S T IJ DIE S 
IN 
pathological |atabmg 
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FRANCIS DEJLAFI ELD, M.D. 
PROEE8SOR OK PATHOLOGY AND PRACTICAL MEDICINE. 
COLLEGE OF PHYSICIANS AND SURGEONS. 
VOLUME II. 
PART I. 
Broncho-Pneumonta Plates i-xii. 
NOVEMBER, 1883. 
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-TOTERJST^.x H STUDIES 
IN 
PATHOLOGICAL ANATOMY. 
BRON OHO-PNEUMONIA. 
Before proceeding farther with the study of phthisis, it is neces- 
sary to consider more particularly some of the forms of non-tubercular 
broncho-pneumonia. 
Whenever the parenchyma of the lung is inflamed there is regu- 
larly some degree of bronchitis present, so that, strictly speaking, every 
pneumonia is a broncho-pneumonia. In most of such cases, however, 
the changes in the bronchi are superficial. Mucus, pus, or fibrine are 
found on the surface of the mucous membrane; the epithelial cells 
undergo various changes, the mucous glands are swollen, the blood- 
vessels are congested, but the wall of the bronchus is not changed 
except by the infiltration of a few pus-cells. 
There are cases, however, in which the wall of the bronchus does 
undergo well marked changes; it is thickened and markedly infiltrated 
with cells. The inflammatory process then does not usually remain 
confined to the bronchus, but extends to the air-vesicles surrounding it. 
The extension of the inflammation is not to the air-vesicles which 
empty into the bronchus, but into those which are in contact with it. 
It is as if a red-hot needle were thrust through the lung, making a 
track of charred tissue around it. So each of these inflamed bronchi 
along its whole length is surrounded by a zone of inflamed air-vesicles. 6 
STUDIES IN PATHOLOGICAL ANATOMY. 
There may, however, be added to this inflammation of air-vesicles in 
other parts of the lung. 
Such a broncho-pneumonia may run an acute course ; or beginning 
acutely, the inflammation may continue and become persistent. 
Children under five years of age are the usual subjects of such a 
broncho-pneumonia. Less frequently adults, especially young adults, 
are affected in the same way. In all the cases the primary inflamma- 
tion seems to be a bronchitis of a severe type, the pneumonia varying 
in its extent and secondary to the bronchitis. 
The condition which is often described under the name of capil- 
lary bronchitis belongs to this class of cases. It is really a severe 
general bronchitis, with more or less peri-bronchitic pneumonia. The 
trachea, the large bronchi, the medium-sized and the smallest bronchi 
are all involved in both lungs. In the trachea and larger bronchi the 
inflammation is simply catarrhal, with very little change in the walls of 
the bronchi. But in the medium-sized and small bronchi the inflam- 
mation is more intense, their walls are thickened and infiltrated with 
cells, they are surrounded by zones of intense congestion or hepatiza- 
tion, and they may be the seat of cylindrical dilatation. The rest of 
the lungs is congested; there are scattered patches of hepatization; 
there may be fibrine on the pulmonary pleura; the bronchial glands 
may be inflamed and swollen. 
The following case will serve as an example of this condition as it 
occurs in the adult: 
A vigorous laboring man, twenty-five years of age, was suddenly at- 
tacked, thirteen days before his death, with repeated rigors followed by 
fever, headache, prostration, cough and mucous expectoration, dyspnoea 
and pain in the chest. I first saw the patient six days before his death. 
He then looked very seriously ill. The face was cyanotic and anxious, 
the tongue dry, the dyspnoea urgent so that he could hardly lie down 
in bed. There were constant cough with very profuse mucous and 
serous expectoration, severe pain and distress all over the chest, a tem- 
perature of 102°, a rapid and full pulse. There was good resonance 
over the whole of both lungs, with numerous coarse and subcrepitant 
rales. The man grew worse, the temperature rose to 105°, the pulse BRONCHO-PNEUMONIA.' 
7 
became more rapid and full, be became delirious, crepitant rales were 
added to the coarse and subcrepitant rales, and he died on the thir- 
teenth day of the disease. 
At the autopsy, except for some venous congestion of the viscera, 
there were no lesions but those of the lungs. These organs were large, 
heavy, and congested, especially the lower lobes. On the pulmonary 
pleura were thin patches of fibrine. The trachea and large bronchi 
were congested and coated with mucus, but their walls were unchanged. 
The smaller bronchi, however, had their walls thickened and infiltrated 
with cells, and around most of them were zones of intense congestion 
or hepatization. The congestion was extreme, the capillaries distended 
with blood, and the air-vesicles partly filled with blood. The hepatiza- 
tion was due to a filling of the air-vesicles with epithelium, red blood- 
globules, and granular matter. Plate I. is a photograph of a large 
section of this lung, with a low magnifying power. It will be seen 
that each bronchus is surrounded by an opaque zone, due either to con- 
gestion or hepatization. 
The pneumonia of children under five years of age belongs, for the 
most part, to the form of broncho-pneumonia of which we are now 
speaking, although the lesions are often more complicated than in the 
class of cases just described. 
In children broncho-pneumonia occurs not only as an idiopathic 
inflammation, but as a frequent complication of whooping-cough, mea- 
sles, scarlatina, and diphtheria. Children also are much more apt to 
suffer from repeated attacks of broncho-pneumonia than are adults 
from repeated attacks of lobar pneumonia. 
In the ordinary broncho-pneumonia of children, the inflammation 
involves regularly the trachea, the large bronchi, most of the small 
bronchi, some of the air-vesicles, the bronchial glands, and, in some 
cases, the pulmonary pleura and the interstitial connective tissue. 
There is much variety in the extent of the inflammatory process 
and in the gross appearance of the lungs. 
(1.) There may be congestion of the mucous membrane of the 
trachea and large bronchi, with changes in their epithelium and an in- 
creased production of mucus. The smaller bronchi contain pus, their 8 
STUDIES IN PATHOLOGICAL ANATOMY. 
walls are thickened and infiltrated with cells, there may be cylindrical 
dilatation. Around many of the small bronchi are narrow zones of 
congestion or hepatization. The rest of the lungs is, to a greater or less 
degree, congested and oedematous. 
(2.) The conditions are the same as those just described, but the 
zones of peri-bronchitic pneumonia are larger, so that a section of the 
lung shows red or grayish peri-bronchitic nodules, like those of acute 
phthisis. 
(3.) To the lesions mentioned above are added diffuse hepatization 
and collapse of groups of air-vesicles. The diffuse hepatization consists 
of masses varying in their size and in their closeness to each other; 
occupying part of a lobule, or a lobule, or several lobules, and separated 
by aerated lung tissue more or less congested. Or the hepatized areas 
will be so close to each other as to render a lobe or part of a lobe uni- 
formly solid. When there is much of this diffuse pneumonia there are 
patches of^ fibrine on the pulmonary pleura. The hepatized portions 
of lung are of smooth, dense consistence, of light or dark red, or pink- 
ish-gray, or livid, bluish color, not like the red hepatization of lobar 
pneumonia. The sections of the inflamed bronchi and peri-bronchitic 
pneumonia give white figures mottling the surrounding diffuse red he- 
patization. 
If we look more closely at the smaller bronchi we see that they 
contain pus and desquamated and altered epithelium in varying 
amount, sometimes enough to fill up the cavity of the bronchus. The 
wall of the bronchus is thickened and infiltrated with cells. Some of 
these cells look like pus-cells, others like the cells of granulation tissue. 
This thickening and cell-growth extend outward from the wall of the 
bronchus to the walls of the adjacent air-vesicles. (Plate II. and Plate 
XLL, Vol. I.) 
The dilatation of the bronchi, when present, is of the cylindrical 
character, and involves the medium-sized bronchi for a considerable 
part of their length, so that sections of the lung give us everywhere 
cavities corresponding to the direction in which the bronchi are cut. 
Such dilated bronchi are surrounded either by congested or hepatized 
lung. BRONCHO-PNEUMONIA. 
9 
Plate III. is a photograph of a child's lung showing sections of a 
number of inflamed and dilated bronchi. The child was three years of 
age, and was attacked with broncho-pneumonia during the second week 
of scarlatina. Throughout both lungs a number of the medium-sized 
and smaller bronchi were dilated. The lung tissue between them was 
in some parts of the lung aerated, in other parts the seat of a diffuse 
red hepatization. It can be seen in the plate that the walls of the 
dilated bronchi are thickened, and that a layer of pus is adherent to 
the inner surface of the mucous membrane. 
In the zones of peri-bronchitic pneumonia the walls of the air- 
vesicles are thickened and swollen, either with or without some cellular 
infiltration. The cavities of the vesicles are filled with epithelial cells 
and pus-cells. 
In the diffuse red hepatization the air-vesicles contain pus, epithe- 
lium, fibrine, and red blood-globules in varying proportion and amount. 
Some vesicles are distended with these inflammatory products, some 
only contain a small amount. In some cases pus, in others epithelium, 
is the predominant inflammatory product. Fibrine, when present, is 
only in small quantities, and is often absent altogether. (Vol. I., 
Plates XXXIX. and XL.) The capillaries in the walls of the ves- 
icles are congested and prominent. 
The portions of lung which are not hepatized are congested and 
cedematous. The cavities of the air-vesicles are diminished by the en- 
larged capillaries, the epithelium of the vesicles is swollen, and in many 
vesicles a few pus or epithelial cells will be found. 
Such a broncho-pneumonia differs from the ordinary lobar pneu- 
monia of adults in several respects, some of which seem to depend on 
the differences between the lungs of children and those of adults. 
In the child's lung the bronchi occupy a relatively larger portion 
of the whole organ; the interstitial connective tissue is present in 
larger amount; the cavities of the air-vesicles are smaller and their 
walls relatively thicker; the epithelial cells lining the air-vesicles are 
present in larger numbers. 
So in the broncho-pneumonia of children the inflammation is a 
diffuse one, following the distribution of the bronchi in both lungs. 10 
STUDIES IN PATHOLOGICAL ANATOMY. 
The congestion of the capillaries in the walls of the air-vesicles is a 
serious part of the lesion on account of the small size of the vesicles. 
The bronchitis is not only general, but is also more severe, affecting the 
walls of the bronchi. Dilatation of the bronchi follows as the result 
of the changes in their walls. Collapse of groups of air-vesicles from 
obstruction of bronchi adds to the danger of the inflammation. The 
products of inflammation are more slowly removed from the air-ves- 
icles, and there is a tendency to the supervention of chronic inflam- 
mation of the connective tissue framework of the lung. Inflammation 
of the bronchial glands, while it is often simple, may be of tubercular 
character and become chronic. 
When a child suffers from an attack of broncho-pneumonia, death 
may ensue within a few hours. More frequently, however, the consti- 
tutional symptoms last for from five to ten days, and from seven to 
fourteen days more are required for the lung to return to its natural 
condition. 
Less frequently a chronic inflammation of the interstitial tissue of 
the lung is developed, and the child goes on to have persistent bron- 
chopneumonia. 
Such a persistent form of the disease may follow a single attack of 
acute broncho-pneumonia, or the patient may suffer from several acute 
attacks before the chronic condition becomes evident. The course of 
the disease varies in the different cases. 
(1.) A child has an ordinary attack of acute broncho-pneumonia, 
with consolidation of some part of the lung. Defervescence takes place, 
and for several days it appears as if convalescence were going on, al- 
though the physical signs of consolidation still persist. But then an ir- 
regular fever returns, the appetite is lost, the child becomes more and 
more emaciated, and finally dies exhausted at the end of several months. 
(2.) The symptoms begin in the same way and continue, but the 
child does not succumb to the disease. It continues to live with the evi- 
dences of a chronic bronchitis, which go on year after year. So the child 
may grow up to adult life, sometimes better, sometimes worse, never en- 
tirely well. Cough, expectoration, dyspnoea, occasional fever, harass 
the patient at intervals. The lung becomes more and more solid, the BRONCHO-PNEUMONIA. 
11 
bronchi more dilated, the pleura thicker, and the affected side more re- 
tracted. 
(3.) After the persistent broncho-pneumonia has lasted for months 
or years, the patient develops acute general miliary tuberculosis. 
(4.) When only small portions of the lungs are affected in this 
way, the child may seem to recover completely. But the diseased por- 
tion of lung does not return to its natural condition. 
In all the cases of persistent broncho-pneumonia the general condi- 
tions are: (1) A chronic bronchitis with or without dilatation of the 
bronchi; (2) the formation of new connective tissue in the walls of 
the bronchi and the air-vesicles, along the course of the blood-vessels, 
in the interlobular septa and pulmonary pleura ; (3) obliteration of air- 
vesicles, the production of epithelium and pus within them. The exact 
conditions in each case depend upon the extent of lung involved. 
Plate IV. is a photograph of a section embracing part of two lobes 
of a child's lung. Two years before its death the child suffered from 
an attack of broncho-pneumonia complicating measles. From this it 
recovered, but continued to be sickly until symptoms of tubercular 
meningitis were developed, and after a week's illness the child died. 
At the autopsy the middle lobe of the right lung was found hard and 
solid, its pulmonary pleura thickened. Miliary tubercles were scattered 
through the rest of the lungs, the pia mater, liver, spleen, and kidneys. 
In the plate are seen part of the solid lobe, and part of an adjoining 
lobe in which are miliary tubercles. In the solid lobe the dilated 
bronchi have the appearance of large rounded cavities. The epithelial 
cells lining the bronchi are much changed and covered with pus-cells. 
The walls of the bronchi are much thickened and infiltrated with cells. 
In some the cell-growth is so great that the inner surface of the 
bronchus is ragged, broken, and denuded of epithelium. The inter- 
lobular septa are much thickened and composed of dense connective 
tissue. There is a diffuse growth of young cellular tissue in the walls 
of the air-vesicles, resulting in the obliteration of most of the vesicles. 
Those which are left are deformed and lined with epithelium. 
Plate V. represents a similar condition to that in Plate IV., more 
highly magnified, and taken from the lung of another patient. The 12 
STUDIES IN PATHOLOGICAL ANATOMY. 
bronchi are dilated, but their epithelium is in place and not much 
changed. Their walls are thickened and infiltrated with cells, their 
mucous glands are enlarged. Between these dilated bronchi the lung 
is completely solid. The solidification is principally due to a diffuse 
growth of connective tissue with obliteration of the air-vesicles. The 
remaining air-vesicles are filled with epithelium and pus. 
Plate VI. is a photograph of a section of the upper lobe of the 
lung of a boy five years of age. The blood-vessels have been artificially 
injected. The patient had pneumonia at the age of two years, the next 
year whooping-cough, the next year measles, during the last year of his 
life two separate attacks of pneumonia, in the last of which he died. 
At the autopsy there were found dense old adhesions over the right 
upper lobe, and the pulmonary pleura of this lobe enormously thick- 
ened. This lobe was contracted, hard, and dense. The larger part of 
the rest of the lungs was the seat of diffuse red hepatization. The plate 
represents a vertical section through the dense right upper lobe. The 
pulmonary pleura is much thickened, and from it dense fibrous septa 
run into the lobe. Near the apex is a small cavity which contained a 
lump of yellow cheesy matter. The bronchi are not dilated. There 
is a diffuse growth of connective tissue, by which most of the air- 
vesicles are obliterated. 
Instead of a whole lobe, or part of a lobe, being converted into 
fibrous tissue, as in the cases just mentioned, there may be peri-bron- 
chitic nodules scattered through one or both lungs, in which there is 
the same chronic interstitial growth. 
Plate VII. is a photograph of a section of part of the lung of a 
boy three years of age. In December, 1881, he had a bad attack of 
diphtheria from which he recovered, but remained feeble and anaemic. 
Toward the end of January, 1882, he developed measles with double 
pneumonia and died on February 7th. Throughout both lungs were 
numerous small whitish nodules, some surrounded by red hepatization, 
some by aerated lung tissue. These white nodules are sections of small 
bronchi and of zones of peri-bronchitic pneumonia. The bronchi con- 
tain pus and fibrine, but their epithelium remains intact. The walls of 
the bronchi are split up by multitudes of cells. The peri-bronchitic BRONCHO-PNEUMONIA. 
13 
zones of pneumonia are composed of a growth of granulation tissue in 
the walls of the air-vesicles, so extensive that but few vesicles are left, 
and these are lined or filled with epithelial cells. The plate shows a 
number of these white nodules, each formed of a thickened bronchus 
with its zone of pneumonia. 
Plate IX. represents a single bronchus with the tissue around it. 
The walls of the bronchus are continuous with the surrounding gran- 
ulation tissue. The air-vesicles are small and widely separated. 
Plate X. is from one of the peri-bronchitic zones of pneumonia. 
It shows one air-vesicle and portions of two others lined with epithe- 
lium. The walls of the vesicles are replaced by granulation tissue 
richly supplied with blood-vessels. 
I have seen two cases of broncho-pneumonia in boys, at the age 
of seventeen and nineteen respectively, in which the lesions resembled 
those of the persistent broncho-pneumonia of children. 
Both the patients were suddenly attacked with prostration, fever, 
cough and profuse muco-purulent expectoration, dyspnoea, pain in the 
chest, coarse rales all over the chest, with dulness over the consolidated 
portions of lung. The temperature was from 97° to 103°, irregular, 
usually higher in the evening, sometimes in the morning; the pulse 
became more rapid as the disease went on. The patients grew more 
and more feeble and emaciated, delirious, and died at the end of four 
and seven weeks respectively. After death the larger bronchi were 
found congested and coated with mucus. There were patches of 
fibrine on the pulmonary pleura, and in one of the cases purulent serum 
in one of the pleural cavities. In both lungs there was an irregular, 
diffuse, red hepatization, mottled with small white nodules from the 
size of a pin's head to that of a pea. Between the areas of red he- 
patization the lung was congested. In the areas of red hepatization 
the air-vesicles were filled with pus, reticulated fibrine, granular mat- 
ter, and epithelial cells. The white nodules corresponded to sec- 
tions of bronchi, with zones of peri-bronchitic pneumonia. These 
bronchi contain pus. Some are still lined with epithelium; in others 
this has disappeared. The walls of the bronchi are thickened and in- 
filtrated with round, polygonal, and nucleated cells. In some this cell- 14 
STUDIES IN PATHOLOGICAL ANATOMY.. 
growth is so extensive that the inner surfaces of the bronchi are ragged 
and irregular, so that they look like little purulent cavities. In the 
peri-bronchitic zones of pneumonia the walls of the vesicles are thick- 
ened and infiltrated with cells, the blood-vessels remain pervious. The 
cavities of the vesicles are filled with a basement-substance of homo- 
geneous, finely fibrillated character, or more dense and opaque, like retic- 
ulated fibrine. In this are embedded polygonal, round, and fusiform 
cells, resembling pus, epithelium, and young connective tissue cells. 
Plate VIII. is a photograph of a section of a bronchus, with the 
surrounding lung. The wall of the bronchus is thickened, as are also 
the walls of the vesicles for some distance around it. The cavities of 
the vesicles are filled with inflammatory products, so that they look 
like dark spots surrounded by the more transparent thickened walls of 
the vesicles. 
Plate XII. represents a section of a bronchus in the same condi- 
tion, but with a higher magnifying power. The vessels have been 
artificially injected. 
Plate XI. represents a single air-vesicle and the peculiar tissue 
with which its cavity is filled. 
It is evident, then, that the characteristic feature of all the forms 
of broncho-pneumonia which I have described is the implication of the 
connective tissue framework of the lung. There is not merely an accu- 
mulation of inflammatory products in the cavities of the bronchi and 
air-vesicles, as in other forms of pneumonia, but also inflammatory 
changes in the walls of the bronchi and vesicles, so that the tissue of 
the lung is much more seriously changed, and changed in a way much 
more likely to remain permanent. 
In this way, also, the lesions of broncho-pneumonia resemble those 
of acute and chronic phthisis. 
In both we find the same combination of peri-bronchitic and dif- 
fuse pneumonia; the peri-bronchitic pneumonia characterized by the 
implication of the walls of the vesicles and the presence of permanent 
tissue in their cavities. 
In both the cellular infiltration of the walls of the bronchi may 
lead to their dilatation and to the formation of cavities. BRONCHO-PNEUMONIA. 
15 
In both there are inflammatory changes involving the connective 
tissue framework of the lung; and when these changes have once com- 
menced, there is the same tendency to a persistence and extension of 
the inflammatory process. 
In both we may have much the same clinical histories. 
But in broncho-pneumonia there are no tubercle tissue, no tubercle 
bacilli, no obliteration of blood-vessels, no areas of coagulation necrosis, 
and comparatively little cheesy degeneration of inflammatory products. Artotype, 
E. Bieratidt, N Y 
Plate I. x 5 
ACUTE BRONCHO-PNEUMONIA Plate II. x 200. 
ACUTE BRONCHO-PNEUMONIA. Artotype, 
E. Bierstadt, N Y. 
Plate III. x 5^ 
ACUTE BRONCHO-PNEUMONIA. Artotype, 
E. Bierstadt, N Y. 
Plate IV. x 5 
PERSISTENT BRONCHO-PNEUMONIA. Artotype, 
E. Bierstadt, N Y 
Plate V. x 6 
PERSISTENT broncho-pneumonia Artotype, 
E. Bierstadt, N Y. 
Plate VI. x 4 
PERSISTENT BRONCHO-PNEUMONIA Artotype, 
E. Bierstadt, N Y. 
Plate VII. x 11 
PERSISTENT BRONCHO-PNEUMONIA. Artotype, 
E. Bierstadt, N Y. 
Plate VIII. x 20 
PERSISTENT BRO N CHO-PN E U MON I A. Artotype, 
Plate IX. x 1 70 
PERSISTENT BRONCHO-PNEUMONIA. 
E. Bierdtadt, N. Y E. Bieratadt, M, Y. 
Artotype, 
P| ate X. x 1 500 
persistent broncho-pneumonia. Artotype, 
E Bieratadt, N. Y 
Plate XI. x850 
persistent broncho-pneumonia. Artotype, 
Plate XII. x 200 
persistent BRONCHO-PNEUMONIA. 
E. Bierstadt, N. Y. CHRONIC PULMONARY PHTHISIS. 
Chronic phthisis is a disease which continues for months and years. 
Its invasion may be acute and well marked, or slow and insidious. Its 
course may be progressive and uninterrupted, or marked by intermis- 
sions and exacerbations. The morbid process may remain confined to 
the lung, or extend, apparently by auto-inoculation, to other parts of 
the body. The patient may entirely recover, and the old pulmonary 
lesion be discovered after his death from some other disease; or he may 
die, while the disease is still active, at almost any period of its develop- 
ment. 
All the lesions of chronic phthisis seem to be the result of inflamma- 
tory processes, but the long duration of the disease is attended with 
marked transformations and degenerations of the inflammatory products. 
It is only, therefore, by examining and comparing a great many lungs 
in different stages of the disease that we are able to determine the real 
character of the lesions. 
