-half to one degree). Quite fre-
quently the course of the disease is apyrexial. Haemoptysis
is common in the early stages, may be recurrent, is usually
slight, may be profuse, but in either case is not connected
with the occurrence of lobular inflammation as it is in the
pneumonic type of the disease. Diarrhoea and night sweats
are usually absent. In advanced cases with marked retrac-
tion of the lung and thickened pleura the cough may be
violent, paroxysmal, and tend to produce vomiting. Dys-
pnoea and rapid pulse may be present in cases where em-
physema has developed. Muco-purulent or fetid expectora-
tion may be present and the cases may ultimately present
the variouscli nical features of advanced sclerosis of the lungs
This form of tuberculosis tends more than any other t(
undergo arrest, or, at least, to run a prolonged course. It
may last from ten to twenty years.
Acute pneumonic tuberculosis (galloping consumption,
phthisis florida, caseous tuberculosis) occurs in two forms:
the disseminated lobular or bronco-pneumonic type, and the
lobar or pneumonic type. The former occurs most often in
children or young people, and in those with a predisposition
to tuberculosis. These two types constitute only about two
and one-half per cent, of the total cases of pulmonary tu-
berculosis. The lobar variety is rare and occurs more often
in adults than in children.
Acute pneumonic tuberculosis is usually primary though
it may occur secondary to chronic pulmonary tuberculosis.
In the lobular type there is acute inflammatory broncho-
pneumonia beginning in the smaller bronchi which are filled
with cheesy substance while the alveoli are filled with
catarrhal products. These areas are first grayish-red and
later become white and caseous. By fusion they may re-
semble the lobar type, but the lobular distribution can usu-
ally be made out. These caseous areas, from 1-3 cm. in
2*4 PULMONARY TUBERCULOSIS.
diameter, may be irregularly scattered throughout the
lungs. Usually they are most numerous at the apex.
Smaller, opaque, gray or caseous nodules may be present.
Small or large cavities may be found at the apex or base of
the lungs. Prudden has demonstrated that these changes
may occur without the agency of a secondary infection.
This form of pneumonia may follow the aspiration of blood
into the bronchi in cases of haemorrhage (tuberculosis aspir-
ation pneumonia.—Baumler).
In the lobar type a single lobe or the entire lung may
be involved. The affected area is gray, yellowish-white
and caseous. The surface is smooth or granular, uniform-
ly changed, and it may be very difficult to detect any tuber-
culous foci. Softening and cavities may be present in the
apex. In some cases the change is less uniform, there be-
ing aggregated masses of caseous areas surrounded by
hyperaemic or consolidated tissue.
The onset of the lobular form is variable. Haemorrhage
may be the initial symptom, followed by chills, high temper-
ature, rapid pulse and respiration, and rapid loss of flesh and
strength. In children the disease usually follows measles
or whooping-cough. While convalescing from these dis-
eases the temperature may rise suddenly, there is cough,
dyspnoea, and signs of consolidation. The case commonly
ends fatally in from a few days to two or three weeks, or,
with the appearance of hectic fever and sweats the disease
may pass into a condition of chronic phthisis.
The temperature in the lobular form is high and of a
remittent type varying from 101-104^ F. In the later
stages with diminished vitality the temperature may range
from 96 or 97° F. in the morning, to 103W F. in the evening
(Fowler).
In the lobar type of the disease the onset is sudden.
There is chill, rapid rise in temperature, pain in the side,
cough, mucoid or rusty sputum, dyspnoea and, perhaps,
cyanosis. In all respects the attack is like an ordinary
pneumonia. At the eighth or tenth day, however, the tem-
perature becomes irregular, the pulse rapid, expectoration
muco-purulent and, perhaps, greenish (Traube), and sweat-
ing may occur. Death may occur in from one to four
weeks; the case may be prolonged for two or three months
or it may become one of chronic phthisis.
Chronic pneumonic tuberculosis (chronic ulcerative tuber-
culosis, fibro-caseous tuberculosis). This form of the disease
constitutes the great majority of the cases of pulmonary
tuberculosis in which caseation and excavation occur.
PULMONARY TUBERCULOSIS.
2*5
While the lesion is primarily tubercular, in nearly all cases
it ultimately becomes a mixed infection, and some of the
best known and most troublesome features of the disease
are due to secondary infection with pyogenic organisms.
The lesions of this variety of tuberculosis show great
variety in nature and distribution. Broncho-pneumonia,
miliary tubercles which are disseminated either by the air
passages or the vessels, sclerosis, caseation and excavation
are the chief changes. The formation of cavities in this
disease is favored by the occurrence of secondary infection
(Prudden). Tubercular changes in the bronchi, bronchial
glands, pleurae, and in the other organs and tissues of the
body are frequent. Tubercular laryngitis is common in this
form of the disease.
The onset of chronic pneumonic tuberculosis is very
varied. It may come on insidiously, and marked changes
may have occurred in the lung before any symptoms de-
velop. Again, the same insidious invasion is accompanied
only by symptoms of anaemia and gastric disturbance, par-
ticularly in young females, or there may be irregular fever
simulating malaria. In any of these types if the tempera-
ture is watched it will usually be found from one-half to one
degree above normal in the afternoon or evening. A per-
sistent temperature of this kind is suspicious of, but does
not necessarily indicate, tubercular infection.
In many cases there is a history of repeated attacks of
bronchitis which gradually become prolonged, or a winter
cough may be protracted through the summer and be ac-
companied by emaciation and night sweats. This is a fre-
quent history following influenza bronchitis occurring dur-
ing the winter or spring months. Many cases present no
history but that of a more>or less constant cough which is
dry and not troublesome. They will often not acknowledge
a cough unless closely questioned.
There is, at times, a history of one or more attacks of
pleurisy, either dry or with effusion; the pleurisy has disap-
peared,'but following it there is a history of cough, fever,
night sweats and emaciation.
In some instances the larynx is the primary seat of the
2*6 PULMONARY TUBERCULOSIS.
disease, though usually it is involved secondarily. There
may be laryngeal irritation and cough, mucoid expectora
tion, huskiness and aphonia.
Haemoptysis may be the first symptom in some cases.
There may be marked haemorrhage followed within a short
time by signs of lesion in the lung, or the haemorrhage may
be slight and the interval before lung symptoms develop
may be long. In other cases there is repeated slight haem-
orrhages. In many cases when any considerable hasmor-
rage occurs there is already disease of the lungs. Haemor-
rhage is present in from sixty to eighty per cent. ■ of the
cases of pulmonary tuberculosis (Osier).* In most cases
it recurs, and may be a prominent feature (haemorrhagic
phthisis). The bleeding is usually sudden, the first intima-
tion the patient has of it is a salty, warm taste in the mouth.
The haemorrhage may come on while coughing but more
often does not. The amount is usually small especially in
the early history of the case. [In 69 per cent, of 4,125 cases
of haemoptysis in the Brompton Hospital the quantity of
blood expectorated was less than one-half of an ounce.]
Cervical or axillary tuberculous adenitis may precede
by months or years the development of pulmonary lesion,
though in some cases the development of the two conditions
is coincident.
Pain is frequently complained of and is usually con-
nected with pleurisy. It is most often felt in the lower and
lateral regions of the chest, or beneath the upper portion of
the scapula.
Cough is a very variable symptom. It may be dry and
hacking at first, later it is loose, with muco-purulent expec-
toration. It may be paroxysmal if there are cavities. Par-
oxysmal morning cough may be followed by nausea and
vomiting.
The respiration is usually increased, somewhat in pro-
portion to the amount of tissue involved and to the degree
of fever. It may be 26-30 per minute during the exacerba-
*Stricker's percentages for soldiers are: without special cause, 86.8 percent.
tuberculous; after exercise, 74.4 per cent, tuberculous; after swimming^ or direct
jurny to the thorax, one-half not tuberculous.
PULMONARY TUBERCULOSIS. 2*7
tion of all symptoms which attend the invasion of new areas
of lung tissue by broncho-pneumonia. Dyspnoea is not
common even when considerable lung tissue is involved, ex-
cept in chronic cases with marked sclerosis and a weak
heart. Nervous dyspnoea may be troublesome at times. Cy-
anosis is rare except where miliary tubercles invade the
sound portion of a lung partly crippled by chronic disease.
Fever is an almost constant element of the clinical his
tory of chronic tuberculosis. There are apyrexial periods,
and in arrested tuberculosis fever will be absent. As a rule
it is a fair indication of the activity of the process in the
lungs. Every variety of range is exhibited. In the early
stage or in quiescent cases the fever may range from 9* to
99° F. As the disease advances and softening occurs, the
fever will range from 99 to 101° F., the morning remission
may be as low as 97w F. A sudden and maintained eleva-
tion of 102-103° F. is indicative of a new area of lobular in-
flammation or a new tract of miliary infiltration. Whatever
type the temperature may exhibit it may maintain this type
for weeks or months at a time if there are no disturbing el-
ements.* Towards the termination of a fatal case the tem-
perature may be subnormal for a day or two. The cases
exhibiting the most irregular and fluctuating temperature
are those in which secondary infection exists.
The pulse is very variable. It is rapid with consider-
able fever or with extension of the disease. According to
Wilson Fox it is influenced more by the patient's strength
than by the degree of fever.
The quickest pulse is usually observed in the morning
(Smith, Fox). There is no reliable relation between the
pulse and the respiration. Nervous influences affect the
pulse greatly. In the late stages the puis© is very rapid
and of low tension. Pseudo-angina and palpitation are fre-
quent. According to Powell palpitation is most frequent in
patients with considerable retraction of the left lung.
Night sweats occur in most cases though some patients
escape entirely. They occur towards morning when the
*Maragliano, Stern and Erbman believe that hectic fever is due to secondary
nfection ahd not to tubercular infection. Fowler dissents strongly from this view
2**
PULMONARY TUBERCULOSIS.
fever drops, or at any time when the patient sleeps there
may be sweating. Sweating may appear early and be per-
sistent, but its appearance usually coincides with the begin-
ning of softening. The severest sweating may disappear
late in the disease without any reference to treatment.
Emaciation is usually progressive as long as the pro-
cess in the lung is advancing, though increase in weight
may occur while the disease is progressing if the patient's
nutrition is forced. As a rule stationary or increased
wTeight is a sign of quiescence of the disease.
Gastric crises may occur, especially in neurotic subjects
and insane delusions and halucinations are sometimes pres-
ent.
Diarrhoea may occur early from errors in diet. Occur-
ing late in the disease it is indicative of intestinal ulceration.
Constipation may be troublesome at times. Anal fistula
usually occurs late in the disease and is much more common
in males than in females.
Symptoms and diagnosis.—In miliary tuberculosis
besides the dyspnoea, cyanosis and peculiar type of fever,
we have the physical signs of bronchitis combined with those
of a varying degree of empysema, and, perhaps, those of
irregular areas of broncho-pneumonia. The percussion note
may be irregularly dull at the base; in the anterior regions
of the chest it may be hyperresonant. Sibilant, sonorous,
and fine mucous and subcrepitant rales may be present.
Pleuritic crepitations may occur from local tubercles (Jiir-
gensen). High-pitched, tubular breathing may be heard at
the base of the lungs; in front and above the breathing may
be low in pitch and expiration may be somewhat prolonged.
Daily alteration in the percussion pitch may be due to the
re-expansion of collapsed areas (Eustace Smith). Miliary
tuberculosis associated with chronic lesion of the lungs may
present few recognizable alterations in the physical signs.
The degree of dyspnoea and cyanosis; the temperature
range; together with the discrepancy between the physical
signs and the general condition of the patient are important
aids in diagnosis. Bacilli are often absent from the sputum.
and frequently there is no sputum. Choroidal tubercles
PULMONARY TUBERCULOSIS.
2*9
may be present, and signs of meningeal tuberculosis or other
forms of general infection wTill aid in the diagnosis. When
the lung is involved in connection with acute general tuber-
culosis the case may resemble typhoid fever, but the tem-
perature is less regular, may assume the inverse type or may
be sub-normal in the morning. The Widal test may decide,
though a negative result in the first four or five days does
not exclude typhoid fever.
Acute bronchiolitis in children and after measles or
whooping-cough, may resemble acute miliary tuberculosis of
the lung. The temperature range is more irregular in mil-
iary tuberculosis, and in bronchiolitis the correspondence
between the dyspnoea and the degree of pulmonary involve-
ment is more evident.
Fibroid tuberculosis. The symptoms of this form of tu-
berculosis are those of sclerosis of the lungs with which it
is clinically identical. In some cases there is an alar or
pterygoid conformation of the chest (Galen, Aretaeus) char-
acterized by winged scapulas, oblique ribs, increased length
of chest, depressed shoulders and diminished anteroposte-
rior diameter of the thorax. The costal interspaces are de-
pressed and the inferior ones show inspiratory recession.
The lateral expansion is diminished, the movement being
mainly perpendicular. Depression of the supra and infra-
clavicular spaces is present and the sterum may be de-
pressed. The heart may be displaced and epigastric pulsa-
tion may be present. The vocal fremitus may be increased
or diminished, depending on the degree of induration, its
proximity to the surface and the degree of emphysema pres-
ent. Moderate induration and emphysema may give more
marked fremitus than a more solid and airless portion of the
lung.
The percussion note may be high-pitched and hard, or
resonant from emphysema. The respiration is weak with
prolonged, high-pitched expiration. Wavy, interrupted or
cog-wheeled respiration may be present. Fine, crackling
rales may be heard in various portions of the lungs. If cav-
ities are present they are usually dry and present the usua.
signs which are apt to have an amphoric character. These
290 PULMONARY TUBERCULOSIS.
changes in the lung are most marked in the apices. Retrac-
tion of the apex below the upper level of the clavicle with
signs of induration is decidedly indicative of tubercular dis-
ease. Local changes with collateral emphysema may be
difficult to detect.
Repeated examinations of the sputum may fail to show
bacilli, but sooner or later they can usually be found. In
primary or secondary basic tuberculosis of a fibroid nature
the diagnosis may be difficult, the only positive proof of its
nature being the presence of tubercle bacilli. The pres-
ence of old lesions in the apices may aid in the diagnosis.
In chronic miliary tuberculosis of the lungs associated with
mesenteric or intestinal tuberculosis the physical signs may
be very indefinite.
Acute pneumonic tuberculosis. In the lobar form the physi-
cal signs may be those or ordinary pneumonia, i. e., dullness,
bronchial breathing and bronchophony. Pleuritic friction
may be present. The breath sounds may be feeble or, at
times, absent. The diagnosis may be aided by a more re-
mittent temperature than is common in pneumonia. The
absence of crisis; the presence of rapid pulse, sweating,
emaciation, mucopurulent expectoration, and, sooner or
later, the presence of bacilli in the sputum will establish
the diagnosis. The diagnosis must often be necessarily de-
ferred till after the acute stage. Fowler remarks that "These
cases are of very rare occurence, and any one who feared
that every case of ordinary pneumonia he observed might
prove to be of this nature would by his unusual alertness
do more harm than good."
In the lobular or disseminated form of the disease the
first signs may be fine, crackling, metallic rales at the apex.
just outside of the nipple, or diffuse rales all through the
lungs. Local signs of consolidation, particularly breathing
of a bronchial character and bronchophony may be heard,
but if the consolidated area is not near the surface of the
lung these signs are indefinite. Several disseminated areas
of consolidation can sometimes be made out. If cavities are
present they will manifest the usual signs.
The diagnosis rests on the presence of bacilli in the spu-
PULMONARY TUBERCULOSIS.
291
turn, or of elastic tissue if the lung is breaking down. Or-
dinary broncho-pneumonia in children may, when attended
with dilation of the tubes, be indistinguishable from tuber-
cular pneumonia. If the sputum cannot be obtained it is
well to withhold opinion as to the exact nature of the case.
Chronic pneumonic tuberculosis. The subjects of this
form of the disease present the pale, loose, dry skin, blue
veins, flushed cheeks, pearly conjunctivae and pale mem
branes which make up the composite general appearance
popularly known as "consumptive-looking," which, taken
with the clinical history, is often almost sufficient for a di-
agnosis.
Cough, which is one of the earliest symptoms, varies
greatly in character and constancy. In some cases there may
be little or no expectoration. The early history of fibrous,
miliary, or caseous tuberculosis without softening is much
more likely to show expectoration than is that of chronic
pneumonic tuberculosis. When bronchitis precedes the dis-
ease the expectoration is likely to be profuse. In the early
stages it may consist of viscid, glairy, or watery mucus:
later it contains small gray, greenish, purulent masses. If
softening has occurred the sputum is muco-purulent and
yellow or greenish in color and may contain flattened
masses (numular sputum). Sputum of this kind is likely to
come from cavities and has been considered characteristic
of phthisis, but it may be present from chronic bronchitis.
This sputum is heavy and sinks in water, a fact of much
concern to some patients. The character of the sputum is
changed by haemorrhage, gangrene, bronchiectasis and vari-
ous other associated conditions.
The sputum should be examined in every case for tu-
bercle bacilli. They are most apt to be found in the small
gray or yellowish-green masses found in the sputum. The
examiner will use whichever of the various methods of
staining that appears to him to be the most convenient
and reliable. There is no constant relation between the
number of bacilli and the activity of the process in the lung,
nor does the continued presence of bacilli necessarily mean
that the disease is progressing actively. As a rule dlminu-
292
PULMONARY TUBERCULOSIS.
tion in the amount and purulency of the sputum and in the
number of the bacilli indicates a lessened activity of the
disease.
Elastic tissue is an important element in phthisical
sputum at times. It may come from the bronchi, alveoli,
or from the arterial wall. That from the bronchi presents
as a long net-wTork or as three or four long fibers lying close
together; that from the alveoli shows bunched fibers with a
curled or alveolar arrangement; that from the arteries may
showT as a sheet of fibers. In order to examine the fibers
place some of the purulent material upon a glass plate
about four inches square and press it out into a thin
layer with another plate about three inches square. Shown
against a black background the elastic tissue appears as
grayish-yellow spots which can be removed to an ordinary
slide for further examination. (Andrew Clark's method.)*
The curved and alveolar arrangement of the fibers is
the most reliable evidence of destructive processes which
are almost always due to tuberculosis. This method, howT-
ever, is of less importance than formerly, owing to the
more definite, reliable, and earlier information given by the
presence of bacilli. Calcareous fragments are sometimes
expectorated along with the sputum.
According to Cabot the red corpuscles of the blood are
normal in pulmonary tuberculosis and the haemoglobin
diminished. Stein and Erbmann show that leucocytosis
is present under certain condicions. They think it is not
connected with tubercular infection but is due to secondary
infection. The physical signs of chronic pneumonic tuber-
culosis vary with the stage and extent of the disease.
Inspection. The conformation of the chest may be indi-
cative of disease though this form of tuberculosis occurs in
chests of any shape or build. In the earlier stages inspec-
tion may be negative through a loss of expansion of the
apices is noted very early in most cases. It is often best
*Fen wick's method is to boil equal parts of sputum and a solution of caustic
soda (20 grains to the ounce) for a few minutes, Let stand for 24 hours in a conical
glass. Examine sediment, The centrifuge will facilitate this process.
PULMONARY TUBERCULOSIS^ 293
observed from behind the patient. As the disease progres-
ses there is retraction of the supra and infraclavicular re-
gions, flattening and widening of the second and third in-
terspaces below the clavicle, marked loss of motion and
drooping of the shoulders. If the upper lobes are emphy-
sematous the scapulae may be raised and the shoulders have
an elevated appearance. The apex of the heart may be
slightly raised, or displaced into the axillary region if much
retraction of the left lung is present. When a considerable
cavity has formed in the apex the chest wall from the second
to the fourth interspaces will be markedly flattened especially
if there is induration and contraction of the tissues around
the cavity.
Palpation is very important in the early stages. Slight
increase in fremitus is obtained early. From the anatomical
conformation and distribution of the right bronchus the
right apex exhibits normally a better marked fremitus
than the left apex If the fremitus in the left apex is equal
to that in the right it indicates disease; if it is greater, the
indication is all the stronger. We must remember that a
local area of moderate fibrosis combined with some degree
of emphysema may, through better conduction facilities,
give more marked fremitus than an area more advanced
toward caseation but less easily vibrated. When a cavity
has formed at the apex the fremitus is markedly increased.
Palpation of the apices and lateral regions often gives a
clear idea of the relative expansion of the two sides.
Percussion. Slight increase in the pitch of the percus-
sion note over the clavicles or in the supra or infraclavicu-
lar spaces is one of the earliest signs of the disease. It is
often best appreciated when the breath is held after a full
inspiration. Loss of resonance above the clavicle from re-
traction of the apex is often the earliest sign of a localized
apical focus of disease. [There should normally be about
a finger's breadth of resonance above the clavicle.] Dull-
ness on firm percussion in the supraspinous fossa? may be
present before it is apparent in front. If a cavity is formed
the percussion note will be high-pitched, short, wooden, and
tubular or tympanitic if the cavity is empty and the sur-
294
PULMONARY TUBERCULOSIS.
rounding tissue is indurated. If the cavity is near the sur-
face the cracked-pot sound may be obtained.
Auscultation. Increased vocal resonance is an early sign
of consolidation. Usually there is the same relative differ-
ence in the vocal resonance of the two apices as is found in
the percussion pitch. The right apex often shows some in-
crease in the vocal resonance without the presence of dis-
ease,—that is, above the accepted normal standard. In-
creased resonance is often best heard behind over the snpra-
spinous fossa or toward the point of the shoulder. Again,
it may be best marked in the apex of the axillary space.
Over a cavity the various sounds are cavernous or amphoric
in character, and pectoriloquy may be obtained, often best
heard with the whispered voice.
The earliest change in the respiratory murmur is often
a feebleness or partial suppression of the inspiratory sound
with prolongation of the expiration which is slightly higher
in pitch than normal. Again, both sounds may be harsh
and higher-pitched, the greatest elevation in the pitch being
during expiration. Later, both sounds are much increased
in pitch, the exjfiration is much prolonged and is tubular
and blowing in character. Over areas of lobular consolida-
tion bronchial breathing and bronchophony may be heard.
In the tissue adjacent to the diseased areas wavy, interrupted
or cogwheel breathing may be heard, especially if there
is a tendency to fibrosis. It is often obtained in the lower
and lateral regions of the chest. Over a cavicy the typical
breath sounds are cavernous in character,—a tubular, high-
pitched inspiration followed by a prolonged, blowing ex-
piration which is empty and tubular in quality and lower in
pitch than the inspiration. The breath sounds may be
markedly amphoric in quality..
Fine, crackling, subcrepitant, localized rales may be
heard early, or more diffuse, moist rales may be present.
As softening progresses the rales become more numerous,
larger, softer and liquid in character. When rales are in-
distinct and doubtful in character they are heard more
plainly with the respiration which follows the act of cough-
ing. Gurgles and tinkling may be heard at times in cavi-
PULMONARY TUBERCULOSIS. 29")
ties. Large cavities in the left apex may present the
heart sounds very plainly, or even a transmitted systolic
murmur. Systolic gurgles and clicks may be heard in a
cavity if it is near the heart. A large cavity with thin
walls and fluid contents may give a succussion sound
(Walshe). Cardiorespiratory murmurs, and pleuro-pericar-
dial friction sounds are frequently heard.
Areas of consolidation close to a large or dilated bron-
chus may give auscultatory sounds simulating those of a
cavity in the lung tissue. Extensive retraction of the
lower lobe with an emphysematous condition of the
upper lobe may give auscultatory signs simulating those of
a cavity in the region of the interlobular septum. The lat-
eral extension of these signs and the comparative condition
' of the two lobes v\ ill differentiate.
An absolute diagnosis may rest on the presence of ba-
cilli in the sputum. While our knowledge of the relation of
this organism to tuberculosis of the lungs greatly facilitates
our diagnostic ability in doubtful cases, it is often the case
that great attention is given to the demonstration of bacilli
to the neglect of careful study of the physical signs and clin-
ical history which is even more necessary to a thorough
appreciation of the individual case.
Many cases of insidious advent can be diagnosed by the
physical signs before eruption into the bronchial tract ex-
hibits bacilli in the sputum. Again, bacilli are sometimes
absent from the sputum when there is well-marked local
evidence of disease. Even in cases of moderately acute
bronchial invasion bacilli may be temporarily absent while
the apical localization makes it certain that the process is
tubercular. We occasionally see local catarrhs in the apex
presenting rales but no change in percussion pitch; which
show no bacilli and which get well without leaving any evi-
dence of permanent disease. However, any local change in
the apex presenting raise in the pitch of the percussion note
should be regarded as tubercular until it is proven other-
wise.
In all cases of pulmonary tuberculosis bacilli will be
found sooner or later if sought for, and in primary basic
296 PULMONARY TUBERCULOSIS.
tuberculosis or in secondary tuberculous processes engraft-
ed on chronic non-tuberculous basic lesions, the detection of
bacilli may be the only way of deciding the nature of the
process. In fibroid lesions—syphilitic or otherwise—ac-
companied with cavities the demonstration of the persistent
absence of bacilli may be the sole means of proving the
non-tubercular nature of the case. In cases with haemor-
rhagic onset the early presence of bacilli may decide the
nature of the case long before any local change can be de-
tected.
Complications.—The complications which, most often
modify the course of pulmonary tuberculosis are pneumonia.
bronchitis, pleurisy, pneumothorax, haemoptysis, laryngeal
tuberculosis, peritonitis, albuminuria and diarrhoea.
Pneumonia. Acute pneumonia is rare in pulmonary
tuberculosis. It is a dangerous complication and while re-
covery may occur, the progress of the tuberculous lesion is
hastened; markedly so if softening of the pneumonic area
occurs.
Bronchitis. The danger from bronchitis usually lies in
its liability to cause broncho-pneumonia or extensive em-
physema. When bronchitis is extensive it may be the di-
rect cause of death.
Pleurisy. The association of pleurisy with tuberculosis
of the lung is frequent and its exact bearing on the history of
the latter is not easy to define. Occurring early in the history
of the case it gives, according to Osier, "a stamp of chronicity
to the case.'' Sero-fibrinous effusion may be absorbed.
Purulent or haemorrhagic effusions are very unfavorable.
In general miliary tuberculosis, sero-fibrinous effusions may
be an expression of the general disease.
In basic tuberculosis of the lungs- the occurrence of
pleurisy, if not purulent or haemorrhagic, may modify the
activity of the tuberculous process in the lungs.
Pneumothorax. The acute pneumonic form of tuberculo-
sis is more apt to be complicated by pneumothorax than are
he chronic forms. In rare instances of disease of the
PULMONARY TUBERCULOSIS. _:9/
middle or lower lung the collapse of the lung incident to the
occurrence of pneumothorax may limit the extension of the
lesion of the lung.
When tuberculosis is limited to one lung the occurrence
of pneumothorax may not be immediately dangerous, the
air may be absorbed and partial re-expansion of the lung
may take place. When the opposite lung is extensively
diseased the occurrence of pneumothorax is dangerous and
may be fatal in a few minutes. (In 39 cases of death after
pneumothorax, the average duration of life was 27 days.—
Douglass-Powell.) In some cases life may be prolonged
for years.
