WITH AUTHOR’S COMPLIMENTS. 
A CONSPECTUS 
OF THE 
Different Forms of Phthisis, 
Intended as an aid to Differential Diagnosis. 
BY ROSWELL PARK, A. M„ M. D.. 
DEMONSTRATOR OF ANATOMY, WOMAN’S MEDICAL COLLEGE; SURGEON TO THE 
SOUTH SIDE DISPENSARY. 
Reprinted from the Chicago Medical Journal and Examiner, for September, 1878. 
CHICAGO: 
Bulletin Printing Company, 113 Madison Street: 
1878. A CONSPECTUS OF THE DIFFERENT FORMS 
CONSUMPTION, INTENDED AS AN AID TO 
DIFFERENTIAL DIAGNOSIS. 
By Boswell Park, A. M., M. D., 
Demonstrator of Anatomy, Woman's Medical College; Surgeon to the South Side Dispensary. 
(Based upon the labors of Niemeyer, Wagner, Kindfleisch, Ruehle and Virchow.) 
The writer assumes that no apology is needed for any article 
calculated to throw any light upon the early recognition or differ- 
ential diagnosis of the different forms of that dread malady— 
consumption. In the following contribution his sole endeavor 
has been to be practical. It would be impossible to present a 
complete picture of the disease within the limits allowed; much 
that is omitted must, therefore, be excused on that ground. The 
determination as to wThether a case of phthisis before us is in a 
tuberculous condition; even further than this—to diagnose ex- 
actly the condition it may be in, is, as every one ■will recognize, 
of vast importance, especially as bearing on our prognosis and 
treatment.* That many advances have of late been made in this 
direction, we have reason to congratulate ourselves. Altogether 
too much carelessness exists in confounding the words “ consump- 
tion ” and “tuberculosis,” “consolidation” and “ deposit of tu- 
bercle,” their indiscriminate use betraying some uncertainty in 
the minds of those who thus employ them. 
So-called consumption, when advanced, can usually be diag- 
* For an excellent summary of the benefits of change of climate in the different forms of 
phthisis, with advice as to choice of localities, see the address of Prof. Loomis before Section I. 
of the American Medical Association during its recent meeting at Buffalo; reported in the July 
number of this journal. 2 
nosed by the merest tyro, but to recognize it in its formative 
stage, to differentiate it from other pulmonary complaints, to dis- 
cern the tubercular element, are often matters requiring most 
careful scrutiny. 
That patients live and die with phthisis without the formation 
of a particle of tubercle is an established fact; that others de- 
velop tubercle in the course of the complaint, and that in yet 
others the tuberculous process is the initiative step, are equally 
true. 
Any assistance, therefore, to the separation and identification 
of each class of cases, is of practical importance. As a contri- 
bution in this direction, the writer submits the subjoined tabular 
views, hoping that they may prove as useful to others as they 
have been to himself. 
But there are many points in the general appearance of a 
patient with incipient phthisis which may be regarded as aiding 
in the diagnosis or showing a condition of system favorable to its 
development. At the risk of being prolix, the writer desires to 
mention the following : slender bones, thin skin, delicate hue of 
cheeks, large eyes, bluish sclerotic, long eyelids, pale face which 
blushes readily, little subcutaneous fat, thin, slender hands with 
incurvated nails (the clubbed fingers are not distinctive of phthisis 
as many suppose; they are noticed in several chronic complaints), 
sharply defined red line at the edge of the gums opposite the 
canines and incisors ; poorly-shaped muscles—especially those of 
the neck which allow the thorax to sink and thus cause the neck to 
appear long, small antero-posterior diameter of thorax, wide in- 
terspaces, acute angle of junction of ribs to sternum—causing 
the chest to seem long, flat and narrow, shoulders tipped forward 
and inner angles of scapulae tipped up like wings; abdominal 
character of respiration, spots of pityriasis (tinea) versicolor or 
lentigo hepatica on back and chest; rise of temperature ( 38.5 C.) 
with flushed cheeks and hot hands at evening, gradual emacia- 
tion, wandering pains in chest and shoulders, etc. 