The one essential feature of chronic phthisis is the presence of tuber- 
cular inflammation; without this there is no phthisis. Such a tubercular 
inflammation is not only an essential, but also a primary, part of chronic 
phthisis ; it exists from the very commencement of the disease. Phthi- 
sis is not an ordinary form of chronic inflammation of the lungs, to 
which tubercles may or may not be added ; it is primarily a tubercular 
affection. 
But although tubercular inflammation is the essential and primary 
lesion of phthisis, its products may be small in quantity and changed 
in character by age. On the other hand, the other forms of associated 
inflammation may reach such a degree of development as to obscure the 
tubercular part of the lesion. 
The changes in the lung which may be associated with tubercular 18 
CHRONIC PULMONARY PHTHISIS. 
inflammation are numerous and varied: Pleurisy, bronchitis, broncho- 
pneumonia, lobar pneumonia, interstitial pneumonia, obliterating endar- 
teritis, and emphysema, may each or all be present; they do not differ 
anatomically from the same lesions when they exist without phthisis; 
they may constitute the principal part of the changes in the lungs ; but 
yet, that well-marked combination of clinical symptoms and anatomical 
lesions which marks chronic phthisis is never effected without the pres- 
ence of tubercular inflammation. This is the leaven which gives the 
character to the whole process. Still, the lesions, the symptoms, and the 
treatment of chronic phthisis often depend much more upon the asso- 
ciated inflammations than upon the tuberculosis. 
Not only is there a difference in the different cases as to the rela- 
tive importance of the tubercular and the associated inflammations, but 
there seems also to be a difference in the way in which the disease 
spreads in the lungs. In some patients the extension of the disease in 
the lungs is not continuous, but at intervals fresh portions of the lung 
are invaded by the disease. In some persons each fresh invasion seems 
to be due to a fresh bronchitis or pneumonia ; in other persons there is 
simply the formation of more miliary tubercles in a new part of the 
lung, as if by auto-inoculation. 
The tubercle bacilli are regularly found associated with the lesions 
of chronic phthisis. On the walls of necrotic cavities and of dilated 
bronchi, and in the sputa, they are abundant. Wherever the inflamma- 
tory products are necrotic and degenerative they may also be found, but 
in the well-formed products of the tubercular and allied inflammations 
the bacilli are but few in number. 
The simplest form of chronic phthisis is that in which the tubercu- 
lar inflammation results in the formation of miliary tubercules, while the 
only associated lesions are bronchitis, emphysema, and pleurisy. 
Somewhat more complicated are the cases in which, besides the miliary 
tubercles, the bronchitis, the emphysema, and the pleurisy, there is also 
an interstitial pneumonia with the production of tubercle tissue and 
connective tissue, and the formation of cavities by dilatation of the 
bronchi. Both these forms of chronic phthisis have been described in 
Volume I. under the name of " Chronic Miliary Tuberculosis." CHRONIC PULMONARY PHTHISIS. 
19 
The still more complicated forms of the disease are yet to be de- 
scribed. 
In. studying these more obscure forms of chronic phthisis we are fur- 
nished with a sort of guide by the lesions of acute phthisis. In both, the 
morbid processes seem to be essentially the same, but in the chronic dis- 
ease these processes are altered by their slow development and long con- 
tinuance. 
We will, therefore, first describe separately the different lesions 
which are associated together in chronic phthisis. 
I. The Diffuse Hepatization.-This is effected either by the filling of 
the cavities of the air-spaces with inflammatory products, or by the 
growth of tissue in their walls, or by a combination of both these con- 
ditions. 
When the hepatization is effected only by changes within the cavities 
of the air-spaces, the affected portions of lung is solid, increased in size, 
of red, gray, white, or yellow color. It may resemble the red or gray 
hepatization of lobar pneumonia, it may be of a peculiar semi-trans- 
lucent appearance, or it may look as if it had undergone cheesy degen- 
eration. 
When the hepatization is due to interstitial inflammation, the 
affected portion of lung is dense, but may still be partly aerated; it is 
diminished in size, and looks like fibrous tissue or granulation tissue, 
sometimes changed in color by the deposition of black pigment. 
A combination of the intra-alveolar and interstitial changes gives us 
a great variety of pictures, according to the exact development of the 
processes. 
In the intra-alveolar pneumonia there is a variety in the character 
of the inflammatory products which fill the air-spaces. Some of the air- 
spaces are filled with large, epithelial cells, which are well formed, or 
in the condition of fatty degeneration. Plate (XIII.) 
Some contain an amorphous granular matter (Vol. I., Plate LX VIL), 
or a peculiar, translucent, coagulated substance. 
Some contain fibrine, pus, and epithelium, and resemble exactly the 
air-spaces filled with inflammatory products which we regularly find in 
lobar pneumonia. In both acute and chronic phthisis this form of 20 
CHRONIC PULMONARY PHTHISIS. 
hepatization, anatomically identical with that which exists in lobar 
pneumonia, is of ordinary occurrence. In some cases it is developed to 
an unusual degree, and some of these lungs have been described as ex- 
amples of a " croupous phthisis." 
Such an intra-alveolar pneumonia forming part of the lesions of 
phthisis is not to be confounded with a real lobar pneumonia occurring 
in a patient already suffering from chronic phthisis. 
Some parts of these lungs are the seat of a dense, dry hepatization 
of gray, white, or yellow color. If we try to inject the lung artificially, 
these portions are only incompletely injected. The air-spaces are filled 
and distended with inflammatory products-pus, epithelium, and fibrine 
-but these products have undergone cheesy degeneration. The pus and 
epithelial cells are small and shrivelled, granular matter is present, the 
net-work of fibrine is indistinct, and all the products are so closely 
compacted together that it is only in very thin sections and favorable 
specimens that we can make out anything more than an amorphous 
mass. The walls of the air-spaces are compressed and thinned; in some 
of them the capillaries can be partially or completely injected; or, in- 
stead of being thinned, the walls of the air-spaces may be thickened 
and infiltrated with cells. Plate XIV. represents a section of air- 
vesicles distended with degenerated inflammatory products, their walls 
thin and compressed, the capillaries only partly injected. 
The interstitial pneumonia affects the walls of the air-spaces, the 
bronchi, the blood-vessels, and the septa between the lobules. In all 
these situations the inflammation results in the production of new con- 
nective tissue, of round-celled tissue, and of tubercle tissue, either sepa- 
rately or together. By this growth the air-spaces are compressed, 
deformed, and obliterated in a variety of ways. The cavities of the 
air-spaces may remain empty, or the epithelial cells or their walls may 
be increased in size and number, or they may contain pus, fibrine, or 
new connective tissue, or there may be polypoid growths from the walls 
of the air-spaces into their cavities. In this way the entire tissue of 
the lung becomes profoundly changed. 
In some places there will be a dense mass of fibrous tissue, well sup- 
plied with blood-vessels, replacing a considerable part of the lung, and CHRONIC PULMONARY PHTHISIS. 
21 
completely obliterating all traces of the original lung-structure. Such 
a condition is found especially around the outside of old cavities. 
In other places the growth of new tissue is not as extensive as this : 
a larger or smaller number of the air-spaces and bronchi are left de- 
formed and altered in various ways. 
In Plate XV. may be seen such an interstitial growth of connective 
tissue, with air-spaces changed into long, narrow cavities lined with 
epithelial cells. 
Plate XVI. represents a section of a portion of hepatized lung 
which does not resemble lung-tissue at all. There is a stroma of con- 
nective tissue enclosing small cavities filled with epithelial cells. 
In Plate XVII. is shown a section of an hepatization which was com- 
posed of a large mass of new, dense connective tissue. In this dense 
tissue were scattered irregularly small areas composed of round-celled 
tissue surrounding cavities of irregular shape. 
Plate XVIIL, taken from a section of another lung in the same con- 
dition, shows one of the cavities with the surrounding granulation tissue 
more highly magnified. 
In many cases of chronic phthisis the hepatization is effected in part 
by a production of new connective tissue within the cavities of the air- 
spaces. This new tissue is composed of a basement substance and cells, 
and may contain blood-vessels. It may be formed as an outgrowth from 
the wall of an air-space, or may seem to be produced free within its 
cavity, only touching its wall at a few points. This new connective tis- 
sue may partly fill the cavity of an air-space and the rest of the cavity 
may remain empty, or contain epithelial cells, or the cavity is completely 
filled with the new growth. The walls of these air-spaces may remain 
but little changed, or they may be thickened and infiltrated with cells. 
Where the process is far advanced, the thickening of the walls of the 
air-spaces and the growth of connective tissue within their cavities results 
in the formation of a diffuse mass of connective tissue, in which the 
structure of the lung can hardly be made out. 
Plate XIX. represents an air-vesicle with thickened walls and a 
growth of connective tissue from the wall projecting into its cavity. 
Plate XX. represents an air-vesicle, of which the walls are but little 22 
CHRONIC PULMONARY PHTHISIS. 
changed. Its cavity is partly filled by new connective tissue, which 
seems to be formed free within it. 
Plate XXL represents a large air-space, its walls somewhat thick- 
ened, and its cavity partly filled with a curious branching growth of 
connective tissue. 
II. The Morbid Changes in the Air-tubes.-The larynx, the trachea, 
and the bronchi are frequently inflamed in cases of chronic phthisis; 
sometimes slightly, sometimes in a marked degree. Indeed, there are 
many cases in which the lesions of the air-passages are of much more im- 
portance than those of the lungs. 
The structure of the walls of the air-passages is of much the same 
character throughout their whole extent. 
On the inside is a layer of epithelial cells. In the smallest bronchi 
this layer is composed of a single layer of epithelial cells of cuboidal 
shape. In the larger bronchi and the trachea the epithelium consists of 
several layers of cells one over the other. The superficial cells are of 
the ciliated, cylindrical type; the deeper cells are polygonal. In the 
larynx the epithelium is in some portions like that of the trachea, in 
other portions it is a flat-celled epithelium like that of the pharynx. 
The stroma of the mucous membrane is composed of loose connective 
tissue containing a considerable number of small cells. Except in the 
smaller bronchi, the portion of the stroma immediately beneath the epi- 
thelium is in the form of a homogeneous basement membrane. 
The stroma contains numerous blood-vessels, some of them of large 
size, and the endothelial cells lining these vessels are apt to be unusually 
prominent. In the larger and medium-sized bronchi the size and num- 
ber of the blood-vessels is especially noticeable. It looks as if marked 
changes in the thickness of the walls of these bronchi could readily be 
effected by a simple congestion or anaemia of the vessels. 
The mucous glands, of the racemose type, are numerous and large 
everywhere except in the smaller bronchi. 
Their ducts open on the free surface of the mucous membrane, and 
are lined with epithelium of the same type as that of the mucous mem- 
brane. 
Not infrequently these ducts contain mucus. The follicles of the CHRONIC PULMONARY PHTHISIS. 
23 
glands are lined with cylindrical cells, which are granular or distended 
with mucus and transparent. 
In the region about the vocal cords the stroma is infiltrated here and 
there with masses of lymphatic glandular tissue. 
Outside of the stroma of the mucous membrane we find muscle, con- 
nective tissue, cartilage, or lung-tissue, as the case may be. The general 
arrangement of the tissues composing the walls of the air-tubes can be 
seen in Plate XXII.-a vertical section of the wall of the trachea, the 
seat of acute catarrhal inflammation. 
The most common form of inflammation of the air-tubes in chronic 
phthisis is the catarrhal. This regularly runs a chronic course, with 
frequent exacerbations. The larynx, the trachea, and the large and 
medium-sized bronchi may be affected either separately or together. 
Such a catarrhal inflammation is responsible for the cough and ex- 
pectoration, and also for other symptoms in many cases of phthisis. 
In its milder forms it is amenable to treatment, and may disappear alto- 
gether. 
The cases vary as to the severity and duration of the inflammatory 
process. 
1. The Mild Cases.-After death we find the mucous membrane 
coated with mucus or muco-pus in variable quantity. The mem- 
brane itself may be either congested or anaemic. On minute examina- 
tion we find a layer of coagulated mucus or muco-pus adherent to the 
free surface of the epithelium, and dipping down into the ducts of the 
mucous glands. This layer is composed of mucus alone, or of mucus 
and pus. Embedded in it are desquamated and degenerated epithelial 
cells from the surface of the membrane, and from the mucous glands. 
The mucous glands are somewhat swollen, and often distended with 
mucus. Plate XXIII. represents a vertical section of the wall of a 
lar^e bronchus in such a condition of mild catarrhal inflammation. It 
is to be remembered that even this mild form, with very slight ana- 
tomical changes, may be associated during life with an harassing cough 
and the expectoration of large quantities of mucus. 
2. The More Severe Cases.-In these, besides the increased produc- 
tion of mucus, there are changes in the epithelial cells. The superficial 24 
CHRONIC PULMONARY PHTHISIS. 
epithelial cells are changed in a variety of ways. Some are swollen, 
some contain large cavities in which are a number of round cells, some 
are dead, shrunken, and deformed, and desquamate in numbers. The 
deep polygonal cells are increased in number, approach the surface, and 
replace to some extent the superficial cells. The stroma remains un- 
changed, but the swelling of the endothelium of the blood-vessels is 
often quite marked. Plate XXIV. represents a vertical section of the 
inner part of the wall of a large bronchus. On the inside is the layer 
of mucus, pus, and desquamated epithelium; in which can also be seen 
the large transparent globules which come from the mucous glands. 
Beneath this is the epithelial layer. Of the superficial cells some are 
normal, some are swollen, some contain cavities, some are necrotic and 
deformed. Beneath the necrotic cells the cells of the deep layer are 
seen to be increased in number. Beneath the epithelium is the stroma 
of the mucous membrane, unchanged except for the swelling of the en- 
dothelium of the blood-vessels. Such changes in the epithelium are 
found in the larynx, trachea, and bronchi. They do not usually involve 
any large area of the mucous membrane, but occur in small isolated 
patches at irregular intervals. 
3. The Long-continued Cases.-When the changes in the mucous 
membrane just described have lasted for a sufficient length of time, there 
are regularly added changes in the walls of the air-tubes. This is es- 
pecially apt to be the case in the old cases of chronic miliary tuber- 
culosis and emphysema. The larger and medium-sized bronchi are the 
parts usually affected. In these we find the wall of the bronchus thick- 
ened and thrown inward in folds and projections of considerable size. 
There is a simple hypertrophy of the connective tissue beneath the 
epithelium, sometimes of the muscular coat also. The blood-vessels may 
be increased in size and number. Plate XXV. is a photograph of a sec- 
tion of a small bronchus in this condition of thickening. 
Of more importance than the changes produced by catarrhal inflam- 
mation are those produced by the inflammation of the walls of the air- 
tubes. Such an inflammation is most frequently associated with catarrhal 
inflammation, but may occur by itself. 
This interstitial inflammation of the air-tubes may have the char- CHRONIC PULMONARY PHTHISIS. 
25 
acter of a simple inflammation, with the production of small cells, or it 
may be a tubercular process. Both forms frequently involve the upper 
part of the larynx and the larger bronchi within the lungs. 
1. Interstitial Inflammation without Tubercle.-The simplest form 
of this is like the broncho-pneumonia of children, an infiltration of the 
wall of the bronchus with small round and polygonal cells, and an ex- 
tension of the inflammation to the surrounding zone of air-vesicles. 
A more severe and complicated form is produced by an excessive cell- 
growth and a disposition to necrosis. The new cells are formed in large 
numbers, the epithelium over them desquamates, the outer cells die, and 
so are formed, in the larynx, superficial ulcers; in the bronchi, sacculated 
bronchiectasige. 
Plate XXVI. is a photograph of a vertical section of such an ulcer 
in the larynx. Plate XXVII. is a drawing of a vertical section of the 
edge of a smaller ulcer of the same character situated a little below the 
vocal cords. Over the edge of the ulcer the epithelial layer is replaced 
by a single layer of large polygonal cells. The stroma beneath is infil- 
trated with small cells, which become more numerous as they approach 
the ulcer, while the floor of the ulcer is formed of a sort of granulation 
tissue, of which the superficial portions are necrotic. 
In the bronchi these changes are apt not to be developed symmetri- 
cally, but to involve especially a part of the wall of the bronchus; for 
this reason the resulting dilatations are sacculated rather than cylindrical. 
The bronchiectasise are rendered still larger by the extension of similar 
changes to the surrounding air-vesicles. Plate XXVIII. is a photograph 
of a section of the whole of a small bronchiectasia produced in this way. 
The wall of the bronchus is thickened and infiltrated with cells. On one 
side the layer of epithelium, although ragged, is still in place. Over the 
rest of the bronchus the epithelium has disappeared. In some places, even 
where the epithelium has disappeared, the infiltrated wall has not become 
necrotic. But in many other places necrosis, either superficial or deep, has 
taken place, so that the wall of the bronchus is fairly broken through.'] 
The air-vesicles surrounding the bronchus contain pus and fibrine, 
and their walls are infiltrated with cells. At some points the necrosis 
has extended to them also, so as to make the cavity still larger and more 26 
CHRONIC PULMONARY PHTHISIS. 
ragged. Plate XXIX. is a drawing of a vertical section of the wall of 
a similar bronchiectasia at a point where the layer of epithelium, al- 
though much altered in character, is still preserved. 
2. Tubercular Inflammation.-Tubercular inflammation of the air- 
tubes involves most frequently the bronchi within the lungs and the 
upper part of the larynx, less frequently the trachea and the large bron- 
chi without the lungs. The cases vary as to the extent of the associated 
inflammation, and the tendency to necrosis of the tubercle tissue and of 
the other inflammatory products. 
The simplest anatomical conditions are seen when there is a moderate 
catarrhal inflammation, a production of new cells in the stroma without 
necrosis, and the formation of tubercle-granula which do not become 
necrotic. Then a vertical section of the wall of the larynx, photo- 
graphed with a low power, will give us such a picture as is seen in Plate 
XXX. The layer of epithelium is still intact, coated on its inner surface 
with a layer of mucus, pus, and desquamated epithelium. From the epi- 
thelial layer down to the mucous glands the stroma is thickly infiltrated 
with cells, and scattered here and there are tubercle granula either single 
or in groups. Plate XXXI. is a more highly magnified drawing from 
another larynx in the same condition. The tubercle granula can be seen 
in the stroma just beneath the epithelium. 
When there are added to the production of tubercle-tissue an ex- 
cessive formation of cells and a tendency to necrosis, the conditions may 
become much more serious and complicated. The catarrhal inflammation 
is intense, with the production of large quantities of pus and mucus. 
The necrosis forms ulcers of different sizes and shapes. The inflamma- 
tion and necrosis extend from the walls of the air-tubes to the surround- 
ing tissues, and in this way are effected some of the most serious of the 
lesions of chronic phthisis. 
In the larynx we find the epiglottis, the vocal cords, and the ad- 
jacent mucous membrane coated with muco-pus, their surfaces ragged 
and irregular. In places the mucous membrane is destroyed so that 
ulcers are formed, in it is places thickened and infiltrated with cells and 
tubercle tissue, in places necrotic. In bad cases the entire thickness of 
the wall of the larynx, with its cartilages, becomes involved. 27 
CHRONIC PULMONARY PHTHISIS. 
In the trachea and large bronchi without the lungs, large ulcers* are 
formed, which may extend to the cartilages. 
The bronchi within the lungs are sometimes the seat of a bron- 
chitis and peribronchitis such as are shown in Plates LXXVII. and 
LXXVIII., Vol. I. In other cases the changes are such as are seen in 
Plate LXXX., Vol I. Both these changes are the same as those in 
acute phthisis, and have been already described in Vol. I. 
The most common change in the walls of the bronchi in chronic 
phthisis, however, consists in an infiltration of the wall of the bronchus 
with small cells and tubercle tissue. This infiltration is not symmetri- 
cal, but affects a bronchus in some particular portion of its length, and 
in this portion some parts of the circumference of the bronchus are 
affected more than others. As a result of this irregular infiltration the 
wall of the bronchus yields here and there, and small sacculated dilata- 
tions are formed. In some cases, especially in chronic miliary tuber- 
culosis, the cavities thus formed simply become larger and larger, 
compressing the surrounding lung. More frequently, however, the pro- 
cess extends from the wall of the bronchus to the surrounding vesicles, 
and areas of coagulation necrosis and miliary tubercles are formed in 
the lung close to the bronchus. The epithelium of the dilated bronchus 
disappears, portions of its walls become necrotic, the cavity increases in 
size partly by simple dilatation, partly by the destruction of its walls. 
Then as the dilatation becomes larger its walls touch the adjacent 
miliary tubercles and areas of coagulation necrosis; these also soften, 
and so the cavity becomes still larger and more irregular. 
Plate XXXII. is a photograph of such a bronchiectasia, the section 
being parallel to the long axis of the bronchus. In the lower part of 
the picture is the bronchus, of its normal size, and still covered with epi- 
thelium, although its wall is infiltrated. This bronchus terminates 
abruptly in a large sacculated dilatation with ragged walls. All about 
the lung tissue is solid with pneumonia, miliary tubercles, and areas of 
coagulation necrosis. 
Some of the cavities in chronic phthisis seem to be formed simply by 
the softening of areas of coagulation necrosis, as in acute phthisis, but the 
larger number seem to be bronchiectasiae, such as have been just described. 28 
CHRONIC PULMONARY PHTHISIS. 
The cavities which are formed principally by dilatation, without 
much necrosis of their walls may be developed with hardly any cough 
or expectoration. And as we examine the patient from time to time, 
the change in the percussion note and the character of the breathing show 
the increasing size of a cavity which remains nearly dry and empty. 
The cavities formed both by dilatation and necrosis, on the contrary, 
are regularly accompanied by a harassing cough and a profuse expec- 
toration. They contain pus, mucus, fragments of dead tissue, and great 
numbers of tubercle bacilli. Their walls are ragged and irregular, 
partly necrotic, partly a sort of suppurative granulation tissue. In this 
active condition the cavities may remain up to the time of the patient's 
death. Or, .instead of this, the active processes may subside, the pro- 
duction of pus and the death of tissue will cease, the cavity becomes dry, 
its walls are changed into fibrous tissue. 
III. The Miliary Tubercles.-These are regularly present in chronic 
phthisis, but vary as to their number, size, and distribution. They are 
of the same characters as the miliary tubercles which have already been 
described with acute phthisis and chronic miliary tuberculosis. 
IV. Ihe Areas of Coagulation Necrosis.-1These have the same 
characters as in acute phthisis. Some are found in the condition of 
coagulation necrosis, some have undergone cheesy degeneration, some 
have become infiltrated with the salts of lime, some have softened and 
broken down. They are not present in all the cases of chronic phthisis, 
but belong especially to those cases which begin as acute phthisis. 
In different cases of chronic phthisis, therefore, we find associated 
together these different lesions: the diffuse hepatization, the changes in 
the air-tubes, the miliary tubercles, and the areas of coagulation necro- 
sis. Sometimes one, sometimes another, of these lesions is especially de- 
veloped and gives its character to the particular case. 
At the time of the patient's death the inflammatory processes may 
still be active, or they may have entirely ceased. A large part of one 
or both lungs may be involved, or only a circumscribed area. In most 
cases the pulmonary pleura is thickened and covered with permanent 
adhesions. So we may find only a small area of consolidation, with 
thickened pleura, and perhaps a dilated bronchus at one apex. Or the CHRONIC PULMONARY PHTHISIS. 