Hemoptysis. In the ear y stages of tuberculosis the oc-
currence of haemoptysis is not of immediate danger, in the
later stages it is of grave import on account of the possibil-
ity of pulmonary aneurism. According to Williams, the
percentage of deaths in a series of cases of haemorrhage in
the various stages was: in the stage of infiltration, 13.95;
in the stage of softening, 24.61; and in the stage of excava-
tion, 67.74.
Laryngeal Tuberculosis. This complication is generally
unfavorable. It is usually of late occurrence. In cases
where the lesion in the larynx is primary the course of the
disease may be very rapid, while in other rare instances it
may run a protracted course. The lactic acid treatment for
laryngeal tuberculosis has modified the unfavorableness of
the prognosis to some extent.
Peritonitis. Any form of peritonitis constitutes a very
unfavorable complication of pulmonary tuberculosis. The
most dangerous form is acute general peritonitis from in-
testinal ulceration with or without perforation. General
tuberculosis of the peritoneum is rarely recovered from as a
complication of pulmonary tuberculosis. Chronic localized
tubercular peritonitis is less dangerous than the previous
forms.
Albuminuria. The importance of albumen in the urine
depends entirely on the cause as determined by careful
analysis of the urine, and on the presence of changes in the
vessels, heart, and other organs. According to Fowler, in
29* PULMONARY TUBERCULOSIS.
cases of albuminuria associated with pulmonary tuberculo-
sis, amyloid disease of the kidney wras present in 6.1 per
cent., parenchymatous nephritis, or interstitial nephritis in
6.7 per cent., and either miliary or caseous tubercles of the
kidney in 6.5 per cent, of the cases.
Diarrhoea. Severe diarrhoea may be fatal in the late
stages of pulmonary tuberculosis. It is commonly due to
ulceration of the intestine, or to lardaceous disease. In
either event the prognosis is very unfavorable.
Treatment.—In the treatment of pulmonary tuberculo-
sis we include such measures of prophylaxis as are appli-
cable to individuals who by birth or acquirement are predis-
posed to the disease, also such means of prevention of direct
infection as apply with more or less direct force to every in-
dividual whether there be predisposition or not, and whose
observance is demanded by public hygiene in order that the
spread of pulmonary tuberculosis may be controlled.
As our inherent vis medicatrix naturaj yet remains the
only specific we possess against pulmonary tuberculosis it
follows that the treatment of the disease consists in aiding
the forces of nature in every way possible to develop indi-
vidual resistance against the disease.
The frequency with which quiescent tubercular lesions
are found in the lungs of persons dying from other diseases
emphasizes the potency of the natural cure of tuberculosis.
According to Heitler the Vienna post mortem records showred
that in 4.7 per cent, of 19,292 deaths not directly due to tu-
berculosis the lungs contained old tuberculous lesions.
Harris gives the percentage as 3*.* in 200 autopsies.
Prophylaxis. The prophylactic measures against tuber-
culosis should begin with the birth of the predisposed in-
dividual, if, indeed, they should not begin sooner. The re-
sults of sanitorium treatment in pregnant tuberculous fe-
males and their issue gives force to the statement of Knopp
that the "State and municipal care of consumptives should
begin with the child in utero."
As far as the legal restriction of the marriage of tuber-
culous subjects is concerned there can be no question of the
abstract benefit of requiring a clean bill of health in this
PULMONARY TUBERCULOSIS.
299
particular despite disturbance of social ethics. The ques-
tion of the marriage of persons with arrested tuberculosis of
the lungs is not so simple. Females run much greater risks
than males. It is better to give a straight-forward opinion
on the subject—which is usually disregarded—and place the
responsibility wiiere it belongs.
The child of a tuberculous mother should be suckled by
a wet nurse or be fed artificially. Special attention must be
given the dietary during the first few years of life. When
fed on cow's milk it is best to boil the milk. Attention
should be given to the nose and throat, to the bronchial af-
fections of childhood, and to the general health after the
infectious diseases of early life. The best prophylactic
measure for these children is an out-door life. They should.
be literally turned out of doors to live in fresh air and sun-
shine. They should sleep in wTell ventilated rooms and have
a daily cold sponge bath. As the period of puberty ap-
proaches we should be on the watch for conditions of anae-
mia especially in girls. Syrup of the iodide of iron, cod-
liver oil, and arsenic are useful at this period. Later on, in
early adult life, those who are predisposed to tuberculosis
should be advised to remove to a suitable climate for a per-
manent residence.
Measures of prevention include the careful inspection
of dairies, abattoirs and their products, by competent officers.
This is a matter of vast importance and one which state and
municipal governments are coming to appreciate. Atten-
tion to the sanitary condition of public places and convey-
ances is also a matter where municipal regulations may be
productive of much benefit.
The compulsory notification of pulmonary tuberculosis
is a municipal question which has received considerable dis-
cussion. As an abstract question of public health there is
much to be said in its favor. On the other hand the parallel
as to the necessity of notification, between tuberculosis and
the infectious diseases already on the notifiable list, is not
readily apparent to the mind of the layman as the direct ori-
gin of the infection can usuallv not be demonstrated.
Neither is the parallel a just one as far as the benefits ac-
300 PULMONARY TUBERCULOSIS.
cruing to the infected individual are concerned, nor will it
be until there are state and municipal institutions for the
treatment of indigent tuberculous subjects. Sir Richard
Thorne thinks compulsory notification does more harm than
good, that New York's experience demonstrates it to be ex-
tremely partial, only effectual against tenement classes, and
that the diminution of the death rate was already in prog-
ress. In the absence of the ability of departments of
health to do anything more than furnish gratuitous informa-
tion, it is doubtful if compulsory notification is advisable.
The information can be equally well distributed through the
visiting and out-departments of medical institutions and
such distribution should be required of them.
It should be impressed on the tuberculous subject that
carelessness in his habits is dangerous to himself as well as
to others. He should expectorate only into a- sputum cup
or cuspidor containing a five per cent, solution of carbolic
acid, or into a small cloth which is to be immediately burned.
He should under no circumstances swallow his sputum. The
contents of the sputum cup should be burned twTo or three
times daily and the cup boiled and disinfected. All eating
utensils used by the patient should be washed separately
and thoroughly boiled, as should also all soiled linen worn
by the patient. Tuberculous subjects should sleep alone.
Under proper precautions the dust from hospital wards
containing tuberculous patients does not contain bacilli.
The same precautions applied to the home life of patients
would render the danger of infecting others practically ob-
solete.
Our measures of treatment may be classed as general,
special and symptomatic.
General Measures of Treatment. General methods consist
in diet, tonic medication, antiseptic medication and open-air,
sanitorium, and climatic treatment.
Diet. The nutrition of tuberculous patients is a most
important matter. The dietetic rules must be adapted to
the state of the patient's digestion. If the digestion is good
a liberal, mixed diet is advisable. If the digestion is poor
every effort must be made to improve it, and with this end
PULMONARY TUBERCULOSIS.
301
in view a change of climate or a sea voyage may be under-
taken with great benefit. When this is impossible the pa
tient should be kept at rest, if there is fever, and fed every
three or four hours with small quantities of milk, butter-
milk, koumyss, eggs, meat extracts or powTdered meat. As
much time should be spent in the open air as possible.
When the stomach is irritable the method of forced feeding
recommended by Debove is useful. The stomach is washed
out and a litre of milk containing an egg and 100 grammes
of finely powdered meat is introduced through the tube
thrice daily. If the patient is able to dispense with the
tube the administration of a pint of milk containing an egg
and a teaspoonful of somatose every four hours may be pref-
erable.
Patients with active tubercular disease require a great-
er amount of nourishment than a healthy individual in order
to compensate for the bodily waste. The results of forcing
the amount of food as practiced at such sanitoria as that of
Nordach in the Baden Black Forest are very encouraging
when combined with the proper amount of fresh air and
exercise.
A couple of teaspoonfuls of milkine in eight ounces of hot
water taken at bed time or during the night often relieves
the cough and promotes rest better than a sedative draught.
The same potion in the morning promotes expectoration and
counteracts the depression so common at this period of the
day.
The routine administration of alcohol in tuberculosis is
not advisable. Dry wines may be allowed with benefit in
some cases. In advanced stages a little champagne or
whisky or rum taken in a hot drink may be of occasional
benefit.
Tonic medication. The most reliable tonic remedies
are cod-liver oil, strychnia, hypophosphites, iron, and ar-
senic. These remedies, as a class, are not adapted for the
periods of high fever.
Cod-liver oil is of benefit, when easily assimilated, in
improving nutrition. It is more acceptable to children than
ot adults and is better tolerated in winter than in summer.
3(>2 PULMONARY TUBERCULOSIS.
Its value in tuberculosis has been much over-estimated in the
past. The oil alone generally disturbs the digestion before
enough has been taken to be of any great benefit. It is best
administered in capsules in combination with creasote, or
some of the many "tasteless"' preparations may be used.
The dose should not be large enough to disturb the stomach.
The so-called extracts of cod-liver oil appear to be as bene-
ficial as the oil itself. After several years continuous use
of them I am convinced that they stimulate digestion and
improve the bronchial catarrh associated with tuberculosis
to as great an extent as the oil itself when the latter is well
borne. They are not irritating to the stomach and can be
given to children without difficulty and can be given contin-
uously at any stage of the disease with great benefit.
Strychnia is a valuable remedy in tuberculosis. Williams
regards it as a specific for the retching of phthisical patients,
and says it enables them to take cod-liver oil continuously
without gastric derangement when given in doses of from
3^ to ¥1¥ of a grain. Mays gives strychnia an importance
next to rest and nutrition in phthisis. He gives it in doses
as high as 4- of a grain. Pepper has reported excellent re-
sults from the continuous use of strychnia. While Mays'
estimate is an exaggerated one, strychnia is a very useful
remedy. All other medicines seem to have a better influence
when the patient is under the effect of stimulating doses of
strychnia. A convenient method of administration is to be-
gin with six drops, thrice daily, of a solution containing two
grains to the ounce; increase one drop every third day until
the patient is taking as much as is well borne (usually about
15 to 1* drops). Insomnia is sometimes the first symptom of
overdosing.
The alkaline hypophosphHes are valuable in pulmonary
tuberculosis. The combined bypophosphites have, after a
long period of t: ial, seemed to me to be of little use, indeed,
in many instances, seemed to be distinctly harmful. On the
other hand the hypophosphite of soda is of great benefit in
many cases. It should be given in doses not to exceed two
grains thrice daily, and is adapted to cases with little rise in
temperature. If a temperature of 100-101° F. is present the
PULMONARY TUBERCULOSIS.
303
hypophosphite of quinia may be used. Hypophosphites are
beneficial chiefly through their influence on nutrition.
Darenberg says there is a great loss of hypophosphites from
the body in phthisis and thinks that they aid the forma-
tion of fibrous tissue and the calcification of tuberculous for-
mations. Hodgkinson concurs in this opinion.
Iron is a valuable tonic in tuberculosis. According to
MacKenzie the neutral preparations are best, and fever is
regarded as a contraindication. Fowler recommends the
syrup of the iodide, or the phosphate, in cases with glandu-
lar enlargement in young subjects. He thinks Blaud's pill
is useful if cough is not severe, but thinks that iron increases
the cough and the tendency to haemorrhage. I have found
the so-called "tasteless"tincture or the citro-muriate of iron,
combined with the compound tincture of cinchona, of value
in tuberculous cases.
Arsenic is of use in some cases. Williams recommends it
in the early periods and in cases combined with asthmatic
conditions. Osier advises the use of Fowler's solution in all
varieties of tuberculosis. Fowier and Burney Yeo have not
seen much benefit from the use of arsenic. Arsenic is of
particular value in anaemic cases and the iodide of arsenic is
sometimes of special value. On the whole arsenic does not
seem to be as efficient in combating the malnutrition of tu-
berculosis as it is in the malnutrition of other conditions and
Jaccoud's statement that "It would be difficult to find an
agent more capable of combating the malnutrition always
existent in the disease" seems to be an overestimate of the
value of the drug.
Iodoform is, according to Ransome, one of the best
drugs for aiding nutrition and relieving cough. Europhen
may be used as a substitute for iodoform. Flick uses an in-
unction composed of
Europhen, 3i
Oil of rose, gtt. i
Oil of anise, 3i
Olive oil, §iiss
A tablespoonful of this is rubbed into the arm-pits and
thighs at night. The odor may be removed in the morning
by sponging with bay rum.
304
PULMONARY TUBERCULOSIS.
Antiseptic Medication. It is generally admitted at pres-
ent that it is impossible to directly inhibit the tubercle bacil-
lus through the internal administration of anti-bacillary
remedies, and that the good effect of these remedies when
given internally is through their effect on nutrition by stim-
ulating digestion and assimilation.
Creasote is the principal remedy of this class. Known
since 1*30, and its use in tuberculosis described by Bouchard
and Timbert in 1*77, it was not much in use until Summer-
brodt in 1**7 gave the results of the treatment of 5,000 cases
with creasote. Summerbrodt believed in its specific proper-
ties and ardently advocated its use in immense doses. It is
generally conceded that moderate doses give better results
than are obtained by attempting to saturate the system with
the drug. The best results seem to be obtained from doses
not to exceed from five to ten minims. Pure beechwood
creasote is best. It may be given m capsules, or the crea
sote "perles" may be used, or it may be given in cod-liver
oil, malt, or wine with vegetable bitters. The most conven-
ient method is to drop it into empty capsules and follow its
administration with a glass of milkine. Carbonate of crea-
sote (creasotal) is a more eligible preparation in that it has
not the disagreeable odor of creasote and is not so irritating
to the stomach. It is a liquid, has little taste, is said to
contain 92 per cent, of creasote, and in the intestinal canal
it splits up into creasote and carbonic acid. It may be given
beaten up with the yolk of an egg, or may be given in cap-
sules. The dose is, at first, five drops after meals. Leyden's
method is to increase three drops daily up to twenty-five
drops; after two or three weeks it is reduced gradually to
ten drops, and subsequently the dose is again increased.
Guaiacol, a derivative of creasote, is much used as a
substitute for the latter. Aside from its odor it is a more
eligible preparation than creasote. It agrees better with
the stomach, and it has seemed to me, after several years
continuous use of guaiacol, that the results were better than
with any other .preparation of this class except with the
pure creasote in such patients as tolerated the creasote un-
usually well. Guaiacol may be administered in the same
PULMONARY TUBERCULOSIS.
305
way as creasote and in about the same dose. From five to
ten drops appear to give about the best results. The follow-
ing is a useful formula:
Guaiacol, lii
Alcohol, 3v
Wine of cod-liver oil, Ixii
*Dose,.a tablespoonful.
Guaiacol may be given hypodermically, using 1 to 7
minims of sterilized guaiacol and injecting deeply. It may
also be used by inunction, giving, once in two or three days,
10 to 60 minims either undiluted or with olive oil, glycerine,
or tincture of iodine. These are, however, objectionable
methods with no obvious advantages.
Carbonate of guaiacol may be given in cachets, or in
capsules in doses of from five to fifteen grains thrice daily.
It is well borne by the patient but does not appear to be as
efficacious as liquid guaiacol. Benzosol is an antiseptic of
value but in my experience has not been of special value in
tuberculosis. The dose is from five to ten grains. Guaiaco
late of piperidine is recommended in doses of from five to
twenty-five grains. According to Chaplin and Tunnicliffe
it is safe, causes no unpleasant effects, is exceedingly well
borne, and patients under its influence improve in appetite
and strength. Iodo-guaiacol camphorate, eosote (valerianic
acid ester of creasote) and various other combinations of
creasote are recommended but do not appear to have special
therapeutical advantages or power over those already men-
tioned.
The use of antiseptic inhalations and sprays is of ad-
vantage in pulmonary tuberculosis in lessening the amount
of expectoration, modifying the cough, and preventing in-
*The following formula is ax eligible one for preparing the above preparation.
Gaduol, 64 grains.
Guaiacol, 128 minims.
Alcohol, 1 fl. oz.
Fuller's earth, 4 drams.
Peptonized manganese, 2 drams.
Water, 2 fl. oz.
Sugar. 2 oz.
Port wine, q. s, to 1 pint.
Mix the gaduol. guaiacol and alcohol and triturate thoroughly with the Fuller's
earth. Dissolve the pep. manganese In the water, add the wine and sugar and mix
thoroughly with the gaduol and guaiacol mixture. Let this mixture stand for a day,
shaking occasionally. Filter nnd pass enough wine through the filter to preserve
the volume.
306
PULMONARY TUBERCULOSIS.
fection of the larynx. Burney Yeo recommends creasote,
carbolic acid and chloroform for the latter purpose. Fox
thinks antiseptic inhalations of value. Eucalyptol, iodine
in ether, menthol, aristol, oleum pini sylvestris, camphor
etc., may be used. Douglass recommends the use of euca-
lyptus oil made from the leaves of the eucalyptus globulus
and administered by saturating the air of the patient's room
by means of suspended cloths dipped in the oil, and by the
inunction of three or four drams of lanoline ointment con-
taining three drams of oil to the ounce.
Inhalations of the oil of cinnamon is highly recommend-
ed by Lucas-Championniere, and by Hilton Thompson. The
results are said to be diminution of cough, expectoration,
temperature, number of bacilli, and increase in weight.
Intra-tracheal injections of eucalyptol, menthol and other
substances have been practiced with alleged good results.
While this method is of benefit in bronchiectatic conditions
in phthisical cases, it does not appear to be of any special
benefit to the disease of the lung. Injections of a dram of a
solution composed of guaiacol, 2 parts; menthol, 10 parts;
olive oil, 88 parts may be used.
The direct injection into the lung tissue of iodine, car-
bolic acid, creasote (3 per cent. sol. in sterilized olive oil),
iodoform and other substances has bee^a practiced and is
strongly recommended by Pepper. When carefully admin-
istered such injections are, as a rule, not dangerous though
serious results may follow them. Treatment by compressed
air either pure or saturated with creasote has been attended
with benefit in some cases. It has, however, not yet been
demonstrated that the introduction of antiseptic substances
into the lungs by any of these methods is attended with any
permanent improvement of the diseased area of lung tissue.
and while it is possible to introduce, by inhalation, oil solu-
tions directly into the smaller bronchi, and, possibly, the al-
veoli also, the benefit, in phthisis, is probably confined to
those tissues which are in direct contiguity with the patent
air passages.
When we carefully review the equivocal position of the
old and tried medicaments for pulmonary tuberculosis, as
PULMONARY TUBERCULOSIS. 307
well as the thousand-and-one modern "cures," we are
obliged to admit that we are not yet in position to dispute
Laennec's statement that "although the cure of tuberculosis
is possible for nature, it is not so for medicine. "
Fresh Air Treatment. The benefit to the tuberculous
subject of the systematic indulgence in fresh, pure air is
universally conceded by all observers. This recognition of
the power of fresh air is admitted in no equivocal terms
Wilks says ' 'The only remedy known for consumption is
air, air, fresh air." Ransome says "Fresh air night and
day before .everything else." Trudeau's experiments on
confined and unconfined rabbits illustrate the value of the
open-air treatment of tuberculosis.
The fresh air treatment may be carried on with the pa-
tient at home or at a suitable sanitorium, without a change
in climate. At home the fresh air treatment is more or less
difficult to manage, especially in the cities. A partially
successful attempt, however, is better than to.house a pa-
tient in a stuffy, ill-ventilated room, dope him with medicine
and blame nature for the result. The patient should have
the sunniest, brightest room obtainable. The windows
should be kept open during the day, and partially so at
•night. If there is active disease with fever the patient
should be kept in bed, or if there is a porch or yard avail-
able he may be wrapped up and placed in an invalid's chair
and allowed to spend four or five hours daily in the open
air. Neither cough, fever, night sweats, or haemorrhage
contraindicate fresh air. Ransome says that nothing re-
lieves the fever so much as fresh air. Moderately low tem-
perature is not important, but wetness and high winds
should be guarded against. If the patient is well enough to
be about he should spend six to eight hours daily in the
open air and take a daily amount of exercise which must
be specified by his physician.
The sanitorium treatment of tuberculosis has risen in
importance because of the results obtained at such institu-
tions as those of Nordach, Falkenstein, Gobersdorf, Davos,
etc., in Europe, and at the Sharon sanitarium near Boston,
the Adirondack sanitarium, the Asheville sanitorium, the
:;os
PULMONARY TUBERCULOSIS.
Aiken sanitarium, etc., in this country, and various institu-
tions in Canada. To obtain good results it is not necessary
that the sanitaria be situated in an ideal climate. Burton-
Fanning says that good results are obtained where climatic
conditions are only moderately favorable, though the con-
ditions most conducive to good results are pure, cool, brac-
ing air, abundance of sunshine, dryness of soil, and eleva-
tion above the sea. At the Victoria hospital for consump-
tives, near Edinburgh, where the climate is by no means
ideal, and the patients not of the most favorable class, with
an average residence of less than three months, the results
are said by Philip to be very encouraging. The plan of
treatment in these sanitoria is to keep the patient in the
open air during the day as much as possible without regard
to the weather except in special cases. Very liberal diet is
given. The windows of the patient's room are wide open
all day, and sufficiently so at night to insure good ventila-
tion. The average temperature of the rooms is kept at
from 60-65° F. Exercise, bathing, medication and all
auxilliary means are employed to hasten recovery. Daily
observation is given each patient. These institutions, con-
ducted under the supervision of competent and reliable men,
in whom the profession may repose confidence, furnish bet-
ter opportunity for recovery to a patient than he will find
by adopting climatic treatment in his own way, and without
intelligent direction.
There is great need in this country for sanitoria near
our large cities where patients with moderate incomes may
be treated at a small expense. It is to be hoped that the
state and municipal governments will soon realize that there
is not only humanity, but also economy, in the establish-
ment of public institutions on the sanitorium plan for the
treatment of their indigent tuberculous residents.
In the climatic treatment of tuberculosis the open air
feature must not be neglected. Patients sometimes have
the idea that if they make a suitable change in climate they
must perforce get well without any effort on their part.
The value of any climate is in direct ratio to the number of
days throughout the year which the patient can be in the
PULMONARY TUBERCULOSIS.
309
open air and sunshine. The average temperature is of
secondary importance. The majority of the patients with
good family history and in the early stage of the disease
will get well in any climate if they live an outdoor life.
Proper accomodations and diet are not always obtain-
able in desirable climates and this must be considered when
patients are not able to endure an out-door life. Those
who can live out doors can usually get along with such food
as can be obtained. A camping trip across our western or
southwestern states is one of the best methods of utilizing
the fresh air and climatic methods of treatment.
The earlier the climatic change is made the better the
chances for recovery. It is very difficult to persuade patients
to break up business and social associations early enough to
give them the best results from climatic treatment. Later,
they are not only willing, but insist, against advice, on a
change of climate. In case of improvement it is difficult to
keep patients in a proper climate for a sufficient length of
time. Properly conducted sanitoria in our own localities
would obviate some of these difficulties by affording a place
where patients could be kept under proper conditions for a
portion of the year.
In deciding the advisability of a change of climate we
must be governed entirely by the patient's condition, and
not by the anxiety of himself and friends. Patients with
high fever, night sweats, loss of flesh, extensive areas of
lung involvement, or cavity formation, should not be allowed
to go away from home.
The various climates may be divided into those of high
altitudes, the dry, warm climates, and the moist, warm
climates.
High altitudes possess, according to Williams, dim-
inished barometric pressure—rare atmosphere, and dia-
thermacy or increased facility of transmission of the sun's
rays which causes an increase in the difference between sun
and shade temperature of 1° F. for every rise of 23r> feet.
The o-eneral result in selected cases of chronic tuberculosis
being excellent: improvement in K-J per cent,, great im-
provement in 74 per cent., disappearance of all symptoms
310 PULMONARY TUBERCULOSIS.
in 41 percent.; local conditions show 75.5 per cent, im-
proved, 5.5 per cent, stationary, and 19.18 per cent, worse.
Both sexes do well. The most favorable age is from 20 to
30, and those with hereditary disease are especially ben-
efited.
Cases of incipient disease, with haemorrhagic tendency,
are often much benefited by high altitudes, though such per-
sons should not be suddenly changed from a low to a high
altitude. Patients with a temperature above 101° F. should
not be sent into high altitudes, and the latter is contra-
indicated in patients with extensive lung involvement, cav-
ities, aneurysm, laryngeal involvements, catarrhal tubercu-
losis, all varieties of acute disease, weak heart, emphysema,
and chronic varieties of tuberculosis when much lung tissue
is involved or there is extensive degree of fibrosis of the
lung, particularly where the heart is weak.
A residence of from eight to twelve months at least is
necessary in order to obtain benefit from high altitude. Of
the higher altitudes in this country the Colorado, New
Mexico and Arizona resorts are the best. Asheville and the
Adirondacks are the best of the more moderate elevations.
Such moist, warm climates as Florida (Gulf coast), the
Bermudas, the Maderia Islands, Malaga, the Island of Cor-
sica, and Falmouth in Great Britain are the best. They are
adapted to cases with limited lung space, emphysematous
and bronchial conditions, and weak hearts.
Dry, warm climates, like the lower portion of the Rio
Grande Valley, southwestern Arizona, southern California,
various points in Georgia, the Carolinas and eastern Ten-
nessee in this country; the Riviera, Egypt and Algiers are
the most noted points. According to Foster it is doubtful
if the Mediterranean offers the best climate for the majority
of cases. Hillier praises South Africa, and Sand with
enumerates the advantages of the Egyptian deserts.
Ocean voyages, while beneficial in some cases, are con-
traindicated, according to Parkes Weber, in advanced cases,
cases with fever, in laryngeal and in intestinal tuberculosis,
and in cases associated with advanced arterial sclerosis or
cardiac disease.
PULMONARY TUBERCULOSIS. 311
Special Treatment. The treatment of tuberculosis with
special preparations like the new (T. R.) tuberculin, Mar-
agliano's anti-tuberculosis serum, Hirschfelder's oxytoxins,
etc., is yet in an experimental stage, and the one thing
definite in regard to it is that the literature of the past five
years on this subject will make curious reading half a cen-
tury hence. Trudeau, whose experimental work with
various serums at the Saranac laboratory gives his opinion
weight, thinks that the outlook for an efficient tuberculosis
antitoxin is not entirely hopeless.
Symptomatic Treatment. The symptoms which most
often demand attention are the fever, cough, sweating,
diarrhoea, haemorrhage, and gastric disturbances.
Fever is almost constantly present in pulmonary tuber-
culosis and is, to some extent, a measure of the intensity of
the disease. Its reduction is a most difficult therapeutic
measure, indeed, so little is accomplished toward the well-
being of the patient by the reduction of the fever by drugs
that it is only when the fever is unusually high that it
should be attempted. The depression resulting from the
use of the coal tar products overbalances the slight benefit
derived from them. The combination of two and a half
grains each of phenacetine and quinine is often of use given
every three or four hours or every two hours for three doses
just before the rise in temperature in a septic type of fever.