Among the physical signs may be mentioned—special excita- 
bility of the heart in anaemic persons, continuous acceleration of 
the pulse without evidence (except by the thermometer) of increased 
temperature, systolic murmur in the subclavian, becoming louder or heard only during expiration (a sign of adhesion of pleural 
surfaces at apices). The pulse is not only rapid, but soft and 
empty, and even when there is fever it has not the usual sthenic 
characteristics. Enlargement of glands may cause venous com- 
pression with dilatation of veins of neck and face, or even cya- 
nosis. Depression of supra and infra-clavicular spaces does not 
always of itself indicate any variety of phthisis; it is due to in- 
duration or shrinking of the apex of the lung (from pneumonic- 
cirrhotic—processes) and may predispose. But when it appears 
by itself without other signs to indicate phthisis, it more often 
indicates a partial cure of the nutritive changes which of them- 
selves predispose to that disease. A feebleness of respiration in 
the same locality and with similar accompaniments is of similar 
import. So also is a wide extension of cardiac shock and dislo- 
cation outward of apex beat. These latter signs, therefore, are 
by no means pathognomonic of phthisis unless accompanied by 
other signs, as above. 
Caution is required if one would not be misled by too great 
reliance on physical signs. Puerile respiration and increased 
vocal resonance in right infra-clavicular and supra-spinous regions, 
often alluded to as signs of incipient phthisis, are met with in 
healthy lungs, and should not be regarded as suspicious sounds 
unless accompanied as above. So, too, with regard to fever; a 
fever which has no obvious cause, and which persists, points to 
phthisis; if there be absence of fever and suspicious physical 
signs, even though there be emaciation and cough (often caused 
by tracheal catarrh or chronic tonsilitis), the fear of phthisis may 
be dismissed. 
Anaemia, combined with dyspepsia and hysteria, may simulate 
phthisis; here the thermometer should decide. Chronic bron- 
chial catarrh may cause needless alarm ; but this need not be un- 
less it shall have attacked the apices ; its usual manifestations are 
confined to the lower lobes, and as improvement occurs it takes 
place from above downward. 
Phthisis may be strongly suspected when a patient with a cough 
has or has had an uncontrollable diarrhoea, or non-specific aphonia 
or when fever is present without other cause. 
Without going at all deeply into the consideration of the seti- 4 
ology of consumption, certain factors in which are mentioned in 
the tabular statements, a few either of the more prominent points, 
or of those too often overlooked, will bear mention in this connec- 
tion ; consideration of these points not infrequently influencing 
our diagnosis. 
A sudden chilling of the stomach or of the skin may be suffi- 
cient to set up catarrhal or pneumonic processes whose termina- 
tion we cannot forsee. Children fed on pap instead of being 
nourished at the breast, are more apt to react poorly against such 
disease. Diseases such as syphilis, typhoid, diabetes, chlorosis, 
etc, predispose, inasmuch as they cause malassimilation. Puny, 
badly nourished subjects, are more susceptible, because among 
such, inflammatory nutritive disorders show greater tendency to 
cell formation and subsequent caseous degeneration. Great al- 
terations of temperature and a high degree of moisture each 
predispose, as do previous and frequent catarrhs. 
Lack of expansibility of chest apices owing to change in the 
cartilages of the first ribs, congenital or occurring in early youth 
(e. g. ossification or shortening), faulty carriage of body, dimin- 
ished respiratory capacity, due to feebleness of respiratory mus- 
cles, are all prominent factors. Bronchial catarrh and usually 
associated disease of the bronchial glands attending measles, es- 
pecially when epidemic, and the frequent general glandular 
troubles also attending it, make it a frequent cause. The con- 
nection between phthisis and pertussis is, for the same rea- 
son, equally manifest. That between phthisis and the later stage 
of diabetes mellitus is more obscure. 
Haemorrhage, as such, does not predispose except as its result- 
ing clots fail to be resolved and absorbed ; clots or fragments of 
clots remaining may be regarded with considerable concern. 
There is no evidence that the milk of consumptives can excite 
the disease. 
On the other hand, malaria and valvular heart disease are said 
to confer some immunity. While the phthisical lung is the more 
vascular, emphysematous lungs are more dry and bloodless and 
rarely inflame; but when once inflamed they degenerate rapidly. 
With regard to the cough, almost always a distressing feature, 
it may be regarded as the expression of (a.) the extent of impli- cation of the bronchial mucous membrane; (b.) the extent of 
implication of the lymphatic (bronchial) glands; (c.) nervous 
reflex excitability ; (d.) the proximity of the lesion to the larynx. 