29 
upper half, or the whole, of one or both upper lobes is shrunken, its sur- 
face puckered, and fastened here and there by adhesions to the chest 
wall. It is rendered solid and unaerated by the intra-alveolar and inter- 
stitial pneumonia and the miliary tubercles. It is traversed by cavities 
formed by the dilatation of bronchi. In the lower lobes will be patches 
of miliary tubercles. 
Instead of this, either the whole or part of a lung will be increased 
in size, and solid, except for cavities of different sizes. The intra-alveolar 
pneumonia and the areas of coagulation necrosis form the principal part 
of the morbid process. 
If the patient has recovered, bands and patches of fibrous* tissue, 
small cheesy or calcified areas, fibrous tubercles, cavities with fibrous 
walls, are left as the result of the morbid process. 
There is hardly any limit to the diversity and extent of these differ- 
ent morbid changes in the different cases of chronic phthisis. 
If now we look back at the different forms of tubercular inflamma- 
tion of the lungs, we find : 
I. Acute Miliary Tuberculosis.-Here the inflammation of the lung 
is only part of the lesion of a general disease, miliary tubercles being de- 
veloped at the same time in many other parts of the body. 
The miliary tubercles conform to several different types: 
1. Little masses of amorphous granular matter composed of a group 
of vesicles filled with granular matter, their walls thinned, or thickened, 
or necrotic. In these tubercles the bacilli are present in large numbers. 
Plate XXXIII. is a drawing of part of such a miliary tubercle, the ba- 
cilli stained by Gram's method. 
2. Miliary tubercles formed by the infiltration of the walls of a group 
of air-vesicles with tubercle tissue or granulation tissue, while their cav- 
ities are filled with tubercle tissue or with fibrine, pus, and epithelium. 
Plate XXXIV. is a drawing of a very small miliary tubercle of this kind. 
The blood-vessels have been artificially injected with blue. Two air- 
vesicles have their walls infiltrated and their cavities filled with tuber- 
cle tissue. In Volume I. similar tubercles are shown in Plates XLIII. 
and XLV. 
3. Miliary tubercles formed by the infiltration of the walls of bron- 30 
CHRONIC PULMONARY PHTHISIS. 
chioles or air-passages with tubercle tissue, their cavities remaining 
empty, or filled with tubercle tissue or pus, fibrine, and epithelium. 
Plate XXXV. is a drawing of such a tubercle formed by the infiltration 
of the walls of two bronchioles. 
4. Miliary tubercles formed by the infiltration of the walls of small 
bronchi and of the walls and cavities of a number of air-vesicles partly 
with tubercle tissue, partly with other inflammatory products. In this 
way masses of considerable size are formed, which soon undergo cheesy 
degeneration. 
5. Miliary tubercles formed in the pleura, the septa, and the connec- 
tive tissue along the walls of the blood-vessels. 
II. Acute Phthisis.-This is a localized tubercular inflammation in- 
volving the lungs-either one or both. It is characterized by the very 
great development of the accompanying inflammatory processes, and the 
necrosis of considerable portions of the lung tissue. The invasion of the 
disease is acute, and its course is rapid. 
III. Chronic Phthisis.-This is also a localized tubercular inflamma- 
tion of the lungs. 
In some of the cases in addition to the miliary tubercles we find but 
few other lesions, and these cases, for convenience, we include under the 
name of " Chronic Miliary Tuberculosis." 
In other cases we find, besides the tubercles, a very marked develop- 
ment of other inflammatory changes, as in acute phthisis. These cases we 
may call simply " Chronic Phthisis," or " Chronic Pneumonic Phthisis." APPENDIX. 
LOBAR PNEUMONIA. 
Since describing the regular lesions of lobar pneumonia, I have seen 
several examples of the disease which merit a special description. 
We have seen that in ordinary lobar pneumonia the cavities of the 
air-spaces are filled with fibrine, pus, and epithelium; and that if the 
patient die these products are found after death ; if he recover, they 
are absorbed, and the lung returns to its natural condition. 
We have also seen that in broncho-pneumonia and in phthisis there 
may be interstitial changes in the walls of the air-passages and the 
formation of organized connective tissue in their cavities. 
A number of observers have described cases of pneumonia which 
ran a chronic course, lasted for a long time, and in which, after death, 
organized tissue was found in the cavities of the air-spaces. 
I have seen four cases of lobar-pneumonia in adults in which the 
disease ran an acute course, lasted but a short time, and yet, after death, 
the air-spaces were found to contain organized new connective tissue. 
Case I.-A male, forty-three years of age, was admitted to the Roose- 
velt Hospital on February 8, 1881. Five days before, after sleeping 
in a cold room, he was attacked with a rigor, followed by fever, cough, 
loss of appetite, sleeplessness, and prostration. On admission he pre- 
sented the ordinary rational symptoms of lobar pneumonia and the 
physical signs of consolidation of the upper lobe of the right lung. 
On February 15th there was an exacerbation of the symptoms, and the 
physical signs of commencing consolidation of the lower lobe of the 
left lung were present. 
On February 16th the physical signs of the consolidation of the 
right lung were becoming less distinct. On the evening of February 
16th he died. 32 
LOBAR PNEUMONIA. 
At the autopsy the lower lobe of the left lung was found to be in 
the condition of red hepatization. The minute lesions were the ordi- 
nary ones of lobar pneumonia, the air-spaces being filled with pus and 
fibrine. 
The right upper lobe was partly consolidated and partly aerated. 
The hepatized portions were of gray color and irregular shape, and 
the lobe looked as if it was in the condition of gray hepatization going 
on to resolution. 
In the hepatized portions some of the air-spaces contained granular 
matter, and fatty and degenerated epithelium and pus-the ordinary 
condition of a resolving pneumonia. But many other of the air-spaces 
contained irregular masses of tissue which was not degenerated, but 
was apparently organized. In each of these vesicles was an irregular 
mass partly filling its cavity and touching its wall on several points, 
often anastomosing with similar masses in other vesicles. These masses 
did not look like outgrowths from the walls of the vesicles, nor were 
the walls altered. Each little mass was composed of a finely fibrillated 
basement substance in which were embedded round, oval, polygonal, and 
fusiform cells. Swollen epithelial cells adhered to the wall of the vesi- 
cle, and were found free in its cavity (Plate XXXVI.). 
Case II.-A male, thirty-nine years of age, came to the outdoor de- 
partment of the Roosevelt Hospital on December 24, 1883, complaining 
that he had been vomiting for several days. On December 25th he was 
attacked with pain in the side, chill, dyspnoea, and fever; crepitant rales 
were heard over the right middle lobe. On December 29th the man was 
admitted to the hospital in an intoxicated condition. His face was flushed, 
his tongue coated and dry, and he was mildly delirious. There was con- 
solidation of the middle lobe of the right lung. December 30th delir- 
ium alternating with stupor continued, and it was evident that the lower 
lobe of the right lung had also become consolidated. On January 1st 
the lower lobe of the left lung also was consolidated. The patient 
passed into the typhoid state, and died on January 8th. During the 
course of the disease the physical signs of lobar 'pneumonia were well 
marked. The cough was infrequent and the expectoration scanty. The 
temperature was never very high, nor were the breathing or pulse very LOBAR PNEUMONIA. 
33 
rapid until the close of the~ disease. The most marked symptoms were 
the delirium, stupor, prostration, and typhoid state. 
At the autopsy the only morbid changes found were in the pia mater, 
the spleen, and the lungs. 
The pia mater was infiltrated with serum and with new connective- 
tissue cells. The spleen was large and soft. 
The lower lobe of the left lung was small, dense, partly aerated, of 
red color, mottled with small gray patches. The bronchi were con- 
gested, and the pulmonary pleura was coated with fibrine. The middle 
and lower lobes of the right lung were consolidated, but diminished in 
size. The blood-vessels of this lung were injected with blue gelatine. 
The consolidation of the lungs was effected, as in ordinary lobar pneu- 
monia, by plugs of inflammatory matter within the air-spaces. In ordi- 
nary lobar pneumonia these plugs are so large as to distend the air-spaces, 
and in this way the hepatized portions of lung are regularly increased 
in size. 
In this case, however, the plugs were small and did not distend the 
air-spaces. This small size of the plugs made it easy to see in sections 
the inflammatory material in a number of air-spaces joined together by 
prolongations. 
Some of the air-vesicles contained only pus and fibrine. In others 
the fibrine ran more in straight lines and was stiffer, so that the plugs 
were of irregularly triangular shape, only touching the walls of the vesi- 
cles at their angles (Plate XXXVII.). 
Many of the plugs were composed of a homogeneous or finely fibril- 
lated basement^ substance, in which were embedded fusiform, polygonal, 
round, and oval cells. In some of these plugs were large blood-vessels 
with thin walls into which the blue injection had run. This new tissue 
was not an outgrowth from the walls of the vesicles, but was formed 
within their cavities. The walls of these vesicles were thickened and in- 
filtrated with round cells (Plate XXXVIII.). 
In still other vesicles both the organized tissue, and pus, and fibrine 
were found. 
Case III.-A female, forty-five years 'of age, was admitted to Belle- 
vue Hospital on November 27, 1883. 34 
LOBAR PNEUMONIA. 
On November 17th she was exposed to the weather for a long time. 
Soon^ after she came home she was attacked with a chill, fever, head- 
ache, and prostration. The next day she had cough, with brownish sputa, 
dyspnoea, and was obliged to go to bed, where she has remained ever 
since. When the patient was first seen, on November 27th, she looked 
seriously ill. Her face was flushed, she was dull and apathetic, her 
tongue was coated and dry, there was pain over the right lung, dysp- 
noea, cough, and profuse muco-purulent expectoration. There was con- 
solidation of the upper lobe of the right lung. She passed into the 
typhoid state, and died on December 5th. 
At the autopsy no lesions were found except in the upper lobe of 
the right lung. This lobe was consolidated, but not enlarged. There 
was a little fibrine on the pulmonary pleura. The cut surface of the 
lung had the appearance of a smooth, red hepatization, mottled with 
minute white dots. 
Minute examination showed a diffuse interstitial growth of connec- 
tive tissue around the blood-vessels, in the septa, and in the walls of the 
air-spaces. These walls are symmetrically thickened and infiltrated 
with round cells. The cavities of the vesicles are only partly filled 
with the inflammatory products, which can be seen extending from one 
vesicle into another. Some of the vesicles contain nothing but epithelial 
cells. Others contain a finely fibrillated basement substance, in which 
are imbedded epithelial cells, small round cells, and large shining bodies, 
which look like altered epithelial cells (Plate XXXIX.). Altogether 
the appearances were essentially the same as in the lungs of Case II. 
Case IV.-A male, sixty-three years of age, was admitted to the 
Roosevelt Hospital on April 17, 1885. He said that he had been sick 
all winter with dyspnoea, attacks of asthma, cough, and muco-purulent 
expectoration. He is now anaemic and emaciated, with some oedema of 
the legs. There are sibilant and sonorous rales over both lungs, except 
over the lower part of both lungs behind, where there is absence of 
breathing and flatness on percussion. The urine contains albumen and 
casts. Pulse 72, temperature 98.6° F. On April 20th the man seemed 
worse, the dyspnoea was greater, the sputa were reddish-brown. On 
April 21st the temperature rose to 100.4° F., and there were dulness LOBAR PNEUMONIA. 
35 
and bronchial breathing over the upper lobe of the left lung. The 
temperature continued at from 99°-101.4° until April 25th, when it fell 
to the normal. The man continued to become more feeble, the physical 
signs of consolidation of the left upper lobe continued, and he died on 
May 18th. After death the right lung presented the lesions of chronic 
bronchitis, with some old fibrous tissue at the apex. The upper lobe of 
the left lung was small, in the condition of gray hepatization, with a 
good deal of black pigment. At the apex there were a few old miliary 
tubercles and some diffuse fibrous tissue. In the hepatized portion of 
the lung the lesions were the same as in Cases II. and III. The walls 
of the air-spaces were thickened, and their cavities were incompletely 
filled. The filling was effected partly by epithelium, pus, and fibrine, 
partly by organized tissue composed of a basement substance and cells, 
and in some places of new blood-vessels. 
It seems, then, that there is a form of lobar pneumonia characterized 
by the production of new connective tissue within the cavities of the 
air-spaces a few days after the invasion of the inflammatory process. PLATE XIII. 
CHRONIC PHTHISIS. 
X 800 PLATE XIV- 
CHRONIC PHTHISIS. 
X 800 PLATE XV. 
CHRONIC PHTHISIS. 
X 750 PLATE XVI. 
CHRONIC PHTHISIS, 
x 75 0. PLATE XVII. 
CHRONIC PHTHISIS. 
X 750 PLATE XVIII. 
CHRONIC PHTHISIS. 
X 800 PLATE XIX 
CHRONIC PHTHISIS. 
X 750 E.uATE XX. 
CHROMIC PHTHISIS. 
X850 PLATE XXI. 
CHRONIC PHTHISIS. 
X45O Artotype. 
E. Bierstadt, N. Y. 
Plate XXII. x20 
VERTICAL SECTION OF THE WALL OF THE TRACHEA. PLATE XXIII. 
CATARRHAL BRONCHITIS. 
X 90 PLATE XXIV 
CATARRHAL BRONCHITIS 
X 800 Artotype. 
E. Bierstadt, N. Y. 
Plate XXV. x10 
CATARRHAL BRONCHITIS. Artotype, 
E. Bieretadt, N. V. 
Plate XXVI. x27 
AN ULCER OF THE LARYNX. PLATE XXVII. 
AN ULCER OF THE LARYNX. 
X 800 Artotype, 
E. Bierstadt, N. Y- 
Plate XXVIII x10 
A BRONCHT-ECTASIA. PLATE XXIX. 
THE WALL OF A BRONCHI ECTASIA. 
X 800 Artotype, 
E. Bierstadt, N. Y. 
Plate XXX x27 
TUBERCULAR LARYNGITIS. PLATE XXXI. 
TUBERCULAR LARYNGITIS. 
X 2 5 0 Artotype, 
E. Bierstadt, N. Y. 
Plate XXXII. x10 
BRONCHI-ECTASIAE. PLATE XXXIII. 
PART OF A MILIARY TUBERCLE. BACILLI. 
X 800 PLATE XXXIV. 
A MILIARY TUBERCLE 
x 2 0 0 PLATE XXXV. 
a miliary tubercle around two bronchioles. 
X 150 PLATE XXXVI. 
LOBAR PNEUMONIA. 
x 750. PLATE XXXVII. 
LOBAR PNEUMONIA, 
x 35 0. PT,ATT. XXXVIII. 
lobar pneumonia. 
X 300 ELAIE XXXIX. 
LOBAR PNEUMONIA. 
X 350 BRIGHT'S DISEASE OF THE KIDNEYS. 
The recognition of the group of diseases, which still bears the name 
of its discoverer, dates back only to the year 1827, when Richard 
Bright published his first paper on the subject. This first paper was 
followed by others, and in 1829 Christison published, in the Edinburgh 
Medical and Surgical Review, his account of the same disease. Both 
these authors regarded the disease as a morbid change in the kidneys, 
which was the cause of the accompanying symptoms. 
Very soon, however (in 1831), we find Graves, Gubler, and Jaccoud 
looking at the disease from exactly the opposite point of view, and 
teaching that the kidney lesions were not the cause of the disease, but 
the result of it, and that the cause was to be looked for in some morbid 
change of the blood. 
In 1842 Rokitansky recognized the waxy, or amyloid kidneys as 
presenting different lesions from those found in other examples of 
Bright's Disease. 
Frerichs, in 1851, published his monograph on Bright's Disease, 
and gave a systematic account of the disease which has had a decided 
effect on the minds of most subsequent observers. While he describes 
with care the different forms of the disease, the different circumstances 
under which it arises, and the variety of symptoms produced by it, he 
regards the kidneys as all constituting merely the stages of one morbid 
process. So far as the lesions are concerned, he teaches that there are 
three stages of Bright's Disease: 1. The stage of hyperaemia and of 
commencing exudation. 2. The stage of exudation and of commencino- 
transformation of the exudation. 3. The stage of atrophy. 
The first stage is characterized by increase of the size of the kidney, 38 
BRIGHT'S DISEASE OF THE KIDNEYS. 
especially of the cortex; by general congestion; by extravasations of 
blood in the Malpighian bodies, the tubes, and the kidney tissue; and 
by filling of tubes with coagulated fibrine. The epithelium of the 
tubes is unaltered. 
In the second stage, the congestion diminishes while the exudation 
increases. The exudation is found in the tubules and in the interstitial 
tissue. The epithelium of the tubes and the exuded fibrine within 
them breaks down into fatty granules. The exudation between the 
tubes is sometimes organized into connective tissue. The cortex be- 
comes of a white-yellowish color, and remains thickened. The surface 
of the kidney is smooth or slightly granular. The pyramids are of a 
reddish color. Some of the Malpighian bodies are normal, others are 
enlarged, and filled with exudation. In the cortex the epithelium of the 
tubes is swollen and granular, and may break down altogether, or it 
simply shrivels and atrophies. The tubes are filled with degenerated 
epithelium, granular matter, and fat-globules, or with homogeneous exu- 
dation. The tubes are dilated. The dilatation of the tubes is the prin- 
cipal or only cause of the increased size of the kidney. 
In the third stage, the kidneys are smaller, or of normal size, or even 
larger than normal. The capsule is adherent. The surface of the 
kidney is irregular and granular, its color a dusky yellow. Its con- 
sistence is hard. The cortex is thinned. The pyramids are smaller. 
The fat about the pelvis is increased in amount. The tubes are dilated 
and filled as in the second stage, or are collapsed and folded together. 
Most of the Malpighian bodies are shrivelled and fatty. If the exuda- 
tion between the tubes has become organized, we find masses of con- 
nective-tissue cells and fibres. 
This description of the lesions, taken as it was from nature, is as 
true now as when it was written. But yet our present pathological 
knowledge makes us interpret these lesions somewhat differently. 
In 1852 Dr. George Johnson published a work on kidney diseases 
which, like that of Frerichs, has had a durable effect on medical opin- 
ions. He distinguishes five forms of Bright's Disease. 
1. Acute Desquamative Nephritis.-The form of disease occurring 
after scarlet fever, exposures to cold, etc. This corresponds to Frerichs's BRIGHT'S DISEASE OF THE KIDNEYS. 
39 
first stage. Johnson,'however, lays most stress upon the desquamation 
of the epithelium, and but little on the exudation in the tubes. Exuda- 
tion between the tubes he does not mention. 
2. Chronic Desquamative Nephritis.-This corresponds to the sec- 
ond and third stages of Frerichs. Johnson describes the degeneration 
of the epithelium, the denudation of the tubes of their epithelium, their 
dilatation and collapse, and the presence of coagulated material within 
them. The Malpighian tufts are thickened or atrophied. The arteries 
are thickened. He regards the production of new fibrous tissue as an 
accidental and unessential phenomenon. 
3. Waxy Degeneration of the Kidney.-Under this name Johnson 
describes kidneys which are of large size, their cortex thick and white, 
their tubes filled with waxy material. This waxy material he supposes 
to be produced by a degeneration of the epithelium. The large hyaline 
casts found in the urine he calls waxy, and seems to consider them 
diagnostic of this form of kidney disease. 
4. Acute Non-desquamative Disease of the Kidney.-This is charac- 
terized during life by scanty or suppressed urine, but containing no albu- 
men, and no casts, or only a few waxy ones. The kidneys are of normal 
size; the epithelium of the tubes is somewhat altered. 
5. Chronic Non-desquamative Disease.-The kidneys are usually 
large, very rarely atrophied. The cortex is thick and white. The con- 
voluted tubes are more opaque than usual. The Malpighian bodies and 
arteries are thickened. 
6. The Granular Fat Kidney .-This form may be a consequence of 
the non-desquamative disease, of acute desquamative inflammation, and 
rarely of chronic desquamative disease. The kidneys are large, the 
cortex white, mottled with yellowish granulations. These yellow gran- 
ulations are formed of tubes, containing oil-globules. The vessels and 
Malpighian bodies are thickened. Sometimes the same yellow, fatty 
granulations are found in atrophied kidneys. 
7. The Mottled Fat Kidney.-KA the tubes of the cortex contain oil- 
globules, and there are red spots of congestion or extravasation. 
To Traube (1856) belongs the merit of recognizing chronic congestion 
of the kidney as a lesion with an entirely different cause from that of 40 
BRIGHT'S DISEASE OF THE KIDNEYS. 
other forms of Bright's Disease ; and also of calling attention to the 
fact that blood-contamination cannot be the only cause of the cerebral 
symptoms. 
Grainger Stewart distinguishes: 
1. The Inflammatory Form.-This has three stages : (1.) That of 
inflammation; (2.) That of fatty transformation; (3.) That of atrophy. 
These correspond very closely with the three stages described by Frerichs. 
2. The Waxy Form..-This also has three stages: (1.) That of 
simple degeneration of the vessels; (2.) That in which a secondary 
alteration of the tubes is superadded; and (3.) That of atrophy. 
In the first stage, the kidney is of normal size, the tubes are un- 
altered ; only the Malpighian bodies and small arteries have undergone 
waxy degeneration. 
In the second stage, the kidney is enlarged, the cortex thick and 
white, with Malpighian bodies and small vessels waxy; the tubes con- 
tain hyaline casts; their epithelium is swollen ; their basement mem- 
brane may be waxy. 
In the third stage, the kidney is small. The surface is rough, gran- 
ular, and pale. The tubular structures are swollen. The tufts and ves- 
sels are waxy. A few tubes are distended, most are collapsed, and are 
represented only by fibrous tissues. 
3. The Cirrhotic or Contracting Form.-This consists of an 
hypertrophy of the connective tissue of the organ, and a consequent 
atrophy of all the other structures. 
There is at first little diminution of the size of the organ, but the 
capsule is thickened and adherent, and the surface is rough and granu- 
lar. The color is pale and reddish. The arteries are prominent, their 
walls thickened, and their cavities often dilated. On the surface, and 
in the substance, cysts are often seen. Some are produced by dilatation 
of the Malpighian capsules, some by dilatation of the tubes, some from 
morbid growth of epithelial elements. The tubes are compressed and 
atrophied by the new fibrous tissue. They contain little opaque ma- 
terial, but often hyaline matter. Sometimes urate of soda is found in 
the stroma and tubes of the pyramids. The disease is a non-inflamma- 
tory increase of connective tissue. BRIGHT'S DISEASE OF THE KIDNEYS. 
41 
Both the waxy and contracting forms may be secondarily affected 
with the inflammatory disease. 
4. Simple Fatty Degeneration.-The kidneys are of about the nor- 
mal size. The surface is smooth, the capsule not adherent. Their text- 
ure is soft, the cortex is pale and mottled, with sebaceous-looking de- 
posits. The epithelium of the tubes is fatty. 