Quinine alone must be given in large doses which are not
always well borne. When the fever is above 101° F. the
patient should be kept at rest, with as much fresh air as
possible. Ransome says that nothing, in his experience,
relieves the fever so much as fresh air and sponging with
cold water and vinegar. Fever is no contraindication to
fresh air and as much of the latter should be had as is pos-
sible without overexertion. Sponging with tepid cologne
water is grateful and useful.
Cough is a troublesome symptom and one which patients
are usually anxious about. It is well with the cough, or
with the fever, to trust to general measures as much as pos-
sible for relief. If cough is troublesome at bed time, or
paroxysmal in the morning, a cup of hot milkine will often
312 PULMONARY TUBERCULOSIS.
afford much relief. Nauseous cough mixtures are to be
avoided, and when cough medicines are prescribed the}
should be as simple as possible. In nervous, irritable peo-
ple Hoffman's anqjlyne is often very useful. A mixture con-
taining to each dose | gr. of morphia or \ gr. of codeia, 10
drops of dilute hydrobromic acid, and syrup of tolu q. s ,will
be taken longer, with more relief and less complaint, than
most other cough mixtures. If the cough is hacking and
very persistent we may use i gr. of codeia, 1 gtt. of fl. ext.
of cannabis indica, 3 grs. of muriate of ammonia, and syrup
of tolu q. s. In cases with considerable bronchitis and scanty
expectoration we may use muriate of ammonia, gr. 5; codeia,
gr. I; tincture of Pulsatilla, gtt. 6 to H;liq. am. acetat., gtt. 20;
elix. simp., q. s. In laryngeal cough we may use inhalations.
sprays and sedative troches. Oil solutions of the various
antiseptic drugs are of great use in relieving cough and ex-
pectoration when given by inhalation. Warm applications
or counter-irritation to the chest may be useful. Lozenges
of acacia and licorice are useful in laryngeal cough. Spray-
ing with a 2 to 3 per cent, solution of menthol or aristol; in-
halations of 20 drops of a saturated solution of menthol, or
a like amount of equal parts of creasote or guaiacol with
spirit of chloroform when the membrane is dry and irritated
may be of use. With laryngeal catarrh we may use a tea-
spoonful of compound tincture of benzoin in a pint of water
near the boiling point for inhalation. With profuse secre-
tion from the mucous membrane we may find 3 to 5 drops of
tincture of belladonna and half a teaspoonful of syrup of
senega every four hours of value.
Night sweats are a troublesome through erratic symp-
tom in tuberculosis. When regular and severe they weaken
the patient and should be stopped if possible. A cool
sponge bath in the morning followed by thorough friction of
the body will often lessen the sweating. Atropine is the
most useful remedy. It should be given at bed time in ^ to
T\ grain doses. Camphoric acid is, next to atropine, the
best remedy for sweating. It is best given in three doses
of five or ten grains each (in capsule) at 5, 7 and 9 o'clock
in the evening. Agaricin (TyTV g*-) may be given six hours
PULMONARY TUBERCULOSIS. 313
before the sweating takes place, or, as I have found useful,
T\ of a grain may be given at 2 and 7 P. M., followed by
thirty drops of fluid extract of pinus canadensis at bed time.
Picrotoxin (^ gr.) may be given at bed time. Zinc oxide
(5 gr. in pill) is sometimes useful. If profuse sweating oc-
curs whenever the patient sleeps it is an indication for stim-
ulants and nourishing drinks.
Diarrhoea may be troublesome when there is acute or
chronic ulceration of the intestines. In the acute form ten
grain doses of bismuth (sub-carbonate or sub-gallate) with
five drops of deodorized tincture of opium and a like amount
of spirits of camphor every three or four hours is useful.
Dover's powder with bismuth is of service. Starch enemata,
plain or with opium, may be used. The acetate of lead and
opium pill is useful. If the discharge is watery and profuse
ten drops of dilute nitric acid with five drops each of tinc-
ture of opium and tincture of camphor given in simple elixir
will be of use. In the diarrhoea of chronic ulceration the
diet is very important. Such drugs as acetate of lead (2 to 3
gr.), sulphate of copper {i to i gr.) combined with opium in
pill form, are of use. Bismuth (gr. 20), and co. ipecac pulv.
(gr. x) may be given in milk every 4 to 6 hours. Tincture of
catechu, gtt. 20; tinct. opii deodor., m 5; mist, creatae, 5 iv,
may be tried. Fluid extract of coto bark in five minim
doses may be useful. When the lower intestine is affected
lead and opium pill combined with starch enemata (tr. opii,
gtt. xx too ss; mucil. amyli 5 ii) is of great service.
Haemorrhage is to be treated by rest and opium (mor-
phine hypodermically). If the vascular tension is high
lower it with aconite and sodium bromide. No stimulants
should be given. Tincture of hamamelis in 20 to 60 minim
doses is recommended. In profuse haemorrhage, with low
temperature, we may use ergotin hypodermically. Tempora-
ry ligation of the four extremities is efficacious in profuse
haemorrhage, and from j\ to -g\ of a grain of atropia may be
given hypodermically. Astringents, as a rule, do no good
in the pulmonary haemorrhage of tuberculosis.
Gastric disturbances are to be avoided, to a large ex-
tent, by the general treatment and attention to diet. Acidi-
314
PULMONARY TUBERCULOSIS.
ty and flatulence may be relieved by bismuth and bromide
of sodium or strontium. For loss of appetite without di-
gestive disturbance Fowler recommends bicarbonate of soda,
gr. xv.; dilute hydrocyanic acid, m iii; comp. inf. of gen-
tian 5i.
Gastric crises may occur which must be tided over by
restricting the diet to liquid food. Vomiting may occur
through the irritation produced by the severe coughing or
through some sore spot or sensitive area in the throat, at-
tention to which will relieve the vomiting. The nausea so
frequently present may be controlled by small and frequent
doses of lime water containing one drop of carbolic acid to
the ounce, or by small doses of calomel and soda.
Pain from pleurisy may be controlled by strapping the
chest, painting the surface with tincture of iodine, applying
belladonna plasters, small blisters, or hot applications.
The experimental work of Biondi, Schmidt, Gluck and
others show that a portion or the whole of a lung may be
removed without fatal results. Lowson and Tuffier have
successfully removed a tuberculous portion of the human
lung with good results. While these cases demonstrate
the possibilities of lung surgery, the application of such
methods must be extremely limited in the treatment of tu-
berculosis of the lungs. The surgical drainage of tubercu-
lar cavities of the lung has generally been regarded with
disfavor. It is not beyond argument, however, that this
may be the most advantageous way of treating single cav-
ities properly situated. Should the future discover a reli-
able bacillicide for the after treatment of drained tubercu-
lar cavities the question of operation would assume a differ-
ent aspect.
CHAPTER XIV.
ACTINOMYCOSIS OF THE LUNGS.
Bollinger described actinomycosis in 1877, and. in 1878
Israel described it as affecting the lungs, though the disease
had previously been observed in man by von Langenbeck in
1845, and by Lebert in 1857. The disease is said to be some-
what more common in Germany and Russia than in this
country, and to be rare in England. It is much more com-
mon in men than in women. The total number of cases of
actinomycosis now on record is comparatively small.
Pulmonary actinomycosis is an infectious disease of
chronic course caused «by the actinomyces, or ray-fungus
(strejttothrix actinomyces).
^Etiology.—The fungus which causes the disease gains
entrance to the body through the respiratory or alimentary
tracts. In the latter case the symptoms may be chiefly
thoracic, as, when the disease affects the liver it may extend
to the pleura and lungs and open through the ribs. The or-
ganism has not been recognized outside of the body. There is
no direct proof of infection through the flesh or milk of dis-
eased animals. It is most likely that the infection occurs
through the medium of the food.
It is not positive as to just which group of bacteria the
organism belongs, though it is credited to the streptothrix
group. It is markedly polymorphous and occurs as small
spherical or irregularly-shaped grains or masses of a
sulphur-yellow color, and from one-half to two millimetres in
diameter. These bodies present an internal granular mass
and an outer zone of radiating mycelia which may present
bulbous terminations. According to Bostrom the clubbing
is due to hyaline degeneration of the filaments. These small
masses which are characteristic of the disease are found in
the granulations of the diseased area, or in pus from such
316 ACTINOMYCOSIS OF THE LUNGS.
area. In the early stages of their formation they may be
grayishin color.
Morbid anatomy.—The lesions of pulmonary actino-
mycosis are unilateral in the majority of instances. Accord-
ing to Hodenpyl there are three groups of lesions: lesions of
chronic bronchitis; miliary lesions resembling miliary tu-
berculosis, the nodules are composed of groups of fungi sur-
rounded by granulation tissue; destructive lesions of the
lungs characterized by broncho-pneumonia, interstitial
fibrosis, and abscess of the lungs.
When the chest wall becomes involved there is enlarge-
ment of the affected side, effacement of the intercostal spaces,
the soft tissues become discolored and cedematous, the skin
becomes red in spots, and abscesses form and discharge a
small amount of pus. Fungoid masses of red and yellow
granulation tissue form around the openings.
Actinomycosis of other organs and tissues is frequently
associated with the pulmonary form of the disease Necro-
sis and erosion of the ribs, vertebras or sternum;subcutaneous
abscesses, and metastases to other portions of the body occur.
Clinical history.—The clinical history Qf pulmonary
actinomycosis maybe similar to that of pulmonary tubercu-
losis, tumors of the lungs, or chronic pleurisy. The fact
that actinomycotic and tuberculous processes maybe associ-
ated in the lungs tends towards ambiguity of the clinical
history.
The onset of the disease is gradual and is accompanied
by an insidious cough, with, perhaps, slight expectoration.
There is general weakness with loss of weight. Pleurisy,
with or without effusion, may be a feature of the early stages.
The patient becomes pale and anaemic and loses flesh; cough
becomes more troublesome, and the sputum becomes muco-
purulent, more abundant, and may contain the yellow gran-
ules which are characteristic of the disease. The tempera-
ture is more or less elevated and gradually assumes a hectic
type.
When the chest wall becomes involved there is a change
in the contour of the affected side. Scoliosis may develop
The soft tissue becomes swollen and inflamed, abscesses
ACTINOMYCOSIS of the lungs. 317
form and discharge pus and the sinuses are surrounded by
granulation tissue. The clinical history is now much like
that of caries of the ribs or vertebrae. The symptoms may
resemble those of emphysema, or may simulate those of
typhoid fever.
The course of the disease is progressive. The average
duration is about one year. Recovery is very rare. Death
is preceded by general septic conditions.
Symptoms and diagnosis.—Cough, fever, emaciation;
with muco-purulent' or perhaps fetid expectoration are the
principal symptoms. Cough and expectoration are im-
portant symptoms as in some cases the diagnosis may be
reached through the presence of the actinomyces in the
sputum. Bizzozero cautions against mistaking degenerated
epithelial cells in the sputum for the organism of the dis-
ease. The fever is irregular in type and eventually be-
comes hectic. The physical signs are usually indefinite.
The lower portion of the lungs is the part usually affected,
and the disease is generally confined to one side of the chest.
More or less localized dullness will be present and there
will be a corresponding loss of respiratory sounds. Signs
characteristic of pleural effusion may be present. There
may be signs of a cavity in the lung. As the disease pro-
gresses and the chest walls become affected there will be
much restriction of motion and the voice and respiratory
sounds will be weak and indefinite.
In the early stages it may be impossible to differentiate
the disease from tuberculosis, or from chronic pleurisy.
The presence of actinomyces in the sputum, or in the dis-
charge from the chest wall may be the only means of mak-
ing a positive diagnosis. If the disease has extended from
the liver the latter will be enlarged. Extension from the
upper respiratory tract, or from the mouth may render the
diagnosis less difficult than usual.
Godlee says that if, on opening an abscess connected
with the ribs, pleural cavity, or spine, the amount of pus is
small and haemorrhage unusually free, and especially if
subsequent insidious burrowing of pus beneath the skin oc-
curs, we should be suspicious of actinomycosis.
318
MYCOSIS PULMONUM.
Treatment—The medicinal treatment of actinomycosis
of the lungs is symptomatic only. Large doses of iodide of
potash (20 to 40 grains t. i. d.) are recommended but it is
doubtful if it does any real good. Injections of iodide of
potash have also been recommended.
Surgical measures are the only means that may avail
against the inevitably fatal results, and on this account
much greater risk may be assumed than is justifiable in
other pulmonary diseases. We must bear in mind the
great danger of haemorrhage during operation, and also
the possibility that the disease has extended to places and
tissues where surgical intervention cannot follow'.
MYCOSIS PULMONUM.
Pulmonary mycosis (pneumonomycosis) is a disease of
the lungs caused by the presence of fungi. The disease
may be primary or secondary (fungus growth in the cavities
of phthisical lungs.)
Virchow first recognized the disease in 1*54. The
principal form of the disease is that due to the aspergillus
fumigatus. Other forms may be due to sarcinae (p. sarcinica),
to an oidium said to be allied to the yeast fungus*, to an
organism called by Flexner the streptothrix pseudo-
tuberculosaf, and, according to some observers, to some
of the mucosinae or moulds. Rixford and Gilchrist have
reported cases of protozoic infection of the lungs. \
These various infections of the lungs are followed by
changes in the lung tissue which are very similar to those
occurring with tuberculosis. The symptoms and clinical
history are those of chronic lung disease and may closely
simulate those ©f tuberculosis, chronic bronchitis, asthma
haemoptysis, etc. The diagnosis depends on the demon-
stration of the nature of the infection.
*Gilchrist and Stokes—Bui. Johns Hopkins Hospital vol. vii, No. 64: July 1896.
tPseudo-tuberculosis hominis stroptothrica,—Flexner, Johns Hopkins Hospital
Bui: June 1897.
jProtozoan or coccidioidal pseudo-tuberculosis. Johns Hopkins Hospital Rep.
896,1, 209.i v v
HYDATIDS OF THE LUNGS. 319
Renon and Dieulafoy hold that the aspergillus fumiga-
tus may be a pathogenic organism, though in some cases it
is secondary. Virchow and others maintain that it is al-
ways saprophytic, and the lesions are secondary to other
processes.
Secondary aspergillo-mycosis may occur in connection
with pulmonary tuberculosis, chronic bronchitis, bron-
chiectasis, haemorrhagic infarction of the lungs, malignant
growths in the lungs, and to valvular lesions of the heart.
HYDATIDS OF THE LUNGS.
Hydatids of the lungs (echinococcus of the lungs) is due
to the presence in the lungs of the larvae of the taenia
echinococcus. The disease is most common in Iceland
Australia, and some European countries where there is close
association between men and dogs. It is rare on this conti-
nent, though Ferguson states that a number of cases have
been observed in Winnipeg since the Icelandic immigration
in 1844.
^Etiology.-—The cestode of the taenia echinococcus is
four or five mm, long and consists of three or four seg-
ments. The terminal segment is mature and may contain
5,000 eggs. The head is small and has four sucking disks sur-
rounded by a double row of hooklets. The ova are acci-
dentally ingested by man, chiefly through the medium of
the drinking water.
The ovum having reached the stomach is relieved of its
envelope by digestion and the embryo makes its way
through the coats of the stomach or intestines and may
reach the lungs, after passing through the capillaries of
the portal or hepatic veins, by way of the pulmonary
artery, or, it may enter a systemic vein after leaving the
stomach, and thence gain the pulmonary artery. Accord-
ing to Bird, hydatid disease of the lung may occur through
inhaling dust containing the ova of the echinococcus. in
which case they might enter the bronchial arteries. It is
not definitely known, however, how much of their move
ment is to be attributed to migration and how much to vas-
cular transportation.
320
HYDATIDS OF THE LUNGS.
Echinococci are more frequent in the lung than in the
pleura, but the liver is the favorite seat of the affection.
In this country about seven per cent, of the cases have oc-
curred in the lungs or pleurae. In 1,862 cases collected by
several observers the lungs and pleurae were affected in 153
cases, Thomas' collection of 809 cases show the lungs to have
been affected in 134 cases, and the pleurae in 2 cases.
Morbid anatomy.—When the embryo has reached its
destination its hooklets disappear and it is gradually
changed into a small cyst containing a clear fluid. The wall
of the cyst is composed of an external thick, transparent,
elastic, laminated layer (ectocyst); and an internal granular,
parenchymatous layer (endocyst). This cyst determines
more or less formative inflammation in the surrounding
tissue, and becomes enveloped in a fibrous capsule. This
capsule is rarely as dense as it is in hydatids of the liver,
and frequently it is slight or absent altogether.
The method of development of the cysts is the same as
in other tissues and need not be considered here. The fluid
contained in the cysts is clear and limpid and has a specific
gravity of 1.005 to 1.015. It contains no albumen, or at
most only a trace. There may be traces of sugar. Usually
the cysts contain scolices and the characteristic hooklets.
As the cysts grow they compress the lung tissue; cause
inflammation of the surrounding tissue, gangrene, and the
formation of cavities which may be connected with the
bronchi. The bronchi may be patent directly to the sur-
face of the cyst, but as long as the latter is tense with fluid
the bronchi will not open directly into the cyst. If the
cyst collapses the bronchi open and the air enters the cyst
cavity.
Rupture into a bronchus may occur with discharge of
the cyst contents, or even of the cyst itself, in which case
the cavity may become obliterated. This result is rare,
however, for, if the cyst is surrounded by a fibrous wall the
cavity continues to discharge pus. Rupture into the pleura
is followed by pneumothorax, and pleurisy with serous or
purulent effusion. Rupture into the pericardium is usually
rapidly fatal.
HYDATIDS OF THE LUNGS.
321
The lung tissue surrounding a cyst may become pneu-
monic, gangrenous (if the cyst is dead), or fibrotic. These
changes may lead to the death of the cyst which may in
time be followed by suppuration and decomposition of its
contents. It thus becomes an abscess which may discharge
in any direction. If the cyst dies, its contents become tur-
bid and albuminous. The adult cyst may become glutinous,
opaque and m ay break up into fragments. If there are daughter
cysts, they will later pursue the same course. In rare in-
stances the cyst contents may undergo fatty degeneration
and the cyst dries up.
Hydatid cysts of the lung are usually single. The
multilocular variety is very rare. Both lungs may be in-
volved, and there may be more than one cyst in a lung.
The right lung is more often affected than the left; and the
lower lobes more frequently than the upper. Very few
cases of hydatids of the lungs recover.
Clinical history.—Small cysts in the lung may give
very indefinite symptoms, or none at all. There may be a
history resembling that of tuberculosis. Usually there is a
dry, hacking, paroxysmal cough with some mucoid expec-
toration. Slight haemoptysis is quite common in the early
stages; later on it may be profuse. Fever is generally ab
sent unless inflammation is present in the lung, Moderate
dyspnoea may be present, but the dyspnoea is not trouble-
some unless pressure is exerted on large vessels. Pain is
slight or absent unless the pleura is involved. There may
be a sense of weight or constriction about the chest. Loss
of flesh and weight is common. Rupture of a cyst into
a bronchus is attended with severe, sudden pain in
the chest, violent cough, marked dyspnoea, the expectora-
tion of watery fluid which contains the characteristic hook-
lets, and possibly by severe haemorrhage. Small pieces of
hydatid membrane may be present in the expectorated fluid.
If the bronchus opening into the cyst is small the escape of
the contents of the cavity may be gradual and accompanied
by less severe symptoms. If daughter cysts are present in
the expectorated fluid the bronchus entering the cavity is
probably a large one. Haemorrhage may occur at intervals
322
HYDATIDS OF THE LUNGS.
after the rupture. Death may occur at the time of rupture
of the cyst. If communication be established with the pleu-
ral cavity the signs of pneumothorax and pleurisy will
follow.
After rupture of the cyst the violent, severe and par-
oxysmal coughing spells may continue, the expectorated
matter containing fragments of membrane and daughter
cysts. The expectoration may become purulent and fetid,
or it may be dark-colored and resemble pus from an hepatic
abscess, while the clinical history may be similar to that of
gangrene of the lungs. Hectic fever, loss of flesh, and club
bing of the finger ends may occur. In some cases the symp-
tom s are much less severe, and aside from the dyspnoea
which may attend the expectoration of cysts or fragments
of cyst wall the history may not be distinctive.
Symptoms and diagnosis.—A small, deeply-seated
cyst may give no symptoms. If a large cyst exists there
may be diminished chest expansion and respiratory mur-
mur. If the cyst is near the surface there will be loss of
expansion, diminished voice and respiratory sounds, slightly
tympanitic or a flat percussion note, and diminished or absent
vocal fremitus. The cardiac impulse may be displaced and
the chest wall may show local prominence andeffacement of
the intercostal spaces, or the cyst may project through a
space and form a round tumor on the chest wall. According
to Fowler, the most characteristic sign is a round area of
dullness on percussion showing absolute dullness in the cen-
ter with gradually increasing resonance toward the margin;
the breath sounds and vocal resonance being absent over
this area. If the cyst is near the chest wall the so-called
hydatid thrill may be felt.
Sub-crepitant rales from cedema and congestion of lung
tissue may be heard. Signs of pressure on the vessels,
pneumogastric nerves, or on the oesophagus may be present.
The differentiation from tuberculosis rests on the location
of the lesion, its failure to involve other portions of the
lungs, by the absence of bacilli and by the greater effect of
tuberculosis on the general health.
Signs of a cavity may be obtained soon after rupture
TUMORS OF THE LUNGS.
323
and before contraction has occurred. If the cavity is active-
ly secreting, the diagnosis may be difficult if the expectora-
tion contains nothing characteristic, and the signs may re-
semble those of tuberculosis, abscess, or gangrene of the
lungs.
Sudden and severe pain and dyspnoea with signs of air
and fluid in the pleural cavity characterize rupture into that
cavity. Rupture into the pericardial sac may be immediate-
ly fatal. If not, there will be increased praecordial dullness
with diminished or absent cardiac impulse. A cyst of the
liver projecting into the lung may rupture into a bronchus,
in which case the expectoration will be stained with bile.
When cysts of the right lobe of the liver project upward it
may be difficult to determine whether the cyst is above or
below the diaphragm. Pressure effects on the structures
within the chest are not so common with hydatid cysts as
with other forms of tumors. If fluctuation is present and
pleural effusion can be excluded, the fluctuation is most
likely due to an hydatid cyst.
Treatment.—The medical treatment of hydatids of the
lungs is symptomatic only. Surgical measures alone can
hope to effect a cure. While paracentesis has resulted in a
cure in a few instances, it is regarded by most observers as
a dangerous procedure, as the fluid may escape into the
bronchi and cause a fatal result. The same surgical course
should be pursued as in dealing with a pulmonary abscess or
other lung cavity. The question of whether to simply drain
the cavity, or to remove also the ectocyst, is one which
must be decided by the conditions of the tissues and the sur-
geon's experience.
TUMORS OF THE LUNGS.
Tumors of the lungs may be primary or secondary.
Primary growths are rare in the lungs. Secondary growths
are more common. [In 112 cases of tumors of the lungs the
disease was primary in 38, and secondary in 64.—Wilson
Fox.] The primary growths are usually epithelioma, en
cephaloid, or scirrhus, the first named being the most com-
mon. Sarcoma may occasionally be found in the lungs as a
324 TUMORS OF THE LUNGS.
primary growth, and enchondroma very rarely occurs as
such. Primary cancerous growths may originate in the
glands of the bronchi, or in the alveolar epithelium. They
may spread along the lymph channels.
Sarcomata are most often secondary though they may
be primary. The most frequent variety is the round-cell
form, though spindle-celled, myeloid, melanotic, and osteo-
sarcomatous forms are also met with.
The secondary growths may be encephaloid, scirrhus,
epithelioma, colloid, enchondroma, melano-sarcoma, or
osteoma. Enchondroma may occur in the bronchial carti-
lages.
^Etiology.—Tumor of the lungs is most common be-
tween the fortieth and sixtieth years of life. The primary
form affects the sexes equally (Walshe). The secondary
form is most common in women. It is not clear that the
fact pointed out by Williams that in cancerous disease gen-
erally there is a family history of tuberculosis rather than
one of malignant disease, will apply to primary malignant
disease of the lungs. It is claimed that a large proportion
of the deaths of persons over forty years of age who are
employed in the cobalt mines of Schneeberg, is due to ma-
lignant disease of the lungs.
The secondary growths usually follow disease of the
genito-urinary system, digestive tract, or of the bones.
Morbid anatomy.—Primary carcinoma and sarcoma
usually occur in but one lung and may form large masses
involving the greater portion of the lung. Secondary
growths are usually distributed through both lungs though
they may be localized and involve chiefly the pleura. Met-
astatic growths are usually disseminated and may involve
arge portions of the lungs. Primary growths when limited
to a single lung generally affect the right lung. Secondary
multiple growths usually affect both lungs alike.
Primary growths may occur as well-defined tumors or
as infiltrations, the latter being most common. All traces
of lung tissue may be destroyed. The growth may extend
into the lung tissue along the perivascular and peribronchial
lymph spaces. Cancerous growths may be soft and fleshy
TUMORS OF THE LUNGS.
325
in appearance, or may be hard, solid, white masses. The
site of the bronchial glands may be marked by pigmentation.
Sarcomata may form masses an inch or two in diameter,
or there may be numerous nodules scattered through the
lung tissue. They are well-defined, soft, and have a fleshy
appearance. The sub-pleural and pulmonary lymphatics
are usually infiltrated.
Secondary growths usually form small, multiple, dis-
seminated nodules in both lungs. They may resemble tu-
bercles. Large, single masses may be present.
With widely disseminated growths or with dense infil-
trations the lungs may be enlarged, though some retraction
may at times be present. Softening, excoriation, and pus
coliections may occur. Cancerous, sero-fibrinous,or haemor-
rhagic pleurisy may be an associated lesion. The mediasti-
nal and bronchial glands are usually affected, less frequently
the cervical glands are involved, and rarely the inguinal
glands are enlarged.
Clinical history.—The clinical history of tumors of
the lungs may be very indefinite, especially with primary
growths. There may be no symptoms of a lesion in the
chest (Walshe). Pain may be an important symptom if the
pleura is involved. Dyspnoea may be troublesome and may
be paroxysmal if there is pressure on the trachea. Dry,
painful cough, mucoid expectoration may be present, Stokes
has called attention to "prune-juice" expectoration in some
cases of primary cancer of the lung, Passive congestion of
the face and of one or both upper extremities may occur
from pressure, The pneumogastric or recurrent laryngeal
nerves may show pressure effects. If the mediastinum is
not involved the pressure effects will be absent. The rapid
dissemination of the lung lesions may be attended with
pneumonic symptoms and albuminuria (Wunderlich), Emaci-
ation may or may not be considerable.
The duration of the disease is from six to eight months.
It may run a very acute course, Jaccoud observed a case
which lasted only a week from the onset of the symptoms.