Table I. gives, side by side, the features of the three different 
forms of inflammatory phthisis uncomplicated by tubercle; the 
site of the primary lesions being respectively in the interstitial 
connective tissue, the acini or alveoli and the bronchioles. The 
second class of cases can usually be more easily differentiated from 
the first than from the third ; while in many cases there are such 
a variety of pathological processes taking place consentaneously 
that it may be impossible to assign the patient a place in any one 
class. 
But that cases are frequently met with where this classification 
can be made, I trust no one will deny. It is taken for granted 
that the tubercular element has been excluded (though perhaps 
this is not essential); this is done chiefly by aid of the thermom- 
eter (vide Table II.) This table is founded principally upon the 
monograph of Ruehle. (Ziemssen’s Cyclop). Apicial Catarrh. 
Beginning in the bronchi, producing 
inflammatory infiltration and swelling of 
the entire thickness of their walls, with 
caseation and dilatation. Degeneration 
then takes place, pneumonic processes are 
set up by extension into the parenchyma, 
and the inflammatory products either 
necrose or undergo induration resulting in 
limitation and cure. 
First shades of dulness develop very 
gradually in apices, and sometimes a little 
further down. 
Signs of bronchitis predominate over 
those of infiltration. 
Uncomplicated Inilammatory Phthisis. 
Lobular Disease Characterized by 
Foci:—Broncho Pneumonia. 
• Changes consist of formation of clusters 
of nodular foci which excite inflammation 
in surrounding parts and coalesce with the 
inflammatory products thus formed. The 
whole mass then becomes caseous, and 
breaking down forms ulcers, and so the 
destructive processes advance; or they may 
be arrested by the recurrence of simple 
inflammation with resulting induration. 
Slight dulness, with sunken supra- 
clavicular fossae; apices of lungs lowered. 
(Best ascertained by percussion in front, 
with patient’s mouth open.) 
Narrowed chest, with imperfect and 
unequal expansion. 
Signs of infiltration predominate over 
those of bronchitis. 
Table I. 
Simple Chronic Apicial Pneumonia. 
Changes consist of simple, chronic, 
indurative inflammation. 
The most important physical sign is 
dullness in the supra, and infra-clavicular 
and supra, and infra-spinous fossae. The 
more intense and extended this dullness, 
the greater the probability that this is the 
form of the disease. 
Later the altered shape of affected side 
and impeded respiration show that shrink- 
ing has supervened. This sinking above 
and below the clavicle and the flattening of 
the whole upper part of the thorax indicate 
chronic pneumonia. Non-sibilant crackling rales are heard 
from the outset, at least on deep inspiration 
and coughing. Later the rales may become 
sibilant. 
Same. 
Same. 
Cough, with moderate expectoration, one 
of the first'symptoms. 
Expectoration accompanies the cough; 
sputa frequently contain streaks of blood. 
Sputa contain also yellowish-white, non- 
aerated streaks, and much amorphous 
matter, together with small detached 
particles which sink in water. 
Haemoptysis not as likely to occur. 
More or less pain. 
Expiratory sound is usually bronchial; 
and in many cases the inspiratory sound 
has an uninterrupted, vesicular character 
for an appreciable time before the sound 
becomes bronchial. 
Crackling rales are scanty at the outset; 
but when softening takes place, they are 
abundant, and mixed with a sibilant, 
bubbling sound. 
Course more rapid. 
As the disease advances (vid. supra) 
auscultatory and other signs of cavities are 
discerned; e. y., tympanitic and “ cracked- 
pot” resonance. 
Dry cough from the outset, with scanty 
expectoration. 
When expectoration is a feature, the 
sputa are gelatinous, of reddish tint, and 
contain elastic fibers early in the disease. 
Later the sputa are more solid and 
globular, and contain more or less blood. 
Haemoptysis may cause the first alarm. 
More or less pain. 
Respiratory murmur changes gradually 
from a puerile respiration to a loud, harsh, 
bronchial sound, heard both during inspir- 
ation and expiration. 
Crepitant rales may be heard at times; 
if present, they are rather sibilant in 
character. If any catarrh be present, these 
may be abundant. 