Dickinson describes tubal nephritis, granular degeneration, and de- 
purative infiltration : 
1. Acute Tubal Nephritis.-This, the nephritis of scarlet fever and 
of exposure to cold, is described in very much the same terms as the 
acute desquamative nephritis of Johnson. 
2. Chronic Tubal Nephritis.-The kidney is large, the cortex of an 
opaque white or buff-color, the pyramids pink. The surface is smooth, 
the capsule not adherent. The convoluted tubes are distended with 
granular and'fatty epithelium and with fibrinous exudation. The 
straight tubes are packed with the products of epithelial growth, while 
others contain transparent fibrine. The tubes are not changed, save as 
regards their contents. The Malpighian bodies are normal or some- 
what dilated. There is no increase of inter-tubular tissue. These kid- 
neys remain large and smooth to the last, unless complicated with the 
depurative change. 
Sometimes the cortex is sprinkled with white, sharply-defined 
specks, like bits of bran. This change is characteristic of a great 
amount of fatty change in the accumulated epithelium. 
3. Granular Degeneration.-The kidneys may be of normal, or even 
increased size, but are usually small. The capsule is adherent. The 
surface is irregular and covered with little rounded nodules. The cor- 
tex is thin. Cysts are often found in the cortex and cones. There is 
an increase of fibrous tissue around the Malpighian bodies and vessels, 
and beneath the capsule and deeper in the cortex. The cortical tubes 
are atrophied or dilated, but many tubes may remain unchanged. The 
tubes may be filled with epithelium, or with transparent, fibrinous ma- 
terial. In the majority of cases the epithelium is exactly such as is 
found in normal kidneys. "When changed, it is by an alteration m its 
regularity of form, becoming somewhat angular, as if cramped in grow- 42 
BRIGHT'S DISEASE OF THE KIDNEYS. 
ing space. The circulation through the blood-vessels is much ob- 
structed. The formation of cysts is due to dilatation of the tubes, or of 
the Malpighian capsules. 
4. Depurative Infiltration.-The kidney is at first of normal size, 
pale, and its surface smooth. The only change is in the Malpighian 
tufts, which react with iodine. As the disease goes on, the kidney be- 
comes larger and its capsule adherent. The cortex is of a pale, opaque 
fawn-color, or has a pinkish or gray translucency. Afterward the kid- 
ney atrophies and its surface becomes nodulated. There may be small 
cysts. In cases of long standing, almost the entire organ gives the 
characteristic reaction with iodine. The first change is the infiltration 
of the Malpighian bodies and vessels. Afterward new fibrous tissue is 
formed between the tubes, the epithelium degenerates; the tubes are 
dilated and contain fibrinous casts. 
It will be seen that the name of " depurative infiltration " is given 
to the same form of kidney disease which is called by others waxy or 
amyloid. 
Klebs describes : 
1. Diffuse Granular Degeneration of the Epithelium.-This condi- 
tion is found by itself, and in connection with lesions, in the interstitial 
tissue. By itself, it occurs with pyaemia, phthisis, rheumatism, typhoid 
and typhus fevers, the malarial fevers, the acute exanthemata, extensive 
burns, poisoning with phosphorus, and the mineral acids. During life 
the urine may contain granular casts and albumen. The kidney is some- 
what enlarged, the cortex grayish yellow, the pyramids bluish red. 
There may be little extravasations of blood in the convoluted tubes. 
The epithelium of the tubes is granular and may distend them. The 
tubes may contain casts. These changes are most frequent in the con- 
voluted tubes, but are sometimes confined to the straight tubes of the 
pyramids. The entire process is a degenerative and not an inflammatory 
one. 
2. Cyanotic Induration of the Kidneys.--This condition is produced 
by any long-continued obstruction to the escape of venous blood from the 
kidneys, most frequently by heart disease. The kidneys are increased 
in size, the surface smooth, the capsule not adherent. The organ is hard, BRIGHT'S DISEASE OE THE KIDNEYS. 
43 
the cortex and pyramids congested, and of a dark-red color. The epi- 
thelium of the tubes is not altered. The interstitial tissue is harder, but 
not increased in amount. The continued congestion may, after a time, 
produce further changes. The epithelium of the convoluted tubes may 
undergo granular degeneration, and the cortex becomes paler. Or there 
may be an increase of interstitial tissue, and the surface becomes nodular. 
3. Interstitial Nephritis.-This has two stages: (1.) That of cell- 
infiltration; (2.) That of atrophy. 
(a.) The Stage of Cellular Infiltration of the Interstitial Connective 
Tissue. The kidney is increased in size. The surface is smooth, the 
capsule not adherent. The cortex is of a whitish or yellowish color, the 
pyramids red. In the cortex the tissue between the tubes is everywhere 
increased from two to four fold. This increase is due to the presence 
q-£ lymphatic elements and of cleai serum, bheie is at first an exuda- 
tion of lymphatic fluid, which dilates the lymphatic vessels of the inter- 
stitial tissue, and is accompanied by an emigration of white blood- 
globules, which finally fill all the spaces in the interstitial tissue. The 
epithelium of the convoluted tubes undergoes granular degeneration in 
consequence of its disturbed nutrition. The increased pressure of blood 
causes an exudation of the elements of the blood from the Malpighian 
tufts, namely, fibrinogenic material which coagulates in the tubes, albu- 
men, and red blood-globules. The lymphatic cells perforate the base- 
ment membrane of the tubes, and become adherent to the fibrinous 
casts. 
(6.) The Stage of Atrophy.-The preceding stage may terminate in 
resolution and recovery. If it does not, it is succeeded either by a 
hyperplasia of connective tissue or by granular atrophy. 
If there is a hyperplasia of connective tissue, the kidneys are of nor- 
mal size, or slightly atrophied. The capsule is somewhat adherent. 
The cortex is whitish, yellowish, or mottled. The pyramids are con- 
gested. There is a uniform increase of connective tissue between the 
tubes. The tubes are unaltered or somewhat narrowed. 
Granular atrophy is more common. The kidney is atrophied. The 
capsule is very adherent. The surface is uneven and nodular. The 
change of the lymphatic cells into connective tissue is accompanied by 44 
BRIGHT'S DISEASE OF THE KIDNEYS. 
fatty degeneration of the cells. In the atrophied spots the tubes and 
glomeruli become impervious. The tubes contain hyaline casts. The 
basement membrane of the atrophied tubes becomes thick and fibrous. 
The glomeruli are atrophied, their capsules thickened, their vessels oblit- 
erated. The larger arteries are thickened. 
Glomerulo-nephritis.-Klebs gives this name to a form of disease 
which he has observed in scarlatina cases. The kidneys are of medium 
size, the capsule not adherent, the surface smooth, the parenchyma con- 
gested. There are no changes except in the glomeruli. These appear 
as opaque, white points. On minute examination, it is found that there 
are large numbers of small, rounded cells about the loops of the Mal- 
pighian tuft, while the epithelium of the capsule is unaltered. 
Amyloid degeneration is described in much the same way as by other 
authors. 
Rindfleisch describes : 
1. Acute Parenchymatous Nephritis.-In the milder form the kid- 
ney is of normal size, the surface smooth, the cortex of a yellowish-gray 
color. There is a moderate degree of cloudy swelling of the epithelium 
of the convoluted tubes. 
In the severer form the kidney has the same appearance, but is in- 
creased in size and the cortex thickened. 
Both these forms occur with the acute exanthemata, typhus, pyaemia, 
etc. 
2. Diffuse Interstitial Nephritis.-This corresponds very closely with 
the description given by Klebs. 
He states that the disease may begin as a parenchymatous nephritis, 
and afterward become interstitial, but that the two forms also occur in- 
dependently of each other. 
Amyloid degeneration is usually accompanied by interstitial neph- 
ritis. The amyloid degeneration is the primary change, and the nephritis 
follows it as a secondary lesion. 
Rosenstein describes : 
1. Chronic Congestion of the Kidney.-This condition is described 
in much the same way as by the preceding authors. 
2. Catarrhal Nephritis.-The kidney is of normal size, or slightly BRIGHT'S DISEASE OF THE KIDNEYS. 
45 
enlarged; in severe cases congested and mottled with small ecchymoses. 
The process begins at the apices of the pyramids, which are at first con- 
gested, afterward pale. After a time we find the pyramids divided into 
red and white striae, running from the apex to the base of the pyramids. 
The red striae are the portions more recently congested ; the white are 
the tubes distended by an increase of epithelium. 
The urine contains a little albumen, hyaline, granular, and epithelial 
casts, and blood-globules. 
The symptoms during life are not marked. The lesion is seldom 
primary. It may follow catarrhal inflammation of the urethra, bladder, 
or ureters; the use of cantharides, copaiba, and cubebs ; typhoid and 
typhus fever, cholera, etc. 
3. Diffuse Nephritis, Parenchymatous Nephritis, Bright's Disease, 
Granular Degeneration of-the kidney.-This form has three stages. 
The first stage is that of hyperaemia. The kidney is of normal size, 
or enlarged, congested, and red ; there is blood in the tubes, and swelling 
of the epithelium of the convoluted tubes. 
The second stage is that of exudation. The kidney is enlarged, 
the cortex pale, the pyramids red. The epithelium of the convo- 
luted tubes is swollen and granular. The tubes are dilated and 
contain casts. There is usually an increase of cells in the interstitial 
tissue. 
The third stage is that of atrophy. The kidney becomes smaller, its 
surface nodular. The atrophy may take place without any change in 
the interstitial tissue, simply as a result of the destruction of the epithe- 
lium. Usually, however, the retraction of the new interstitial tissue as- 
sists in producing the atrophy. 
The epithelium is granular or fatty. The Malpighian bodies are 
atrophied, their capsules thickened and surrounded with new connective 
tissue. The basement membranes of the tubes are thickened, and are 
accompanied by bands of connective tissue. The intertubular capillaries 
are partly dilated, partly small and fatty. 
The atrophy consists, therefore, in a suppression of the function of a 
number of the tubes, with obliteration of some of the blood-vessels and 
increase of the interstitial tissue. 46 
BRIGHTS DISEASE OF THE KIDNEYS. 
Both processes, that in the ephithelium and that in the connective 
tissue, can occur separately, but are usually combined. 
4. Amyloid Degeneration.-He describes this form in much the 
same way as other authors. He regards the degeneration of the vessels 
only as a complication of the parenchymatous and interstitial change. 
5. The Fatty Kidney.-There is an infiltration of the epithelium 
with fat, or a fatty degeneration. The condition is described in the 
same way as the diffuse granular degeneration of Klebs 
Weigert divides Bright's Disease into parenchymatous degeneration 
and true nephritis. He does not distinguish between interstitial and 
parenchymatous forms of nephritis, but believes that in all cases the 
disease begins with degeneration of the epithelium, which is followed 
by inflammatory interstitial processes. 
Gull and Sutton have shown very clearly the frequency with which 
changes in the arteries and capillaries-arterio-capillary fibrous-are 
associated with the atrophic form of Bright's Disease; and that these 
changes in the arteries and capillaries may also exist and give symp- 
toms without any lesions of the kidneys. From these facts they have 
drawn the conclusion that this form of Bright's Disease is not, properly 
speaking, a disease of the kidneys, but rather one of the arteries and 
capillaries. 
Bartels uses the name of " The Diffuse Diseases of the Kidneys," 
with the subdivisions of Hyperaemia, Ischaemia, Acute Parenchymatous 
Nephritis, Chronic Parenchymatous Nephritis, Kenai Cirrhosis, and 
Amyloid Degeneration. 
Active hyperaemia is, he says, a condition which arises solely as the 
result of some toxic influence, most frequently from the use of canthar- 
ides. Apparently he has little or no personal experience of the ana- 
tomical changes found in the kidneys. 
Passive hyperaemia is the same condition as that also called 
" chronic congestion of the kidney," and cyanotic induration of the 
kidney. Its most important form is that due to valvular lesions of the 
heart and to certain affections of the lungs. He makes no new state- 
ments concerning the pathological changes. 
Ischaemia is the condition of more or less complete stoppage of the BRIGHT'S DISEASE OF THE KIDNEYS. 
47 
arterial blood-supply to the kidneys, occurring independently of conges- 
tion of the nervous system. It occurs only in the asphyxia stage of 
cholera. 
Acute Parenchymatous Nephritis.-Under this name Bartels in- 
cludes all the cases of acute Bright's Disease. He says that the only 
essential and constant microscopical appearances are the changes in the 
epithelium of the tubes. The epithelial cells are swollen and cloudy, 
they are infiltrated with granules of fat, and are broken down. To 
these changes in the epithelium are frequently added a swelling and in- 
filtration of the stroma, casts in the tubes, and extravasations of blood. 
Chronic P arenchymatous Nephritis.-This may follow acute paren- 
chymatous inflammation or may begin as a chronic process. The kid- 
neys are large, white, and smooth. The tubes are dilated; the epithe- 
lium is only partly preserved, and the cells which remain are large, 
granular, and fatty. In many places the epithelium is completely gone 
and in its stead the tubes are entirely filled with masses of detritus 
mixed with oil-globules; casts are found in many of the tubes. The 
stroma is thickened by fluid exudation, by an emigration of white 
blood-cells, and by a growth of new connective tissue. The small ar- 
teries and Malpighian tufts are often the seat of waxy degeneration. 
Penal Cirrhosis.-The kidney is very much diminished in size, es- 
pecially the cortex. This diminution in size is due to the wasting of 
the glandular tissue, while at the same time there is an extensive 
growth of new fibrous tissue. The change in the kidney is due to a 
primary growth of the intertubular connective tissue, and this leads to 
the dwindling of the substance of the gland, a wasting preceded by no 
inflammatory swelling of the organ. 
To Cohnheim belongs the merit of drawing attention to the importance 
of the glomeruli in acute nephritis, and to the changes which are found 
in them. He also points out clearly that well-marked symptoms of acute 
nephritis may exist during life, although no structural changes are found 
in the kidneys after death. 
Langhans, Nauwerck, and Friedlander have developed still further 
the doctrine of glomerulo nephritis, and have described in detail the 
lesions found in the glomeruli. 48 
BRIGHT'S DISEASE OF THE KIDNEYS. 
Ziegler describes 
1. Glomerulo-nephritis^ occurring either by itself or combined with 
changes in the epithelium of the tubes, or wfith exudation of inflamma- 
tory products into the stroma. 
2. Chronic Parenchymatous Nephritis.-The common feature of this 
form of nephritis is that from the blood-vessels there is a continued 
inflammatory exudation, and that changes go on in the epithelium of the 
kidney. 
As subdivisions of parenchymatous nephritis he distinguishes: 
The inflammatory, fatty kidney; 
Chronic hemorrhagic nephritis; 
Chronic glomerulo-nephritis. 
3. Chronic Indurative Nephritis.-The inflammation leads to a new 
growth of connective tissue in the stroma, and an atrophy of the tubes 
and the glomeruli. 
4. The Arteriosclerotic Contracted Kidney.-In this the changes be- 
gin in the walls of the arteries; they are thickened, their lumen narrowed 
or obliterated. As a result, smaller or larger numbers of glomeruli become 
atrophied, with the kidney tissue belonging to them. The stroma is not 
much thickened. 
As wTe look back over the history of the disease, it is easy to 
recognize the points of difference and the progress which has been 
made. 
From the very first we find authors looking at the disease from two 
points of view: that of the symptoms and that of the lesions. So that, 
while some regard Bright's Disease as a nephritis with its attendant 
symptoms, others regard it as a disease of the blood, or of the arteries 
and capillaries, with which a nephritis may or may not be associated. 
At the time when Frerichs wrote, it was customary to regard a great 
many morbid conditions of an inflammatory character, and to think that 
every inflammation went regularly through three stages. So we find 
Frerichs arranging all the lesions of Bright's Disease as belonging to 
the stages of congestion, exudation, and contraction of a nephritis, and 
teaching that all the forms of acute and chronic Bright's Disease were 
different stages of one and the same morbid process. BRIGHT'S DISEASE OF THE KIDNEYS. 
49 
Then we find in England, first, Johnson, and then Dickinson, referring 
most of the kidney lesions to changes in the epithelium of the tubes. 
Here, again, it soon became evident, that although changes in the 
epithelium exist and are of importance yet Johnson and his school had 
taken too one-sided a view of the subject. 
That in some cases of Bright's Disease there is waxy degeneration 
of the walls of the arteries and Malpighian tufts was early recognized 
by Rokitansky. As these kidneys have been more studied, it has been 
found that there may be : 
1. Waxy degeneration of the arteries and glomeruli, without any 
change in the other parts of the kidney or any disturbance of its func- 
tions. 
2. Waxy degeneration of the arteries and tufts, followed by chronic 
changes in the rest of the kidneys. 
3. Waxy degeneration of the arteries and tufts, forming an unimpor- 
tant part of a chronic nephritis. 
The next step forward was the recognition by Traube of the condition 
of chronic congestion of the kidney, its dependence on heart disease, and 
its termination in changes in the structure of the kidney. 
Then we find an attempt by Grainger Stewart to go back to Frerichs's 
classification of an inflammation in three stages, but separating the waxy 
and the cirrhotic kidneys. 
Among English writers we find a disposition to class the kidneys 
according to their gross appearance, and to speak of the large white kid- 
ney and the contracted kidney, and to regard the cirrhotic kidney as 
not inflammatory. In England, also, we find especial attention drawn 
to the condition of the arteries and capillaries in the kidneys and in 
the rest of the body as a cause of the kidney lesions and of the 
symptoms. 
The next step forward was the recognition of the changes in the 
glomeruli, first by Klebs, then by Cohnheim, Friedlander, and others. 
At the same time there has been an attempt, especially in Germany, 
to class together the changes in the epithelium, the exudation of inflam- 
matory products, and the formation of new connective tissue under the 
one head of parenchymatous inflammation, teaching that the morbid 50 
BRIGHT'S DISEASE OF THE KIDNEYS. 
process originates in the epithelium, and that the other changes are sec- 
ondary to this. 
Further modifications have been introduced into this doctrine of 
a parenchymatous nephritis, by the contention that changes in the 
epithelium alone are not of inflammatory, but of degenerative nat- 
ure. 
Incidentally Cohnheim brings out well the important point that 
with well-marked changes in the urine and constitutional symptoms we 
may find no structural changes in the kidneys; in other words, that the 
morbid changes in these kidneys must have been confined to the blood- 
vessels. 
Although so much has been done in the study of the lesions of 
Bright's Disease, it must be confessed that the ideas of the profession in 
general concerning it are still somewhat crude. 
As regards Acute Bright's Disease, we often find the belief: 
That the kidneys are large, and either white or congested ; that the 
chief change is in the epithelium of the tubes, which is swollen and de- 
tached and blocks up the tubes; that there is some change in the glom- 
eruli which allows albumen to pass through the walls of the capillaries ; 
that the patients pass too little urine; that in consequence of this dimin- 
ished production of urine there may be developed dropsy or cerebral 
symptoms ; that the chief object of treatment is to make them pass more 
urine, or, failing this, to purge or sweat them. 
As regards Chronic Bright's Disease, it is generally believed that there 
are two principal forms : one, in which the kidney is more or less large 
and white, while during life there is dropsy, and much albumen in the 
urine ; and one in which the kidney is more or less contracted and red 
and there is little or no albumen in the urine, or dropsy. 
It has appeared to me that the principal reason for the general ig- 
norance concerning Bright's Disease is, that although good descriptions 
exist of nearly all the morbid changes in the kidney, yet they are in the 
form of isolated facts and separate names, with but little to bring them 
together or unite them in any orderly classification. 
I believe that such a classification can be made, and that the principle 
on which to make it is to think of the kidney lesions as examples of the BRIGHT'S DISEASE OF THE KIDNEYS. 
51 
same morbid changes that are common to the whole body and not of 
conditions peculiar to the kidney. 
I make the attempt, therefore, to describe and classify in this way 
first, the lesions of Acute Bright's Disease, and, secondly, those of Chronic 
Bright's Disease. 
ACUTE BRIGHT'S DISEASE. 
There is a general agreement, at the present time, that there is cer- 
tainly one morbid condition to which the name of inflammation can 
properly be applied. This condition is characterized by an accumu- 
lation of blood in the vessels and an escape of the plasma, white cells 
and red cells, from the vessels into the surrounding tissues. The inflam- 
mation is, therefore, called an exudative inflammation. 
It may be that the congestion and escape of the elements of the blood 
from the vessels will be the only morbid change ; or there may be added 
degeneration or death of the surrounding tissues, or a growth of new 
tissue. It is evident, in such an inflammation, that it is the blood- 
vessels which are principally concerned. How and why it is that 
their walls are so changed that they allow the elements of the blood 
to pass through them we do not know, but the ordinary production 
of serum, fibrine, and pus in this way is a matter of every-day obser- 
vation. 
The introduction of certain poisons into the body is regularly fol- 
lowed by changes in the cells of the viscera. The poisons which exert 
this effect are ordinarily mineral poisons, such as arsenic, mercury, and 
phosphorus; or the poisons of infectious diseases, such as diphtheria, 
typhoid fever, etc. According to the quantity and virulence of the 
poison received into the body, there are more or less marked changes 
produced in the cells of the viscera. 
Small doses of such poisons, acting only for a moderate length of 
time, produce a simple swelling of these cells. The cells are swollen, 
more opaque, more coarsely granular. They are not dead, nor broken 
down, nor do they contain any new substances ; the change in their ap- 
pearance is due to the swelling of the net-work which forms a part of 
every cell. Under these circumstances there are either no changes at 52 
BRIGHT'S DISEASE OF THE KIDNEYS. 
all in the blood-vessels of the viscera, or a slight congestion, with, per- 
haps, a little exudation of serum. 
Larger doses of such poisons, or more virulent poisons, or a longer 
duration of the action of a poison, are attended by the deposition in the 
cell-bodies of granules of albuminous matter and globules of fat. At 
the same time there is a change in the nutrition of the cells, and they 
are often broken and disintegrated. Under these conditions there 
may be a considerable congestion of the vessels and an exudation of 
serum. 
Very large doses of such poisons cause the death of the cells of the 
viscera, a death which may take the form of coagulation-necrosis or of 
disintegration and breaking down of the cell. With these changes 
there will often be an excessive congestion of the vessels and a large 
exudation of serum. 
In many examples of acute exudative inflammation the only re- 
sults of the inflammation are the inflammatory products and the death 
or degeneration of the tissues. Such an inflammation is regularly a 
transitory process; if it is not so severe as to cause death, it runs a 
limited course, the congestion subsides, the escape of the elements of the 
blood from the vessels ceases, and the tissues return to their natural con- 
dition. It may, however, happen that in an exudative inflammation there 
will be, from the very first, not only a production of serum, fibrine, and 
pus, but also a growth of new tissue. This new tissue, when once pro- 
duced, is permanent and remains during the rest of the patient's life. 
Not only is this the case, but such an inflammation, instead of running a 
short and limited course, is apt to continue for months and years, with 
the continued production of more and more new tissue. The new tissue 
seems to originate in the connective tissue of the inflamed part. It is 
composed at first largely of cells, with but little basement substance; 
later it resembles more closely ordinary connective tissue. Such an in- 
flammation may be called " productive," or " diffuse " inflammation. 