Symptoms and diagnosis.—Primary growths not in-
volving the mediastinum are so rare, and, pressure effects
326
TUMORS OF THE LUNGS.
being absent, their symptoms so indefinite, that they are
often not recognized when present. When an intrapulmo-
nary growth is large there may be some bulging of the side,
though retraction may be present from extensive infiltra-
tion or from collapse due to bronchial obstruction. The
heart may be displaced. Vocal fremitus may be normal,
increased, or absent. Pulsation may occur from transmitted
heart's action. The percussion note may present any quali-
ty from normality to absolute dullness. Extension of dull-
ness beyond the median line is as important, but of less
common occurrence, as in mediastinal tumors. The breath-
sounds are usually diminished in intensity. Bronchial
breathing may be present.
The diagnosis is not difficult in secondary growths, as
the history of the patient will be suggestive. Progressive
emaciation, involvement of the cervical glands, especially
the clavicular, dark-colored expectoration, and anomalous
physical signs will suggest the nature of the trouble.
Treatment.—The treatment of tumors of the lung is
symptomatic. In special cases it is possible that surgical
measures might be considered with advantage.
CHAPTER XV.
PLEURISY.
Inflammation of the pleura may be primary or second
ary, As to its cause it may be acute or chronic. From an
anatomical point pleurisy may be divided into dry pleurisy,
fibrinous, plastic or adhesive pleurisy, and pleurisy with
effusion. According to the character of the effusion pleurisy
is spoken of as serous, sero-fibrinous, sero-purulent, puru-
lent (empyema), haemorrhagic, and putrid. The terms trau-
matic, diaphragmatic or phrenic, cancerous, tubercular etc.,
are sometimes used to indicate special features of individual
cases. Attempts have been made to classify pleurisy from
a bacteriological standpoint, and there has been described
a pneumococcus pleurisy, a streptococcus pleurisy, a sapro-
genic pleurisy, a staphylococcus pleurisy, a tubercular
pleurisy, and pleurisy due to such organisms as the typhoid
bacillus, the influenza bacillus etc.
While in many instances of tubercular and of pneumo-
coccus infection of the pleura a characteristic inflammation
results which can be defined clinically, in the majority of
cases the part played by the various infections cannot, as
yet, be outlined clinically with sufficient clearness to make
such a classification of practical utility. Regarding the
disease purely from a clinical standpoint the simplest classi-
fication is one under which may be included the greatest
number of cases without the subdivision which is necessary
when we attempt an aetiological classification. Dividing
pleurisy, then, into fibrinous or plastic pleurisy, sero-
fibrinous pleurisy, and purulent pleurisy, we have a classi-
fication embracing the clinical features of the majority of
cases and which is more definite than the simple division
into acute and chronic pleurisy, and which is less elaborate
and confusing than a classification based on the numerous
aetiological factors of inflammations of the pleura.
328
FIBRINOUS PLEURISY.
Fibrinous (plastic, adhesive) pleurisy may be primary
or secondary, acute or chronic (prifiiative dry pleursy). It
may occur in any degree from the slight inflammation with
little or no exudation (dry pleurisy), to extensive plastic
exudations resulting in considerable induration of the
pleurae. It is probable that the pleuritic adhesions so fre-
quently found post mortem in subjects in whom there has
been no history of pleural disease are the result of the
milder degrees of fibrinous pleurisy.
^Etiology.—Primary, fibrinous pleurisy may occur as
an independent affection, in persons of good health, from
exposure to cold. It is not clearly understood just how the
disease is thus brought about, though we have bacteriologi-
cal evidence of the loss of resistance in tissues after exposure
to cold, and we know that individual resistance in this
repect varies greatly. It is not improbable that a clearer
appreciation of the practical workings of pneumo-dynamics
might explain some of this class of cases. All constitutional
conditions which lower the vitality of the individual may
predispose toward plastic inflammation of the pleura.
Some cases of primary, plastic pleurisy are undoubtedly
tubercular in origin. The exact proportion is difficult to
estimate. In general serous-membrane tuberculosis the
pleura may be involved simultaneously with the peritoneum.
In tubercular pleurisy the visceral pleura is infected
through the sub-pleural lymphatics or from the bronchial
or tracheal lymph glands. The parietal pleura may be
infected from the cervical, vertebral, or mediastinal lymph
glands, or through the diaphragm from the lymphatics of
the peritoneum. The frequent impossibility of demonstrat-
ing the tubercular nature of the adhesions which are often
present in cases of pulmonary tuberculosis shows the
difficulty of recognizing the tubercular nature of a primary
pleurisy. While the adhesions which are associated with
pulmonary tuberculosis may be due, in some instances, to
associated infections, it is altogether likely that in the great
majority of cases they are tubercular in origin. This latter
is more readily demonstrated, according to Fowler, by ex-
FIBRINOUS PLEURISY. 329
amination of the pleural surfaces of the interlobar fissures
where the tubercular granulations are most distinct.
Secondary, fibrinous pleurisy occurs in connection with
acute diseases of the lungs such as pneumonia, tuberculosis,
cancer, abscess, gangrene; to inflammations of the pericar-
dium and mediastinum. Bright's disease, and acute rheu-
matism may precede this form of pleurisy. Fractures of
the ribs,' injuries of the chest walls, gun-shot and other
perforating wounds of the pleura may cause plastic pleurisy
when the injury is not septic in character.
Morbid anatomy.—In fibrinous pleurisy there is a
fibrinous exudate upon the pleural surface. Leucocytes and
blood corpuscles are enclosed in the muscles of this exuda-
tion. Preceding the appearance of this fibrinous exudate
there is injection of the subserous vessels, loss of lustre of
the membrane, proliferation of the nuclei of the endothe-
lial cells of the pleura, and blocking of the stomata of the
membrane and-of the adjacent lymphatics with fibrin and
corpuscles. The layer of coagulable lymph varies in thick-
ness with the amount of cellular elements and fibrin poured
out. The layers of lymph nearest the pleural membrane
may be dense and laminated; superficially the lymph is
trabeculated with a fine net work of fibrin enclosing corpus-
cles. If the inflammatory process ceases at this point
(dry pleurisy) the exudation may become vascularised and
form connective tissue with more or less union of the sur-
faces of the pleura. The exudation may become absorbed
without the formation of adhesions, and some thickening and
opacity of the pleura may be the only result of its presence.
Thickening of the interlobular septa is a frequent result. In
chronic tubercular pleurisies of this type the layers of ex-
udation may be very thick and laminated and may be gran-
ular in appearance from prolonged friction of the surfaces
of the pleura. In tubercular pleurisy particularly, the
pleural membrane lining the interlobar fissures is fre-
quently much thickened and closely adherent. In the
chronic forms of fibrinous pleurisy great induration of the
visceral pleura may result, and the adjacent interlobular
lung tissue may be involved. In fibrinous pleurisy the
330 fibrinous pleurisy
visceral pleura is much more frequently involved than the
parietal pleura owing to the frequency of the occurrence of
pleurisy secondarily to inflammations of the lung. The
lower portion of the pleura is much more frequently affected
than the upper especially in tuberculous cases, though in
apical tuberculosis of the lung the pleura is affected more
often than has been supposed. In some cases the inflamma-
tion is limited to the diaphragmatic pleura (diaphragmatic
pleurisy), and though any variety of pleurisy may be limited
to the diaphragmatic pleura, such an inflammation is usually
of a fibrinous nature.
Clinical history.—The clinical history of acute plas-
tic pleurisy is usually distinctive. Pain in the side is the
earliest and most prominent symptom. Preceding or accom-
panying the onset of the pain there may or may not have
been chilliness or a chill. If the latter occurs it is usually
of a nervous character. The pain is sharp and piercing, and
usually begins very suddenly at about the middle of inspira-
tion and ceases with the beginning of expiration. In some
cases, especially in the apical pleurisies accompanying
pneumonia of the same region in children, the pain may be
more or less continuous.
Dry, hacking cough is present. It is apt to be constant
and causes considerable pain. Dyspnoea, if present, is ir-
regular and results largely from fear of pain. The temper-
ature is usually elevated two or three degrees. The pulse is
rapid (from 100-120) quick, small and irregular in force. In
some cases of limited inflammation there may be no history
except that of slight cough, slight pain on deep inspiration,
and a slight febrile rise. In pleurisy secondary to other dis-
eases of the chest the occurrence of the above symptoms
will be readily understood though they be masked by the
symptoms of the original disease. The majority of cases of
fibrinous pleurisy which are observed in this stage are not
followed by effusion: the symptoms subside within two weeks
and the patient is apparently as well as ever. If the inflam-
mation has been extensive, recovery may be slow and there
may be more or less thickening of the pleura with perma-
nent loss of expansion of the affected side. In some of these
FIBRINOUS PLEURISY.
331
cases of acute plastic pleurisy, liquid effusion will result, or
rather the plastic exudation and the sero-fibrinous effusion
are practically simultaneous in their appearance, as in the
following case.
Man aged thirty-five years. Three days ago developed
a sharp pain in right side. Pain has continued ever since
and is still severe when he coughs or breathes deeply.
Temperature 101°; pulse 100. Examination shows loss
of motion of lower right side. Heart apex displaced one
inch to the left. Fremitus absent below sixth rib on right
side. Partial dullness on right side between fifth and sixth
interspaces; flatness below sixth rib. Well marked friction
sound from fifth to seventh ribs on right side. Explora-
tory puncture in seventh interspace obtains fluid of a turbid
character containing flakes of lymph.
In this case the plastic exudate was considerable, and
the liquid effusion moderate in amount, as sufficient time
had not elapsed, in all probability, for the effusion to reach
its extent. The friction sound, which is usually absent
when sufficient fluid is present to be readily recognized, was
therefore well marked.
Primary, plastic pleurisy may result in great thicken-
ing of the pleural membranes and result in cirrhotic pro-
cesses in the lungs (Sir Andrew Clark). This condition
is clinically identical with like conditions which result from
chronic empyema, long standing encysted serous effusions,
or primary pulmonary cirrhosis, and its occurrence as
a pathological or clinical entity has been denied.
In primary, plastic pleurisy of tubercular origin there
may be great thickening of both pleural layers, eventually
much retraction of the side, and a history of "stitch in the
side," moderate cough, slight fever, gradual loss of
strength, etc., extending over a period of a year or two.
The following case was of this nature:
Young woman twenty-two years old. Sick eleven
months, previous health good. Family history good except
as to an aunt wiio died of phthisis. About a year ago
patient began to have pain in the left side extending from
the nipple line around to the point of the scapula. This
was followed by slight cough, gradual loss of flesh, and for
the last two months, amenorrhoea. Her temperature was
99.8°; pulse 100. The left side shows slight retraction
332
FIBRINOUS PLEURISY.
below the level of the fifth rib, considerable loss of ex-
pansion over same area with inspiratory recession of the
interspaces. Deep inspiration causes pain and cough.
Fremitus, pitch of voice and inspiratory sounds, pitch of
percussion note all markedly increased over this area.
Very little air enters the lo'ver portion of the left lung.
No bacilli could be found in the sputum until within the
last two months. During this period, however, there have
been signs of consolidation and catarrh of the left
apex.
Symptoms and diagnosis.—The pain of acute, plastic
pleurisy is severe and lancinating. It usually catches
the patient suddenly at about the middle of the inspiratory
act. It is ordinarily felt in the axillary region or just
below che nipple at the level ofthe fourth or fifth inter-
space. In secondary, apical pleurisy the pain is felt at
the top of the shoulder and beneath the upper portion
of the scapula In diaphragmatic pleurisy the pain may
be felt lower down in the back or in the abdomen and pres-
sure over the diaphragmatic insertion at the tenth rib
increases the pain. The pain of pleurisy is increased by
deep breathing and by coughing. The patient adjusts his
position so as to limit the motion of the affected side,
usually by flexing his body, leaning toward the affected
side, and clasping the ribs by one or both hands when
he coughs. His face has an anxious, pained expression.
There is moderate elevation of temperature and a quick-
ened pulse, The cough is spasmodic, hacking, and painful.
Expectoration is scanty or absent.
The respiration is jerky, and the motion of the affected
side is diminished in acute cases largely from fear of pain
though in chronic cases there may be much loss of ex-
pansion, and even retraction of the chest wall, from thick-
ness and induration of the pleural and sub-pleural tissues-
The fremitus is unchanged in acute cases. In chronic cases
it may be increased over the lower portion of the chest
wall. The percussion note is usually not perceptibly altered
unless there has been considerable plastic exudate when it
may be slightly dull.
On auscultation we obtain the only definite sign of this
FIBRINOUS PLEURISY.
333
variety of pleurisy i. e., the friction sound. Pleural friction
sounds may be grazing, rubbing, or grating in character.
They are heard about the middle of the inspiratory act and
cease before the inspiration is completed. The grazing or
fine crepitating sounds are obtained m the earliest stage
before much exudation is present. They may last but a
short time. They may closely resemble the crepitating
rale of pneumonia but occur earlier in the inspiratory act
and are distributed over a longer period of time than the
latter. The sounds are also not so distinctly individual as
are the numerous, bunched crepitations of pneumonia. If
there is moderate plastic exudate the sounds become
rubbing or grating in character. If considerable exudation
occurs the friction sound disappears. If there is fluid
effusion the sounds may disappear early if the effusion is
abundant and they may reappear when the fluid is absorbed
in which event they will be dry and rubbing in character
(reduction rales). With considerable plastic exudate and
liquid effusion of moderate amount the friction sounds may
remain throughout the course of the disease. If the exuda-
tion is entirely plastic the friction sounds gradually become
rubbing in character and more dry in quality and disappear
within a week or two.
The voice sounds and respiratory murmur are usually
diminished except in chronic cases with thickened pleura
and adhesions. They will then be raised in pitch but
diminished in volume. Loss of expansion, inspiratory re-
cession of intercostal spaces, increased tactile fremitus,
diminution in volume and increase in pitch of the vocal and
respiratory sounds may indicate pleural adhesions, but, as
these symptoms may be present without adhesions, the lat-
ter can only be diagnosed provisionally, seldom posi-
tively.
In diaphragmatic pleurisy the respiration is usually
short, and is thoracic in type. The motion of the diaphragm
is limited. Severe dyspnoea may be present with attacks
resembling angina (Andral). Objectively it is difficult to
explain the severity of the subjective symptoms of dia-
phragmatic pleurisy.
334
FIBRINOUS PLEURISY.
The diagnosis of acute plastic pleurisy is usually not
difficult. In interlobar pleurisy if there are encysted col-
lections of fluid the diagnosis may be difficult. In some in-
stances the onset of plastic pleurisy may resemble that of
pneumonia to a marked degree with the exception of the re-
lation of the pulse and respiration rate which is less dis-
tinctive than in pneumonia.
The following case illustrates this type of the onset of
pleurisy:
Man aged 45, large and fleshy. Previous health good.
Was taken ill suddenly with a chill followed by fever and
pain in the side, cough, slight expectoration, and dyspnoea.
Temperature 102.8°, pulse 100, respiration 32. On examina-
tion there were bronchial rales in the left lung; no consoli-
dation. Over the lower portion of the left pleura, anteriorly,
then was a very rough, grating friction sound. In twenty-
four hours the temperature came down to^ 100.5° and the
cough and dyspnoea were relieved. The frction sound be-
came less rough and disappeared in five or six days.
The pain of myalgia or of intercostal neuralgia may
simulate that of pleurisy but the tender spots may be
definitely outlined and friction sounds are absent. The
chronic types of fibrinous pleurisy may, especially when
tubercular in nature, furnish the signs of encysted collec-
tions of fluid, and the only definite means of differentiation
may be the use of the exploring needle.
Treatment.—The treatment of fibrinous pleurisy is
largely symptomatic. For the pain the most efficient rem-
edy is one-fourth of a grain of morphia hypodermically. In
diaphragmatic pleurisy morphia is generally a necessity.
Next to morphine the quickest relief is afforded by a good-
sized fly blister. When these means are ojectionable, es-
pecially in children, the hot poultice, mustard plaster, or
hot applications are very useful. Blisters, while relieving
pain, seem, also, to have some modifying action on the in-
tensity of the inflammatory process, and their application
is, therefore, good treatment in cases of active inflamma-
tion. A single blister, 4x5 or 5x6, is better than several, or
a succession of, small ones. Leeches, cupping, cauterization,
etc.. are troublesome and inefficient methods compared with
SERO-FIBRINOUS PLEURISY. 335
the above treatment. Leeches are better than cupping for
the relief of pain.
Fixing the side by means of long strips of adhesive
plaster passing over the median line and drawn tightly is
highly recommended by Roberts and others. It certainly
gives much relief. The ice bag is recommended, but does
not seem to be of much service. The fever and cough
should be treated symptomatically. The bowels should be
managed by a little calomel followed by a saline. The use
of large doses of salicylate of soda has been recommended
for the limitation of the inflammation and the prevention of
liquid effusion, but they do not seem to have such effects
and are apparently useless. Iron, quinine and strychnine
are very useful in overcoming the depression which follows
the attack.
SERO-FIBRINOUS PLEURISY.
Sero-fibrinous effusion occurs in pleural inflammation
of a somewhat more severe character than that in which
fibrinous exudation alone occurs. This form of pleurisy
occurs at any time of life, though most common in adults.
Men are more frequently affected than women.
^Etiology.—All the causes of acute plastic pleurisy are
factors in the production of the sero-fibrinous variety, as
more or less plastic exudation precedes or accompanies sero-
fibrinous effusions. Rheumatism, Bright's disease, inflam-
mations of the lungs, pericardium, or mediastinum may be
accompanied by sero-fibrinous pleurisy. A large proportion
of the cases of this variety of pleurisy belong to the so-called
idiopathic pleurisies. Bacteriological research has shown
that most of these cases are due to certain organisms. The
bacillus tuberculosis is the organism most frequently caus-
ng seto-fibrinous pleurisy, while in some few instances the
pneumococcus appears to be the causative agent. Cover-
slip preparations, cultures and ordinary inoculation tests
may fail to show the tubercle bacillus as they are often very
few in number. Eichorst found that by injecting 15 cc. of
fluid exudate into test animals 62 per cent, of the cases were
shown to be tuberculous. Le Damany, by injecting large
quantities of fluid, demonstrated all but four of fifty-five
336
SERO-FIBRINOUS PLEURISY.
cases to be tuberculous. Bowditch traced the history of
ninety cases occurring between 1849 and 1879, and found that
thirty had died of tuberculosis. Of 101 cases of fibrinous,
sero-fibrinous, haemorrhagic and purulent pleurisy, Osier
found thirty-two cases to be definitely tubercular. From
the statements of French authors it would appear that from
70 to 75 per cent, of the cases of acute pleurisy are tubercu-
lous. Observations of series of cases by Kelsch and Vallard,
Lemoine, Netter, Chaufford and Gombault, Thue, Fiedler,
Barrs, Richochon and others have shown, either through
inoculation experiments or through the subsequent history
of the cases, that from one-third to one-half of the cases
were tubercular. Staphylococci, streptococci, pneumococci
Eberth's typhoid bacillus, and other micrococci have been
found in the effusion of pleurisy by Thue, Fernet, Sidney
Martin and others.
The clinical fact that pleurisy often will rapidly follow
a sudden exposure, wetting, or chill is not denied by those
who are the strongest advocates of the growing belief that
these cases are, as S£e expresses it, ' 'tubercular pleurisy,
the nature of which has been misunderstood." We cannot,
at present ascribe all sero-fibrinous pleurisies to microbic
infection, but as far as their tubercular nature is concerned,
the following may be accepted: That a considerable pro-
portion of the cases which come on suddenly in healthy
people are of a tuberculous nature; that a somewhat larger
proportion of the sub-acute or insidiously appearing cases
in persons whose present health is not of the best are tu-
berculous in nature; and that sero-fibrinous pleurisy second-
ary to chronic diseases are also frequently tubercular in
origin.
The difficulty of proving the tubercular nature of some
cases, which eventually exhibit their tubercular nature by
examination of the fluid or by inoculation experiments,
causes the subsequent history of these cases to be of special
interest. The fact that many cases recover and never ex-
hibit any evidence of tuberculosis is rather an argument in
favor of the curability of this variety of tuberculosis of the
pleural, serous membrane than an indication of its non-tu-
SERO-FIBRINOUS PLEURISY.
337
bercular nature. Yet it is difficult to exclude the doubtful
element of subsequent infection in those cases where con-
siderable time has intervened between the recovery from
the pleural inflammation and the appearance of recognizable
tuberculosis. We must know something of the liability to
subsequent infection, the character of the morbid process,
and the nature of its onset in the inlividual cases before we
can estimate the value of statistics bearing on the fact of
the subsequent development of tuberculosis in persons with
a previous history of pleural inflammation.
It is a perfectly safe clinical rule to regard persons who
have had sero-fibrinous pleural effusions, especially when
such effusions come on insidiously without evident cause in
persons of an indifferent state of health, as candidates for
tuberculosis, and to frame our advice and medication on
that basis.
Sero-fibrinous effusions may occur after pneumonia
though such occurrence is rare, metapneumonic pleurisy
being usually purulent. Sero-fibrinous effusions may occur
in the free pleural cavity adjacent to encysted purulent
effusions.
Morbid anatomy.—In sero-fibrinous pleurisy the pro-
portion of serum and fibrin varies greatly. The fibrin
will be found on the surfaces of the pleura or may be float-
ing as floculi in the liquid effusion. It may be very scanty
in amount or may form thick layers or masses. It may de-
posit as thick, curdy masses or layers at the most dependent
portion of the pleural cavity. The liquid effusion may be
clear, or slightly turbid; lemon-yellow, greenish, dark brown
or red (haemorrhagic pleurisy) in color. The usual color is
light yellow with a greenish tinge. The fluid is alkaline in
reaction and has a specific gravity of from 1.005 to 1.030
(Fraentzel). It contains leucocytes, large cells probably
derived from the pleural endothelium, red blood corpuscles,
and shreds of fibrin. If the corpuscular elements are few,
the fluid is clear and translucent; if they are numerous, the
fluid is opalescent or turbid. Urea, uric acid, sugar, choles-
terine, leucine, ty rosin and xanthoxine may also be found
in the fluid. The fluid is albuminous, the amount of albu-
rJ,">S
SERC-FIBRINOUS PLEURISY.
men varying from 31 to 77 per cent. (Walsh). After with-
drawal of the fluid it may coagulate spontaneously. Haem-
orrhagic effusion is rare. It may occur in connection with
cancer, tuberculosis, Bright's disease, cirrhosis of the liver,
with malignant types of specific fevers, or independently of
any of these affectior s. The quantity of fluid present varies
from a few ounces to several pints. The fluid may be locu-
lated or encysted in small sacs by means of masses of lymph
or by adhesions. These small collections of fluid usually
occur in the lower portions of the pleural cavity, but may
occur in any part. One sac,or portion of the pleural cavity,
may contain serous effusion, and at the same time another
portion of the pleural cavity may be occupied by a purulent
collection of fluid. The displacement of the organs within
the chest which results from effusion is readily reduced upon
removal of the fluid unless prevented by extensive deposi-
tion of lymph or failure of the collapsed lung to expand.
In large effusions the heart and mediastinum are dis-
placed toward the sound side unless retained by adhesions.
This occurs early and does not represent the degree of pos-
itive pressure within the pleura as closely as does the dowm-
wrard displacement of the diaphragm or liver. The apex of
the heart may be raised and the heart may lie more trans-
versely, in left-sided effusions. In effusions of the right
side the heart is displaced to the left without much or any
change in level. The heart does not rotate on its axis in
these displacements. A large portion, or the whole, of the
lung may be collapsed, airless, bloodless, grayish in color
and lie close to the spine.
The displacement of the heart is due in part to the loss
of the usual elastic traction of the lung of the affected side
and may be present in small localized collections of fluid
which could not possibly exert much pressure on the heart.
The collapse of the lung is likewise due in part to the loss
of expansion and tractile force in the lung of the affected
tide and to the elasticity of the lung tissue which causes it
to retract, as the fluid accumulating in the pleural cavity
alters the state of the intra-pleural tension, and as the air
remaining in the alveoli is absorbed. With small effusions,
SERO-FIBRINOUS PLEURISY. 339
especially localized ones occupying the lower portion of the
pleural cavity, that portion of the lower lobe in contact with
the effusion is usually collapsed. When these collections
occur in the anterior part of the left pleura the heart may
be displaced upward and inward without there being any
other marked evidence of pleurisy. Thus, in a young man
this displacement of the heart led to the discovery of a
localized collection of fluid in the lower anterior part of the
left pleural cavity, and from which the withdrawal of four
ounces of fluid wras followed by a reposition of the heart to
its normal situation.
Clinical history.- The clinical history of sero-fibrin-
ous pleurisy varies with the nature of the case. Prodro-
mal symptoms may or may not be present. In some instan-
ces the onset is abrupt, with chill, fever, and pain in the
side,—the manifestations of acute plastic pleurisy. These
are followed by a more or less rapidly accumulating fluid
effusion. The fever may reach 102° or 103° at first and drop
a degree or so when the effusion is established. In cases
where plastic exudation and sero-flbrinous effusion are both
well marked we will get pronounced subjective symptoms
of the former and definite objective evidences of the latter.
In many cases with considerable effusion the onset is
insidious, and there is an entire absence of definite history.
the patient going about his usual avocations, if they do not
entail physical labor, without great difficulty, suffering only
slight shortness of breath, some cough, and general weak-
ness.
A physician'recently presented himself, stating that he
"did not feel quite right," and thought he would come in
and see what was the matter. He was attending to a fairly
large general practice without special difficulty except for
feeling weak and having some shortness of breath when he
hurried. He had a slight cough, and his temperature was
100.5W. His left pleural cavity contained over three pints
of fluid.
A boy sixteen years old came into the clinic having ar-
rived in Chicago two days previously from Philadelphia.
He complained of feeling weak during the journey and was
short of breath after his arrival. His previous health had
340
SERO-FIBRINOUS pleurisy.
been good. His temperature was 101°. Forty -two ounces
of fluid was withdrawn from his left pleural cavity.
In this class of cases the fluid may accumulate quite
rapidly.
An office patient complained of slight cough, general
weakness, and exhibited two and a half degrees of fever.
Examination of his chest determined nothing of special in-
terest. He returned two days later no better. A second
examination was negative as far as his pleurae were con-
cerned. Two days later he returned in the same condition,
and as he was a complaining aud loquacious individual he
was prescribed for and dismissed without further examina-
tion. The next day he consulted another physician who
withdrew over three pints of fluid from his chest.
In the so-called "latent" type of pleurisy, especially
when tubercular in nature, there may be simply a history of
slight cough, slight dyspnoea, and a low grade of fever con-
tinuing for long periods. There may be slight retraction
of the side. In other cases, especially of encysted tubercu-
lar effusions, there may be a febrile history resembling mild
remittent malarial fever, or irregular typhoid. In a recent
case of this kind in a woman who had exhibited an irregu-
lar fever for four or five weeks, the removal of a few7 ounces
of fluid from an encysted effusion in the left pleural cavity
resulted in immediate improvement.