The local signs extend very slowly, or as 
gradually become confined and fixed. 
If bronchiectases are produced by the 
cirrhosis and retraction of the connective 
tissue, signs of cavities of corresponding 
size will be found. 
Cough is usually of moderate severity, 
or may be absent. 
Expectoration scanty; but in case there 
be inter-current bronchial catarrh, it is 
more abundant, catarrhal in character and 
muco-purulent. 
Sputa contain no blood. 
Haemoptysis rarely or never. 
Pains—supposed often to be rheumatic— 
frequently occur on affected side. Laryngeal and intestinal complications 
make their appearance late. 
Fever inconsiderable until the disease is 
advanced. 
Emaciation and loss of strength, with 
constitutional symptoms, are among the 
first suspicious signs noticed. 
Heredity plays a conspicuous part, espec- 
ially in “scrofulous” patients, or those 
who have frequent attacks of catarrh. 
Same. 
Derangement of appetite and digestion 
frequent. Functions of larynx and in- 
testines rarely undisturbed. 
Fever — at evening — is present, with 
night sweats. 
Emaciation one of the earliest and most 
prominent symptoms; advances pari passu 
with the fever and complication. 
Heredity plays an important part, as do 
rapid growth, poor development, and such 
diseases as typhoid, morbilli, pertussis, etc. 
Local irritating causes arc a much less 
important factor. 
Usually no complications. 
Fever—at evening—absent or inconsider- 
able. 
Emaciation — at first only slight—in- 
creases very slowly or disappears. 
Heredity plays an unimportant part. 
Local irritating causes are a much more 
important factor. Thus much for the cases of purely inflammatory phthisis. The 
frequent complication of such cases by the neoplastic element, 
tubercle, makes possible yet another grouping between, on the 
one hand, those cases included in Table I, and, on the other, 
certain cases where the appearance of miliary tubercle is, so far 
as can be determined, the first pulmonary lesion. Between these 
two strongly contrasted forms occurs one where tubercle is found 
in products of previous inflammatory change. 
Our knowledge of tubercle is yet far from exact, and the divid- 
ing line between it and scrofulous and other affections not clearly 
drawn. But the writer may be allowed to define the position 
taken in preparing this paper. With regard to scrofula, Ruehle’s 
views seem so just and well-founded, that they are given almost 
verbatim. 
By scrofula is meant—not any particular feebleness or sickli- 
ness of body, but rather a tendency to certain forms of disease, 
e. g., inflammations of mucous membranes and skin, whose pro- 
ducts are abnormal in character, and which being carried to the 
lymphatics excite in them inflammation or hyperplasia. These 
inflammations are characterized by abundant cell proliferation. 
According to Rindfleisch, one fundamental characteristic of scrof- 
ulous affections is the accompanying disproportion between the 
volume of the blood and the weight of the body. 
Scrofulous, as well as other inflammations lead often to the 
formation of cheesy masses. Tnese are described by Wagner as 
being results of inflammation where the purulent or fibrino-puru- 
lent exudation, or the desquammated epithelium have, in conse- 
quence of anaemia, lost so much liquid that there results a dry, 
grayish or yellowish mass, firmly imbedded in the tissues. Even 
tubercle itself, as well as old cancerous nodules, haemorrhagic in- 
farctions, incapsulated collections of pus, etc., may undergo this 
change as well as fatty metamorphosis. There is no yellow tu- 
bercle as formerly spoken of; when such is found, it is the pro- 
duct of the cheesy atrophy just mentioned. 
Now these cheesy infiltrations and suppurations of mucous 
membranes, by some unknown means, elaborate a poison which, 
when re-absorbed, produces tubercle. The source of tubercular 
infection is, therefore, thus furnished by the patient himself. 
(Rindfleisch.) 10 
Probably the best idea or definition of tubercle may be gath- 
ered from the description of Wagner, who considers it an infil- 
trated, multiple, usually miliary, non-vascular neo-plasm, consist- 
ing especially of nuclei of varying sizes, indifferent and giant 
cells—all imbedded in a reticular tissue, and which constantly 
tends to pass into cheesy atrophy or softening. The basis for its 
development—the cheesy focus—is most frequent in connective 
tissue, previously irritated (“ scrofulous ”) glands, bones, testicles, 
etc. This cheesy focus may be incompletely encapsuled, the cap- 
sule being only a relative and Considerable but not absolute obsta- 
cle to resorption. Tubercle probably originates from (fixed) 
connective tissue corpuscles, and the endothelium connected there- 
with ; it grows by division of the nuclei and extends along con- 
nective tissue, lymphatics and blood-vessels. 