The three morbid conditions just described are the morbid conditions 
which affect the kidneys in acute Bright's disease. All the cases of 
this disease are examples of an acute exudative inflammation, or of an 
acute degeneration, or of an acute or sub-acute diffuse inflammation. BRIGHT'S DISEASE OF THE KIDNEYS. 
53 
We divide acute Bright's disease, therefore, into three classes and 
describe : 
Acute Exudative Nephritis; 
Acute Degeneration of the Kidney; 
Acute Diffuse Nephritis. 
I. Acute Exudative Nephritis.-This is an acute inflammation of the 
kidney characterized by congestion, an exudation of plasma, an emigra- 
tion of white blood-cells, and a cliapedesis of red blood-cells from the 
vessels ; to which may be added swelling or necrosis of the renal epithe- 
lium and changes in the glomeruli. 
Of such a nephritis we may distinguish three varieties : 
1. A mild form, which gives symptoms during life, but leaves no 
lesions in the kidney after death. 
2. A more severe form, in which we find inflammatory changes in 
the kidney after death. 
3. A form characterized by the excessive production of pus cells. 
Lesions.- In a nephritis of this type we should expect that the inflam- 
matory products, the serum, white and red blood-cells, and coagulable 
matter from the blood-plasma, would collect in the Malpighian bodies 
and tubes, or infiltrate the stroma between the tubes; and that of the 
inflammatory products in the tubes and Malpighian bodies, a part 
would be discharged with the urine and a part found in the kidney after 
death. We should also expect that the quantity of inflammatory products 
would be in proportion to the severity of the inflammation, and that an 
excessive number of pus-cells would belong to the especially severe 
forms of the disease. Still further, it is evident that, with the milder 
examples of nephritis, with but little exudation, no inflammatory prod- 
ucts might be found in the kidney after death, all having been dis- 
charged into the urine during life. 
As a matter of fact, the kidneys do present just such changes. In 
the mild cases we find no decided lesions in the kidney after death. 
In the more severe cases the kidneys are increased in size, their sur- 
faces are smooth, the cortical portion is thick and white, or white 
mottled with red, or the entire kidney is intensely congested. If the 
stroma is infiltrated with serum the kidney is succulent and wet; if the 54 
BRIGHT'S DISEASE OF THE KIDNEYS. 
number of pus cells is very great, there will be little whitish foci in the 
cortex. 
In such kidneys we find the evidences of exudative inflammation in 
the tubes, the stroma, and the glomeruli, all the changes being most 
marked in the cortical portion of the kidney. 
Plates XL. to L. are all taken from normal kidneys, the autopsies 
made within six hours after death. They represent the normal appear- 
ance of the tubes, glomeruli, and stroma, and are to be compared with 
the plates which show their appearance in disease. 
The epithelium of the convoluted tubes is often simply flattened. 
As this same appearance is also found in the chronic congestion of heart 
disease, it seems probable that this change of the shape of the cells is 
merely due to the inflammatory congestion. 
In other cases, not only is the epithelium flattened but there is also a 
real dilatation of the cortex-tubes. This dilatation does not involve 
groups of tubes, but all the cortex-tubes uniformly. 
In other cases, the epithelium of the convoluted tubes is swollen, 
opaque, degenerated, and detached from the tubes. But in fresh kid- 
neys, properly preserved, this degeneration and desquamation of the 
epithelium is not nearly as constant or as marked a feature as would be 
supposed from the descriptions of some English observers. 
The tubes, whether with flattened epithelium or dilated, may be 
empty. More frequently, however, they contain coagulated matter in 
the form of irregular masses and of hyaline cylinders. The irregular 
masses are found principally in the convoluted tubes; they seem to be 
formed by a coagulation of substances contained in the exuded blood- 
plasma, and are not to be confounded with the hyaline globules so often 
found in normal convoluted tubes. The cylinders are more numerous in 
the straight tubes, but are also found in the convoluted tubes. They 
also are evidently formed of matter coagulated from the exuded blood - 
plasma, and are identical with the casts found in the urine. 
The tubes may also contain red and white blood-cells. 
Plates LI. to LIV. illustrate these changes in the tubes. Plate LV. 
shows the casts and white and red blood-cells as they are found in the 
urine. BRIGHT'S DISEASE OF THE KIDNEYS. 
55 
In the cases in which there is an excessive emigration of white blood- 
cells, we find these cells in the tubes, in the stroma, or distending the 
capillary veins. This excessive emigration is not necessarily attended 
with exudation of the blood-serum, and so the urine of these patients 
may contain no albumen. The white blood-cells are not usually found 
equally diffused through the kidneys, but are collected in foci in the 
cortex. These foci may be very minute, or may attain a considerable 
size. Plates LVI. and LVII. show this condition. 
In the glomeruli we find changes which, at first sight, seem peculiar, 
but are really similar to the changes which we find in arteries and cap- 
illaries in many inflamed tissues, and in the tubes. The cavities of 
the capsules may contain coagulated matter and white and red blood- 
cells, just as do the tubes. The capsular epithelium may be swollen, 
sometimes so much so as to resemble the tubular epithelium, and this 
chano-e is most marked in the capsular epithelium near the entrance 
of the tubes. Plate LVIIL is a photograph of a glomerulus in acute 
exudative nephritis complicating typhoid fever. Plate LIX. is a draw- 
iim of a glomerulus from the kidney of a young child with scarlatinal 
nephritis. 
The most noticeable change, however, is in the capillary tufts of the 
glomeruli. These capillaries are normally covered on their outer sur- 
faces by flat, nucleated cells, so that the tuft is not made up of naked 
capillaries, but each separate capillary throughout its entire length is 
covered over with these cells. There are also flat cells which line the 
inner surfaces of the capillaries, although not uniformly, as is the case in 
capillaries in other parts of the body. Still, in spite of the presence of 
all these cells, the outlines of the walls of the capillaries are fairly dis- 
tinct. 
In exudative nephritis the swelling and growth of cells on and in 
the capillaries change the appearance of the glomeruli. They are 
larger, more opaque, the outlines of the main divisions of the tuft are 
visible, but those of the individual capillaries are lost. Plate LX. is a 
photograph of a glomerulus and tubes from the scarlatinal nephritis of 
a child. The glomerulus is swollen, opaque, the cells more prominent; 
the outlines of the capillaries are indistinct. Plate LXL and LXII. are 56 
BRIGHT'S DISEASE OF THE KIDNEYS. 
photographs of glomeruli from scarlatinal nephritis, which show still 
better these changes. Plate LXIII. is a drawing of part of the glomer- 
ulus seen in Plate LXL, more highly magnified. It shows the growth 
of the cells in and between the capillaries. Plate LXIV. is a drawing 
of fragments of another glomerulus showing the same cell-growth. 
It is difficult to tell how much these changes in the glomeruli inter- 
fere with the passage of the blood through their capillaries. 
In most cases of exudative nephritis the patients recover, and the 
glomeruli return to their natural condition; but in the cases which are 
protracted for months, we find the glomeruli still presenting the same 
changes which have just been described, or with thickened capsules, or 
with the tufts in various stages of atrophy and obliteration. 
In some examples of exudative nephritis we also find a thickening of 
the walls of the branches of the renal artery within the kidney. This 
thickening is principally due to a swelling of the muscle-cells in the 
walls of these vessels. 
. Etiology.-Acute exudative nephritis is frequently a primary disease, 
either occurring after exposure to cold, or without discoverable cause. 
It complicates scarlatina, measles, diphtheria, typhoid fever, acute general 
tuberculosis, pneumonia, acute endocarditis, acute peritonitis, dysentery, 
erysipelas, diabetes, and many other of the infectious diseases and severe 
inflammations. It is one of the forms of nephritis which complicate the 
puerperal condition. 
Symptoms.-In the milder cases the only symptoms are the changes 
in the urine. This is somewhat diminished in quantity, of normal or 
high specific gravity; it contains albumen in moderate quantities, a few 
casts, sometimes blood. 
In the more severe cases the changes in the urine are more decided. 
It is diminished in quantity, or even suppressed ; its specific gravity is 
normal or high; the quantity of albumen is very large; the casts are 
numerous-hyaline, granular, containing white or red blood-cells or 
epithelium ; there are also free white and red blood-cells and epithelial 
cells from the kidney and the bladder. As a rule, the quantity of albu- 
men and the number of casts are in proportion to the severity of the 
nephritis, but this is not always the case. Large quantities of albumen, BRIGHT'S DISEASE OF THE KIDNEYS. 
57 
numerous casts, and many white and red blood-cells may be found in 
the urine of kidneys which, after death, show no structural changes ; 
while, on the other hand, small quantities of albumen and a few 
hyaline casts are compatible with a severe nephritis. Still further, the 
number of casts found in the urine during life is not always in propor- 
tion to the number of casts and quantity of coagulated matter found in 
the corresponding kidneys after death. 
. In addition to the changes in the quantity and composition of the 
urine, the patients present constitutional symptoms which vary, in the 
different cases, as to their number and their severity. A febrile move- 
ment, with more or less prostration; stupor, headache, sleeplessness, 
restlessness, muscular twitchings, and general convulsions; dyspnoea, 
loss of appetite, nausea, and vomiting; a pulse of high tension with 
exaggerated heart-action, or hypertrophy of the left ventricle; dropsy 
and anaemia-these may be called the characteristic symptoms of acute 
exudative nephritis. Of these symptoms a certain number-the fever, 
the prostration, the loss of appetite and nausea, the anaemia, the diminu- 
tion in the quantity of urine, the albumen and casts in the urine-are 
such as would naturally accompany an acute inflammation of the kid- 
ney, and very often they are the only symptoms which do accompany 
it. 
But with this same kidney lesion a certain number of patients will 
present, besides the symptoms just mentioned, the additional features of 
cerebral symptoms, changes in the heart and circulation, and dropsy. 
We might, indeed, think that the cerebral symptoms and the dropsy 
were due to the diminished excretion of urine; but when these condi- 
tions occur, as they often do, in patients who are passing large quantities 
of urine of good specific gravity; and when they are absent, as they 
often are, in patients who are hardly passing any urine at all, it is evi- 
dent that these symptoms are not directly due to the nephritis, but con- 
stitute a separate, complicating set of symptoms, which may be present 
or absent in any given case of the disease. 
What the complicating lesion is which produces these symptoms we 
do not fully know; but the changes in the action of the heart and the 
dropsy, naturally direct our attention to the arteries and capillaries, 58 
BRIGHT'S DISEASE OF THE KIDNEYS. 
with the expectation of finding in them some morbid condition which 
will hinder the passage of the blood through them. Whether the mor- 
bid condition is of an inflammatory nature, or whether it is only a spas- 
modic contraction, we are as yet ignorant. 
The cases of exudative nephritis, with an excessive production of pus- 
cells, have a somewhat different clinical history. Such a nephritis oc- 
curs both in children and adults ; it may be primary, or complicate 
scarlatina, diphtheria, or measles. 
The invasion is sudden, with a high temperature and marked pros- 
tration. Restlessness, delirium, headache, and stupor are soon developed, 
and continue throughout the disease. The patients lose flesh and 
strength and pass into the typhoid state. Dropsy is slight, or absent 
altogether. The urine is not so much diminished in quantity as one 
would expect; its specific gravity is not changed; albumen, casts, and 
red and white blood-cells are present in considerable quantities, but not 
always early in the disease, and may even be abseht altogether. 
It is a very fatal form of nephritis, and yet one easily misunderstood 
on account of the resemblance of its symptoms to those of an acute 
meningitis. 
IL Acute Degeneration of the Kidney.-This is an acute change in 
the kidney characterized by degeneration or death of the epithelial cells 
of the tubules. 
Lesions.--After death the gross appearance of the kidneys varies 
with the intensity of the morbid process and with the presence or 
absence of secondary changes on the part of the blood-vessels. In the 
milder cases the kidney is a little swollen and the cortex is pale ; in the 
severe cases the kidney is much enlarged and the cortex is either white 
or congested, 
o 
The changes in the renal epithelial cells are : A simple swelling of 
the cell-body, especially of its net-work, causing it to look larger and 
more opaque and to take on irregular shapes; an infiltration of the cell- 
bodies with granules of albuminoid matter and fat; a death of the cells, 
which may take the form of coagulation-necrosis, or of a disintegration 
and crumbling of the cell-bodies; a desquamation of the dead cells; a 
formation of hyaline masses in the cells; a growth of new cells to take BRIGHT'S DISEASE OF THE KIDNEYS. 
59 
the place of the dead epithelium. All these changes are most marked 
in the convoluted tubes. 
The more marked and rapid is the degeneration of the cells, so much 
the more likely is there to be added a secondary exudative inflammation 
with congestion, and exudation into the tubes. 
Plate LXV. is a photograph of a mild acute degeneration of the kid- 
ney, complicating lobar pneumonia. The only change is a moderate 
swelling of the renal epithelium. Plate LXVL is a more highly magni- 
fied drawing of the same condition, also complicating pneumonia. Plate 
LXVIL is a photograph of a more intense degeneration, with more de- 
cided swelling of the renal epithelium. It complicated an acute peri- 
tonitis of twelve days' duration. Plate LXVIII. is a photograph of a 
well-marked acute degeneration due to phosphorous poisoning; the epi- 
thelial cells are swollen and contain globules of fat. Plate LXIX. is a 
drawing of the degeneration of yellow fever with marked swelling of the 
cells. In one of the tubes are seen some of the concretions which are so 
often present with this disease. Plate LXX. is a photograph of the in- 
tense degeneration produced by arsenic. The renal epithelium is swollen 
and necrotic, while the blood-vessels are congested. Plate LXXI. is a 
more highly magnified drawing of some of the tubes from the same kid- 
ney. The tubes are filled and distended with the swollen and necrotic 
cells. Plate LXXII. is a drawing of the kidney tubes from a long-pro- 
tracted case of typhoid fever. The epithelium has become necrotic and 
broken down and occupies the tubes in the shape of irregular granular 
masses. Plate LXXIII. is a photograph of acute degeneration of the 
kidney, complicating acute yellow atrophy of the liver. The tubes are 
filled with necrotic and desquamated epithelium and cast matter. Plate 
LXXIV. is a drawing of the cortex-tubes from a patient who died with 
chronic dysentery. It shows the hyaline globules in the epithelium. 
Plate LXXV. is from a patient who died six days after taking corrosive 
sublimate. It shows the growth of new cells on the walls of the tubes 
to take the place of the necrotic and desquamated epithelium. 
Causes.-The regular causes of acute degeneration are the infectious 
diseases, the severe inflammations, and poisons such as arsenic, mercury, 
and phosphorus. 60 
BRIGHT'S DISEASE OF THE KIDNEYS. 
Symptoms.-The quantity of the urine is unchanged, oris diminished, 
or suppressed according to the severity of the lesion. Its specific grav- 
ity is but little changed. In most of the cases albumen and casts are 
absent, or present only in small quantities. In the more intense cases 
with secondary exudative inflammation, albumen in large quantities, 
numerous casts, and red and white blood-cells are found. 
So many of the examples of this lesion are secondary to other dis- 
eases, and are of so mild a type, that they can hardly be said to have 
any symptoms of their own. The severer forms are indeed danger- 
ous to life, but dropsy and disturbances of the circulation are not as- 
sociated with them. 
III. Acute Diffuse Nephritis. 
This is the most serious and important of all the forms of acute 
nephritis, not only for the reason that it involves so many of the struct- 
ures of the kidney, but because its lesions are from the first of a per- 
manent character, and because disturbances of the circulation are so fre- 
quently associated with it. 
It is one of the forms of scarlatinal nephritis, it occurs early and 
late in the course of diphtheria, it is the most important variety of 
the nephritis of pregnancy, and it is especially frequent as a primary 
nephritis with or without a history of exposure to cold. 
The changes in the kidneys are extensive and well marked. 
The kidneys are large, at first smooth, later sometimes a little rough- 
ened ; the cortical portion is thick, white, or mottled with yellow or red, 
or congested ; the pyramids are red. 
In these kidneys we find the same lesions as have been described as 
belonging to exudative nephritis, but with two additional changes- 
changes which are found in the earliest stages of the inflammation and 
which give the characteristic stamp to the lesion : first, a growth of 
connective tissue in the stroma; second, a growth of the capsule-cells of 
the Malpighian bodies. 
Both these changes do not involve the whole of the kidney, but 
symmetrical strips or wedges in the cortex, which follow the line of the 
arteries. These wedges are small or large, few or numerous, regular or 
irregular, in the different kidneys. But in every wedge we find the BRIGHT'S DISEASE OF THE KIDNEYS. 
61 
same general characters : one or more arteries of which the walls are 
thickened, the Malpighian bodies belonging to this artery show an 
enormous growth of capsule-cells, with compression of the tufts; run- 
ning parallel to these arteries a growth of connective-tissue cells and 
basement substance in the stroma. Between the wedges we find at first 
only the changes of exudative nephritis; later, a growth of diffuse con- 
nective tissue. 
Sometimes we find these wedges small, symmetrical, and at consider- 
able distances from each other, as in Plate LXXVI., a photograph of a 
vertical section of the cortex of a scarlatinal kidney. The patient first 
showed albumen in the urine on the twenty-first day of the scarlatina, 
and died six days later. More frequently the wedges are much closer 
together, sometimes even becoming continuous. 
If the nephritis is of acute type and recent, the new tissue between 
the tubes consists largely of cells; if the nephritis is of subacute type 
and longer duration, the tissue is denser and has more basement sub- 
stance. Where the growth of new tissue is abundant, the tubes become 
small and atrophied. Plate LXXVII. is a photograph of a vertical 
section of a post-scarlatinal nephritis of about three weeks' duration. 
The lesion follows the wedge-type, but the wedges are so close to- 
gether that the changes seem to be continuous. The interstitial tissue 
is largely composed of cells, the changes in the glomeruli are well 
marked. 
Plate LXXVIII. is a photograph of a vertical section from an idi- 
opathic nephritis of four months' duration. The wedges follow with 
some regularity the line of each artery with its glomeruli, while between 
the wedges we find dilated tubes and diffuse connective tissue. 
In these wedges the constant change is the growth of new tissue in 
the stroma between the tubes, not an infiltration of the stroma with 
pus-cells, as in exudative nephritis, but a new growth of cells and base- 
ment substance. The tubes seem to become compressed and atrophied 
between the new tissue. 
In each wedge is one or more of the arteries which run up into the 
cortex and give off the little branches ending in glomeruli. The walls 
of these arteries are thickened. 62 
BRIGHT'S DISEASE OF THE KIDNEYS. 
The glomeruli belonging to these arteries become the seat of changes 
of a permanent character. There is the same growth of the cells cover- 
ing the vessels, and of the cells within them, as in exudative nephritis, 
reaching even a greater development. In addition, there is a growth 
of the cells lining the capsules to such a degree as to form a mass of 
cells compressing the tuft. The tuft, apparently, never returns again to 
its natural condition, but, as time goes on, the vessels are obliterated, the 
capsule-cells are changed into connective tissue, and the glomeruli are 
finally transformed into little balls of fibrous tissue. 
Plate LXXIX. is a photograph of a glomerulus with the growth of 
capsule-cells from the same kidney as Plate LXXVIL 
Plate LXXX. is a photograph of a glomerulus from the same kidney 
as is shown in Plate LXXVIII. The growth of capsule-cells is very 
considerable. 
Plate LXXXI. is a photograph of a glomerulus, with its growth 
of capsule-cells, which has become changed into a ball of fibrous 
tissue. 
When this form of nephritis is continued, as it sometimes is, for years, 
the acute nephritis succeeded by chronic inflammation, the changes in 
the tissue of the kidney are very marked. Many of the glomeruli are 
atrophied, the walls of the arteries are thickened, the new connective 
tissue formed in the stroma is large, dense, and replaces much of the 
kidney tissue. The tubes are obliterated or dilated or deformed. The 
kidneys may retain their large size, or become atrophied; the cortex of 
the kidneys remains white. 
Plate LXXXII. is a photograph of a vertical section of a kidney from 
a woman who suffered from a subacute diffuse nephritis following 
pregnancy, and lasting for four years. She was under observation dur- 
ing the entire course of the disease. 
Symptoms.-The urine during the acute periods of the nephritis is 
scanty, colored by blood, of high specific gravity. It contains much 
albumen, numerous casts of all kinds, and red and white blood-cells. 
Exceptionally, the casts are few or absent. Later in the disease, or when 
it is of a more subacute type, the urine is more abundant, the specific 
gravity falls, the albumen and the casts continue. In the protracted BRIGHT'S DISEASE OF THE KIDNEYS. 
63 
cases, the albumen and casts may for a time diminish or even dis- 
appear. 
The patients develop all the symptoms which we are accustomed to 
associate with Bright's Disease : Headache, restlessness, neuralgic pains, 
delirium, stupor, coma, muscular twitchings, and general convulsions; 
dyspnoea and cough; loss of appetite, nausea, and vomiting; neuro- 
retinitis ; diarrhoea; increased arterial tension and hypertrophy of the 
left ventricle of the heart; anaemia, loss of flesh and strength ; and 
dropsy, often developed to an extreme degree. 
The course of the disease varies with the intensity with which it is 
developed, and the rapidity with which it proceeds. 
The invasion may be sudden, the symptoms marked, and the dura- 
tion of the disease short, with a fatal termination. Or with the same 
acute invasion, the disease may be protracted over many months. Or 
the invasion may be gradual, the course of the disease subacute, the 
symptoms not continuous, but with periods of improvement or even ap- 
parent recovery, and the duration of the disease protracted for months 
and years. 
The prognosis of this form of nephritis is bad. The lesion is a per- 
manent and a progressive one. It is, indeed, apparently possible to re- 
cover from it, although with damaged kidneys, but this is the excep- 
tion. The rule is that, sooner or later, the disease proves fatal, although 
it may well happen that periods of improvement give rise to false hopes 
of recovery. 
Treatment.-From what has been said concerning the nature of 
acute Bright's disease, some general conclusions may be drawn as to its 
treatment. 
In acute degeneration of the kidney, it does not seem probable that 
any treatment can be of avail. We are not possessed of means by 
which we can affect acute morbid changes in the epithelium of the 
kidneys. 
In exudative nephritis two separate sets of symptoms present them- 
selves to us for treatment; those due to the nephritis, and those due to 
the complicating disturbances of the circulation. For the nephritis we 
naturally employ the methods of treatment which are appropriate to an 64 
BRIGHT'S DISEASE OF THE KIDNEYS. 
acute exudative inflammation in any part of the body; for the disturb- 
ance of the circulation we use the means by which we can regulate 
the action of the heart, and put a stop to contraction of the arteries. 
In acute diffuse nephritis the problem of treatment becomes much 
more complicated. The inflammation of the kidneys may be at the first 
of an acute, or of a subacute type; the complicating disturbances of 
the circulation are developed to a great degree; the long continuance 
of the disease has its effect on the entire nutrition of the patient; the 
character of the lesion is such that we hope for the alleviation of 
symptoms and the prolongation of life rather than for the cure of the 
disease. PLATE XL. x 50. 