When sero-fibrinous effusions are associated with en-
cysted purulent effusion the history of the latter will pre-
dominate, and the diagnosis of the former will rest entirely
on the physical examination. The persistence of fever and
rapid pulse after thorough drainage of the empyema, may
serve to direct attention to the serous effusion, as in the
following case;
Man aged 35. Encysted empyema in right pleural
cavity. Excision of a portion of the seventh rib
and drainasre. Pus cavity well contracted, small and well
drained. Temperature and pulse remained high notwith-
standing the good drainage. Palpation of the cavity showed
it to be completely walled off from the remainder of the
pleural cavity by dense adhesions Examination of the
upper portion of the right chest showed evidences of fluid
above the fifth interspace—the upper boundary of the wall
SEROFIBRINOUS pleurisy. 341
of adhesions surrounding the drained cavity. Puncture in
the third interspace obtained sero-fibrinous fluid, about a
pint of which was withdrawn. The temperature and pulse
improved but the patient died from general sepsis.
The course of sero-fibrinous pleurisy is variable. In
acute cases the fever may disappear in a week and slight or
moderate effusions may be absorbed. In others the effusion
gradually increases, the pain and fever continuing for from
twelve to sixteen days when improvement will begin. In
the sub-acute cases when the effusion reaches as high as
the third rib recovery will be slowr. These cases may have
lasted two or three weeks before coming under observation,
and while the natural tendency is toward absorption this
may not take place until a portion of the fluid is removed
by aspiration or otherwise. Absorption is then slow and is
followed by rough friction crepitus when the pleural sur-
faces come in contact. As a rule there is loss of resonance,
and feeble breathing over the base of the lung for a consid-
erable period.
A sero-fibrinous effusion may last for months without
change, particularly in encysted tubercular pleurisy.
Loculated effusions consisting of a pint or so of fluid are
more apt to recur than are small effusions of from four to
eight ounces. Large free effusions are not so apt to
re-accumulate though they do so in a small proportion of
cases. In some cases effusions will recur repeatedly in
spite of aspiration and all other treatment. Cases of
perforation and discharge of the effusion though the lung
or chest wall have been reported (Sahli, Harris).
Sero-fibrinous effusion, when not treated, may gradually
increase for one or two weeks. There is then a stationary
period lasting a fewT days which is followed by gradual
absorption. Some cases of large effusions may disappear
rapidly, and, again, they may last for months without a
change. Spontaneous absorption rarely takes place during
the period of marked fever, though this may occur in tuber-
culous cases. The moderate temperature of sub-acute cases
usually disappears soon after aspiration. In acute cases
the fever is slower to disappear after aspiration.
342
SERO-FIBRINOUS PLEURISY.
When a pleural cavity is full of fluid and the heart is
greatly displaced, there will be, as a rule, comparatively
little disturbance. There may, however, be danger of
sudden death from syncope caused by some slight exertion.
According to Weil, fatal syncope may be due to thrombosis
or embolism of the heart or pulmonary artery, cedema of
the opposite lung, or to degeneration of the heart muscle.
He thinks that the mechanical effect of the displacement of
the heart, or of the twisting of the great vessels, in the
production of syncope, is not clearly demonstrated.
Sudden death has in some instances been preceded by
paroxysmal attacks of dyspnoea, or attacks of syncope. In
some cases sudden death occurs without premonitory
symptoms.
Symptoms and diagnosis.—The subjective symptoms
of sero-fibrinous pleurisy may be very variable as shown by
the clinical history already detailed. Moderate fever,
dyspnoea, slight cough, pain and weakness are the chief
complaints. The fever range varies greatly with the nature
of the case. Usually it is not a prominent symptom. The
pain usually ceases when the effusion becomes considerable,
but may return to some extent wiien absorption is effected.
In cases of slight effusion and considerable plastic exudation
the pain may be continued during the course of the disease.
The cough is usually a characteristically short, hacking
affair to wirich little attention is paid. Dyspnoea is trouble
some on exertion. There may be a tendency to attacks of
syncope. In subacute cases with large effusions the weak-
ness, dyspnoea on exertion, and short, dry cough are the
symptoms most likely to be remarked on by the patient in
describing his condition.
The physical signs of effusion within the pleural cavity
may or may not be determinate and conclusive. Large
effusions are usually recognized with ease, but small effu-
sions, or loculated ones, may be very difficult to determine
by the physical signs alone. Thickening of the visceral
pleura from induration subsequent to the deposit of quanti-
ties of exudate in acute plastic pleurisy, and consecutive in-
terstitial fibrosis of the lung with partial collapse may fur-
SERO-FIBRINOUS PLEURISV. 343
nish conditions which produce physical signs in every way
similar to those of encapsulated effusion of moderate di-
mensions.
Inspection is important in effusions of any extent. If
there is a large effusion the shape of the chest may be al-
tered, the affected side appearing larger and its outline
rounded. The depressions of the intercostal spaces may be
effaced, or, rarely, the intercostal spaces may be bulging.
(According to Stokes, bulging of the intercostal spaces is
due to inflammatory paralysis rather than to intra-thoracic
pressure alone, and indicates a severe lesion.) Measure-
ments and cyrtometer tracings show that the enlargement
of the side is more apparent than real, though according to
Powell the total circumference of the chest is always in-
creased. The patient may lean toward the affected side and
there may be an evident degree of scoliosis. Extensive
effusions in the right side may cause a fullness of the side
from displacement of the liver. In small, loculated effusions
in the lower portion of the pleural cavity the chest wall may
be retracted and measure less than the opposite side and
there may be depression and inspiratory retraction of the
interspaces.
In large effusions the loss of respiratory excursion on
the affected side is at once apparent. Expansion of the
affected side may be limited to the upper portion, or the
whole side may appear motionless. In encapsulated effu-
sions the loss of motion is limited to the area affected, gen-
erally tne lower portion of the chest.
Cardiac displacement, as shown by dislocation of the
apex beat, is one of the most reliable evidences of pleural
effusion. In effusion on the right side the displacement is
less, relative to the amount of effusion, than in left effusions.
In right effusions the apex is displaced to the left and
slightly upwrards, and may be displaced as far as the ante-
rior axillary line. In left effusions if the apex is under-
neath the sternum it may not be discernible. It may be
displaced to the right as far as the right nipple line. I en-
tirely agree with Powell in his view as to the importance of
cardiac displacement as an early and constant sign of pleur-
344
SEROFIBRINOUS PLEURISY.
al effusion, but not with his statement that it occurs /;r/W
passu with the extent of the effusion. In this respect the
degree of displacement is not to be regarded as strictly re-
lated to the amount of effusion in all instances. There are
pneumo-dynamic forces other than positive increase in in-
trapleural tension which cause the cardiac displacement—
such as the elastic traction force of the opposite lung—
hence, as in cases already cited, we may get displacement
of the heart with very small encapsulated effusions. This
absence of ratio between the extent of the effusion and de-
gree of displacement of the heart renders the latter all the
more valuable as a sign of pleural effusion, as displacement
of the diaphragm, liver, and other organs which is depen-
dent on positive intrapleural tension are late signs of effu-
sion and only obtained, as a rule, in large effusions and
where other positive signs have been previously obtained.
By palpation we can at times more clearly determine
the variations in chest expansion, the alteration in the in-
tercostal spaces, or the displacement of the apex beat, than
we can by inspection. We have, besides, absence of vocal
fremitus over the area occupied by the fluid. This is the
rule, though in small effusions where there are adhesions
and especially in encapsulated effusions, the fremitus may
be present or even increased if the lung has not collapsed
and has undergone a moderate degree of fibrosis. It is very
rare that fluctuation can be detected. Pulsation may very
rarely be felt in sero fibrinous effusions. CEdema of the
chest wall is seldom found. In children vocal fremitus may
be present over the area of effusion in the absence of any
adhesions.
Percussion affords us valuable evidence of the presence
of effusion. Percussion over the area of fluid gives a pecu-
liarly toneless, flat note. The lack of tone is distinctive,
though in small or loculated effusions the note may be mod-
ified to such an extent that it differs but little from that
given forth by collapsed or extensively indurated lung
tissue.
The limits .of the dullness are important and are best
determined by light percussion. In encapsulated effusions
the limits of dullness will have no distinctive features. In
SERO-FIBRINOUS PLEURISY. 345
moderate sized or large, free effusions the upper and lower
borders are important. The upper border of flatness may
be found at any elevation according to the amount of effu-
sion. With moderate effusion, no adhesions, and an elastic
lung the line of flatness may be lower in the axillary and
mammary regions when the patient is lying dowm than
when sitting or standing. This is a positive evidence of
fluid, but it is seldom that it can be definitely determined.
With considerable effusion the upper border of flatness is
irregular and has been described as Damoiseau's curve, or
the letter S curved line of Ellis. It is highest in the axil-
lary and scapular regions and dips dowmward in the inter-
scapular region leaving a tongue of comparative dullness in
the postero-median line winch Garland has called the "dull
triangle." Anteriorly the line declines gradually until it
reaches the sternum. According to Garland the line alwTays
begins at a lower level behind than in front. In some cases
of considerable effusion this line can be readily made out,
in many it cannot be definitely determined. The lower
border of flatness is outlined by the curved line of the
diaphragmatic arch on the left side, while on the right the
flatness runs into that of the liver. In large effusions of the
left side the lower line of flatness may be straightened and
much depressed and the tympanitic note of Traube's semi-
lunar space may be obliterated. In very extensive effusions
the flatness may extend to the clavicle, and, transversely,
beyond the opposite side of the sternum. According to
Pitres, Damoiseau's curve is not observed in small effusions,
and in moderate sized effusions the anterior and lateral por-
tions of the upper border of flatness form a horizontal line,
while the posterior portion falls abruptly.
Above the level of the fluid in cases of moderately ex-
tensive effusion the percussion note may have a peculiar
quality of tympany—the so-called Skodiac resonance. This
is obtained in the sub-clavicular region and gradually dis-
appears into dullness in the axillary and mammary regions.
In front this resonance may cover a triangular area with
the sternal border as the base. Skodiac resonance may be
obtained behind above the level of the fluid but not so clear-
346 SERO-FIBRINOUS PLEURISY.
ly as in front. Even in cases of very extensive effusion a
modified form of Skodiac resonance will be obtained in the
infraclavicular region. This variety of resonance over the
upper portion of theichest, with marked dullness or flat-
ness over the lowTer portion, strongly indicates pleural effu-
sion and becomes positive with alteration in the upper level
of the flatness with change in the position of the patient.
With extensive effusions the tympanitic note in the first
or second interspaces.may change in pitch when the mouth
is opened, due to transmission of vibrations from the pri-
mary bronchus (the tracheal tone of Williams). A cracked-
pot sound may also be obtained in the same situation
(Shattuck).
During the absorption'of the] fluid the dullness gradu-
ally descends, but remains, in some degree, over the lower
portion of the chest even after the fluid has been entirely
absorbed, and may persist for a long time in the event of
adhesions or induration of the;pleura occurring, or any lung
C3ndiiion which interferes with expansion.
In regard to the value of evidence obtained by percus-
sion relative to the amount of effusion present in a given
case, we may note that Garland has pointed out that
stomach tympany may be obtained at the level of the sixth
rib in the nipple line in the presence of large effusions of
th3 left side, and that similar effusions on the right side
may not appreciably lower the liver dullness. PowTell
maintains that the clinical'-evidence of the conversion of
negative into positive intra-thoracic pressure though the
extent of the effusion is (1) by the dullness extending above
the third cartilage—the'patient being in the sitting posi-
tion, and (2) by the Skodiac resonancejbecoming tubular in
quality, or extinguished. He thinks a negative pressure is
necessary for the development of the full-toned Skodiac
note, and that tubular, cavernous, or tracheo-bronchial re-
sonance in the region of the sterno-clavicular angle is
indicative of positive pressure, and of a greater degree of
effusion.
By auscultation we may obtain valuable evidence of
effusion through both the voice and the respiratory sounds.
SERO-FIBRINOUS PLEURISY. 347
The voice sound, in large effusions, may be entirely absent
below the level of the fluid, more particularly so over the
front and sides of the caest. In large effusions we canal-
most always obtain a modified form of bronchophony just
above the lower angle of the scapula, and in moderate effu-
sions the voice sounds usually have the same character just
above the level of the fluid.
iEgophdny is sometimes heard over pleural effusion and
was thought by Laennec to be diagnostic, but it may be
obtained over cavities, or consolidated lung. It is thought
by some to be of value in distinguishing localized effusion
from consolidated lung tissue. It is a sign of little value in
pleural effusion. In some cases whispering pectoriloquy,
Baccelli's sign {pectorilogue aphoni(juc), is clearly heard
through the fluid by means of direct auscultation. It was
thought by Baccelli to be diagnostic of serous, in contradis-
tinction to purulent, effusions. In most cases of localized
effusion, and in some cases of large effusion, high-pitched
voice sounds can be heard over the area of effusion. While
typical aegophony is not common in effusion the voice
sounds often have a peculiar nasal twang or lisp.
The respiratory sounds are absent below the level of
the fluid in typical cases of considerable effusion. In the
early stages the respiratory murmur is more intense above
than below the fluid, and as the fluid increases
in amount the sounds below the fluid become tub-
ular in quality and eventually are bronchial or dis
appear altogether. In front and at the sides of the
chest the respiratory sounds are usually absent, while
behind about the lowTer angle of the scapula there can usu-
ally be heard a bronchial type of breathing, particularly
on expiration, as the cartilages of the larger bronchi keep
them from collapsing. These sounds are not so soft as the
bronchial breathing of pneumonia and do not seem to be so
distant from the ear. In localized effusions the respiratory
sounds may be high-pitched and clearly heard over the area
of the effusion. Bronchial rales, and fine, crackling rales
from partial expansion of collapsed lung may be heard on
deep inspiration. In some cases of considerable effusio n
34*
SERO-FIBRINOUS PLEURISY.
fine crepitating rales may oe heard on full inspiration due
to congestion or oedema of compressed lung tissue. In mod-
erate effusions friction sounds may be heard just above the
level of the fluid, and where the pleura covering the tongue
of lung which overlies the heart is involved there may be a
pleuro-pericardial friction sound. The respiratory murmur
in the opposite lung is increased in intensity—puerile type.
The occurrence of congestion rales in the sound lung, to-
gether with the cough of congestion, blood-tinged expec-
toration, great dyspnoea and cyanosis indicates great pres-
sure and a corresponding danger of syncope. When there
is considerable displacement of the heart a systolic mur-
mur may be heard at ics base which will disappear with
removal of a portion of the fluid. With small effusions the
breathing may be tubular, metallic or amphoric in quality,
and there may be loud, resonant rales suggestive of a cavity.
As the fluid is removed the respiratory sounds gradually
return to the normal, though they may be feeble and sup-
pressed for a long time in the lower portion of the lung.
The diagnosis of sero fibrinous pleurisy is usually not
difficult in typical cases of moderate or large effusions.
They are most likely to be confounded with pneumonia, but
a careful consideration of both subjective and objective
signs will prevent mistakes. In pleurisy the onset is apt to
be insidious, the temperature is lower, the ratio of pulse to
respiration is not distinctive, the cough is less troublesome,
the sputum is not rusty or sticky, the surface of the body is
not markedly hot or flushed; the affected side is enlarged,
the heart is displaced, fremitus is absent, percussion dull-
ness is more absolute even to flatness, voice and respiratory
sounds are lessened or absent, bronchial breathing and
bronchophony, if present, are feeble and not marked as in
pneumonia, pneumonic crepitation is absent, the upper out-
line of dullness and its alteration with change of position
are distinctive of pleurisy. Skodiac resonance is more pro-
nounced in pleurisy.
In localized effusions the diagnosis may be difficult and
only to be S( tied by the exploring needle. Pulmonary col-
lapse, fibiosis, hydatids, and new growths in the pleura may
SEROFIBRINOUS PLEURISY. 34'. I
simulate localized pleurisy. In all cases of lonbt, explora-
tion should be made with the hypoder dc n 3edle. The use
of the exploring needle has become almost a routine meas-
ure by many who would not admit doubt or lack of precision
as to their methods of diagnosis. The information which it
"supplies as to the quality, not to say the nature, of the fluid
may be useful from a therapeutic standpoint, and as it is a
harmless measure when properly used, it should not be de-
cried. In localized pleurisy the exploring needle is almost
always necessary as the symptoms are so often indefinite we
are seldom positive about the presence of fluid until we see
it.
The signs to be considered in differentiating serous
from purulent effusions will be considered hereafter,though
the exploring needle is practically always r3lied on to de-
termine this question.
Treatment.—In the treatment of sero-fibrin >us jjleuri
sy there is opportunity for the exercise of judgment with
respect to the course to be pursued in the individual case.
There is a somewhat widespread tendency to resort to as-
piration in all cases of effusion which are susceptible of
diagnosis. There is a subtle temptation in this method in
that it enhances the patient's appreciation of the physician's
skill as well as of his own moral and financial obligations in
the matter, besides giving him the mental satisfaction of an
ocular demonstration of the cause of his trouble as well as
more or less physical relief. On the other hand the con-
servatism which advocates waiting a month or six weeks
for the absorption of an effusion is not supported by our
modern ideas of the aetiology of sero-fibrinous pleurisy.
The views of H. I. Bowditch, the pioneer of the surgical
treatment of serous effusions, which were considered some-
what radical in his day, are now regarded as correct.
Medicinally we may use hydragogue cathartics, diure-
tics and diaphoretics for the removal of effusio is, but their
action is uncertain and not much reliance is to be placed on
them. Placing the patient on a dry diet and administering
saline purgatives to deplete the serum of the blood, after
the manner of Hay (k to H ounces of Epsom salts in con-
:350
SERO-FIBRINOUS PLEURISY
centrated solution every morning or second morning before
breakfast), may cause considerable effusions to disappear
rapidly. Salty diet may be allowed. Regular dosing with
salt is recommended by some. Tonic medication is indicated
and greatly favors the chances of absorption. Iodide of
potassium and salicylate of sodium are recommended for
the promotion of absorption and rather extravagant claims
have been made for salicylate of soda in this respect. I
have never been able to see that either of these remedies
was of any particular value in promoting the absorption of
pleural effusions.
There is as much difference of opinion as to the power
of medicinal measures to promote the absorption of effusions
as there is about the efficacy of antiphlogistic treatment in
preventing effusion. Laennec, Guerin, and Peter believed
in our ability to prevent effusions, while Rickard expressed
his unbelief. Beaumetz, Dieulafoy, Montuard Martin, Fais-
ans and others are non-committal. For the promotion of
absorption Hayem, Koster, and Deri recommend salicylate
of sodium. Huchard advocates the use of diuretics for the
same purpose, while Rickard, Faisans, Talamon, Vincent,
Harris and many others disclaim any faith in the power of
drugs to promote absorption. Potain recommends .sodium
chloride in teaspoonful doses every few hours to prevent
the reaccumulation of effusions.
The important question of which cases of effusion are
suitable ones for aspiration relates mainly to free effusions.
Localized effusions should always be aspirated when it is
possible to do so as there- is little prospect of the fluid ab-
sorbing until at least a portion of it is removed. An en-
capsulated effusion of only a few ounces may cause the per-
sistence of pain, cough, dyspnoea and temperature eleva-
tion, and all of them are much relieved by the removal of
the fluid. It is claimed that as these cases are usually
tubercular the effusion acts as a splint to the lung and by
lessening functional activity constitutas a conservative pro-
cess which should not be interfered with. In many of these
cases there is no history of tuberculosis, and such a condi-
tion cannot be demonstrated. The continued presence of a
SERO-FIBRINOUS PLEURISY.
351
localized collection of fluid will result in changes in the
pleura and lung which will permanently interfere with ex-
pansion. Even in cases of well advanced tuberculosis of
the lungs the occurrence of an effusion may produce symp-
toms which demand its removal, as occurred in the follow-
ing case:
Young man 20 years old. Family history of consump-
tion. Sick ten months with tuberculosis of the left lung,
the upper lobe being consolidated down to the upper border
of the third rib. Temperature ranged from 99.5° to 101".
Became worse rather suddenly. Temperature rose to lo3~
and pulse to 120. Examination showed a lobular pneu-
monia of apex of lower lobe. Pain in the side, cough and
dyspnoea were distressing. These symptoms continued for
more than a week, the temperature not going below 102".
Examination showed evidences of a local collection of fluid
anteriorly below the fourth rib on the left side. By
aspiration eight ounces of. fluid was removed. The symp-
toms improved at once and in two or three days the patient
was quite comfortable.
In regard to free effusions we find many rules as to
which cases should be operated and when to interfere.
The nature of the fluid, the extent of the effusion, the age.
personal and family history of the patient are important in
determining for or against interference. In inflammatory
cases with moderate effusion, where friction sounds can be
heard at the upper border of the fluid, and when the fluid
contains many flakes of lymph, it is likely that the fluid
affords protection to the inflamed surfaces of the pleurae
and that the early removal may favor the formation of
adhesions. In these cases it is best to depend on tonics and
eliminatives for awhils and not to interfere unless the fluid
tends to increase rapilly, or in case it remains stationary
for two weeks.
According to Pow^ell if there is good Skodiac resonance
down to the third rib the lung is in a condition of physio-
logical rest and interference is uncalled for; if pyrexia
•continues at the end of the second week we should wait a
week longer before operating; if the patient's family history
is unfavorable we should interfere early unless the effusion
352
SERO-FIBRINOUS PLEURISY.
is in the same side with pre-existing lung disease; if the
effusion extends up to the second rib or higher, extinguish-
ing Skodiac resonance and causing decided increase in the
measurement of the side, especially if there is retching
cough,frothy, viscid expectoration speckled with blood, and
fine crepitations in the healthy lung, we should interfere at
once without regard to the stage of effusion.
In a large percentage of cases of sero-fibrinous effusions
of insidious onset the pressure symptoms as defined by
PowTell do not present, nor does absorption occur. While
it is true that in most of these cases the presence of a
considerable amount of fluid in the chest for three or four
weeks does not necessarily compromise the lung to any
extent, it does the general condition of the patient. In
view of the relief afforded the patient, as well as the
avoidance of permanent injury to the lung by the early
removal of a portion of the fluid, it is not clear that we are
justified i:i waiting the appearance of pressure symptoms
or of delaying for three weeks in the hope that absorption
may take place. It is undoubtedly better to act within the
shorter period stated by Bowditch, who says: "I cannot see
any valid reason for continuing any active treatment more
than one, two or three weeks without puncturing." This is
all the more clear when we note the clinical history of
these cases after partial aspiration, and how it emphasizes
the force of Trousseau's observation that the "slowness in the
absorption is, perhaps, as much dependent on the pressure
exerted by the excess of fluid upon the serous membrane by
which absorption has to be performed, as by the mere
greatness of the quantity." The force of this observation
is exemplified in the case of encapsulated effusions which,
however small, are not absorbed, as a rule, until partially
removed.
Free, sero-fibrinous effusions, especially those of
insidious onset, should be aspirated as soon as there is
sufficient accumulation of fluid to cause prostration, dys-
pnoea, much compensatory action of the opposite lung, and
displacement of the heart, though, as before remarked, the
latter symptom cannot always be regajded as directly pro-
SERO-FIBRINOUS PLEUK1SY. 353~
portionate to the extent of the effusion. Dieulafoy would
aspirate an effusion of three or four pints, while Peter
would not interfere with one of 1,000 grammes, but would
aspirate one of 2,000 grammes, and Hardy operates if
suffocation threatens. Peter would not operate until after
the twentieth day, while See thinks the effusion is sure to
return if not operated on before the twentieth or thirtieth
day. Rickards thinks the effusion not likely to return if aspi.
rated during decline of the temperature. Talamon thinks
that a serous pleurisy which is not tapped is recovered
from more completely than one which has been tapped.
No definite rule can be formulated regarding the time
to interfere with an effusion. Each case presents its own
indications. Subacute cases of insidious onset and with
considerable effusion can usually be aspirated with advan-
tage without special regard to the temperature or to the
length of time the effusion has existed. The fever will
generally decline rapidly after aspiration. In cases with
more acute onset, high temperature, and exhibiting friction
sounds denoting considerable plastic exudation, as well as
considerable effusion, it is well to wait a week or two until
the activity of the process subsides, before aspirating, as
absorption of the balance of the effusion is not likely to
occur during the active stage, and reaccumulation of the
fluid is quite likely to take place, as occurred in the follow-
ing case recently under observation:
Man aged thirty-three years. Laborer. Sick for a
week with pain in the side, cough, dyspnoea and fever.
Pulse 110; temperatorel03°. Examination showed the left
pleural cavity to be filled to the level of the fourth rib with
fluid. Friction sounds could be heard from the third to the
fourth ribs. Four days later there was no change in the
amount of fluid and the temperature was the same. As the
patient was attending the out-department of the clinic and
was quite weak and suffering from dyspnoea, it was decided
to aspirate the fluid although the activity of the process had
not yet modified. Thirty-eight ounces of fluid were re-
moved. Four days later the fluid had reaccumulated and
the temperature was still high (102.8°). Ten days later the
temperature had declined to 101° and the patient felt much
better although the amount of fluid was fully as great as at
354
SERO-FIBRINOUS PLEURISY.
the time of aspiration. Thirty-six ounces of fluid were now
removed and recovery ensued without further trouble.
In the above class of cases the fever maybe accepted as
a rough clinical guide to the stage and intensity of the in-
flammatory process, and as such, may be taken as an indi-
cation for or against aspiration.
As to the dangers accompanying aspiration, they are,
according to Potain, chiefly pulmonary congestion, svn
cope, embolism, and cardiac weakness. Samuel Gee points
out the danger of death from serous expectoration immed-
iately or shortly after operation and resulting from
oedema of the lungs, also the danger of pneumothorax from
puncture of the lung or from spontaneous rupture of the
lung; of haemorrhage from the pleural membranes, and of
embolism of distant arteries, the most common result being
hemiplegia. Pneumothorax may develop after operation,
it rarely appears at the time. Subcutaneous emplrysema
may occur without pneumothorax. Free albuminous
expectoration, associated with dyspnoea and likely to prove
fatal, is described by French authors. It comes on after
operation. These dangers are not imminent if aspiration
is carefully performed. At the same time we must bear in
mind the possibility of fatal syncoi)e occurring in any case.
The liability of transforming a sero-fibrinous effusion into a
purulent one by aspiration was emphasized by Verneuil,
Le Fort and others. Modern experience confirms the
view of Beaumetz, Dieulafoy and others that this danger is
insignificant with aseptically performed operations.
In encapsulated effusions it is evident that there can be
no elective point for puncture. In free effusions we select
the point at which we can most readily gain access to the
fluid. This is usually in the fifth, sixth or seventh inter-
space just anterior to the axillary region, or about half
way between the nipple line and the mid-axillary line. The
interspaces are widest in this situation and the muscular
tissues are thinnest. This region is most easy of access
with the patient in the recumbent or semi-recumbent
position. Another point often selected for puncture is
posteriorly just below the angle of the scapula. There is
SERO-FIBRINOUS PLEURISY.