Tuberculosis has its analogies to miliary carcinosis ; is proba- 
bly transmissible, like glanders, syphilis, etc., and is not usually 
found with other infectious diseases. 
With regard to the prognosis of cases of consumption thus 
eomplicated, resorption of tubercle, accompanied usually by fatty 
atrophy, takes place very rarely indeed ; calcification, softening 
and liquefaction (ulceration), much more frequently. But there 
is never a chance that the lung can return to its normal condition. 
The best that can be hoped for is that the lesions already existing 
may be rendered innocuous ; this happens by shrinkage of the 
infiltration and formation of blood-vessels which do not penetrate 
deeply, but supply constant though scanty nourishment. (Rind- 
fleisch, Wagner.) Of course this applies only to cases referred 
to in the second column of Table II. 
These remarks will suffice to explain more fully the following 
table. If there be any one point in it upon which sufficient stress 
has not been laid, it is that in reference to the constant use of 
the thermometer as an aid to diagnosis. The writer deems it 
possible by its aid, and by the other signs given in the same table, 
to group four-fifths, at least, of cases of consumption in their 
proper place; and of those coming under the heading of the first 
column probably one half can, by the use of Table I, be again 
classified. Acute Miliary Tuberculosis. 
Supervention or Formation of Miliary 
Tubercle during Apparent Good Health. 
Much resembles an acute infectious 
disease. 
AEtiology, etc. 
But one cause is known; the absorption 
of caseous matter. Most cases present some 
antecedent lesion of some organ; but often 
not recognized. 
Persons predisposed to inflammatory 
action suffer from acute and primary tuber- 
culosis with greater relative frequency. 
Where measles, etc., or “ scrofulous ” af- 
fections have caused enlarged lymphatics, 
bronchial glands, etc., or where there are 
caries of bone, caseous testicle, pros- 
tate or bladder, remains of inspissated ab- 
cesses, remains of serous inflammations or 
ulcerations, or the like, there may be said 
to be cause for development of miliary 
tubercle. When it assumes the form of an 
Non- Tubercular Compared with Tubercular Phthisis. 
Tubercular. 
Adventitious Deposit of Tubercle (Miliary) 
following Caseous Metamorphosis of Pro- 
ducts of Inflammation. Always second- 
ary to the inflammatory variety. 
AETIOLOGY, etc. 
A sort of middle ground between the 
forms on either side. 
Occurs in connection with pre-existing 
lesions of the apices. 
The greatest danger for consumptives is 
that they may become tuberculous. Incap- 
sulation of caseous masses affords some 
protection against this. 
Next after the caseous products of pneu- 
monia in liability to tubercular infection 
come the exudates of pleurisy and pericar- 
ditis; caseous, lymphatic and bronchial 
glands, etc. 
Table II. 
Inflammatory. 
Purely and Directly the Residt of Inflam- 
matory processes. May be either one or 
a complication of all the forms mentioned 
in Table I. 
AETIOLOGY, etc. 
Exciting causes: anything which pro- 
duces congestion and bronchial catarrh. 
(Vid. supra.) 
Pneumonia, catarrhal or croupous, when 
it has attacked the apex. 
Croup, cerebral irritation, or moist erup- 
tions,[may be followed, after puberty, by 
bronchial haemorrhage and inflammatory 
lung disorder. acute disease, these foci may be considered 
as having for some time remained non- 
infective. 
Same. 
Pathology. 
Is the result of a neoplasm; is rapidly 
acute, and is a resorption disease. 
The focus of attraction for the acute pro- 
duction of tubercle in the lungs is usually 
a pre-existing chronic tuberculosis of those 
organs; when miliary tubercle forms the 
only lesion we have to do with the acute in- 
fectious disease. 
There is no chronic miliary tuberculosis 
in the old sense of the word. 
Same. 
Pertussis, morbilli, scarlatina, etc., may 
lead to this form by producing a “scrofu- 
lous ” condition and glandular tuberculosis, 
thus supplying foci for subsequent general 
infection. 