VERTICAL SECTION OF A NORMAL KIDNEY. 
Photo-Gravure Co., N. Y. PI.ATE XLI. x 430. 
NORMAL CONVOLUTED TUBES. 
Photo-Gravure Co., N. Y. PLATE XLII x 430. 
NORMAL CONVOLUTED TUBES. 
Photo-Gravure Co., N. Y. PLATE XLIII. x 1500. REDUCED. 
A CONVOLUTED TUBE. 
Photo-Gravure Co., N. Y. PLATE XLIV. X 850. REDUCED. 
NORMAL CORTEX TUBES. 
Photo-Gravure Co., N. Y. PLATE XLV x 850. REDUCED. 
NORMAL PYRAMID TUBES. 
Photo-Gravure Co., N. Y. PLATE XLVL x 1500. REDUCED. 
A PYRAMID TUBE. 
Photo-Gravure Co., N. Y. PLATE XL VIL x 430. 
A NORMAL GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE XLVIII. x 430. 
A NORMAL GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE XLIX. x 850. REDUCED. 
A NORMAL GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE L. x 430. 
A NORMAL GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE LI. x 50. 
VERTICAL SECTION, ACUTE EXUDATIVE NEPHRITIS. 
Photo-Gravure Co., N. Y. PLATE LIL x 450. 
ACUTE EXUDATIVE NEPHRITIS, ACUTE TUBERCULOSIS. 
Photo-Gravure Co., N. Y. PLATE LIII. x 400. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LIV. x 50 
VERTICAL SECTION. ACUTE EXUDATIVE NEPHRITIS. 
Photo-Gravure Co., N. Y. PLATE LV. x 850. REDUCED. 
CASTS, EXUDATIVE NEPHRITIS. 
Photo-Gravure Co. N. Y. PLATE LVI. x 850. REDUCED. 
ACUTE EXUDATIVE NEPHRITIS, EXCESS OF PUS CELLS. 
Photo-Gravure Co., N. Y. PLATE LVIL x 850. REDUCED. 
ACUTE EXUDATIVE NEPHRITIS, EXCESS OF PUS CELLS. 
Photo-Gravure Co., N. Y. PLATE LVUI. x 280. 
ACUTE EXUDATIVE NEPHRITIS, TYPHOID FEVER. 
Photo-Gravure Co., N. Y. PLATE LTX. x 850. REDUCED. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LX. x 220. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LXI. x 300. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LXII. x 400. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LXIII. x 1600. REDUCED. 
ACUTE EXUDATIVE NEPHRITIS, SCARLATINA 
Photo-Gravure Co., N. Y. PLATE LXIV. x 1500. REDUCED. 
PORTIONS OF AN INFLAMED GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE LXV. x 50. 
ACUTE DEGENERATION OF THE KIDNEY. 
Photo-Gravure Co., N. Y. PLATE LXVI. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, PNEUMONIA 
Photo-Gravure Co., N. Y. PLATE LXVIL x 220. 
ACUTE DEGENERATION OF THE KIDNEY, 
PERITONITIS. 
Photo-Gravure Co., N. Y. PLATE LXVIII. x 430. 
ACUTE DEGENERATION OF THE KIDNEY, 
PHOSPHORUS POISONING. 
Photo-Gravure Co., N. Y. PLATE LXIX. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, YELLOW FEVER. 
Photo-Gravure Co., N. Y. PLATE LXX. x 50. 
ACUTE DEGENERATION OF THE KIDNEY, 
ARSENIC POISONING. 
Photo-Gravure Co., N. Y. PLATE LXXI. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, ARSENIC. 
Photo-Gravure Co., N. Y. PLATE LXXII. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, TYPHOID FEVER, 
Photo-Gravure Co., N. Y. PLATE LXXIII. x 50. 
ACUTE DEGENERATION OF THE KIDNEY, 
YELLOW ATROPHY OF LIVER. 
Photo-Gravure Co., N. Y. PT ATE LXXIV. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, DYSENTERY. 
Photo-Gravure Co., N. Y. PLATE LXXV. x 850. REDUCED. 
ACUTE DEGENERATION OF THE KIDNEY, 
CORROSIVE SUBLIMATE. 
Photo-Gravure Co., N. Y. PLATE LXXVI. x 30. 
ACUTE DIFFUSE NEPHRITIS. 
Photo-Gravure Co., N. Y. PLATE LXXVII. x 50. 
ACUTE DIFFUSE NEPHRITIS, SCARLATINA. 
Photo-Gravure Co., N. Y. PLATE LXXVIII. x 30. 
SUB ACUTE DIFFUSE NEPHRITIS, FOUR MONTHS. 
Photo-Gravure Co., N. Y. PLATE LXXIX. x 280. 
ACUTE DIFFUSE NEPHRITIS. 
Photo-Gravure Co., N. Y. PI,ATE LXXX. x 350. 
ACUTE DIFFUSE NEPHRITIS, GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE LXXXI. x 220. 
ACUTE DIFFUSE NEPHRITIS, AN ATROPHIED GLOMERULUS. 
Photo-Gravure Co., N. Y. PLATE LXXXIL x 50. 
ACUTE DIFFUSE NEPHRITIS, AFTER FOUR YEARS. 
Photo-Gravure Co., N. Y. CHRONIC BRIGHT'S DISEASE. 
The chronic forms of Bright's disease are of much more frequent oc- 
currence than are the acute forms. The cases of the disease are very 
numerous, they present a good deal of variety in their lesions and in 
their symptoms, but they can all be conveniently grouped under the 
three heads of: 
Chronic Congestion of the Kidney. 
Chronic Degeneration of the Kidney. 
Chronic Diffuse Nephritis. 
I. Chronic Congestion of the Kidney. 
This condition of the kidneys can be produced by any mechanical 
cause which interferes with the circulation of the blood in such a way 
as to cause venous congestion of the viscera. The most common of such 
causes are: Chronic inflammation of the mitral or aortic valves, dilata- 
tion of the heart, aneurisms of the arch of the aorta, pulmonary emphy- 
sema, and'large accumulations of fluid in the pleural cavities. 
The congested kidneys remain of their natural size, or become some- 
what larger. They are heavy in proportion to their size. They are of 
hard consistence, of dark-red color, or the cortex is pink or white, while 
the pyramids are dark red. The capsules are not adherent, the surfaces 
are smooth. 66 
CHRONIC BRIGHT'S DISEASE. 
The epithelium of the cortex-tubes remains like that of the normal 
kidney, or the cells are flattened with ciliae on their free surfaces (Plate 
LXXXIII.). These tubes are from the kidney of a man thirty-one years 
old, who had suffered for three years from palpitation of the heart. 
Three months before his death his heart was enlarged, with a mitral 
systolic murmur. The urine was of a specific gravity of 1.030 and con- 
tained no albumin. One month before his death he had severe dyspnoea, 
vomiting, dropsy of the face and legs, cough with mucous and bloody 
sputa, sibilant and sonorous rAles, a temperature of 101° F., scanty 
urine, the specific gravity from 1.016 to 1.026, containing from five to 
twenty per cent, of albumin. The dyspnoea and dropsy continued, and 
he died suddenly. On the. aortic valves were two large, soft vegetations, 
the mitral valve was thickened and fringed with small vegetations, 
both ventricles were dilated and hypertrophied. The kidneys weighed 
16 ounces, their surfaces were smooth, the cortex thick and pale. There 
were no changes in the stroma or arteries. The epithelium of most of 
the cortex-tubes was flattened, and the free surfaces of the cells looked 
as if they were covered with ciliae. The glomeruli were large, their 
capillaries somewhat dilated, their walls thickened, and the cells which 
covered them swollen. 
Instead of being flattened the epithelial cells maybe swollen, and the 
separate cells more distinct from each other, than is the case in the nor- 
mal kidney (Plate LXXXIV.). 
Of the glomeruli some remain unchanged, but a considerable number 
in each kidney are large, their capillaries are a little dilated with their 
walls a little thickened, the cells which cover the capillaries are a little 
swollen. Plate LXXXV. is from the kidney of a male, twenty-seven 
years old, who for about fifteen years had an insufficient mitral valve 
with attacks of cough, dyspnoea, palpitation on exertion, and occasional 
oedema of the feet. Two months before his death the dyspnoea and 
dropsy became worse, and continued to increase until he died. During 
these two months the urine was of a specific gravity of 1.030 and con- 
tained a considerable quantity of albumin with granular casts. After 
death the mitral valve was found to be thickened and insufficient and 
both ventricles were dilated. The kidneys were somewhat enlarged, CHRONIC BRIGHT'S DISEASE. 
67 
their surfaces smooth, the cortex thick and pink. The glomeruli were 
large, their capillaries a little dilated and thickened, the tuft-cells swollen. 
The veins in the pyramids were distended with blood. The epithelium 
of the cortex tubes was swollen. There were no changes in the stroma. 
The dilatation of the capillaries of the glomeruli persists if the 
chronic congestion is succeeded by chronic nephritis, but there is added 
a growth of the tuft-cells, and sometimes atrophy of the glomeruli 
(Plates CXXV., CXXVI., and CXXVIL). 
There are no changes in the stroma, except in some cases an increase 
in the size of the normal areas of subcapsular connnective tissue. 
The arteries are, as a rule, unchanged, but sometimes the small arter- 
ies of the cortex are dilated and their walls thickened. 
The veins in the pyramids are regularly congested and sometimes di- 
lated. Much less frequently the capillary veins of the cortex are also 
dilated. 
The principal effect of chronic congestion of the kidneys is to dimin- 
ish the quantity of urine. Although the kidneys are always congested, 
they are much more so at some times than at others, so the quantity of 
urine is sometimes normal, sometimes diminished, sometimes suppressed. 
Under the effect of drugs the quantity of the urine may be for a time 
increased. The specific gravity of the urine varies from 1.020 to 1.025, 
but it may for a time be down to 1.010 or up to 1.035. The quantity of 
urea is rarely less than 10 grains to the ounce of urine, it may be as 
high as 21 grains. Albumin and casts are not a prominent feature of 
the disease. They may be entirely absent, but more frequently, when 
the heart-action is at its worst, they are present in moderate quantities. 
The effect of the congestion of the kidneys on their functions is, 
therefore, simply to diminish the quantity of the urine; its quality re- 
mains good, and the exudation from the blood-vessels is inconsiderable. 
The most serious feature of chronic congestion is its liability to be 
succeeded by chronic nephritis. 
II. Chronic Degeneration of the Kidney. 
The same mechanical causes which produce chronic congestion of the 
kidneys may produce chronic degeneration. It is also produced by the 68 
CHRONIC BRIGHT'S DISEASE. 
chronic diseases, by chronic alcoholism, and by vicious modes of life. 
The lesion is, therefore, regularly a secondary one, and is not to be con- 
founded with the forms of chronic nephritis. 
The kidneys are, as a rule, considerably increased in size, weighing 
together from 16 to 20 ounces. Sometimes, however, they are of me- 
dium size, or even quite small. Their surfaces are smooth, the cortex is 
pink, white, or yellow, the pyramids are red. 
The epithelium of the cortex-tubes is swollen, coarsely granular, or 
infiltrated with fat-globules. Plates LXXXVI. and LXXXVII. are from 
the kidney of a man, forty-seven years old, who for five weeks before 
death suffered from headache, vertigo, dyspnoea, and oedema of the feet. 
Eleven days before death he had an attack of right hemiplegia, hemiopia, 
and aphasia, which only lasted for a few hours. The urine was of a 
specific gravity of 1.012, contained a trace of albumin and a few granular 
casts. Seven days before death he passed into the typhoid condition. 
After death the large arteries at the base of the brain were found to be 
small, but their walls were not changed, nor did they contain thrombi. 
The'small arteries in the brain and pia mater were normal. In the lower 
part of the left anterior ascending central convolution a portion of the 
cortex, half an inch in diameter, was infiltrated with blood. In the right 
occipital lobe, in the lower part of the left frontal lobe, and in the upper 
surface of the right lobe of the cerebellum were similar small extravasa- 
tions of blood. Both ventricles of the heart were dilated, the coronary 
arteries were normal, there was interstitial myocarditis of the wall of 
the left ventricle near the apex, with small thrombi in the ventricle. 
The kidneys were of medium size, hard, red, and smooth. The epithelium 
of the cortex tubes was much swollen, coarsely granular, and somewhat 
infiltrated with fat. The glomeruli were large, with dilated capillaries 
and swollen tuft-cells. The stroma was normal. The muscular coat of 
the arteries was somewhat thickened. 
The glomeruli, in chronic degeneration, are unchanged unless the de- 
generation is due to venous congestion. If this is the case the glomeruli 
are changed as in chronic congestion (Plate LXXXV.). 
There are no changes in the stroma; the arteries are normal, or 
their walls may be a little thickened. CHRONIC BRIGHT'S DISEASE. 
69 
The quantity of the urine varies at different times in the same case, 
and also in different cases; it may be abundant, scanty, or suppressed. 
Its quality is not changed, as one would expect from the degeneration of 
the epithelium, the specific gravity is not diminished, nor is the propor- 
tion of urea to the ounce of urine decreased. 
Albumin and casts in moderate quantities are more frequently pres- 
ent than with chronic congestion. 
Besides the changes in the urine, the degeneration of the kidneys 
seems to decidedly impair the nutrition of the patients. As the kidney 
lesion is always secondary to some other serious morbid condition, it is 
difficult to tell how much of the existing troubles are caused by the 
kidneys. Anaemia, loss of flesh and strength, delirium, stupor, and the 
typhoid condition are developed in the bad cases, and the condition of 
the kidney seems to be, at least in part, answerable for their develop- 
ment. 
ITT. Chronic Diffuse Nephritis. 
In all advanced cases of chronic Bright's disease, excluding chronic 
congestion and chronic degeneration, we find changes in the kidneys 
which-correspond to our ideas of the changes produced by chronic in- 
flammation. There is a growth of new connective tissue in the stroma, a 
growth of new cells in the glomeruli, exudates in the tubes and in the 
urine, and changes in the walls of the arteries. 
During the lives of the patients we observe a number of symptoms 
which constantly accompany the disease of the kidneys. The cases 
vary, not as to the kind of symptoms, but as to the degree of their 
development and the number which are present in each case. 
The regular symptoms of chronic Bright's disease are : 
Changes in the quantity of the urine: a diminution in the quan- 
tity of solids which it contains, and the presence in it of albumin, casts, 
and red and white blood-cells. 
Dropsy of the subcutaneous connective tissue and of the serous 
cavities. 
Disturbances of the functions of the stomach and intestines. 
Dyspnoea due to fluid in the pleural cavities, to infiltration of the 
lungs with serum, to contraction of the arteries, or to heart-failure. 70 
CHRONIC BRIGHT'S DISEASE. 
Neuro-retinitis, or nephritic neuro-retinitis. 
Diminution in the quantity of haemoglobin and the number of red 
blood-cells. 
Contraction of the arteries, with headache, sleeplessness, delirium, 
stupor, muscular twitchings, general convulsions, coma, hemiplegia, 
blindness, dyspnoea, vomiting, and a rise of temperature. 
Chronic uraemia with dulness and apathy, mild delirium, stupor, 
and the typhoid condition. 
Loss of flesh and strength. 
It must be admitted that each one of these symptoms can exist 
(except the changes in the urine) without disease of the kidneys; that 
the changes described in the kidneys can exist without any of these 
symptoms; and that when these symptoms do exist they are not always 
in proportion to the changes in the kidneys. But yet, when we study a 
sufficient number of cases it is evident that these are only exceptions, 
and that, as a rule, kidney lesions and kidney symptoms correspond to 
each other. 
Although all these cases are evidently examples of a chronic 
nephritis, yet there is enough diversity in the course of the disease to 
make it necessary to subdivide them. In order to do this it is a 
natural instinct to try and carry out such a subdivision with reference 
to the different portions of the kidney, and to distinguish a tubal, an 
interstitial, a glomerulo-, and an arterio-sclerotic nephritis. 
From the point of view of the pathologist such a subdivision can be 
carried out. It is very easy to find kidneys in which the changes in the 
tubes, the stroma, the glomeruli, or the arteries are the most marked. 
But yet, even from this point of view, the examination of a sufficient 
number of kidneys rather leads to the belief that, after all, the lesion of 
the kidneys is really the same, and that the predominance of the changes 
in the tubes, the stroma, the glomeruli, or the arteries is accidental 
rather than essential. 
From the point of view of the clinician the attempt to subdivide the 
disease in this way simply leads to hopeless confusion. 
It has seemed to me, therefore, that for the present the most practical 
way of looking at the matter is to regard all the cases of chronic CHRONIC BRIGHT'S DISEASE. 
71 
Bright's disease, excepting chronic congestion and chronic degeneration, 
as examples of chronic nephritis; and to subdivide the cases of such 
chronic nephritis according to the presence or absence of exudation 
from the blood-vessels, and the rapidity or slowness of the development 
of the nephritis. We can in this way distinguish : 
Chronic nephritis with exudation, running a subacute or a very 
slow course. 
Chronic nephritis without exudation, running a slow, or a very slow, 
course. 
In speaking of the exudation of serum from the vessels and its pre- 
sence in the urine, we speak of it as it occurs during the whole course of 
the disease, and not as it occurs for short periods. We mean that in an 
exudative chronic nephritis there is usually a large quantity of albumin 
in the urine, but that in the protracted cases there may be periods dur- 
ing which the albumin diminishes or entirely disappears. In the same 
way, in a non-exudative nephritis there may be periods during which 
albumin is present in considerable quantities. It is interesting to notice, 
in some of the cases in which the quantity of albumin varies very much 
at different times, how the character of the symptoms also varies with 
the presence or absence of the albumin. 
I must reiterate that, in describing exudative and non-exudative 
chronic nephritis, I am not describing separate lesions of the kidneys, but 
merely varieties of the same lesion ; and that it is perfectly possible for 
the same kidneys to be affected at different times by both these forms of 
inflammation. For in all the kidneys one form of inflammation-the 
productive with the formation of new tissue-is present. The exuda- 
tion from the vessels is something which is added to this, but does not 
change it. 
In the same way, in a tubercular peritonitis the tubercular inflam- 
mation of the peritoneum is always present, but in some cases a large 
exudation of serum in the peritoneal cavity is present, in others it is 
absent, and this presence or absence of the serum makes a difference in 
the clinical history of the case. 
(a) Chronic Diffuse Nephritis with Exudation. Lesions.-The 
largest number of the kidneys are found after death to be large, smooth, 72 
CHRONIC BRIGHT'S DISEASE. 
with a thickened cortex of white, or mottled white, yellow, and red 
color. 
A small number are atrophied with a white cortex, and seem to be a 
possible later stage of the large white kidney. 
A considerable number are of about the size of a normal kidney, 
with nodular surfaces and the cortex of gray and red color. 
When the nephritis follows chronic congestion the kidneys remain 
hard, the cortex is pink or white. 
In a few cases the kidneys are very small, weighing together not 
over four ounces, with a red cortex. 
The growth of new connective tissue in the stroma of the cortex is 
considerable. It is diffuse, separating the tubes symmetrically from 
each other; or in wedges running down from the surface of the kidney; 
or in irregular patches in the cortex. 
When the growth of new connective tissue is diffuse there is a 
moderate general and symmetrical dilatation of the tubes. When the 
growth of new connective tissue is in wedges, or patches, the tubes with- 
in the wedges or patches are atrophied, while the tubes between the 
wedges and patches are irregularly dilated. Plate LXXXVIII. is from 
the kidney of a male, thirty-nine years of age. For about six months 
he suffered from dyspnoea and loss of strength. For about two months 
before his death he had severe headaches, became pale, and developed 
general dropsy. The urine measured about fifty ounces, specific gravity 
1.012, albumin, fifteen to sixty per cent., hyaline and granular casts, red 
and white blood-cells. The kidneys weighed 20 ounces, the cortex was 
thick and white; the cortex-tubes were symmetrically dilated with 
flattened epithelium and contained cast matter and blood; the glomeruli 
were large and showed a marked growth of tuft-cells : in the stroma 
there was an extensive diffuse growth of connective tissue; the arteries 
were normal. 
Plate LXXXIX. is from the kidney of a male, twenty-eight years old, 
who for five years had suffered from weekly attacks of frontal headache, 
nausea, and vomiting. Four days before his death his urine was of a 
specific gravity of 1.008, contained a large quantity of albumin, casts, 
and white and red blood-cells. The patient was anaemic, very drop- CHRONIC BRIGHT'S DISEASE. 
73 
sical, and died comatose. The kidneys were large and smooth, the cortex 
thick and mottled red, white, and gray. There was a large growth of 
new connective tissue in the stroma of the cortex, both in the form of 
wedges and diffuse. The tubes in the wedges were compressed and 
atrophied, those between them were dilated. The epithelium of the 
dilated tubes was flattened. The glomeruli were large, the cells cover- 
ing the capillaries were much increased in number, in some of the 
glomeruli in the wedges there was a marked growth of the capsule-cells. 
The walls of the arteries were somewhat thickened. 
Plate XC. is from a male, twenty-nine years of age, who for eighteen 
months before his death had occasional dropsy of the legs. For six 
months before his death the dropsy increased and was constant. 
During the four months before his death the urine measured from 14 to 
29 ounces, was from 1.012 to 1.016 specific gravity, contained from five 
to twenty per cent, of albumin, granular casts, and white and red blood- 
cells. He died with dropsy and dyspnoea. The kidneys were very 
large and smooth, the cortex thick, mottled red, gray, and yellow. 
There was an extensive growth of new connective tissue in the stroma 
of the cortex, separating the tubes from each other. The cortex-tubes 
were somewhat dilated, the epithelium was flattened and coarsely 
granular, the tubes contained a good deal of coagulated matter. In the 
glomeruli there was a moderate growth of the cells covering the capil- 
laries. The arteries were normal. 
Plate XCI. is from a male, twenty-five years of age, who had his first 
attack of dropsy and vomiting when he was sixteen years of age. He 
had repeated attacks of the same kind afterward. The last attack 
began nine months before his death. During this time the specific 
gravity of the urine was from 1.008 to 1.015, the quantity of urea to the 
ounce of urine was about four grains, the albumin was from twenty to 
thirty per cent., there were but few casts. During the last nine months 
of his life he suffered from headache, nephritic retinitis, vomiting, 
dyspnoea, anaemia, and dropsy. The kidneys were small, their capsules 
adherent, their surfaces nodular, the cortex mottled red and gray. In 
the cortex was a growth of connective tissue so extensive that but few 
tubes were left, and most of these were irregularly dilated. Many of 74 
CHRONIC BRIGHT'S DISEASE. 
the glomeruli were atrophied, in others there was a growth of the tuft- 
cells. The walls of the arteries were a little thickened. 