355
more tissue in the way here, and the interspaces are
narrower; there is likely to be a heavy deposition of lymph
on this portion of the pleural membrane, and, according to
Gee. the lung is more apt to be adherent at this point, and
the consequent danger of pneumothorax or of sloughing of
the lung from perforation is greater.
Various forms of trocar and cannula, and reversible
and rotary pumps, have been devised for the aspiration of
fluids. The simplest means are the best. A trocar and
cannula connected with a long tube in which is placed a
glass coupling may be used. If nothing better is at hand
an ordinary trocar and cannula may be used by fastening
around the mouth of the cannula a piece of gold-beater's skin
for a valve. When wet, this tissue will collapse and pre-
vent the entrance of air. The best instrument is some
aspirator like the Potain modification of the Dieulafoy
instrument.
If the patient is wTeak or nervous a hypodermic injec-
tion of jt to 1 grain of morphia may be given immediately
preceding operation. If the heart is weak 7V grain of
strychnia may be given in addition. The patient should be
in a reclining position with the .shoulders elevated. In
small, or encapsulated effusions, the sitting position, may
be best. Previous exploratory puncture will have told us
how large a needle to use, though any needle may become
blocked by plugs of lymph. The chest wall should be
thoroughly cleansed. Local anaesthesia, and incision of the
chest wall are unnecessary when using ordinary aspirator
needles. If the tissues are indurated it often requires
considerable force to get the needle into the pleural cavity,
entrance to which is immediately appreciated through the
lack of resistance. We should be careful not to injure the
visceral pleura in moving the needle about, though some
scratching of the pleura usually does no great harm. If a
needle with a sliding point is used the danger of injury to
the visceral pleura will be obviated. It is best not to
employ any more suction force than is necessary to keep
the fluid running.
There can be no rule as to the quantity of fluid to be
356 PURULENT PLEURISY.
removed. It is impossible to estimate the quantity of fluid".
in a given case, and we do not expect or desire to remove
all of it. Aspiration should be stopped as soon as the
patient exhibits hurried respiration, cough, or complains of
pain. If the fluid becomes bloody, aspiration should be
stopped. If lymph blocks the needle or if deposits of
lymph interfere with aspiration, the needle should be
withdrawn and subsequent attempts made.
The withdrawal of a very small quantity is often fol-
lowed by absorption of the fluid. If the fluid reaccumulates
it should be aspirated as often as necessary. S. West advo-
cates free incision and drainage in chronic cases of sero-
fibrinous pleurisy which repeated tappings fail to cure.
The after treatment of these cases consists of tonic
medication, pulmonary gymnastics, and, perhaps, change to
a slightly higher altitude for a time. Restricted expansion
of the lower portion of the lung may be present for a
longtime and some degree of loss of expansion maybe
permanent.
PURULENT PLEURISY.
Purulent pleurisy (empyema, suppurative pleurisy) is
the result of an inflammatory process more intense but less
sthenic than that which causes serofibrinous effusions. It
is usually a secondary affection though it may be primary.
Empyema may be acute or chronic, and may be general or
local in extent.
^Etiology.—Empyema arises from infection of the
pleural membranes with some microorganism. Pneumo-
cocci, streptococci, and tubercle bacilli are the usual infective
agents. Tuberculosis does not often cause empyema.
When the latter condition occurs in tuberculosis it is likely '
to be due to pneumococcus or to streptococcus infection.
The streptococcus is the common infecting agent in the
purulent pleurisies of the adult resulting from the various
septic infections of the pleura, and in empyema secondary
to some of the infectious diseases. The pneumococcus is a
common infecting agent in the purulent pleurisies of child-
hood. Meta-pneumonic empyerra is almost always due to
PURULENT PLEURISY.
357
the pneumococcus, and these cases run the most favorable
course. Pneumonia does not always precede the pleurisy.
Primary pneumococcus pleurisy is a not uncommon con-
dition. It must be remembered that pleural effusions after
pneumonia are sometimes serous and may contain pneu-
mococci. Also that serous effusions not secondary to
pneumonia may be due to pneumococci.
The staphylococcus, the typhoid bacillus, the influenza
bacillus, and other organisms may be the infecting agents
in a few instances. In some cases observed by Thue during
an epidemic of influenza, the pneumococcus was the organ-
ism most frequently found.
Empyema occurs as a sequence of acute sero-fibrinous
pleurisy in persons whose general health is not good. It is
difficult to explain the cause of this change in most
instances. Aspiration is a rare cause of a serous effusion
becoming purulent, and is constantly becoming more
infrequent. Primary purulent pleurisy is not uncommon
in children.
Secondary purulent pleurisy is common after pneu-
monia, scarlet fever, and typhoid fever; and more rare
after measles, whooping-cough, diphtheria, erysipelas,
etc. Local conditions such as wounds of the chest, frac-
tures of the ribs, or perforations of the pleura by tubercu-
lous processes in the lung frequently cause empyema.
Pneumonia, bronchiectasis, pulmonary abscess, gangrene,
cancer or tubercle; mediastinal diseases, pericarditis,
diseases of the oesophagus, cervical abscess, cancer or
abscess of the chest wall, tubercle of the bronchial glands,
caries of the vertebras, ribs, or sternum; peritonitis, sub-
phrenic abscess, abscess of the liver, spleen or pancreas,
and perforation from a gastric ulcer may act as causes of
secondary purulent pleurisy.
Morbid anatomy.—Inflammations of the pleura which
are of sufficient intensity from the start, or which develop
sufficient intensity at any period, may be attended by the
formation of pus. In this event the exudation of cor-
puscles is sufficiently free to give the exudate a purulent
character. The effusion usually separates into clear,
35S PURULENT PLEURISY.
greenish-yellow serum in the upper portion, and thick,
creamy pus in the lower part. It may be simply turbid
and contain floculi of lymph. The pus from pneumococcus
pleurisy is usually thick and creamy, is not clotted, and on
standing does not readily separate into clot and serum, but
thin, greenish serum appears on the surface after a time
(Netter).
Pus from streptococcus pleurisy is moderate in quanti-
ty, yellow in color and not very thick. On standing it sep-
arates into two layers: the upper clear and abundant, the
lowTer may contain shreds of false membrane. Pus from an
empyema usually has a sweet, heavy odor. In cases of
wounds of the pleura the pus may be fetid. In gangrene of
the lung or pleura the pus has a markedly offensive odor.
The pus from an empyema may have a gelatinous consist-
ence after withdrawal, or it may contain quantities of gas
which makes it quite foamy in an aspirator bottle.
As the connective tissue of the pleural surfaces be-
comes involved in the process a granulating tissue is formed
which may continue to generate pus. If the pus is drained
its formation will generally cease, the granulation tissue
becomes fibrous, and adhesions of the pleural surfaces oc-
cur. The pleural membranes may become greatly thick-
ened, and form grayish-white layers from 1 to 2 mm. in
thickness. The costal surface may show erosions and fistu-
lous openings. The visceral pleura may show perforations.
The new tissue in the pleural layers undergoes much con-
traction which is followed by various degrees of retraction
of the chest walls. Calcareous plates may form ,in the adhe-
rent pleural layers and may be of considerable size. The
lung may be markedly compressed. Displacement of the
thoracic organs may be considerable. Intra-pleural pres-
sure is usually higher in empyema than in serous effusions.
Loculated empyema (pleural abscess) usually occurs in
the lateral or posterior, lower portion of the chest. It may
occur between the base of the lung and the diaphragm,
usually on one side, rarely on both. Interlobar empyema
may occur and may be discharged through the lung into a
bronchus. Apical empyema is very rare but may occur.
PURULENT PLEURISY.
359
Clinical history.—The clinical history of purulent
pleurisy is quite as variable as that of sero-fibrinous effu-
sions. The onset may be abrupt with high fever, cough,
pain and early dyspnoea. Quite frequently the onset is in-
sidious and takes place during the course of, or following,
some of the acute diseases. There may be no pain, little
or no cough, and no dyspnoea until the pleural cavity be-
comes quite full. The character of the effusion and, to
some extent, its clinical manifestations are largely deter-
mined by the virulence of the infecting organism and the re-
sistance of the individual. Virulent infections cause effusions
rich in cell elements and deficient in fibrin, and are likely f,o be
purulent from the start. This is particularly true of strepto-
coccus infections, though they may be primarily sero-fibrin-
ous. Streptococcus pleurisies are most common in the
adult after the infectious diseases, pneumonic inflammations,
and may occur after pneumothorax from perforation in tu-
berculosis. The onset may be acute, with pain, high and
irregular temperature, and repeated chills. Again the on-
set may be insidious with only moderate temperature.
Absorbtion rarely occurs; they seldom discharge through
the bronchi; reaccumulation after puncture is rapid and
frequent; the course is towTard chronicity, and relapses are
common. The mortality rate is high (25 per cent.—Straus).
Pneumococcus pleurisies may be primary but are usu-
ally secondary to pneumonia, coming on with the onset,
during the course of, or after the crisis of the lung inflam-
mation. They may come on several months afterward
(Straus). Usually they come on immediately after the
crisis The onset may closely resemble that of pneumonia
with the exception of a more rapid pulse. In primary
pneumococcus pleurisies there may be an imperfect crisis
about the seventh day, the dyspnoea, however, persisting.
The temperature in pneumococcus pleurisies usually ranges
from 99" to 102°, and in some instances may be absent
(Straus). The effusion may be primarily se^o-fibrinous and
subsequently become purulent. The prognosis is more
favorable than in any other form of empyema. Absorption
may rarely occur. Simple aspiration may be followed by
360
PURULENT PLEURISY.
recovery. If left untreated they are very likely to» evacu-
ate spontaneously.
The following histories are typical of meta-pneumonic
empyema from pneumococcus infection:
Girl, aged seven years. Left apical pleura-pneumonia.
The pneumonia ran the usual course, being accompanied by
marked pleuritic friction and pain., Crisis on the sixth day,
the temperature going down to normal. On the evening of
the seventh day the temperature rose to 102". On the eighth,
ninth and tenth days the temperature varied from 99.5° in
the morning to 1<>2" in the evening. Moderate sweating
toward morning. On the tenth day there were signs of
fluid in the left side reaching as high as the third rib.
Aspiration of over a pint of pus. On the twelfth day the
fluid had reaccumulated. Siphon drainage instituted and
maintained for four weeks. Complete recovery. Perma-
nent loss of expansion less than one-fourth of an inch, as
observed two years later.
Young woman, seventeen years old. Pneumonia ter-
minating by lysis on the ninth and tenth days. Temperature
normal in the morning, and 99.5° in the evening for three
days. Temperature then rose to 101.5°, and varied from 99°
in the morning, to 101.5° in the evening. Examination
showed the left side to be full of fluid to the upper border
of the third rib. Aspiration of thirty-four ounces of pus.
Five days after, the fluid had reaccumulated. Siphon drain-
age instituted and maintained for four weeks. Complete re-
covery. Loss of expansion, observed twTo years afterwxard.
one-fourth of an inch.
Tubercular empyema may or may not be preceded by
evidences of pulmonary tuberculosis. It may follow tuber-
culosis of the bronchial glands. The effusion may be at
first sero-fibrinous. It may be due to streptococcus or to
pneumococcus infection. The onset may be acute or sub-
acute. The course has a tendency toward chronicity. The
effects of the effusion on the general condition of the patient,
and the pressure effects are often inconsiderable. There
may be little fever. The fluid will usually return after
aspiration. In a large proportion of the cases of tubercu-
lar empyema the various operative measures undertaken
for its relief fail of the desired result because of the inabil-
ity of the lung to expand, and they are converted into cases
PURULENT PLEURISY.
361
of chronic empyema which furnish a varied and irregular
clinical history.
Chronic empyema is essentially a surgical affection
though the responsibility for its occurrence has been laid
at the door of medical unskillfulness (Ewald). That this
charge is not just is pointed out by Curtis who calls atten-
tion to the fact that in some cases the patient has followed
his usual avocation for weeks while ill and before coming
under observation, and that in tubercular cases it may not
be possible to prevent the empyema from assuming a
chronic form.
The history of chronic empyema may be simply that of
loss of flesh and strength, some dyspnoea, slight irregular
fever, and eventually signs of enlargement of the side with,
possibly, pointing of the abscess in some of the intercostal
spaces, as in the following case:
Boy, aged eight years, sick for four months with irreg-
ular fever, shortness of breath, loss of appetite and flesh,
Left side bulging below the fourth rib in front. In the
fifth interspace to the left of the nipple line there is a
prominence over which the skin is tense and reddened. Fluc-
tuation can be detected. Examination shows signs of fluid
as high as the fourth rib.
Symptoms of septic infection are more or less marked
in empyema especially in children. Sweating may or may
not be pronounted. There may be little cough, and the
fever may be very irregular. In chronic cases there will
be various degrees of deformity from contraction of the
chest walls.
If purulent effusions in the pleura are not interfered
with they may affect various tissues within or without the
chest. They may disappear by absorption in a very limited
number of cases, the pus becoming inspissated, lime salts
deposited, and the pleurae greatly thickened. Perforation
into a bronchus may occur, usually in loculated empyema,
in which case pneumothorax generally results. Necrosis
of the visceral pleura may occur and the pus may find its
way into a bronchus without perforation of the latter,
in which case pneumothorax is absent (Traube). Perfora-
3(2 PURULENT PLEURISY.
t'on of the chest wall may occur (empyema necessitatus), us-
ually in the antero-lateral region of the chest (Cruveilhier),
and generally in the fifth interspace (Marshall). The pus
may break into the mediastinum, pericardium, oesophagus,
stomach, or peritoneum. It may pass down along the spine
and psoas muscle into the iliac fossa.
Symptoms and diagnosis.—The subjective symp-
toms of purulent pleurisy differ from those of the serofib-
rinous form chiefly in there being a more irregular, septic
type of fever, greater prostration, less cough, 'greater tend-
ency to sweating, less dyspnoea unless the quantity of fluid
is great, and little or no pain.
Leucocytosis is generally present in purulent pleurisies
and may be marked.
The physical signs are those of general or loculated
effusion and are similar to those of sero-fibrinous effusions.
The main differences in empyema are the greater degree of
enlargement of the affected side, particularly in children
with free, purulent effusion; the greater tendency to oblit-
eration and bulging of the intercostal spaces; the more fre-
quent occurrence of oedema of the chest wall, and enlarge-
ment of the subcutaneous veins; a greater degree of displace-
ment of the heart, liver, or diaphragm, due, according to
Senator, to the greater wTeight of the fluid. The breath
sounds may be loud and tubular over a considerable effusion,
especially in children. According to Baccelli whispering
pectoriloquy is not heard over a purulent effusion.
Pulsation synchronous with the heart's action is a phe-
nomenon occasionally met with. Pulsating pleurisy occurs
in two forms: The intrapleural form in which the whole
side of the chest may pulsate without any bulging or point-
ing of the effusion. Inmost of these cases the pulsation is
confined to the praecordial region or to the lower intercostal
spaces (Gee). In the second form—the pulsating empyema
necessitatus. there is an external, pulsating, bulging tumor
in one or two places. The bulging is rarely larger than an
orange. In either variety the heart is much displaced, and
the heart sounds may be conducted to the bulging area.
There is no thrill on palpation, and no expansion similar to
PURULENT PLEURISY. 363
that of aneurism. Pulsating effusions are usually chronic
and practically always left sided, and may be associated
with pneumothorax, in which case the pulsation is conveyed
by tne fluid alone. The effusion is almost always purulent,
though pulsating, sero-fibrinous effusions have been ob-
served. Loculated empyema may pulsate if situated near
the heart. If so there is always bulging. Intrathoracic
aneurism, and pulsating, cancerous tumor may simulate
pulsating empyema.
In the differential diagnosis from sero-fibrinous effusions
the exploring needle will settle many doubts and prevent
many mistakes. The following characteristics of purulent
effusions may, however, be taken into consideration: They
are most common in children; most often due to pneumo-
coccus or to streptococcus infection; the onset may be of
the pneumonic type in primary pneumococcus infection or
in meta-pneumonic cases, while in the adult it may be insid-
ious; in the later stages the fever is of the hectic type, or,
in some instances, the fever may be absent; the clinical
history shows emaciation, profuse perspiration, febrile
urine, rigors, anaemia, cachexia, and. in adults, great pros-
tration and delirium; leucocytosis is present; fluctuation in
the interspaces, oedema of the chest wall, pointing and
pulsation may occur. In loculated empyema there may be
rupture of the sac. Absorption is rare but may occur in
pneumococcus infections ic children.
In fetid empyema we may have typhoid, septic symp-
toms indicative of infection of the whole body. Similar
symptoms may occur in cases which are not fetid. Coma
and delirium may be present. Enlargement of the spleen,
diarrhoea, and joint symptoms may occur. Death may
take place in ten or fifteen days no matter what treatment
is employed.
Loculated diaphragmatic empyema may be associated
with hepatic or subphrenic abscess. It may be latent and is
difficult to diagnose especiallv wiien it contains gas. Sub-
phrenic abscess usually occurs on the right side. There is
usually pleurisy on the same side, generally empyema
with or without perforation of the diaphragm. The pus is
364
PURULENT PLEURISY.
fetid and may burst into the lung even if there be no em-
pyema. If empyema be present it will be localized and the
physical signs of the two conditions will be practically
identical. There is fulness and tightness of the hypochon-
drium; the liver may be depressed, but is not always so;
besides, it may be depressed in uncomplicated empyema.
In subphrenic abscess there is dullness and signs of effusion
at the base whether effusion be present or not, as the dia-
phragm may be pushed upward and the lung compressed or
collapsed. The heart apex may be displaced without there
being empyema, but usually is not. Puncture or aspiration
may show the presence of pus, but may not indicate its lo-
cation above or below the diaphragm as the needle may
pass through the diaphragm when the latter is much ele-
vated. Even resection of a rib and exploration with the
finger may be indecisive. When a subphrenic abscess con-
tains gas the sounds may have a general amphoric char-
acter and there may even be no liver dullness.
In some cases of long continued abdominal pain the
patient may develop a unilateral type of breathing result-
ing in an elevation of the diaphragm and of the liver
dullness, laterally and behind, of as much as two inches,
the anterior, lower border of liver dullness remaining un-
changed. This area of dullness may resemble that of
hepatic, subplerenic, or localized pleural abscess.
Pyopericardium, suppurating hydatids of the liver,
pleura, or lung; necrosis of the ribs, sternum, or vertebrae,
Wunderlich's "peripleuritis" etc., are conditions to be elimi-
nated in the diagnosis of localized empyema.
Treatment.—The treatment of purulent pleurisy is
altogether surgical. The fact that it is possible in very
rare instances for cases of pneumococcus infection to be-
come absorbed has absolutely no bearing on the indications
for surgical measures. We will not enter here into a discus-
sion of the general surgical treatment of empyema, but
will consider a few points of general interest.
In acute, general empyema the course to be pursued
depends upon the nature of the infection, the age of the
patient, and the character of the effusion. In children and
PURULENT PLEURISY.
365
young people general empyema occasionally recovers by
simple aspiration, though this may have to be repeated
several times. Upon one occasion I performed the ninth
aspiration on a boy for post-scarlatinal empyema. He was
aspirated twice subsequently. About a year afterward I
examined the boy's lungs and found it difficult to tell which
side had been affected. It is generally admitted, however,
that we are not warranted in trusting to simple aspiration
for the cure of purulent effusion, and that drainage is
necessary.
It makes but little difference what methods are pursued
provided that drainage is sufficiently free, though there is
much discussion over the procedures necessary to procure
adequate drainage, particularly in relation to the necessity
for rib resection. Surgeons are generally in favor of resec-
tion in all cases of empyema. Godlee recommends resec-
tioh"as a routine practice to which there are certain except-
ions." The operation is neither difficult nor dangerous, and
while there is no particular objection to it in any case, it is
not necessary in every instance. In empyema in children
general opinion seems to favor incision and drainage up to
the end of the second year. After this period resection is
generally recommended. Koplik recommends simple in-
cision, at least for primary operation, in children under one
year, especially when they are weak; in older and stronger
children he thinks resection may be best. Holt recom-
mends simple incision rather than resection. As the death
rate in children from one to three years old is given as nearly
fifty per cent, it is evident that the best results have not
yet been attained. Bogart thinks that in children resection
of the ninth rib in the posterior axillary line is ordinarily
demanded, and should be preceded by a preliminary aspira-
tion when the collection of fluid is large; primary irrigation,
curettage, and multiple rib lesection is contradicted in
children unless to aid inclosing a persistent cavity or sinus.
Chloroform is not contradicted in operating, though ac-
cording to Winters full anaesthesia should not be induced.
In general cases of empyema secondary to infectious
diseases, especially meta-pneumonic empyema, where by
366 PURULE.VT PLEURISY.
exploratory puncture we know that the effusion is compara-
tively thin and probably does not contain great masses of
lymph, we can, by a simple siphon drainage, obtain more
perfect results than by resection of the ribs. This method
is but little more trouble than aspiration and does not in
anyT way interfere with subsequent resection if the latter is
deemed necessary. The cases whose clinical history is cited
on page 360 were siphoned in the following manner:
A trocar and cannula—the cannula constructed so as to
just admit of the passage of i\ inch tubing—was passed
through the sixth or seventh interspace in the anterior
axillary line. The trocar was withdrawn and some T\ inch
tubing passed into the chest and down almost to the
bottom of the pleural cavity. The cannula was withdrawn
over the tubing. The tube should project about eight
inches from the chest wall. Cotton is packed around the
tube at its point of exit, and a narrow strip of plaster
fastens the latter to the chest wall. Ordinary syringe tubing
is convenient as that portion of the tube which is within the
chest becomes rigid and does not flex on itself as pure
rubber tubing is apt to do. On the outer end of the tube
there should be an ordinary flush-bottle clip and a glass
coupling, When the tube is in place about three yards of
tubing is attached to the coupling and run into a jar of
water at the bed side. With the thumb and finger the air
is then stripped out of several feet of the tube and the clip
is moved down and fastened below. After the pressure is
relieved the pus can be siphoned out rapidly or slowly by
occasionally stripping out a few feet of tubing and fasten-
ing the clip. At the end of a week the tube can be with-
drawn a couple of inches, and by gradual withdrawal the
cavity will become small enough in three or four weeks to
put in a short, open, drainage tube, which can be removed
and the opening allowed to close when the discharge dimin-
ishes to about a dram in twenty-four hours. A slight degree
of chloroform anaesthesia is desirable though not absolutely
necessary in introducing the tube. In a few days the pa-
tient can be placed in a wheel-chair and taken out of doors,
which is a great advantage inchildren in hastening recovery.
PURULENT PLEURISY.
3:57
General effusions of several weeks standing, especially
if there is tendency toward pointing, are better treated by
free incision with or without resection of a rib. Better drain-
age is usually secured in all positions of the patient when
the resection is made at the ninth rib just outside of the line
of the angle of the scapula (Gee), though many surgeons
prefer operating in the anterior axillary line. A chief
danger after operation is pneumonia of the opposite lung.
Considerable elevation of temperature after operation is
usually due to imperfect drainage or to pneumonia. Caille
states that the temperature remains near the normal after
operation in very few cases, but that its elevation always
means something which should be sought for and cor-
rected.
Irrigation of the pleural cavity after operation for free
effusion should not, as a rule, be practised. Offensive ef-
fusions generally become less so soon after free drainage is
established. There is danger of fatal syncope in some cases,
and general opinion is against irrigation.
In localized empyema resection is almost always neces-
sary. Irrigation is frequently indicated but should be used
with caution. Irrigation by submersion in a warm bath is
recommended by Zeman when the opening is large enough
to allow the water to pass freely in and out. This method
is endorsed by Adams. In tubercular empyema the pro-
priety of establishing free drainage may be doubtful. In
many of these cases it is difficult or impossible to close the
cavity, and to produce expansion of the lung under these
circumstances may hasten the destructive process in the
lung. Repeated aspiration may be practiced, and sterilized
or antiseptic solutions may be siphoned in and out of the
cavity. In some cases of tubercular empyema operation
may be indicated.
In cases of double empyema it is safer to drain one side
and aspirate the other if necessary, postponing the drainage
of the opposite side until the patient becomes accustomed
to the change in the respiratory conditions. In case there
are adhesions it may be perfectly safe to drain both cavities
.at once.
368 PURULENT PLEURISY.
Failure of an empyemic cavity to close is met with most
often in tubercular cases. Absence of adhesions, extensive
collapse of the lung, great rigidity of the chest wall, bron-
chial fistula, caries of the spine or ribs, tumors, and foreign
bodies are the conditions which most commonly interfere
with closure of the cavity. In tubercular cases where sup-
puration persists, it may be necessary for the patient to
wear a tube for an indefinite period.
In some long-standing cases incision and drainage fail
to result in closure of the cavity because the changes which
have taken place in the pleurae interfere with expansion of
the lung, retraction of the chest wall etc., which are neces-
sary to the closure of the cavity. These pleural changes
are great thickening (^ to 1 inch), and the development of
calcareous plates which may be large or small and most
often occur in tubercular cases. It may be impossible to
remove them.
If a cavity fails to close in spite of free, single or double
drainage, and particularly when the drainage is not perfect,
the effects of chronic suppuration will appear: The patient
becomes anaemic, exhibits hectic fever and develops amyloid
visceral changes, enlarged liver, diarrhoea, emaciation and
clubbed fingers; the urine is light in weight and may be al-
buminous. These conditions may almost entirely disappear
if perfect drainage is established and the cavity closed.
The possibility of attaining this desirable end by the per-
formance of one of the more extensive operations, such as
Estlander's operation should be considered.*
In cases which exhibit, as a result of blood, poisoning,
the so-called "pulmoval cerebral abscess," the abscess should
be opened if distinct localising symptoms are present, as
they are otherwise fatal. The connection of these- abscesses
with empyema is not clearly understood. According to
Gowers they do not result from true tubercular cavities; the
abscess is single in about half of the cases; it is usually sit-
uated in the posterior lobe of the hemispheres; the cerebel-
lum is seldom affected and never singly,
*For consideratioii of the sreneral sursical treatment of chronic empyema
reference should be made to Pager's "Surgery of the Chest" God !*-»•« nnnti.K.tS
to Fowler and Godlee's Diseases of the Lungs", etc ' U0CUee s contribution:
CHAPTER XVI.
PNEUMOTHORAX.
By pneumothorax we mean the presence of air in the
pleural cavity. The presence of air alone in the pleural sac
is a rare condition, pneumothorax being practically always
associated with serum {hydro-pneumothorax) or with pus {pyo-
pneumothorax), and the term pneumothorax, as ordinarily
employed, applies to either of these conditions.
Pneumothorax occurs more frequently in males than in
females. It occurs chiefly in adults between the ages of
twenty-five and thirty-five years—the period of greatest
mortality from tuberculosis, but may be met with in very
young children.
^Etiology.-—When air enters the pleural cavity the
normal intrapleural tension in the pleural cavity (a nega-
tive force equal to-6 to-8 millimetres of mercury.—S.