Pathology. 
Is the result of a neoplasm; is more or 
less chronic, and is a resorption disease. 
Follows caseous infiltration or degenera- 
ation as a sequel to chronic catarrhal or 
croupous inflammation, tubercles being de- 
posited in the metamorphosed pneumonic 
product. 
Is regarded by some as a combination of 
inflammation and tuberculosis. 
Plays a subordinate role, inasmuch as 
tubercle is an accidental, secondary pro- 
duct. 
The number, size and distribution of 
of miliary tubercles do not necessarily 
Pertussis, morbilli, scarlatina, etc., may 
lead to this form directly. 
Pathology. 
Is the result of inflammatory processes, 
and is a chronic disease with intercurrent 
simple forms of inflammation, which may 
heal by cicatrization. 
Consists in suppuration or caseous degen- 
eration of lobular or lobar infiltration; the 
extension (with exceptions) of a chronic 
catarrh and copious secretion of young 
cells into the bronchioles and finally into 
the air vessicles. In the invasion of miliary tuberculosis 
three stages are often distinguishable: (a.) 
Local scrofulo-tubercular primary infec- 
tion ; (b.) tuberculosis of lymphatic glands; 
(c.) general infection. 
Time is not afforded for these changes. 
Cavities are not formed. 
May be complicated by intestinal as well 
as cerebral or meningeal tubercle. 
aft'ord an expression of the constitutional 
disturbance. 
When upon phthsis tubercle supervenes, 
it usually first develops in the mucous 
membrane of the bronchi, trachea or larynx. 
The most frequent site is the point where 
the bronchiole connects with the acinus. 
Thence it spreads in all directions. 
Same. 
Cavities rarely enlarge by caseous de- 
generation of the tubercular infiltration, 
but by a diphtheritic infiltration with sub- 
sequent decay. 
Often combined with laryngeal disease, 
ulcer of the bowel, intestinal or cerebral 
When the branches of the pulmonary 
artery become obliterated, the bronchial 
arteries enlarge and conduct the supply of 
blood to the lungs. The intercostal arter- 
ies also enlarge and advance through the 
pleuritic exudate; so that the affected lung 
really receives more blood than the sound 
one. Part of this blood is discharged into 
the intercostal veins; this impedes the dis- 
charge of the cutaneous veins into the in- 
tercostal so that the former enlarge; and 
hence the blue network of veins often no- 
ticed on the chest wall. 
Cavities are enlarged by the same pro- 
cesses which assisted in their formation. 
Often accompanied by laryngeal and in- 
testinal diseases, as well as by fatty oramy- Cases cannot be considered protracted; 
nevertheless the same change may occur. 
May occur in early infancy. 
Morbid Anatomy. 
Lungs are congested, oedematous, emphy- 
sematous at edges, and present in the vast 
majority of cases an uniformly studded as- 
pect of miliary tubercles, gray, translucent 
and fresh. Pleurae the same. The perito- 
neum, liver, kidneys and spleen are usually 
covered with the same. Also, in young 
subjects, the parts about the base of the 
brain. The smallest miliary tubercles, 
being invisible to the unaided eye, are often 
overlooked in the glands and viscera. 
The corpse usually resembles that of one 
dead from acute febrile disease, decompo- 
sing rapidly. The blood is dark and liquid 
and settles to dependent parts, causing pul- 
tubercle, and fatty or amyloid liver and 
kidneys. 
Same. 
Same. 
Morbid Anatomy. 
The tubercle of chronic tuberculosis is 
never uniformly disseminated; the gray 
tubercle proper being found along with the 
yellow caseous masses (the so-called “yel- 
low tubercle ”) showing the deposit to have 
gradually taken place. The abdominal 
viscera are less often covered with tubercles. 
Same. 
loid changes in the liver ;"witlx the access 
of the former (fatty change) occurs imper- 
fect assimilation of food and emaciation; 
•with the access of the latter the pulmonary 
symptoms often seem to recede. 
In protracted cases the volume of the 
blood is diminshed and the heart flabby. 
In recent cases the flow of the right heart 
is impeded, and it is therefore dilated and 
hypertrophied. 
Never appears before first dentition. 
Morbid Anatomy. 