Plate XCII. is from the kidney of a man with a long history of 
chronic miliary tuberculosis, dropsy, and albuminous urine. The 
kidneys were small, with white cortices. There was a large growth of 
connective tissue in the stroma of the cortex. Some of the tubes were 
atrophied, others were dilated. In the glomeruli the capillaries were 
the seat of waxy degeneration, the cells covering them were increased in 
number. The walls of the small arteries were the seat of waxy 
degeneration. 
The cortex-tubes may be compressed by the new connective tissue 
and atrophied, or uniformly dilated, or irregularly dilated in groups. 
The epithelium is swollen, granular, degenerated, fatty, broken, or 
flattened (Plates XCIIL, XCIV., XCV, XCVL, and XCVIL). 
The tubes may contain blood, or cast matter, or coagulated matter 
(Plates XCVIII. and XCIX.). 
The glomeruli are changed in several different ways. 
1. There is a growth of the capsule-cells in such numbers that they 
compress the tufts. The cells covering the capillaries are also 
increased in size and number. The capsule-cells may Anally be changed 
into connective tissue and the tufts become atrophied (Plates C. and 
CL). 
2. The glomeruli are of large size, the cells covering the capillaries 
are increased in number so that the outlines of the vessels are lost, but 
yet the capillaries are not compressed nor the glomeruli atrophied 
(Plates CIL and CIIL). 
3. There is a growth of the cells which cover the capillaries and of 
the cells within them. Of the cells which cover the capillaries the cell- 
bodies become very large, the capillaries are compressed, and the 
glomeruli eventually become atrophied (Plates CIV., CV., and CVI.). 
4. The walls of the capillary vessels become the seat of waxy 
degeneration, while the cells which cover them are increased in size 
and number (Plate CVII.). 
5. If the nephritis is the result of venous congestion from an 
obstruction of the circulation, the glomeruli remain large, the capillaries CHRONIC BRIGHT'S DISEASE. 
75 
dilated and with thickened walls, while there is added a growth of the 
cells which cover the capillaries (Plate CXXV). 
The arteries behave in the same way as they do in non-exudative 
nephritis. In some cases they are unchanged: in others they are the 
seat of obliterating endarteritis; in others there is a thickening of the 
muscular coat; in others there is thickening and sclerosis of the entire 
arterial wall; and in still others there is waxy degeneration. 
Causes.--Such a chronic exudative nephritis occurs frequently as a 
primary disease, especially in young adults. It follows acute diffuse 
nephritis, chronic congestion, and chronic degeneration of the kidney. 
It may complicate syphilis, chronic phthisis, chronic endocarditis, 
prolonged suppuration, and chronic inflammations of the bones and 
joints. 
Symptoms - The urine varies in quantity at different times. When 
the nephritis is most quiescent the quantity of urine is normal. 
During the exacerbations of the nephritis the urine is scanty or 
suppressed. When the patients are doing badly, often when they are 
dropsical, the quantity of urine is very much increased. 
The specific gravity and the proportion of urea to the ounce of urine 
slowly diminish. In the cases of shorter duration the specific gravity is 
apt to run between 1.012 and 1.020. In the very chronic cases it will be 
between 1.001 and 1.005. Very low specific gravities regularly indicate 
a large growth of connective tissue in the stroma of the cortex, or waxy 
degeneration of the capillaries of the glomeruli. 
The urine regularly contains albumin and casts. During the ac- 
tive periods of the disease the quantity of albumin is very large; dur- 
ing its quiescent periods it is smaller, and at times may almost entirely 
disappear. The number of casts regularly varies in proportion to the 
quantity of albumin, but occasional exceptions to this rule are seen. 
Dropsy may be considered a regular symptom of chronic exudative 
nephritis. It is rare to find a patient who goes through the disease 
without exhibiting this symptom. It may be developed at any time in 
the disease, continue uninterruptedly, or occur only in attacks. 
A peculiar pallor of the skin and white color of the sclerotic is 
seldom absent, and is quite characteristic of the disease. It corresponds 76 
CHRONIC BBIGHT'S DISEASE. 
to a diminution in the quantity of haemoglobin and in the number of 
red blood-cells. These changes in the blood are not, as a rule, far 
advanced ; but sometimes they are, and some cases even die with the 
symptoms of pernicious anaemia. 
Many of the patients are troubled with headache and sleeplessness. 
Acute uraemic attacks with contraction of the arteries, convulsions, etc., 
may occur in the course of a chronic exudative nephritis, but they are 
of very much more frequent occurrence with the non-exudative form of 
the disease. 
Chronic uraemia, on the contrary, is one of the ordinary ways in 
which an exudative nephritis proves fatal. The patients pass into a 
condition of alternating delirium and stupor, writh a rapid, feeble, soft 
pulse. 
Simple neuro-retinitis, or nephritic retinitis is developed in a 
moderate number of cases. 
Dyspnoea is a nearly constant symptom, but it is not always the 
same kind of dyspnoea, nor always produced by the same cause. There 
seems to be no real difference between the dyspnoea of exudative and 
non-exudative nephritis. In either one the dyspnoea may be due to 
hydrothorax, to oedema of the lungs, to contraction of the arteries, or to 
failure of the heart's action. 
In many patients the dyspnoea due to contraction of the arteries, or 
to failure of the heart's action, is the first symptom which attracts 
attention. It is a dyspnoea which comes on in attacks, especially at 
night and in the early morning, and is regularly worse when the patient 
lies down. It often begins w'hile the patient is apparently in good 
health, but it is a sure premonition of serious disease. 
A catarrhal bronchitis with cough and expectoration is often present. 
Loss of appetite, nausea, and vomiting are frequent symptoms. 
The heart is often affected. There may be hypertrophy of the left 
ventricle, dilatation of both ventricles, chronic endocarditis, myocarditis, 
or a feeble heart. 
Course of the Disease.-There is hardly any limit to the variety of 
the disease, but the most constant symptoms are anaemia, dropsy, and 
albumin in the urine. CHRONIC BRIGHT'S DISEASE. 
77 
1. There are cases in which the symptoms are nearly continuous, the 
patients get steadily worse, and die within one or two years. The 
anaemia, the dropsy, and the albumin are constantly present, and the pa- 
tients die with dropsy or with chronic uraemia. 
2. There are cases in which the anaemia, the dropsy, and the 
dyspnoea come on in attacks which last for weeks or months. Between 
the attacks the patients are comparatively well, often able to work, 
although the urine always contains albumin. 
3. There are cases in which a number of years before death the pa- 
tient has an attack of dropsy, etc., from which he apparently recovers 
and goes on able to work, but with urine of low specific gravity, which 
sometimes contains albumin. After an interval of many years conies the 
fatal attack with all the characteristic symptoms. 
4. There are cases which for years have no symptoms but pallor of 
the skin and urine of low specific gravity containing albumin. These 
patients often for a long time feel so well that they cannot understand 
that they have a serious disease. 
5. Ihere are cases in which the first symptom is the attack of spas- 
modic dyspnoea, the patients otherwise feeling well. It may be months 
or years before the other symptoms are developed. 
6. There may be a history of chronic endocarditis lasting for years 
before the renal symptoms are developed. 
7. There are cases which apparently recover from the disease. 
The prognosis is bad, but life may be prolonged for many years with 
but few symptoms, and recovery seems to be possible. 
(b) Chronic Diffuse Nephritis without Exudation. Lesions.- The 
larger number of these kidneys are found after death to be diminished 
in size, the two kidneys together may not weigh more than two ounces. 
Their capsules are adherent, their surfaces are roughened or nodular, the 
cortex is thin and of red or gray color. 
A considerable number of the kidneys do not differ in their size or 
appearance from normal kidneys, except that the capsules are adherent 
and the surfaces of the kidneys roughened. 
Many examples of chronic non-exudative nephritis follow chronic 78 
CHRONIC BRIGHT'S DISEASE. 
congestion. The kidneys then remain hard, but the cortex becomes 
thinned, the capsules adherent, and the surface roughened. 
Some of the kidneys, instead of becoming atrophied, are increased in 
size, weighing together from 16 to 32 ounces. The surfaces of these 
large kidneys may be smooth or nodular, the cortex is thickened, its 
color is red, gray, or white. 
There is regularly a growth of new connective tissue in the cortex 
and also in the pyramids, which becomes more and more marked as the 
disease goes on. In the cortex the new tissue follows the distribution of 
the normal subcapsular areas of connective tissue, is in the form of 
irregular masses, or is distributed diffusely between the tubes. In the 
pyramids the growth of new connective tissue is diffuse. Plate CVIIL 
is an example of the senile atrophied kidney. The patient was a man 
eighty years of age, who for several months complained of dyspnoea, 
oedema of the feet, cough and expectoration, and loss of flesh and 
strength. He died with an attack of lobar pneumonia. The urine 
before the pneumonia was of a specific gravity of 1.016, and contained 
neither casts nor albumin. After death it was found that the aortic 
valves were calcified and the left ventricle hypertrophied. The aorta 
and large arteries showed the lesions of chronic endarteritis. The lungs 
were emphysematous, with red hepatization of the right lower lobe. 
The kidneys were very small, their capsules were adherent, their sur- 
faces nodular. The epithelium of the cortex tubes was a little swollen, 
this being due to the pneumonia. There was a moderate growth of 
connective tissue in the stroma of the cortex, taking the form of exaggera- 
tions of the normal areas of subcapsular connective tissue. In these 
masses of connective tissue the tubes and glomeruli were atrophied. 
The arteries showed a very considerable thickening and sclerosis of their 
walls. In the glomeruli the walls of the capillaries were thickened and 
the tuft-cells swollen as the result of the cardiac disease. 
Plate CIX. is from the kidney of a male, fifty-four years of age, who 
for eleven weeks suffered from headaches, which increased in severity 
until, for thirteen days before his death, he could hardly sleep at all. 
Six days before death the urine was of a specific gravity of 1.010, con- 
tained a trace of albumin, but no casts. The heart was hypertrophied CHRONIC BRIGHT'S DISEASE. 
79 
and its action exaggerated, the pulse was small and tense. After being 
in the hospital for a week, he fell out of the window, fractured his 
skull, and died within a few hours. The kidneys were small, their 
capsules adherent, their surfaces nodular. There was a very irregular 
growth of connective tissue in the stroma of the cortex. The tubes 
were in some places atrophied, in others moderately dilated with 
flattened epithelium. Some of the glomeruli were atrophied, others 
showed a moderate growth of tuft-cells. The arteries were normal. 
Plate CX. is from the kidney of a male, fifty years of age, who for 
one year had occasional oedema of the legs. Four days before death 
there was a little oedema of the legs, an hypertrophied but feeble and 
rapid heart, a rapid pulse of very high tension, urine 1.010, albumin ten 
per cent., no casts. He died comatose with a temperature of 108° F. 
The brain and membranes were normal. The lungs were emphysema- 
tous. The aortic valves were a little thickened, the left ventricle much 
hypertrophied. The kidneys were small, their capsules adherent, their 
surfaces nodular, their cortices of gray color. There was a consider- 
able irregular growth of connective tissue in the stroma of the cortex. 
Some of the tubes were atrophied, others irregularly dilated. Some of 
the glomeruli were atrophied, others showed a growth of tuft-cells. All 
the coats of the arteries were thickened. 
Plate CXI. is from the kidney of a man, fifty-five years of age, who 
died in a condition of coma. During a few days before death the 
urine was of a specific gravity of 1.021, on some days contained a good 
deal of albumin, on others none at all. The kidneys were atrophied, 
with adherent capsules and thin nodular cortices. There was a great 
deal of new connective tissue irregularly distributed in the stroma of the 
cortex. Some of the tubes were atrophied, others irregularly dilated 
with swollen and granular epithelium. Some of the glomeruli were 
atrophied, in others there was a growth of the tuft-cells. The middle 
and inner coats of the arteries were very much thickened. 
Plate CXI I. is an example of chronic nephritis following chronic 
congestion. The patient was a man, forty years of age, who was under 
observation for ten months. His principal symptoms were dropsy, bron- 
chitis, with dyspnoea and anaemia. These symptoms came on in attacks, 80 
CHRONIC BRIGHT'S DISEASE. 
the first attack occurring fourteen months before death. During the ten 
months before his death the specific gravity of the urine varied from 
1.010 to 1.022. During much of the time, even during the attacks of 
dropsy, there was no albumin in the urine, but on some days there was 
as much as forty per cent. He finally developed contraction of the 
arteries and died in a convulsion. The mitral valve was stenosed, the 
left ventricle dilated and a little hypertrophied, the right ventricle was 
hypertrophied. In the lungs, liver, spleen, and stomach were the ordi- 
nary evidences of chronic congestion. The kidneys were small and hard, 
with adherent capsules and thin, nodular cortices. There were large 
patches of new connective tissue in the stroma of the cortex, and a dif- 
fuse thickening of the stroma of the pyramids. The cortex-tubes were 
irregularly dilated with swollen and granular epithelium. Some of the 
glomeruli were large, as in chronic congestion, with dilated capillaries 
and a growth of tuft-cells. In others the growth of tuft-cells was large 
and compressed the capillaries, the capsules were thickened, and the 
glomeruli showed the different stages of atrophy. The walls of the ar- 
teries were thickened and sclerosed. 
Plate CXIII. is from an atrophied kidney without history. It is a 
good example of the kidneys in which most of the new tissue is just 
beneath the capsule. 
Plate CXIV. is from the kidney of a male, twenty-eight years of age. 
His symptoms were: nephritic retinitis, dyspnoea, gradual loss of flesh 
and .strength, no dropsy, urine of a specific gravity of 1.008, containing 
very little albumin and no casts. He died in the condition of chronic 
uraemia. The kidneys were very small, with adherent capsules and 
atrophied, nodular cortex. The quantity of new connective tissue in the 
cortex was so great that but few tubes were left, these were irregularly 
dilated with flattened epithelium. The glomeruli were in different 
stages of atrophy. The walls of the arteries were thickened. 
Plate CXV. is from the kidney of a male, forty-eight years of age, 
who suffered from headache, dyspnoea, vomiting, anaemia, and gradual 
loss of flesh and strength. The kidneys were atrophied and nodular, 
with adherent capsules. There was a very large, diffuse growth of 
connective tissue in the stroma of the cortex and pyramids. The cortex CHRONIC BRIGHT'S DISEASE. 
81 
tubes which were not obliterated were irregularly dilated with swollen 
and granular epithelium. Some of the glomeruli showed a growth of 
tuft-cells, others were atrophied. The arteries showed a very marked 
development of obliterating endarteritis. 
The tubes, both in the cortex and pyramids, undergo marked changes. 
Those included in the masses of new connective tissue are diminished in 
size, their epithelium is flattened, some contain cast matter, many be- 
come obliterated. The tubes between the masses of new connective 
tissue are more or less dilated, their epithelium is flattened, cuboidal, 
swollen, degenerated, or fatty. The dilatation of the tubes may reach 
such a point as to form cysts of some size, which contain fluid or coagu- 
lated matter. These cysts follow the lines of groups of tubes, or are 
situated near the capsules. 
Plate CXVI. shows a number of large cysts filled with colloid mat- 
ter, formed by dilatation of the tubes. 
Plate CXVII. shows two masses of new connective tissue with atro- 
phied tubes containing cast matter, and between them groups of dilated 
tubes with cuboidal epithelium. 
Of the glomeruli a certain number remain of normal size, but with 
the tuft-cells swollen, or multiplied. 
Many others are found in all stages of atrophy, until they are con- 
verted into little fibrous balls. This seems to depend partly on the 
growth of the tuft-cells and intra-capillary cells, partly on the thicken- 
ing of the capsules, partly on the occlusion of the arteries to which the 
glomeruli belong. 
Plate CXV1II. shows a glomerulus with a marked growth of tuft- 
cells and intra-capillary cells in the earlier stages of atrophy. 
Plate CXIX. is of a glomerulus with a marked growth of tuft-cells 
still farther atrophied. 
Plate CXX. is of a glomerulus with a growth of tuft-cells completely 
atrophied. 
Plates CXXI. and CXXII. are of atrophied glomeruli with a growth 
of tuft-cells and thickened capsules. 
Plate CXXIII. is of a glomerulus completely changed into a little 
ball of connective tissue. 82 
CHRONIC BRIGHT'S DISEASE. 
Plate CXXIV. shows a rather rare change in the glomeruli. It is 
from the kidney of a male, twenty years of age. Seven years before his 
death he had an attack of rheumatism, and ever since has been troubled 
with dyspnoea on exertion and cough. For several months past the 
dyspnoea and cough have grown worse, he lost appetite, vomited, and 
became anaemic, feeble, and emaciated. The urine was of a specific 
gravity of 1.010 and contained a trace of albumin. There was no 
dropsy. He died with dyspnoea. After death the aortic and mitral 
valves were found to be thickened and insufficient, and the left ventricle 
much dilated and a little hypertrophied. The kidneys weighed to- 
gether sixteen ounces. Their surfaces were smooth, their cortices mot- 
tled red and white. The epithelium of the cortex tubes was flattened, a 
few tubes were filled with blood. The arteries were normal. There 
was a very extensive growth of connective tissue in the stroma of the 
cortex. It was diffuse, separating the tubes, and was composed of deli- 
cate reticulated tissue with large meshes. In the capsules of the glom- 
eruli was the same growth of reticulated connective tissue and irregular 
masses of the same tissue projected into the cavities of the capsules. 
There was also a marked growth of tuft-cells compressing the capil- 
laries. 
If the chronic nephritis follows chronic congestion of the kidney the 
glomeruli remain large, but with a marked growth of tuft-cells (Plate 
CXXV.) ; or they become atrophied, but with the dilatation of the capil- 
laries still evident (Plates CXXVL and CXXVIL). 
The capillaries of the glomeruli may be the seat of waxy degenera- 
tion. 
In non-exudative, as in exudative, nephritis, the renal artery and its 
branches are often, but by no means always, diseased. The arteries are 
regularly changed in one of four ways, but several of these changes may 
exist in the different arteries of the same kidney. 
1. A very common condition is a symmetrical thickening of all the 
coats of the artery, with more or less diminution of its calibre. The in- 
ner coat is thickened by the growth in it of connective tissue, the endo- 
thelial cells remain in place and are somewhat swollen. The muscular 
coat is thickened by an increase in the size and number of the smooth CHRONIC BRIGHT'S DISEASE. 
83 
muscle-cells, the outer coat is thickened by a growth of connective tis- 
sue. Plate CXXVIII. shows part of the wall of a small artery with 
thickening of all its coats, that of the muscular coat being especially 
marked. It is from the kidney of a man, sixty-seven years of age. 
The kidneys were small, nodular, with atrophied red cortices. There 
were thickening and insufficiency of the aortic valve, thickening and ste- 
nosis of the mitral valve, and great hypertrophy of the left ventricle. 
Plate CXXIX. shows the whole of a cross-section of a small artery. 
All the coats are thickened, but especially the inner and the muscular 
coat. It is from the kidney of a man, forty-five years of age. The kid- 
neys were large, with adherent capsules, nodular surfaces, and thick, 
red cortices. The left ventricle of the heart was much dilated and hy- 
pertrophied, with but a little thickening of the mitral valve. 
Plate CXXX. shows the whole of the cross-section of a small artery. 
All the coats are thickened, but the inner coat much more than the 
others, with a consequent diminution in the calibre of the artery. It is 
from the kidney of a female, twenty-nine years of age. The kidneys 
were large, their surfaces finely nodular, their cortices thick, pale, and 
hard. The mitral valve was thickened and stenosed, and both ventri- 
cles were dilated and hypertrophied. 
Plate CXXXI. is an example of another artery of the same kind, 
with its calibre still further diminished, but taken from another kidney. 
2. All the coats of the arteries are thickened and converted into a 
uniform mass of dense connective tissue (arterio-capillary sclerosis), as 
in Plate CXXXIL, taken from an atrophied kidney. 
3. There is a regular obliterating endarteritis, with a growth of new 
connective tissue formed on the inner surface of the inner coat of the 
artery, and filling up the lumen of the artery more and more as it in- 
creases in thickness (Plate CXXXIIL). 
4. There is waxy degeneration of the walls of the arteries. 
Complicating Lesions.-Hypertrophy of the left ventricle of the 
heart is frequently caused by exudative nephritis, but still more fre- 
quently by the non-exudative form; but it must be admitted that such 
an hypertrophy, although frequent, is not constant, that both with ex- 
udative and non-exudative nephritis there may be no change in the 84 
CHRONIC BRIGHT'S DISEASE. 
wall of the left ventricle. The hypertrophy of the wall of the ven- 
tricle may after a time be succeeded by dilatation, or chronic degenera- 
tion, or myocarditis. 
Chronic endocarditis is very frequently associated with chronic 
Bright's disease. The valvular lesions may cause chronic congestion, 
chronic degeneration, or chronic nephritis : or the same patient may suf- 
fer from chronic endocarditis, and either form of chronic nephritis, the 
lesions associated possibly due to the same causes, but not dependent 
on each other. 
Pulmonary emphysema, chronic endarteritis, and cirrhosis of the 
liver, all of them examples of chronic productive inflammation, fre- 
quently accompany chronic nephritis. 
With the endarteritis comes the additional danger of cerebral hemor- 
o 
rhage. 
Patients suffering with chronic nephritis are more liable than are 
other persons to attacks of pericarditis, bronchitis, and gastric catarrh. 
Symptoms.-The typical urine of chronic non-exudative nephritis is 
a urine increased in quantity, of a specific gravity of about 1.010, contain- 
ing a diminished quantity of urea, without albumin or casts, or with a 
trace of albumin and a very few casts, except during exacerbations of the 
nephritis, when the quantity of albumin and the number of casts may be 
considerable. But very important modifications of the urine are of ordi- 
nary occurrence. It is quite possible, with nephritis of this type far ad- 
vanced, to have urine not below 1.020 in specific gravity, and without 
albumin or casts. In such cases the diagnosis has to be made without 
reference to the urine. On the other hand, there are cases in which the 
specific gravity of the urine falls very low, almost to 1.000, either with or 
without waxy degeneration of the vessels. There are cases in which the 
quantity of urine is very much increased, several quarts in the twenty- 
four hours. During the attacks of contraction of the arteries, to which 
these patients are liable, the urine may be diminished to a few ounces or 
suppressed. 
In a great many of the cases cerebral symptoms are developed at some 
time in the course of the disease. Headache and sleeplessness are often 
present, the headache sometimes so severe and continuous that the pa- CHRONIC BRIGHT'S DISEASE. 
85 
tient is nearly maniacal; or instead of the headache there are neuralgic 
pains in the different parts of body. 
Muscular twitchings and general convulsions are much more serious; 
they may be an early symptom, or not occur until late in the disease. 
Hemiplegia with or without aphasia may be the first symptom to 
call attention to the nephritis, or may not occur until late in the disease. 
The invasion of the hemiplegia is sudden and is usually accompanied by 
coma. There is loss of motion alone, or of both motion and sensation. 
The hemiplegia, coma, and aphasia may continue up to the time of the 
patient's death, or disappear after a few hours or days. In the latter 
case the patient may have several such attacks. These attacks have 
been ascribed to localized oedema of the brain. In the cases which 
I have seen there were no changes in the brain-tissue, but the cerebral 
arteries were damaged by chronic endarteritis. 