West) which practically equals, but opposes in direction,
the normal elastic recoil of the lung (a positive force equal
to 6 to s millimetres of mercury.—Donders) is relieved and
atmospheric pressure is applied to both surfaces of the vis-
ceral pleura; the normal elastic recoil of the lung will then
cause its collapse. This alteration affects the mediastinum,
which is a movable partition, and its contents. The elas-
ticity of the lung of the opposite side is also a factor in
producing displacement of the organs within the chest. In
explanation of the absence of pneumothorax in cases where
it would appear to be a natural result, West assumes the
presence of a cohesion of the pleurae—equal to ll\5 milli-
metres of mercury—which counteracts the tendency toward
retraction of the lung. If the lung on the affected side is
adherent to the chest wall in part or in whole the elasticity
of the lung is counteracted and the displacement of organs,
dyspnoea, etc., will not be so marked. Thus the effects of
pneumothorax are more marked in a healthy chest than in
370
PNEUMOTHORAX.
one with adhesions between the lung and chest wall. If the
pleura is entirely adherent and the elasticity of the lung
completely negatived, the opposite lung may become con
siderably enlarged. Its elasticity, however, is not dimin-
ished, and it should therefore, according to West, be called
' 'compensatory hypertrophy."
If the opening in the pleura by which the air gains en-
trance becomes closed or has a valvular action, the intra-
thoracic pressure may become greater than that of the at-
mosphere, and the displacement of the organs within the
chest may be increased. The rise in pressure may be due
to rise in pressure from the valvular action of the opening
during expiratory -efforts, rise in temperature of the gas
contained in the pleura, or to compression of the air by
effusion into the pleural cavity.
Pneumothorax occurs from perforation of the costal,
visceral, or diaphragmatic pleurae; and from the spontaneous
development of decomposition in pleural exudates.
Perforation of the costal pleurae may arise from punc-
tured or shot wounds of the chest wall, in which case it may
or may not be associated with extensive emphysema of the
chest wall; from exploratory puncture (Biggs, Osier); rarely
from fracture of the ribs; and occasionally from abscess of
the chest wall. Perforation of the diaphragmatic pleura
from abscess originating in malignant disease of the stomach
or colon, and especially from ulcer of the stomach, may
cause pneumothorax. Perforation of the visceral pleura is
the usual cause of pneumothorax. The most frequent factor
in its production is tuberculosis of the lungs, especially acute
pneumonic tuberculosis. According to various authorities
ninety per cent, of the cases of pneumothorax are due to
pulmonary tuberculosis. [Biach's collection of 918 cases
shows 76 per cent, due to tuberculosis. Saussier's 131 cases
shows phthisis in 81 cases, empyema in 29 cases, and gan-
grene in 7 cases.] The percentage of cases of tuberculosis
which are complicated by pneumothorax is given by Powell
and West as 5 per cent, and by Fowler as 6.5 per cent. Em-
pyema and pulmonary gangrene are the next most frequent
causes of pneumothorax by perforation of the visceral
PNEUMOTHORAX.
371
pleurae. Rarer causes are: abscess or hydatids of the lung
or mediastinum, rupture of the pleura over a septic infarc-
tion, rupture of a haemorrhagic infarction occurring in
chronic heart disease (Osier), rupture of air vessicles of a
normal lung, (West thinks that an undetected lesion is re-
sponsible for these cases), strains from heavy lifting, or
from unusual positions of the body, emphysema, bronchiec-
tasis, disease of the oesophagus or bronchial glands, and
malignant diseases of the lung.
Pneumothorax from decomposition caused by the gas
bacillus {B. aerogenes capsulatus.—Welch) is very rare, and
is denied by some. The objections of Jaccoud, Fagge,
Powell and others, which served to displace Laennec's sim-
ple or essential pneumothorax as being unscientific in the
sense of being non-perf orative, will have to be qualified so as to
admit of a non-perforative form of pneumothorax in view of
the evidence furnished by LeVy, May and Gebhart, Hamil-
ton and others.
Pneumothorax may occur in persons who are apparently in
perfect health, and as such cases generally recover, the lesions
which induce the pneumothorax may not be discoverable.
Morbid anatomy.—In simple pneumothorax the pleural
surfaces may present their usual glistening appearance.
Usually there are the ordinary changes of acute or chronic
inflammation. In perforative cases the opening in the mem-
brane may be very difficult to find, but can usually be de-
tected by forcing air into the main bronchus. There may
be considerable lymph on the pleural surfaces and adhesions
may or may not be present. Serum or pus may be -present
in the pleural cavity if sufficient time has elapsed, since the
perforation took place, for their accumulation. On opening
into the pleural cavity, or on inserting a trocar, there may
be a jet of air strong enough to blow out a lighted match.
On opening the chest 'the lung is found compressed, col-
lapsed, or carnified; the mediastinum and contents are dis-
placed towards the opposite side.
In acute pneumonic tuberculosis a sub-pleural necrotic
area may perforate the pleura during a coughing spell, or,
perforation may occur while the patient is at rest or asleep.
372
PNEUMOTHORAX.
In the more chronic varieties of tuberculosis the involve-
ment of the pleural membrane results in the formation of
adhesions which are likely to prevent the development of
pneumothorax, otherwise the occurrence of the latter condi-
tion would be much more frequent in pulmonary tuberculo-
sis. In rare cases a cavity, or a sinus leading from a cavity,
may rupture through the visceral pleura.
As a rule the affection is unilateral, and the left pleural
cavity is involved more often than the right. (34:29,
Fowler; 83:42, West; 7:1, Louis: 55:30, Walshe; 23:16, Powell;
2:1, Lebert, Regnaud, Wintrich, Weil. Laennec regarded
the right side as most often affected.) The perforation, on
either side occurs most frequently from the upper lobe than
the lower lobe, the usual site being the mid-lateral aspect of
the upper lobe. The middle lobe of the right lung is affected
in a small proportion of instances. There is usually but one
opening which is generally small, though it may be of con-
siderable size. There may be several openings, and they
may be confined to one lobe or may involve different
lobes,
In pneumothorax from punctured wounds the - gas will
be of the same composition as the atmosphere; in perfora-
tions of the visceral pleura the gas will at first be the same
as in the alveoli: N=79.5, Co2=4.38, 0=16.0. If the open-
ing is closed the oxygen will disappear and the carbonic
acid and nitrogen may lincrease. If the effusion present
is fetid there may be sulphuretted hydrogen gas pres-
ent.
In pneumothorax from punctured wounds or from the
rupture of an emphysematous vessicle the opening may be-
come closed and the gas absorbed in the course of four or
five days. In tubercular pneumothorax there may be no
effusion, and little or no inflammation. In the majority of
cases, however, there will be a variable amount of pus of a
yellow, greenish, or grayish color. It may be fetid. The
effusion is usually serous at first, then sero-purulent and then
purulent. It may be purulent from the first. Serous effu-
sions may be clear, turbid, flaky, or blood-stained. The ex-
udate may be gelatinous, or in some cases there may be
PNEUMOTHORAX. 373
exudation of lymph without any fluid effusion. There is no
constant relation between the duration of the condition and
the amount of effusion.
The effect of the collapse of the lung, resulting from
the pneumothorax, on the progress of tubercular disease in
the lung involved, has caused considerable discussion. In
many cases there is, temporarily at least, modification or
arrest of the tubercular process, though this is disputed by
some observers.
Clinical history.—The clinical history of pneumo-
thorax will vary with its type and aetiological relations.
The onset may be sudden with severe symptoms, or the
pneumothorax may be gradually and quietly acquired with-
out special disturbance. This difference in onset depends
on the rapidity with which the air gains entrance to the
pleural cavity, and on the functional activity of the lung
involved If the lung is badly compromised by disease and
is adherent to the parietal pleura, both of the above factors
will operate in modification of the severity of the onset of
the pneumothorax. In severe cases the patient may exper-
ience a sensation as if something within the chest had given
way; there will be severe pain in the back or in the upper
part of the chest, and the patient may recognize the dis-
placement of the heart. There may be severe shock with
temporary heart failure, cold extremities, clammy perspira-
tion, rapid pulse and respiration, and great mental distress.
Dyspnoea is a marked feature, it is sudden and urgent, and
is mainly due, according to Murphy, to the interference
with the piston action of the diaphragm. The degree of
dyspnoea will be in inverse ratio to the functional activity
of the lung involved. Death may soon follow the collapse
of the lung if the lung involved is the one chiefly depended
on for respiration.
In latent cases there may be no history of the onset,
the pneumothorax developing without special disturbance,
and being recognized only on physical examination. These
cases are likely to occur in tubercular pneumothorax, and,
according to West, may occur occasionally in healthy adults.
374
PNEUMOTHORAX.
A recurrent variety of pneumothorax has been described by
Goodhardt, West, and Furney.
The following case illustrates a common development of
pneumothorax in pulmonary tuberculosis:
Man aged 36 years. Primary apical tuberculosis of the
left lung. Secondary involvement of lower, left lobe.
Temperature, 100.5° to 102°. The patient who had been
well enough to be up and about, woke up one morning feel-
ing weak and depressed. His temperature was 99°, and
pulse 120: respiration somewhat more rapid than usual, but
no special dyspnoea. Examination showed a pneumothorax
of the left side. Two days afterward the temperature had
regained its usual elevation. A slight effusion followed the
occurrence of the pneumothorax, subsequently both air and
fluid were absorbed. The patient died about eight months
afterward.
After an attack of pneumothorax the temperature may
show a considerable drop if its range has been previously
high. If it has not been high the drop will be less manifest.
After the shock passes off the temperature will return to its
previous range. Its subsequent range will depend largely
on the nature of the changes in the pleura. In latent cases
not followed by effusion, and where the air is rapidly ab
sorbed, there may be no pyrexia. If pus forms in the pleural
cavity there will be fever of a hectic type. According to
Peters, and Williams, the temperature of the axilla on the
affected side may be temporarily lower than that of the op-
posite side.
As pneumothorax occurs, in most instances, in cases of
advanced lung disease, it may be regarded as an unfavor-
able manifestation, although it may retard the progress of
the lung lesion in some cases. If the mechanical results of
a valvular opening be not too marked, or if the pleural
inflammation or the pressure from effusion tends to close
the opening, recovery from the pneumothorax may ensue.
In cases not followed by effusion the gas may be absorbed
in a few days. Of thirty-nine cases cited by Powell from
post mortem records, the longest duration of life was twelve
months, and the shortest, ten minutes. Pneumothorax
occurring in a healthy person frequently ends in recovery.
Tubercular cases die within a few weeks as a rule. West
PNEUMOTHORAX.
375
places the mortality of pneumothorax at seventy per cent.
Symptoms and diagnosis.—In severe cases, besides
the subjective symptoms already detailed, the patient will
be found sitting, leaning forward with widely dilated alae
nasi, livid or cyanosed face, and unable to articulate clearly.
After the intensity of the symptoms has passed off the
intense dyspnoea may be relieved even though the respira-
tory rate increase with the accumulation of air within the
pleural cavity. With a respiratory rate of fifty-two per
minute the patient may not be conscious of difficulty in
breathing. (Walshe).
On inspection in a case of general pneumothorax of
considerable extent the side will be found to be immovable
and enlarged. Its surface will be smooth from the absence
of intercostal depressions. The shoulder is raised. The
heart impulse may be displaced or may not be visable. If
the pressure is great there may be bulging of the chest and
distension of the superficial veins. In pneumothorax from
perforation of the visceral pleura by an empyema, particu-
larly in chronic empyema, and in cases due to perforation
of the diaphragmatic pleura, if the opening is patent the
side may be diminished in size or retracted. In pneumo-
thorax circumscribed by pleural adhesions, enlargement
may be slight, some expansion will be noticeable, and slight
inspiratory retraction of seme interspaces may occur. The
opposite side may develop compensatory enlargement, but
the interspaces will show inspiratory recession.
Palpation will determine the absence of the cardiac
impulse from its usual situation. Its actual situation is
usually evident, though it may not be. The displacement
of the heart occurs suddenly, may be recognized by the
patient, and is an important symptom whose relation to
pneumothorax was first pointed out by Gaide in 1*28. Its
sudden and early occurrence shows that it is due to the
removal of the elastic-traction force of the collapsed lung
and to the increased effect of the same force in the opposite
lung, rather than to pressure. The liver and spleen may
be depressed, the former may be as low as the iliac crest.
Vocal fremitus is absent over the affected side except in
376
PNEUMOTHORAX.
cases with pleural adhesions, when some fremitus may be
felt.
Percussion over the air-containing cavity gives a tym-
panitic note which may be obtained beyond the mid-sternal
line if the mediastinum and contents are much displaced.
The note may be amphoric in quality; it may be hyper-
resonant as in emphysema, of a flat quality similar to Sko-
diac resonance, or, in rare instances, dull. — ''Muffled, tone-
less, almost dull." (Walshe). It is claimed that with ex-
treme degrees of tension the note may be markedly dull,
but this appears to me to be doubtful, though the pitch is
often considerably raised. Auscultatory percussion may
furnish a note of strongly metallic character. Displace-
ment of the heart, liver, and diaphragm may be recognized
by percussion. In left-sided pneumothorax the area of
praecordial dullness is usually obscured, and the normal
stomach tympany will interfere with our recognizing down-
ward displacement of the diaphragm. It is claimed that a
cracked-pot sound may be obtained if the opening is patent,
if so, it is a very inconstant sound.
If fluid is present there will be dullness or flatness
below, and tympanitic resonance above. The level of the
dullness is more readily altered by a change in the position
of the patient than it is in pleurisy. The upper level of a
given amount of fluid may be much lower than in pleurisy,
owing to the downward displacement of the diaphragm.
Intercostal percussion may give a sense of fluctuation
and a thrill. According to Walshe, the latter is most
marked between the tympanitic and dull areas.
Auscultation of the respiratory sounds shows them to
be suppressed on the affected side. Distant, tubular, or
amphoric breathing may be present. In circumscribed
pneumothorax with a free opening there may be loud am-
phoric breathing. Metallic rales may be present and
metallictinkling(Laennec) may be heard on deep inspiration,
coughing, speaking, swallowing, or may occur from the
movement of the heart. The voice sounds are amphoric or
metallic in quality, and may have an echo-like character.
The so-called coin-sound or bell-sound {bruit d'uitain.__
PNEUMOTHORAX. 377
Trousseau) is a characteristic metallic echo which is one of
the most constant signs of pneumothorax. It is produced
by pressing a coin flat upon the chest, over the pneumo-
thorax, and tapping it with another coin while the ear or
stethoscope is applied to the opposite aspect of the cavity.
If there is fluid in the pleural cavity we may have, in addition
to the above signs, the succussion sound. (Hippocrates).
This splashing sound has the peculiar metallic quality com-
mon to the other signs of pneumothorax, and is caused by
the splashing of liquid effusion in the air cavity. It is
obtained by shaking or jolting the patient while the observ-
er's ear is applied to the chest wall. The patient may
himself recognize the sound.
The diagnosis of pneumothorax is usually not difficult.
The circumscribed variety is most likely to be confused with
other conditions. If the percussion note is dull we may
mistake pneumothorax for pleurisy. Diaphragmatic her-
nia may simulate pneumothorax, but usually has a history
of injury. Very large cavities in the lung may present
metallic tinkling and the amphoric qualities of voice and
respiratory sounds peculiar to rmeumothorax, but there is
absence of dislocation of the organs, of the succussion
splash unless there is an unusually large quantity of liquid
in the lung cavity, and of the coin-sound, though the latter
may be obtained in rare instances over a large cavity.
Findlay has known emphysema to be mistaken for pneumo-
thorax, and points to the bilateral nature of the former,
also the absence of cardiac displacement, of the coin-sound,
and to the less tympanitic percussion note as differential
points.
Pyopneumothorax subphrenicus (Leyden)—a condition
in which an abscess cavity beneath the diaphragm receives
air through a fistulous communication with an air-contain
ing viscus (usually from perforating ulcer of the stomach)—
may simulate pneumothorax, but can usually be recognized
by the history. If the similarity in the voice and respira-
tory sounds sometimes heard over the upper portion of the
lung in eases of pleurisy, or over consolidated lung in pneu-
monia, to those of pneumothorax, confuses us. we may
378
PNEUMOTHORAX.
avoid mistakes by careful consideration of the general con-
dition of the patient, the subjective symptoms of the dis-
ease, and the location of its physical signs. Subjectively,
an asthmatic paroxysm, or hysterical dyspnoea, may. re-
semble pneumothorax, but physical examination readily
removes any doubt.
Treatment.—If the occurrence of pneumothorax is
attended by severe pain, dyspnoea and mental distress, a
hypodermic injection of morphia should be given. If
severe shock results from the severity of the attack we may
give hypodermic injections of ether. Strapping the chest
has been recommended for the relief of pain and dyspnoea,
and in some instances may possibly be of service. Cupping
and venesection had been advised for the relief of the pres-
sure on the right heart in cases associated with lung disease.
These measures, however, are seldom advisable or necessary.
Surgical measures are the only means of giving direct
relief to the conditions resulting from pneumothorax. Va-
rious procedures have been suggested. Potain recom-
mends the substitution of sterilized air for the air and fluid
in the pleural cavity, and good results have been claimed
from it. Evidently such a measure must have a limited ap-
plication.
The surgical indications are much the same as in
pleurisy. In traumatic pneumothorax from perforationjof
the parietal pleura, surgical or otherwise, there is no special
tendency for the air to accumulate in the pleural cavity, and
if sepsis is not induced the air may become absorbed in a
short time. The use of the Tell-0*Dwyer apparatus 'for
maintaining respiration and preventing collapse of the lung
may be of great service in cases of acute traumatic]pneumo-
thorax.
In pneumothorax from a valvular perforation^of^the
visceral pleura there may be rapid accumulation of J air
which produces great distress through collapse and com-
pression of the lung and displacement of the intrathoracic
organs. Aspiration of the air gives only temporary -relief,
and it may be advisable to introduce a small cannula and
leave it in until the opening in the lung has closed. This
pneumothorax.
h79
must be conducted under strict antiseptic precautions. If
these cases are tubercular there will usually be some
serous or sero-purulent fluid present, but the air may be
the chief difficulty.
A pure hydropneumothorax is very rare, but cases have
been reported in association with hydatids of the chest. If
aspiration is followed by increase in the pneumothorax and
reaccumulation of the fluid, a free opening will probably be
necessary.
In tubercular hydro- or pyopneumothorax, if the fluid
is slight in amount and does not tend to increase, and the
patient is fairly comfortable, the case had better be let
alone. If the amount of fluid is large and tends to increase,
aspiration may be tried. If this is not satisfactory Godlee
recommends passing two needles into the pleural cavity,
one in front connected with a bottle of boric acid solution at
a temperature of 100° F., and one behind, which is connected
with an aspirator, or which may be used as a syphon. The
pleural cavity is drained and washed out with the solution
which is also removed, as far as possible.
In all cases of pyopneumothorax, except some cases of
tubercular origin, especially in cases showing septic effusion,
incision and free drainage is indicated. According to
Fraentzel, Senator, and others, the incision should be made
close to the upper margin of the ninth rib just below the
angle of the scapula. Irrigation may be advisable, but fre-
quently is not best.
In pneumothorax resulting from the perforation of
variously situated abscesses into the pleural cavity, or
where gas results from decomposition, the treatment should
be on the same lines as in cases of empyema.
HYDROTHORAX.
Hydrothorax (dropsy of the pleura) is due to non-inflam-
matory transudation of serous fluid into the pleural cavity.
It occurs as a secondary process in many conditions. The
fluid is clear, usually without floculi of lymph, and is mark-
edly albuminous. The amount of albumen varies greatly,
380 hydrothorax.
but according to analyses of Schmidt, Hoppe-Seyler, Leh-
man and others, is greater than in dropsical fluid from other
serous cavities.
^Etiology.-—Cardiac failure from chronic valvular
disease, and Bright's disease are the most common causes
of hydrothorax. Dropsical conditions due to cardiac failure
from any cause may involve the pleural cavities. Hasmic
dropsies may be associated with hydrothorax. Hydrothorax
may be associated with hepatic cirrhosis, mediastinal tumor,
or with aneurism. Intrathoracic tumor may cause hydro-
thorax by pressure on the azygos veins.
Morbid anatomy.—Any degree of effusion may be
present. In recent effusions the pleural membranes retain
their smooth, glistening appearance. In long-standing
effusions the visceral pleura is usually slightly thickened,
and is of a dull, grayish-white color, due to exudation which
changes into a fibrous film of unequal thickness similar to
that found in the peritoneum in chronic ascites (Fowler),
and probably due to slight inflammation of the serous mem-
brane from prolonged contact with the fluid.
With long standing effusion and thickening of the pleura
the lower lobe, or more, of the lung may be collapsed. The
anterior margins of the lower lobe may be thinned out. In
cases of general dropsy in persons with pleural adhesions
of one side, the corresponding lung may be cedematous,
and there may be hydrothorax of the other side.
Clinical history.—Hydrothorax, like other dropsical
developments, may be exceedingly irregular. It may, or
may not, be present in conditions which should, apparently,
affect all of the serous cavities alike, In renal disease it is
usually bilateral, and we would expect the same condition
in connection with heart diseases in which it is often uni-
lateral, and almost always of greater extent on one side
than on the other. Cases of general cedema, with or with-
out ascites, may, or may not, be associated with hydro-
thorax, and the latter may be present in eases which show
little or no oedema. In nephritis following the infectious
diseases, hydrothorax may come on suddenly in advance of
symptoms of general oedema.
HYDROTHORAX.
3H1
There will be a history of dyspnoea gradually or rapidly
acquired. In chronic heart or kidney disease the gradual
increase in the dyspnoea is likely to be attributed to the
gradual failure of the heart, and if examination of the chest
is neglected we may misinterpret the cause of the dyspnoea.
Marked oppression, orthopnoea, or cyanosis maybe present.
Again, a moderate degree of hydrothorax may add but
little to the respiratory distress. This was illustrated in a
case of cardio-renal disease in which several ounces of fluid
had been aspirated from the left pleural cavity in order to
relieve a severe dyspnoea. The dyspnoea was not relieved.
The vascular tension being very high, a vaso-dilator was
administered, and the dyspnoea was rapidly relieved and did
not reappear to a severe extent although the fluid reaccu-
mulated.
Symptoms and diagnosis.—In many instances the
gradual development of hydrothorax allows of the patient
becoming accustomed to the interference with respiration.
The physical inability incident to the chronic diseases with
which hydrothorax is associated also modifies the evidence
of its advent. The subjective symptoms are therefore less
marked and more liable to be overlooked than they other-
wise would be.
The physical signs are those of fluid in the pleural cav-
ity, though because of the absence of any lymph deposit
and of the lesser density of the fluid they are not so pro-
nounced as in cases of sero-fibrinous effusions. The side of
the chest is usually not enlarged. The heart is displaced
but little, and not at all if there is equal bilateral effusion.
Vocal fremitus is absent. The percussion note is dull but
not so absolutely flat as in sero-fibrinous effusion. Whis-
pering pectoriloquy may be heard. Tubular breathing can
usually be heard, and the fine rales of oedema are usually
heard in the lower portion of the lung on deep inspiration.
The clinical history of the case will establish the differ-
ential diagnosis.
Treatment.—The general treatment of cases in which
hydrothorax occurs is not to be considered here. As far as
the effusion is concerned it should be aspirated in any case
3*2
HEMOTHORAX.
of chronic heart or kidney lesion when there is sufficient
fluid to interfere with the proper performance of respiration.
In some cases of chronic heart disease hydrothorax may be
the particular element which interferes with re-establishing
the circulation. The same precautions should be observed
as in aspirating sero-fibrinous effusions.
HEMOTHORAX.
The term haemothorax is applied to a collection of blood
in the pleural cavity. The haemorrhagic forms of sero-
fibrinous effusions which may occur in connection with
Bright's disease, cirrhosis of the liver, pneumonia, malig-
nant types of specific fevers, and with cancer or tuberculosis
of the lungs or pleurae are not included under the designa-
tion of haemothorax.
Etiology.—Injuries of the chest resulting in laceration
of the pleura or lung, fractured ribs, injury of the inter-
costal or internal mammary arteries, rupture of an intra-
thoracic vein may cause haemothorax. Rupture of an intra-
thoracic aneurism may cause sudden and fatal hagmothorax.
A pulmonary infarction may rupture into the pleural cavity.
Scurvy, purpura, and conditions attended by haemorrhagic
diathesis may be associated with haemothorax. Fatal
haemothorax has occurred from the rupture of an aneurism
of the internal mammary artery after operation for pneumo-
thorax (Fowler).
Clinical history.—In traumatic cases a great amount
of blood may collect in the pleural cavity in a short time,
and will be attended by marked symptoms of haemorrhage.
In other cases the bleeding may be slow, and no very active
symptoms will develop. The rupture of an aneurism may
precipitate an extensive and rapidly fatal haemorrhage pre-
ceded by no premonitory symptoms such as may occur when
an aneurism perforates the trachea or oesophagus, when
there may be attacks of moderate haemoptysis.
Syncope, pallor, coldness of the extremities, rapid
breathing, labored dyspnoea, subnormal temperature, and
feeble, rapid pulse mark the development of haemothorax.
In traumatic cases the blood usually coagulates, the
CHYLOTHORAX.
3*3
serum becomes absorbed, and the clot may finally absorb
also. If septic infection occurs there is acute inflammation
and empyema. Blood may remain for a long time unco-
agulated in the pleural cavity.
Symptoms and diagnosis.—Aside from the subjective
symptoms, which may not be very distinctive in cases of
slow bleeding, the signs of effusion beginning at the base
and extending upward, particularly when following the
occurence of an injury, are most important. Friction
sounds are absent. If the blood has coagulated, the per-
cussion note is hard and flat. The area of dullness may
indicate a much larger effusion than is actually present. A
previous diagnosis of intrathoracic aneurism will assist the di-
agnosis in rapidly developed cases not associated with injury.
Treatment.- When the source of the haemorrhage is
not known, the treatment should be expectant. It is not
expedient to remove the fluid unless the severity of the
dyspnoea requires it, and then only sufficient fluid should be
removed to give relief to the symptoms. In traumatic cases,
if the bleeding has been comparatively slight and has ap
parently ceased, the treatment should be expectant. Where
injuries involve blood vessels which can be located, they
should be tied at once, and if necessary a portion of one or
more ribs should be removed in order to get at the point of
haemorrhage.
CHYLOTHORAX.
Chylothorax (chylous pleurisy) is a collection of chylous
fluid in the pleural cavity. The effusion may be found in
the pleural cavity alone or it may occur in connection with
chylous ascites. Chylothorax has been described as a form
of pleurisy, but as the effusion is non-inflammatory in na-
ture it should properly receive an individual description
(Fowler).
Chylothorax is usually caused by obstruction or rup-
ture of the thoracic duct. Obstruction of the duct at its
entrance into the left subclavian vein by narrowing,
thickening, thrombosis, tubercular disease, or new growths'
may cause chylothorax.
3*4 CHYLOTHORAX.