The anatomical appearances are so varied 
and inconstant, and so familiar, that space 
cannot be afforded to describe them. Suf- 
fice it to say, that amongJ all the’ appear 
ances of infiltration, dilatation, caseation, 
ulceration and necrosis, no tubercles are 
found. 
After death the skin is remarkably white 
and covered with scales of pityriasis (tinea) 
tabescentium. Feet and limbs are often monary hypostases and suggillations The 
muscles are friable. The spleen soft and 
enlarged. 
Intestinal ulcers very rarely form. 
Same. 
Same. 
As there has been more or less bronchial 
or tracheal catarrh during life, evidences 
thereof are found after death. 
Symptomatology and Semeiology. 
At outset repeated rigors, without com- 
plete intermission, with rapid pulse in- 
creasing respiratory rate, and severe con- 
stitutional disturbance. 
Very much resembles typhus. 
Anorexia a notable symptom ; mouth 
often dry, at times very moist. 
Rapidly increasing prostration with ag- 
gravated cough and dyspnoea. 
Extremities cool. Slight cyanosis. 
Soon colliquative sweats, pulse more 
Many so-called tuberculous ulcers of the 
intestines are of a lardaceous or catarrhal 
character. 
The center of the tubercle usually degen- 
erates first. 
Caseous bronchial glands frequent. 
Symptomatology and Semeiology. 
Is necessarily preceded by some such 
condition as that just described. 
Pallor, fever, emaciation and night- 
sweats usually appear early with cough 
and expectoration. 
cedematous, and crural veins plugged with 
thrombi. 
A catarrhal ulcer of the intestine should 
not be mistaken for tubercular. 
Caseous bronchial glands infrequent. 
Symptomatology and Semeiology. 
Has a period of percussory catarrh, with 
protracted cough and expectoration, of 
variable duration; this need not necessarily 
commence in the alveoli and bronchioles, 
or connective tissue, but may proceed 
downward from the trachea. 
Fever and wasting deferred. rapid, emaciation from day to day, senso- 
rium deranged and semi-coma. 
Spleen is usually enlarged. 
Are not enough. 
Condition of sputa crude and dependent 
upon the amount and extent of bronchial 
catarrh; they possess no characteristic ap- 
pearances. 
Cough may be distressing, but hoarse- 
ness is rare. 
The cough of this variety may be thus 
accounted for. 
Spleen may be slightly enlarged. 
Same. 
A hoarse or inaudible cough or a dis- 
tressing laryngitis may occur with the ad- 
vent of tubercular complication, and are 
pathognomonic and unfavorable signs. 
The same holds good here; and when 
the sputa of a persistent cough, accom- 
panied by fever, for a long time retain the 
crude character of the mucous sputa of 
acute bronchitis, suspect of 
tubercle, since the existence of tubercle in 
bronchial mucous membrane is generally 
attended with distressing cough and scanty 
sputa. 
Physical signs are enough to explain 
other symptoms. 
Well defined, dark yellow streaks in spu- 
ta, showing that the catarrh has reached the 
finer bronchi; a bad sign. 
Infiltration and caseous degeneration 
may occur without cough or expectoration. 
Should intestinal inflammation complicate 
such cases it may exercise a derivative in- 
fluence on the bronchi. 
Voice and cough rarely hoarse. 
The discovery of elastic fibres in the 
sputa is a positive sign. Temperature is of the remittent type; 
but not infrequently the maximum occurs 
during the morning. It rarely rises very 
high at any time, and towards the end the 
mean temperature may decline. 
Pulse becomes smaller, and yet more 
rapid, while the respiration rate increases; 
oedema of lungs from insufficient filling of 
right heart, and finally palsy of bronchi 
and suffocative effusion; the violence of 
the fever, malignancy of the disease, 
dyspnoea and rapid collapse, affording 
data for differential diagnosis. 
Temperature very seldom reaches 40° C., 
and is out of all proportion to the rapidity 
of the pulse. 
Little or no meteorism or ileo-caeca 
The hectic is of a continued type: 
temperature always above normal, but not 
much higher in the evening than in the 
morning; i. e., the remissions not well 
marked; moreover it resists treatment. 
Same with regard to period of maximum 
temperature; only the temperature range 
does not show such sharp curves. 
Diarrhoea, especially in those of costive 
The appearance of blood in muco-puru 
lent sputa, whereby they acquire a yellow- 
ish-red color, indicates a chronic pneu- 
monia, and shows that catarrh has extended 
to the air vesicles. 
Hounded, nummulated sputa, which sink 
slowly to the bottom, and do not coalesce, 
are sure indications of a cavity, but not 
necessarily of tuberculosis. 
The hectic is more of a remittent or 
intermittent than of a continued type; with 
a range of, say, 1.1° C. between evening 
and morning temperature; the evening 
elevation being a constant feature. 
The fever may present all possible varia- 
tions in the same individual. A sudden 
accession may be regarded as an indication 
of some fresh inflammatory process; e. g., 
pleuritis, pneumonia. 
(In children the invasion of the air 
vesicles by an acute catarrh is accompanied 
by increased temperature and accelerated 
pulse.) 
With marked evening rise of tempera- 
ture, the rate of respiration does not cor- 
respondingly accelerate; hardly ever more 
than six or eight breaths per minute. 
Patients may run through the whole tenderness. Stools are indefinite in color 
and consistence. 
Profuse sweating at no particular time; 
sudamina frequently. 
Little or no pain in shoulders or chest. 
Patient usually succumbs in from two to 
six weeks. 
The disease may be complicated with 
tubercular meningeal trouble, and then be 
even more rapidly fatal. 
Physical Signs. 
Any previous dullness or history of pul- 
monary disorder is of great significance. 
c 
Same. Respirations may run up to 50 
or GO in the minute, but without corres- 
pondingly increased exertion characteristic 
of true dyspnoea. 
Same. 
No solidification or infiltration. 
habit; signs of implication of meninges, 
especially in younger subjects; also 
hoarseness and aphonia. 
Same; with sudamina. 
Pain in shoulders and chest less frequent. 
Same. 
Same. 
Same. 
Physical Signs. 
A feeble respiratory murmur where the 
percussion note is normal or abnormally 
resonant is indicative either of tubercular 
trouble or lobular pneumonia. 
Rapid respiration and even dyspnoea with- 
out dullness.- 
Physical examination usually fails to re- 
veal enough to account for all the symptoms. 
Even after consecutive pneumonia, with 
bronchial breathing and ringing rfiles, 
solidification not extensive. 
course without diarrhoea or evidences of 
meningeal complication. 
Profuse sweating, usually at night. 
Pain in shoulders and chest more frequent. 
A white coat of vegetable spores and 
filaments often found on tongue. 
Painful decubitus in last stage; with 
oedema of feet. 
May terminate with haemorrhage. 
Physical Signs. 
With patient’s mouth open it is not dif- 
ficult to mark out, in front, the upper limits 
of the lungs—an important matter. (Vid. 
Table I). 
Rapid respiration and even dyspnoea with 
dullness. 
Physical examination usually reveals 
enough to account for other symptoms. 
Solidification of lung usually extensive. Seldom any perceptible abnormality of 
percussion note, or but very slight change, 
as compared with the other side. 
Vid. supra. 
Sometimes a soft friction murmur, caused 
by tubercular deposit on pleural surfaces, 
is heard. (Juergensen.) 
The different signs of catarrh, accentuated 
inspiration with audible expiration, whist- 
ling, sonorous bronchi over whole lung; 
and later rales, heard first in dependent 
regions. 
125 State St., Chicago. 
Tubercle of itself never gives rise to suffi- 
cient consolidation to cause dullness. 
The presence of miliary tubercle may, in 
exceptional cases, produce the same per- 
cussion sound. 
Same. 
Same; fremitus may also be exaggerated 
by lobular infiltration and by tuberculosis. 
Same. 
When area of dullness accords with the 
other signs it is a comparatively favorable 
feature. 
The presence of lobular infiltration may, 
in some cases, cause a hollow or tympan- 
itic note. 
‘ Cracked-pot ’ resonance over a cavity 
with thin walls. 
Fremitus is intensified over cavities con- 
necting with bronchi and containing air. 
(Of little value as a sign.) 
Bronchial respiration, broncopliony, and 
sonorous rales are heard after extensive in- 
duration. 
In the first stage, feeble, harsh or puerile 
respiratory sounds are heard, with all the 
signs of catarrh at apices. {Vid. Table I.) THE CHICAGO 
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