When there is obstruction, the thoracic duct may be dis-
tended in its entire course, and the lymphatics of the
lungs, pericardium, and pleurae may be distended. If there
is perforation of the duct without obstruction the lymph-
atics may not show such distension. The pleural mem-
branes may be white and opaque; the pleural lymphatics
milky and arborescent. The lungs may present collapse,
fibrosis, tubercular or other tissue changes.
The fluid may be present in one or in both pleurae. It
varies greatly in amount and contains fat in the form of an
emulsion. Chemically it contains albumen, globulin, fat
and inorganic salts; while microscopically there will be
found small refractive granules and a few leucocytes. Ac-
cording to Sidney Martin the specific gravity of the fluid is
about 1.022, and it consists of about ninety-one per cent, of
water, and contains from eight to nine per cent, of solids,
the fat amounting to about one or two per cent.
The clinical history is such as may pertain to the
nature of the primary lesion and is in no way distinctive as
the nature of the effusion does not influence the character
of the symptoms in any special way. Emaciation does not
appear to be marked even in those cases where considerable
fluid has been removed by repeated aspirations. Dyspnoea
may be marked, and pain may be present when there is
considerable effusion. The pulse is but slightly accelerated,
and the temperature is usually near the normal.
The physical signs are those of pleural effusion and are
not specially indicative of the nature of the fluid. The
diagnosis will rest on exploratory puncture.
The prognosis, while influenced by the nature of the
primary lesion, is generally unfavorable, though according
to Cayley it is possible for anastomosis with the right
lymphatic duct to be established in cases of obstruction
slowly developed.
The treatment of chylothorax is symptomatic. Aspir-
ation should be performed when there is sufficient fluid to
cause the patient to suffer,
385
TUMORS OF THE PLEURA.
Tumors of the pleura may be primary or secondary.
Primary new growths are rare in the pleura, but may
occur in the form of fibroma, sarcoma, or the so-called
endothelial cancer. Secondary growths are not infrequent
as the result of extension from other tissues. They are
usually cancerous or sarcomatous.
Secondary tumors of the pleura usually result from
infiltration of the pleural membranes from malignant
disease of the lungs, mediastinum, or of the chest walls.
Secondary involvement of the pleura is frequent in cases of
carcinoma of the breast, but may occur when the primary
lesion is situated in any portion of the body.
There has been some discussion over the nature of
primary cancerous tumors of the pleura, but as they cannot
be distinguished histologically from other cancerous
growths it is not worth while, from a clinical standpoint, to
discuss the question. They may form flat, multiple nodules
of a white color, connected by bands similar in structure.
They may show clusters of epitheliod cells, with round or
spindle-shaped nuclei, lying in a fibrous stroma. Alveoli
may present at the periphery of, or throughout, the growth,
and may be lined with cylindrical or cuboidal epithelial
cells. The growth may involve the bronchial glands, the
mediastinal tissues, or may extend along the peribronchial
tissues into the lung.
Any variety of sarcoma may occur in the pleura, but
the round-celled variety is most common. Sarcoma may
occur as large masses involving chiefly the parietal pleura,
with a soft infiltration of the pleural membrane, or there
may be a thick, fibrous layer involving the entire pleural
membranes. Secondary involvement may occur in any or
all of the adjacent tissues.
Tumors of the pleura may be essentially fibromatous,
but most cases of this kind are probably examples of mixed
sarcoma and fibroma.
The clinical history of tumors of the pleura may cover
a period ranging from two to three months to one or more
years. The course of primary tumors is generally rapid
386
TUMORS OF THE PLEURA.
and limited by months rather than years. The onset is in-
sidious as a rule. Pain is usually slight or absent, though
it may be severe and persistent. Cough and dyspnoea on
exertion are usually present. Malaise and loss of flesh may
be early symtoms, but extensive emaciation is not reached.
Moderate, irregular fever is present. The fever is usually
not great unless some complicating condition is pres-
ent. Albuminuria may be present. CEdema of the limbs,
and gastric derangement and vomiting may be present. If
the patient has been under treatment there may be a history
of aspiration of albuminous, bloody serum, or of some other
surgical procedure for the relief of the primary disease in
the breast or other tissues.
Pleural effusion is frequently present and the physical
signs of tumors of the pleura are very similar to those of
effusion. The chest may be rounded, bulging, or retracted.
The heart apex may or may not be displaced. Vocal fremi-
tus may be diminished or absent, as may, also, the vocal
and respiratory sounds.
Tumors of the pleura are chiefly confounded with pleu-
risy, from which they differ mainly by their slow onset and
absence of marked pain or fever. Paracentesis may show
the absence of fluid, or if fluid is obtained, its removal is not
followed by disappearance of the dullness, and by reposi-
tion of the heart if the latter is displaced. A haemorrhagic
effusion is not uncommon in connection with tumors of the
pleura, while it is somewhat rare in tuberculous or pneumo-
coccus pleurisy. Pressure symptoms are usually absent un-
less other structures than those of the pleura are involved.
In some cases of chronic tubercular pleurisy the symptoms
may much resemble the early history of tumors of the
pleura, and the diagnosis may be difficult in this stage.
The treatment of tumors of the pleura is symptomatic.
If fluid is present in the pleural cavity it should not be re-
moved unless necessary, as its removal gives little or no re-
lief, may be followed by distressing dyspnoea, and is usually
followed by reaccumulation.
INDEX.
Abscess, of the heart, 21
of the lung, 257
of the pleura, 358
sub-phrenic, 263, 264
Actinomycosis of the lungs, 315
aetiology of, 315
clinical history of, 316
morbid anatomy of, 316
symptoms and diagnosis of, 317
treatment of, 318
Acute endocarditis, 39
Adonis vernalis in endocarditis, 101
Air embolism, 206
Angina pectoris, 132
Adams-Stokes syndrome in, 136
cardiac asthma in, 136
cases of 134, 135
clinical history of, 133
nature of, 132
occurrence of, 133
syncope anginosa in, 136
case of, 136
treatment of, 139
Aneurism of the heart, 23
Angulus Ludovici 192,
Anthracosis, 249
Aortic regurgitation, 66
capillary pulse in, 68
cases of, 69, 70
murmur of, 68
prognosis in, 67
pulse of, 68
sequences of, 66
symptoms of, 67
Aortic stenosis, 62
cases of, 64
compensation in, 62
murmur of, 64
sequences of, 62
symptoms of, 63
Arterial supply of heart, 131
Aspergillus, 318
Aspiration, in pleurisy, 350, 356
in pericarditis, 18
Asthma. 177
aetiology of, 177
case of, 178
clinical history of, 180
dyspnoea in, 182
morbid anatomy of, 179
sputum in, 180
symptoms and diagnosis of, 181
treatment of, 183
Asystolism, 119
Atelectasis, 195
Bacelli'ssicn. 347, 362
Barrel-shaped chest, 191
Baths in cardiac dilatation. 127
[ Bellingham pulse, 68
Bell-sound, 376
Bicycle, use of in cardiopathies, 128
Bilious pneumonia, 223
case of, 224
Bradycardia, nature and cause of, 144
treatment of, 145
Bronchial asthma. 177
Bronchial stenosis, 175
aetiology of, 175
clincal history of, 175
morbid anatomy of, 175
symptoms and diagnosis of, 176
treatment of, 176
Bronchiectasis, 171
aetiology of, 171
case of, 172
clinical history of, 172
morbid anatomy of, 171
sputum of, 172
symptoms and diagnosis of, 173-
treatment of, 173
388
Bronchiolitis, 152
aetiology of, 152
case of, 153
clinical history of, 157
morbid anatomy of, 154
symptoms and diagnosis of, 163
treatment of, 167
Bronchitis, acute, 152
aetiology of, 152
clinical history of, 156
morbid anatomy of, 153
sputum in, 156
symptoms and diagnosis of, 162
treatment of, 166
Bronchitis, chronic, 153
aetiology of, 153
clinical history of, 161
morbid anatomy of, 155
sputum in, 162
symptoms and diagnosis of, 164
treatment of, 169
Bronchitis, fibrinous, 153
aetiology of, 153
cases of, 158, 160
clinical history of, 158
morbid anatomy of, 154
sputum in, 161
symptoms and diagnosis of, 164
treatment of, 168
Broncho-pneumonia, 237
Bronchorrhoea, 162, 170
Brown atrophy of the heart, 31
Brown induration, 200
Brown oedema, 200
Bruit d'airain, 376
Byssinosis, 250
Cactus in endocarditis, 100
Caffein in endocarditis, 99
Capillary bronchitis, 151
Cardiac abscess, 21, 23
Cardiac aneurism, 23, 55
Cardiac arrhythmia, 145
Cardiac asthma, 136, 177
•Cardiac degeneration, 28
aetiology of, 28
brown atrophy in, 31
INDEX.
clinical history of, 31
fatty, 29
granular, 29
symptoms and diagnosis of, 32
treatment of, 36
Cardiac dilatation, 115
aetiology of, 115
atrophic, 115
baths in, 127
cases of, 116
Cheyne-Stokes breathing in, 120
climbine method in, 12(i
clinical history of, 119
gallop rhythm in, 121
hypertrophic, 115
morbid anatomy of, 117
passive exercise in, 126
primary, 115
pulsus bigeminus in, 122
Schott method in, 123
secondary, 115
simple, 115
resistance movements jn, 126
treatment of, 122
Cardiac hypertrophy, 111
aetiology of. Ill
concentric, 110
excentric, 110
• morbid anatomy of, 112
pulse in, 114
simple, 110
symptoms and diagnosis of, 113
Cardiac murmurs, cause of, 59
diagnosis of endo-from exocar-
diac, 60
diagnosis of organic from anor-
ganic, 60
Cardiac thrombosis, 56
Cardiac neuroses, nature of, 129
Casts in fibrinous bronchitis, 154, 159
Catarrhal pneumonia. 237
Charcot-Leyden crystals, 180
Chorea and endocarditis, 54
Chronic endocarditis, 53
Chronic pneumonia, 248
Chylothorax. 383
aetiology of, 383
INDEX.
389
clinical history of, 384-
nature of fluid in, 384
prognosis in, 384
signs of, 384
treatment of, 384
Cirrhosis of the lung, 248
Climbing method in cardiac dilata-
tion, 126. 128
Coin-sound, 376
Compensatory hypertrophy, of lung,
370
of heart, 112
Compressed air baths in emphysema,
194
Consumption Of the lung, 269
Convallaria in endocarditis, 100
Cor hirsutum, case of, 4
Corrigan's pneumonia, 250
Corrigan's pulse, 68
Crepitant rale in pneumonia, 228
Croupous bronchitis, 153
Curshman's spirals, 180
Damoiseau's curve, 345
Delirium cordis, 147
case of, 148
Degeneration of heart, 28
Diaphragmatic pleurisy, 333, 358. 363
Digitalis, in acute endocarditis, 50
in cardiac degeneration, 37, 38
in chronic endocarditis, 94
in myocarditis 27
in pericarditis, 20
in pneumonia, 234, 235
Digitalin, 97
Dilatation, of heart, 115
of lungs, 186
Dropsy in endocarditis, 104
Dust phthisis, 253
Dyspeptic asthma, 177
Dyspnoea, in asthma, 182
in endocarditis, 105
in pneumonia, 221
in pneumothorax, 373
in pulmonary infarction, 207
Elastic tissue, 292
Embolic pneumonitis, 205
Emphysema, pulmonary, 186
Empyema, 356
loculated, 358
necessitatus, 362 •
pulsating, 362
tubercular, 360
Endocarditis1, acute, 39
aetiology of, 39
aortitis in, 47
case of, 43
clinical history of-, 42
infectious, 40, 42, 43, 47, 51
malignant, 40
morbid anatomy of, 40
nature of. 39
symptoms and diagnosis of, 4t
treatment of, 49
ulcerative, 41
valvular localization of, 45
Endocarditis, chronic, 53
adonis in, 100
aetiology of, 53
caffein in, 99
cactus in, 100
Cheyne—Stokes breathing in, 59
clinical history of, 56
convallaria in, 100
cyanosis in, 57
digitalis in, 94
dyspnoea in, 57
'morbid anatomy of, 54
oedema in, 58
orthopnoea in, 57
pain in, 59
palpitation in, 59
spartein in, 100
strophanthus in, 98
strychnia in, 100
symptoms and diagnosis of, 62
treatment of, 87
Endocarditis, foetal, 56
Enlargement of the heart, 109
Epidemic pneumonia, 223,
Excission of ribs in empyema, 365, 367
Exocardial murmurs, 60
390
INDEX.
Fat embolism, 206
Patty degeneration of heart, 29
Infiltration of heart, 28
Fibrinous pericarditis, 3
Fibrinous pleurisy, 328
aetiology of, 328
case of, 331, 334
clinical history of, 330
morbid anatomy of, 329
symptoms and diagnosis of, 332
treatment of, 334
Fibrinous pneumonia, 215
Fibroid phthisis (Sir A. Clark), 254
Fibrosis of the lung, 248
Fibrous myocarditis, 22
Foetal endocarditis. 56
granular degeneration of, 29, 31,
32, 34, 37; case of, 35
hypertrophy of, 110
innervation of, 129
palpitation of, 146
neuroses of, 129
Heredity in tuberculosis, 270
Hydatids of the lungs, 319
aetiology of, 319
clinical history of, 321
morbid anatomy of, 320
symptoms and diagnosis of, 322
treatment of, 323
Hydropneumothorax, 369
Hydrothorax, 379
aetiology of, 380
clinical history of, 380
morbid anatomy of, 380
symptoms and diagnosis of, 381
treatment of, 381
Hyperaemia, compensatory, 199
Hypnotics in endocarditis, 107
Hypertrophy, of heart, 100
of lungs, 193
Hypostatic pneumonia, 200
Induration, brown, of lung, 200
Infarction of the lung. 205
Infection, tubercular, by inhalation, 271
by inoculation, 272
Influenza pneumonia, 224
case of, 224
Interlobular emphysema, 186
Internal mammary artery, 18
Interstitial emphysema, 186
Interstitial endocarditis, 55
Interstitial pneumonia, 248
Intrapleural tension, 369
Intratracheal injections, 306
Irrigation of pleura, 367
Latent pneumonia, 223
Lobar pneumonia, 215
Lobular pneumonia, 237
aetiology of, 237
air embolism of, 206
cases of, 241
clinical history of, 240
Gallop rhythm, 149
Gangrene of lung, 263
Gerhardt's change of pitch, 260
Granular degeneration of heart, 29
Guaiacol in tuberculosis, 304
Hay asthma, 76, 179
Haemoptysis, 209
aetiology of, 209
cases of, 210, 211, 212
clinical history of, 210
morbid anatomy of, 210
symptoms and diagnosis of, 212
treatment of, 213
Hemothorax, 382
aetiology of, 382
clinical history of, 382
symptoms and diagnosis of, 383
treatment of, 383
Heart, abscess of, 21
arrhythmia of, 145
asystolism of, 119
arterial supply of, 131
brown atrophy of, 31
dilatation of, 115
displacement of in pleurisy, 343
enlargement of, 109
fatty degeneration of, 29, 30, 31, 33;
case of, 34
fatty infiltration of, 28, 30, 31, 32,
36; case of, 33
INDEX.
391
morbid anatomy of, 238
symptoms and diagnosis of, 242
treatment of, 245
Lungs, abscess of, 257
anthracosis of, 249
atelectasis of, 195
brown induration of, 200
brown oedema of, 200
byssinosis of, 25»
cancer of, 323
carnified, 200
cavities in, 26\ 280, 294
congestion of, 199
chaliosis of, 250
dilatation of, 186
emphysema of, 356
fat embolism of, 2 »6 '
fibrosis of, 248
gangrene of, 262
hydatids of, 319
hypertrophy of, 193
hypostatic pneumonia of, 200
hypostatic congestion of, 199
infarction of, 205
mycosis of, 318
cedema of, 202
phleboliths in. 206
siderosis of, 250
silicosis of, 250
splenization of, 197
syphilitic gumma of, 249
syphilitic sclerosis of, 248, 249. 254;
case of, 254
tuberculosis of, 269
Mediastinitis, 6
Metallic tinkling, 26C
Migratury pneumonia, 223
Mitral regurgitation, 76
case of, 79
compensation in, 76
dynamic, 78
murmur of, 78
pulse of, 77
relative, 76, 78
sequences of, 76
symptoms of, 76
urine in, 77
Mitral stenosis. 71
case of, 75
in relation to pregnancy, 72
pulse in, 73
sequences of, 71
symptoms of, 72
thrill of, 73
tuberculosis of lung in, 72
Mycosis pulmonum, 318
secondary aspergillo, 319
Myocarditis, 21
acute circumscribed, 23
acute diffuse, 24
aetiology of, 21
chronic circumscribed, 24
chronic diffuse, 24
clinical history of, 23
delirium cordis in, 25
morbid anatomy of, 22
symptoms and diagnosis of, 23
syphilitic, 23
treatment of, 27
varieties of, 21
Murmurs, anaemic, 60
anorganic, 60
cardio-respiratory, 295
disappearance of, 61
exocardial, 60
i organic, 60
' Nasal irritation in asthma, 179
GMema of the lungs, 202
sputum in, 203
(Edema, cardiac, treatment of, 104
Oxygen gas in pneumonia, 235
Palpitation, cardiac, 146
in endocarditis, 101
Paracentesis, pericardii, 18
thoracis, 355
Passive exercise in cardiopathies, 126
Peptic asthma, 178
Pericardial adhesions, 14
Pericardial effusion, 10
Rotch's sign of, 10
symptoms and diagnosis of, 10
treatment of, D
392
INDEX.
Pericardial friction, 18
Pericardium, adherent, 6
case of, 16
carcinoma and sarcoma of, 5
tuberculosis of, 5
Pericarditis, 1
aetiology of, 1
chronic, treatment of, 19
clinical history of, 7
enlargement of heart in, 6
fibrinous, 4; case of, 8
haemorrhagic, 5
morbid anatomy of, 2
pneumonia in, 226
purulent, 4
sero-fibrinous, 3
symptoms of, 8, 10, 14
symptoms of effusion in, 10
% treatment of, 16
treatment of effusion in, 17
tuberculous, 5
sicca, 3
Peripleuritis, 364
Phthisis, 2ft9
fibroid (Sir A. Clark), 254
Plastic bronchitis, 153
Pleura, abscess of, 3p8
adhesion-t of, 333
inflammation of, 327
tuberculosis of, 3 51
tumors of, 385
Pleurisy, 327
chronic, 361
diaphragmatic, 333, 358, 363 .
fibrinous, 328
friction sounds in, "33
purulent, 356
sero-fibrinous, 335
Pleuro-pericardial friction, 9
Pneumoconiosis, 248, 250
case of, 253
Pneumomycosis, 318
Pneumonia, 215
aetiology of, 215
bacteriology of, 216
clinical history of, 220
crisis in. 222
crepitant rale in, 229
complications of, 22(5
cyanosis in, 230
death in, 227
irregular forms of, 222
mixed infections in, 225
morbid anatomy of, 217
pericarditis in, 225
septic, 225
sputum in, 221
symptoms and diagnosis of, 22*
treatment of, 231
types of, 223, 224
unfavorable symptoms in, 230
Pneumonia, bilious, 223
broncho, 237 r
catarrhal, 237
cirrhotic. 248 ,
Corrigan's. 250
chronic, 248
croupous, 215
epidemic. 223
embolic, 205
fibrinous, 215
hypostatic, 200
influenza, 224
interstitial, 248
latent, 223
lobar, 215
lobular, 237
primary parenchymatous. 249
migratory, 223
septic, 224
serosa, 202
subacute indurative, 249
tubercular, 240, 283, 284. 290. 291
Pneumothorax, 369
aetiology of, 369
cause of dyspnoea in, 373
case of, 374
clinical history of, 373
coin-sound in, 376
nature of gas in, 372
side affected in, 372
symptoms and diagnosis of .375
INDEX. 393
treatment of, 378
Praecordial pain, 132
in endocarditis, 102
Pregnancy, effect of in valvular lesions
92
Pressure effects in pleurisy, 343
Prognosis of valvular lesions, 86
Protozoic infection, 318
Pseudo-angina pectoris, 137
Pseudo-tuberculosis, 318
Pulmonary abscess, 257
aetiology of, 257
case of, 259
clinical history of, 258
morbid anatomy of, 257
multiple pyaemic, 258
sputum in, 258 ,
symptoms and diagnosis of, 259
treatment of, 262
Pulmonary apoplexy, 205
Pulmonary collapse, 195
aetiology of, 195 _
clinical history of, 196
morbid anatomy of, 196
ymptoms and diagnosis of, 196
treatment of, 198
Pulmonary congestion, 199
aedology of, 199 •
clinical history of, 201
forms of, 199
morbid anatomy, of, 200
sputum in, 201
symptoms and diagnosis of, 201
treatment of, 201
Pulmonary embolism, 205
Pulmonary emphysema, 186
etiology of. 186
acute vesicular, 190
case of, 191
clinical history of, 190
forms of, 18fi
general, 189
interlobular, 187
local, 189
morbid anatomy of, 187
senile, 189
symptoms and diagnosis of, 191
treatment, 194
vesicular, production of, 187
Pulmonary fibrosis, 248
aetiology of, 248
cases of, 249, 252
clinical history of, 251
haemoptysis in, 251
localized, 254
morbid anatomy of 250
nature of, 248
symptoms and diagnosis of, 252
syphilitic, 249, 254
treatment of, 255
Pulmonary gangrene, 263
aetiology of, 264
clinical history of, 266
diffuse, 266
morbid anatomy of, 265
sputum in, 266
symptoms and diagnosis of, 267
treatment of, 268
Pulmonary infarction, 205
aetiology of, 205
case of, 208
clinical history of, 207
morbid anatomy of, 206
nature of, 205
sputum in, 207
symptoms and diagnosis of, 207
treatment of, 208
Pulmonary mycosis, 318
Pulmonary cedema, 202
aetiology of, 202
aeute case of, 203
clinical history of, 202
crepitating rales of, 203
morbid anatomy of, 202
nature of, 202
sputum of, 203
symptoms and diagnosis of, 203
treatment of, 204
Pulmonary thrombosis, 205
Pulmonary tuberculosis, 269
aetiology of, 270
antiseptic medication in, 304
bacilli in, 291
cavities in, 280, 294
394
INDEX.
climatic treatment in, 308
clinical history of, 28! i
complications of, 296
decrease of, 269
effect of heart disease in, 27
extent of, 269
fever in, 287, 311
fresh air treatment in, 307
general treatment of, 300
haemoptysis in, 286, 297, 313
hereditary transmission of, 270
high altitudes for. 309
inhalations in, 305
infection in, 271
morbid anatomy of. 276
nervous symptoms in, 28*
night sweats in, 287, 312
points of invasion in, 279
prophylaxis in, 298
pulse in, 287
sanatorium treatment in, 307
special treatment of, 311
sputum in, 291
symptoms and diagnosis of, 288
treatment of, 298
Pulmonic regurgitation, *1
"audible capillary pulse" in, 81
causes of, 81
murmur in, 81
relative, 81
signs of, 81
Pulmonic stenosis, 7,9
case of, 80
effects of, 79
murmur of, 80
symptoms of, 80
Pulsus alternans, 145
Pulsus higeminus, 146
Pulsus differens, 74
Pulsus paradoxus, 14
Pulsus rarus, 144
Pulsus trigeminus, 146
Puncture, exploratory, in pleurisy, 349
Purulent Pleurisy. 356
etiology of, 356
cases of, 360
cerebral abscess in, 368
character of pus in, 358
clinical history of, 359
fetid, 363
irrigation in, 367
morbid anatomy of, 357
pulsating, 362
resection for, 367
symptoms and diagnosis of, 362
subphrenic abscess in, 363
treatment of, 364 >■
tubercular, 360
Putrid bronchitis, 156, 162
Pyopericardium, incision for, H)
Pyopneumothorax, 369
Pyopneumothorax subphrenicus, 377
Rales, crepitant, 229
of cedema, 203
redux, 230
Resistance movements in cardiac dis
ease, 126
Resonance, cracked-pot, 260
Skodiac, 342
Rotch's sign, 10
Schott method in cardiac, dilatation, 123
Septic pneumonia, 225
case of, 225
Sero Fibrinous Pleurisy. 335.
aetiology of, 335
BacellTs sign in, 347
bacteriology of, 335
c'inical history of, 339
course of, 341
dangers of puncture in
diagnosis of localized, 34*
latent type of, 340
letter S curve in, 345
morbid anatomy of, 337
Skodiac resonance in. 345
symptoms and diagnosis of. 342
treatment of, 349
when to puncture in, 352
Siderosis, 250
Silicosis, 250
Skodiac resonance, 345
INDEX.
39")
Skoda, veiled puff of. 173
Spartein in endocarditis. 100
Spasmodic asthma, 177
Splenization of lung, 197, 199
Sputum, in asthma, 180
in acute bronchitis, 156
boiled tapioca, 180
in bronchiectasis, 172
in bronchorrhoea, 162
from cavities, 201
in chronic bronchitis. 162
elastic tissue in. 292
fetid. 162
num'ular, 291
in plastic bronchitis, 161
in pneumonia, 221
prune juice, 221
in pulmonary abscess, 258
in pulmonary congestion, 201
in pulmonary gangrene, 266.
in pulmonary infarction, 207
in pulmonary cedema. 203
in tuberculosis, 291
Streptothrix pseudo-tuberculosa, 318
Strophanthus in endocarditis, 98
Strychnia, in endocarditis, 100
in pneumonia, 234
Suffocative catarrh. 151
Subphrenic abscess, 363, 364
Syncope anginosa, 136
Syncope and cyanosis in endocarditis,
103
Syphilitic fibrosis of lung, 249, 254
syphilitic myocarditis, 23
Tachycardia, 141
in Grave's disease, 142
paroxysmal. 143
toxic, 142
treatment of, 143
Thrombosis of heart. 56
Tobacco, effect of on heart. 142
Tremor cordis, 147
Tricuspid regurgitation. 84
associations of, 84
effects of, 85
epigastric pulsation in, 85
jugular pulsation in, 85
murmur of, 86
signs of, 85
Tricuspid stenosis, 82
associations of, 82
case of, 84
diagnosis of, 83
murmur of, 83
symptoms of, 83
Tubercular empyema, 360
Tubercle baccillus in pulmonary tuber-
culosis, 270, 290. 291
in sero-fibrinous pleurisy, 335, 336
Tuberculin, 311
Tuberculosis of the lung, 269
of the pericardium, 5
of the pleura: case of, 331
Tumors of the lungs. 323
aetiology of, 324
clinical history of, 325
morbid anatomy of, 324
symptoms and diagnosis of, 325
treatment of, 326
Tumors of the Pleura. 3*5
etiology of, 385
clinical history of, 3*ii
, morbid i natomy of, 385
nature of, 385
symptoms and diagnosis of. oW
treatment of, 386
Tnrtl^ lung, 171
Toxic asthma, 177. 178
Uraemic asthma, 178
\ Veiled puff, 173
Venesection in pneumonia, 234
Wintrich's change of pitch. 261)
\
NLM051107336