Delirium, mild or violent, stupor, and coma may come on in sudden 
attacks, or be developed slowly and gradually. 
When these cerebral symptoms come on in attacks, the arteries are 
contracted, the temperature is raised, and the patients are said to suffer 
from acute uraemia. Very often they recover from a number of these 
attacks. In the fatal attacks the pulse often loses its tension, but be- 
comes rapid and feeble, and the patients die comatose with a feeble heart. 
Instead of such acute attacks of cerebral symptoms, the symptoms 
may come on gradually in persons already much reduced by the kidney 
disease. The temperature is then apt to be below the normal, and the 
pulse is rapid and feeble. 
Temporary blindness, neuro-retinitis, or nephritic retinitis are de- 
veloped in a moderate number of the patients. 
Chronic bronchitis and emphysema very frequently exist, and the 
symptoms belonging to them often form a large part of the clinical 
history. 
The left ventricle of the heart is regularly hypertrophied. This by 
itself gives no symptoms; but if the arteries become contracted, or if 
the hypertrophied heart becomes feeble, then disturbances of the circu- 
lation are established which cause serious symptoms. 
In the same way, the complicating endocarditis which so often exists 86 
CHRONIC BRIGHT'S DISEASE. 
gives no trouble until the valves are a good deal changed, or the ventri- 
cles dilated, or the heart's action altered, or the arteries contracted ; then 
the circulation is interfered with, and the results of venous congestion 
of different parts of the body show themselves. 
Dyspnoea is a very frequent symptom, often the first symptom no- 
ticed by the patient. It is a spasmodic dyspnoea coming on in attacks 
which last for minutes, hours, or days'. It is regularly made worse by 
mental or bodily exertion, or by the recumbent position. It does not re- 
semble pulmonary asthma. It is apparently due to the association of 
changes in the arteries and in the heart. With contraction of the arte- 
ries alone, or with a feeble heart alone, no dyspncea may exist. But if 
the contraction of the arteries is so great that the hypertrophied and la- 
boring heart is unable to overcome the obstruction; or, if with the con- 
tracted arteries the heart becomes dilated or feeble, then the attacks of 
dyspnoea begin. At first the attacks are not severe and are of short du- 
ration, but if the mechanical conditions which cause them cannot be con- 
trolled they become longer and more distressing. 
Perhaps the most striking examples of this dyspnoea are in the pa- 
tients in whom it is the first symptom of the nephritis. They are apt to 
be middle-aged or elderly men, often engaged in large financial or com- 
mercial enterprises. They profess that they feel quite well and that 
they can attend to their affairs perfectly, but that they are very much 
annoyed because early every morning they have an attack of asthma. 
In spite of their professions of good health, it is evident that they are 
pale and that they have dyspnoea on exertion. The heart is found to be 
enlarged, with or without a murmur, its action either labored or feeble. 
The pulse is tense. The urine is of a specific gravity of 1.010 to 1.030, 
it contains no albumin, or only a trace. In the earlier stages of the dis- 
ease this dyspnoea can be controlled, but later on it is more distressing 
and difficult to remedy. 
The stomach may become the seat of catarrhal gastritis, or of 
spasmodic vomiting. But in some patients it continues to perform its 
functions fairly well. 
Dropsy, as a rule, is absent with non-exudative nephritis, unless it 
is complicated by chronic endocarditis, or cirrhosis of the liver. CHRONIC BRIGHT'S DISEASE. 
87 
Profuse bleeding from atrophied kidneys has been described by 
Bowlby 1 in three cases. 
Regularly, after a time the nephritis exerts its effect upon the 
nutrition of the patient, and the flesh and strength are diminished. On 
the other hand, the patients do not become as pale as they do in exuda- 
tive nephritis. 
Course of the Disease.-It is characteristic of the chronic productive 
inflammations of the lungs, the heart, the arteries, the liver, and the 
kidneys that, while they often exist as serious and fatal diseases, they 
also frequently exist as lesions which do not interfere with general good 
health and long life. This seems to depend, in part at least, on the 
rapidity with which the inflammatory changes in these different parts of 
the body are developed. If they are developed slowly enough the 
functions of the organ continue to be performed in spite of the new- 
growth of connective tissue in it. 
o 
So with the kidneys, it is common enough to find chronic non-exuda- 
tive nephritis far advanced in persons who die from accident or 
intercurrent disease, and have never given symptoms of renal disease. 
In the same way, we can often observe for years persons who have 
urine of low specific gravity, an hypertrophied left ventricle of the heart, 
and occasionally some increase of tension in the arteries, and who yet 
habitually enjoy very fair health. 
But yet these same persons, if they are attacked, with pneumonia, or 
pericarditis, or suffer from a severe accident, will often develop serious, 
or even fatal, renal symptoms. 
A very common form for the disease to take is that of attacks which 
are repeated a number of times, each attack worse than the preced- 
ino* and the general health more and more impaired between the attacks. 
During the attacks there are cerebral symptoms more or less severe- 
headache, sleeplessness, delirium, stupor, coma, convulsions. Dyspnoea 
may be present or absent. The arteries are contracted, with a tense 
pulse. There is loss of appetite, nausea, and vomiting. The urine is of 
low specific gravity and usually contains albumin. Between the attacks 
the patients at first seem to be fairly well, but later they gradually lose 
1 Medical and Surgical Reporter, 1887. 88 
CHRONIC BRIGHT'S DISEASE. 
flesh or strength. The urine between the attacks is of low specific 
gravity and contains little or no albumin. They finally die in one of 
the attacks, or feeble and emaciated. 
In some of the patients spasmodic dyspnoea is the first symptom. 
This can often be controlled for months and years, and the patients then 
seem to be well. But after a time it is more difficult to manage and 
o 
other renal symptoms are added. 
In some cases there are no symptoms for a long time, so that persons 
apparently in good health are attacked without warning by convulsions, 
coma, delirium, or hemiplegia. They may die in the first attack or live 
to go through subsequent ones. 
In some cases the only symptoms up to the time of the patient's death 
are gradual loss of flesh and strength and disturbance of digestion, the 
patient dying feeble and emaciated. These cases are hard to make out, 
unless the specific gravity of the? urine is low and a little albumin pres- 
ent. Otherwise there is nothing to draw attention to the kidneys as 
the cause of the illness. Loss of eyesight from nephritic neuro-retinitis 
may be the first symptom. 
The patients may suffer from the symptoms of cardiac disease for 
years before the congestion or degeneration of the kidney is succeeded 
by chronic nephritis. 
In many cases the course of the nephritis is modified by the compli- 
cating emphysema, phthisis, endocarditis, endarteritis, or cirrhosis of the 
liver. 
In describing these diseases of the kidneys I have followed the old 
plan of speaking of Bright's disease as if it were a real morbid entity 
which could be described and its varieties classified. For my own part 
I do not believe that there is such a disease as Bright's disease, nor- that 
the word should be used except as a popular term. 
It seems to me that, putting aside the idea of Bright's disease, the 
simplest plan is to describe the diseases of the kidneys and of their pelves 
and calyces according to the nature of the morbid process. This plan 
would give us the following classification : 
1. Acute congestion of the kidney. 
• No change in the kidney except an engorgement of the blood-vessels. CHRONIC BRIGHT'S DISEASE. 
89 
Caused by surgical operations, by injuries, by poisons, by extirpa- 
tion of one kidney. 
Produces diminution in the quantity of urine. 
2. Chronic congestion of the kidney. 
Venous congestion, changes in the epithelium, dilatation of the capil- 
laries of the glomeruli and of the capillary veins. 
Caused by any mechanical obstruction of the circulation. 
Produces diminution in the quantity of urine. 
Liable to be followed by chronic nephritis. 
3. Acute degeneration of the kidney. 
Degeneration or necrosis of the renal epithelium, to which may be 
added an exudation of serum from the blood-vessels. 
Caused by the introduction into the body of inorganic poisons, or the 
poisons of the infectious diseases. 
The milder forms give no symptoms. The severe forms are accom- 
panied by scanty urine and constitutional symptoms. 
4, Chronic degeneration of the kidney. 
Degeneration of the renal epithelium. 
Caused by disturbances of the circulation and by chronic diseases. 
Produces a diminution in the quantity of urine. 
May be followed by chronic nephritis. 
5. Acute exudative nephritis. 
Congestion; exudation of serum emigration of white blood-cells, 
diapedesis of red blood-cells into the tubules or in the stroma ; a growth 
of the cells which cover the capillaries of the glomeruli. 
Due to a variety of causes. 
Is accompanied by albumin, casts, and blood-cells in the urine, and 
by constitutional symptoms, is a transitory condition terminating in the 
death of the patient, or his recovery. 
6. Acute productive, or diffuse, nephritis. 
Congestion; exudation of serum, emigration of white blood-cells, dia- 
pedesis of red blood-cells into the tubules, or in the stroma ; a growth of 
the cells which cover the capillaries of the glomeruli and of the cells which 
line their capsules; a growth of new connective tissue in the stroma. 
Due to a variety of causes. 90 
CHRONIC BRIGHT'S DISEASE. 
Is accompanied by albumin, casts, and blood-cells in the urine, and 
by constitutional symptoms. Is apt to be followed by chronic nephritis. 
7. Chronic productive, or diffuse nephritis, with exudation. 
A growth of new connective tissue in the stroma, degeneration of the 
renal epithelium, changes in the glomeruli, changes in the arteries, an 
exudation of serum into the tubules. 
Due to a variety of causes. 
Is accompanied by albumin, casts, and blood-cells in the urine, a 
lowering of the specific gravity of the urine, changes in the quantity of 
the urine, and constitutional symptoms. 
Buns a subacute or chronic course,>and is apt to terminate fatally. 
8. Chronic productive, or diffuse nephritis, without exudation. 
A growth of new connective tissue in the stroma, degeneration of the 
renal epithelium, changes in the glomeruli and in the arteries. 
Due to a variety of causes. 
Is accompanied by urine of low specific gravity and by constitu- 
tional symptoms. Kuns a chronic course and terminates fatally. 
The two forms of chronic nephritis differ from each other anatomi- 
cally only in the presence or absence of exudation from the blood-ves- 
sels. In the same patient, therefore, the nephritis may be at one time 
without exudation, at another time with it. And according to the pres- 
ence or absence of the exudation, there will be a difference in the clini- 
cal symptoms. 
9. Suppurative nephritis. 
10. Tubercular nephritis. 
11. Emboli of the kidneys. 
12. Hydronephrosis. 
13. Pyelitis. 
14. Renal calculi. 
15. New-growths of the kidney. 
16. Displacements of the kidney. PLATE LXXX1I1. X425. 
CHRONIC CONGESTION OF THE KIDNEY. 
N. Y. Photo-Gravure Co. PLATE LXXXIV. X425. 
CHRONIC CONGESTION OF THE KIDNEY. 
N. Y. Photo-Gravure Co. PLATE LXXXV. X 425. 
CHRONIC CONGESTION OF THE KIDNEY. 
N Y. Photo-Gravure Co, PLATE LXXXVI. X425. 
CHRONIC DEGENERATION OF THE KIDNEY. 
N. Y. Photo-Gravure Co. PLATE LXXXVIT. X 25. 
CHRONIC DEGENERATION OF THE KIDNEY. 
N. Y. Photo-Gravure Co PLATE LXXXVI1I. x 25. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N Y. Photo-Gravure Co PLATE LXXX1X. X 25. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. Photo-Gravure Co. PLATE XC. X25. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. Photo-Gravure Co. PLATE XCI. X25. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. PhQto-Qravure Co- PLATE XCII. X 25. 
CHRONIC NEPHRITIS WITH EXUDATION. 
WAXY GLOMERULI. 
N Y. Photo-Gravure Co. PLATE XCIH. X200. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. Photo-Gravure Co. PLATE XCIV. X425. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. Photo-Gravure Co. PLATE XCV. X425. 
CHRONIC NEPHRITIS WITH EXUDATION. 
N. Y. Photo-Gravure Co. PLATE XCVI. X425. 
CHRONIC NEPHRITIS WITH EXUDATION. 
CORTEX TUBES. 
N. Y. Photo-Gravure Co. PLATE XCVII. x 290. 
CHRONIC NEPHRITIS WITH EXUDATION. 
CORTEX TUBES. 
N. Y. Photo-Gravure Co. PLATE XCVIII. X 250. 
CHRONIC NEPHRITIS WITH EXUDATION. 
CORTEX TUBES. 
N. Y. Photo-Gravurs Co. PLATE XCIX. X425. 
CHRONIC NEPHRITIS WITH EXUDATION. 
PYRAMID TUBES. 
N. Y, Photo-Gravure Co. PLATE 0. X 420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A GLOMERULUS WITH THE GROWTH OF CAPSULE CELLS, 
N. Y. Photo-Gravure Co PLATE CI. X420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A GLOMERULUS WITH THE GROWTH OF CAPSULE CELLS. 
N. Y, Photo-Qravure Go- PLATE CH. X420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
N. Y. Photo-Gravure Co. PLATE C1I1. X420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
N. Y, Photo-Gravure Co. PLATE CIV. X475. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
|\l. Y. Photo-Gravure Co. PLATE CV. X420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
AN ATROPHIED GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
N. Y. Photo-Gravure Co. PLATE CV1. X 420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
AN ATROPHIED GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
N Y. Photo-Gravure Co. PLATE CV11. X 420. 
CHRONIC NEPHRITIS WITH EXUDATION. 
A WAXY GLOMERULUS WITH THE GROWTH OF TUFT CELLS. 
N. Y. Photo-Gravure Co. PLATE CVIII. x25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
SENILE ATROPHIED KIDNEY. 
N. Y. Photo-Gravure Co. PLATE CIX. X25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
N. Y. Photo-Gravure Co. PLATE CX. X 25 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
N. Y. Photo-Gravure Co PLATE CXI. x 25 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
N. Y. Photo-Gravura Co. PLATE CXI1. x 25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AFTER CHRONIC CONGESTION. 
N. Y. Photo-Gravure Co. PLATE CXI 11. X 25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
N. Y. Plioto-Gravure Co PLATE CXIV. x 25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
N. Y. Photo-Gravure Co. PLATE CXV. x25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
ATROPHIED KIDNEY. 
hl. Y. Photo-Gravure Co. PLATE CXVI. X25. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
CYSTS. 
N. Y. Photo-Gravure Co. PLATE CXV1I. X 200. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
N. Y. Photo-Gravure Co. PLATE CXVIH. X420. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AN ATROPHIED GLOMERULUS. 
N. Y. Photo-Gravure Co. PLATE CX1X. X 420. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AN ATROPHIED GLOMERULUS. 
N. Y. Photo-Gravure Co. PLATE CXX. X 425. 
CHRONIC NEPHRITIS WITHOUT EXUDATION, 
AN ATROPHIED GLOMERULUS, 
N Y. Photo-Gravure Co. PLATE CXX1. X 425 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AN ATROPHIED GLOMERULUS. 
N. Y. Photo-Gravura Co. PLATE CXXI1. x 425 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AN ATROPHIED GLOMERULUS. 
N. Y, Photo-Gravure Co. PLATE CXXIII. X420. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
AN ATROPHIED GLOMERULUS. 
N. Y. Photo-Gravure Co PLATE CXXIV. X 475. 
CHRONIC NEPHRITIS WITHOUT EXUDATION. 
A GLOMERULUS WITH CHANGES IN ITS CAPSULE. 
N Y. Photo-Gravure Co. PLATE CXXV. X 420. 
CHRONIC NEPHRITIS AFTER CHRONIC CONGESTION. 
A GLOMERULUS. 
N. Y. Photo-Gravure Co. PLATE CXXVI. X 425. 
CHRONIC NEPHRITIS AFTER CHRONIC CONGESTION. 
A GLOMERULUS. 
N. Y. Photo-Gravure Co, PLATE CXXVII. X 425 
CHRONIC NEPHRITIS AFTER CHRONIC CONGESTION. 
A GLOMERULUS. 
N. Y. Photo-Grivurs Co. PLATE CXXVII1. x425. 
PART OF THE WALL OF A SMALL ARTERY. 
THICKENING OF ALL THE COATS. 
N. Y. Photo-Gravure Co. PLATE CXXIX. X425. 
A SMALL ARTERY. 
THICKENING OF ALL THE COATS. 
N- Y. Photo-Gravure Co- PLATE CXXX. X425. 
A SMALL ARTERY. 
THICKENING OF ALL THE COATS. 
N. Y. Photo-Gravure Co. PLATE CXXXI. 
A SMALL ARTERY. 
THICKENING OF ALL THE COATS. 
N. Y. Photo-Gravure Co. PLATE CXXXII. X425. 
A SMALL ARTERY. 
SCLEROSIS. 
N. Y. Photo-Gravure Co. PLATE CXXX11L X 160. 
A SMALL ARTERY. 
OBLITERATING ENDARTERITIS. 
N. Y. Photo-Gravure Co. PRICE, $3.00 
STUDIES 
IN 
p a t h o I o a i c a I 3 n a t o in n 
BY 
FRANCIS DELAFIELD, M.D. 
PROFESSOR OF PATHOLOGY] AND P R AC T IC ALT M E DIC IN E, 
COLLEGE OF PHYSICIANS AND SURGEONS. 
VOLUME II. 
PART 2. 
CHRONIC PHTHISIS 
LOBAR PNEUMONIA 
PLATES XIII-XXXIX 
JUNE, 1886. 
NEW YORK 
wm. wood & co. 
56 <& 58 Lafayette Place 
1886 REFERENCE HANDBOOK 
OF THE 
MEDICAL SCIENCES 
MESSRS WILLIAM WOOD & COMPANY beg leave to announce to the Medical Profession of the United 
States and Canada that they have for several years past been organizing and arranging for the preparation 
of a work differing from all others heretofore published in this country, and balculated, as they believe, from its 
character and the high reputation of its very large staff of learned contributors, to be the most practically and 
generally useful work, to all classes of the Medical Profession of any hitherto presented to their notice. 
It is designed that this superb work shall cover so wide a field, and embrace such a grea 
to make it of the greatest practical utility, not only to the general practitioner,but also to tl 
more particularly in special departments of medical knowledge. 
This work will consist of a collection of consisely written essays on all the 1111 
belonging' to Ilie Broad Domain of Medicine. Its subject matter will be alphabetically arranged 
thus admitting, of instant and ready reference, with no loss of time in reading over page after page to find the 
precise item desired. 
The number of those physicians •who take an interest in the more purely scientific branches of medical know- 
ledge is already quite large, and will undoubtedly increase as time goes on. It has, therefore, been thought 
advisable to devote considerable space to the more important topics belonging to the domain of Anatomy, 
Embryology, Histology, Physiology, Physiological and Pathological Chemistry, 
Pathological Anatomy, Climatology, and Medical Botany. All these topics, as well as those 
belonging to the more directly practical branches of medical knowledge, such as General Pathology and 
Therapeutics, Surgery, Gynaecology, Neurology, Otology, Ophthalmology, Obstet- 
rics, &C., &C., &c., have been assigned to writers who are experts in their respective departments. 
Wood-cut illustrations of the best character and full-page lithographic plates will be a decided feature in the 
work, and will be introduced wherever the authors themselves think that they will serve to elucidate the text. 
Special pains have been taken to secure as large a proportion of original cuts as possible, and no expense has been 
spared in this or in any other branch of the wdrk to secure the highest order of excellence. 
THE REFERENCE HANDBOOK OF THE MEDICAL SCIENCES, will be limited to a series of Eight 
Splendid Imperial Octavo Volumes. 
The pages are of large size, in double columns and the type as small as can be read comfortably by a person 
of ordinary good eyesight. Each page carrying as many words as three ordinary full octavo pages. 
It will be seen that the volumes admit of the introduction of an enormous amount of reading matter (equal 
to the contents of twenty or more of the usual size of octavo volumes), which will be of so practical a nature 
that the entire work will be literally a handbook for the daily, constant reference of the Profession,-a book 
which no physician, whose time is worth anything at all, can afford to be without. 
Large treatises on the Practice of Medicine and Surgery, and on other branches of medical knowledge have 
their appropriate arid necessary place,;-for long, deliberate and patient study,-but this Reference Hand- 
book is designed to furnish not only Thorough and Exhaustive Information, but'to be a con- 
stant daily companion and ready reference on all branches of Medicine and the Collateral 
Sciences. 
A large part of the material contained in this handbook is original work, and upon some subjects, the 
information now to be presented has heretofore been inaccessible, by reason of its being scattered through 
governmental and other manuscript records and archives. 
Prices at which this work wilt be sold: 
In extra English muslin binding, per volume, $6.00 ; in fine leather, raised bands, per volume, 
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Send for a complete Circular giving list of Contributors (300) and 
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VOLUME ONE IS NOW READY. price, $3.50 
STUDIES 
IX 
Anatomy 
BY 
FRANCIS DELAFIELD, M.D. 
PKOSK88OB OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS. 
VOLLJ1\ZEE II. 
PART 3. 
ACUTE BRIGHT'S DISEASE 
PLATES XL-LXXXIL 
NOVEMBER, 1888. 
NEW YORK 
W^ZE. WOOD & CO- 
56 & 58 Lafayette Place 
1888 . REFERENCE HANDBOOK 
OF THE ' 
MEDICAL SCIENCES' 
MESSRS WILLIAM WOOD & COMPANY beg leave to announce to the Medical Profession of the United! 
States and Canada that they have for several years past been organizing and arranging for the preparation 
of a work differing from all others heretofore published in this country, and calculated, as they believe, from its] 
character and the. high reputation of its very large staff of learned contributors, to be the most practically and' 
generally useful work to all classes of the Medical Profession of any hitherto presented to their notice. 
It is designed that this superb work shall cover so wide a field, and embrace such a great variety of topics, as 
to make it of the greatest practical utility, not only to the general practitioner, but also to those who are interested 
more particularly in special departments of medical knowledge. 
This work will consist of a collection of consisely written essays on all the Important Topics 
belonging to the Broad Domain of Medicine. Its subject matter will be alphabetically arranged, 
thus admitting of instant and ready reference, with no loss of time in reading over page after page to find the 
precise item desired. 
The number of those physicians who take an interest in the more purely scientific branches of medical know- 
ledge is already quite large, and will undoubtedly increase as time goes on. It has, therefore, been thought 
advisable to devote considerable' space to the more important topics belonging to the domain of Anatomy, 
Embryology, Histology, Physiology, Physiological and Pathological Chemistry, 
Pathological Anatomy, Climatology, and Medical Botany. All these topics, as well as those 
belonging to the more directly practical branches of medical knowledge, such as General Pathology and 
Therapeutics, Surgery, Gynaecology, Neurology, Otology, Ophthalmology, Obstet- 
rics, &c., &C., &c., have been assigned to writers who are experts in their respective departments. 
Wood-cut illustrations of the best character and full-page lithographic plates will be a decided feature in'the 
work, and will be introduced wherever the authors themselves think that they will serve to elucidate the text. 
Special pains have been taken to secure as large a proportion of original cuts as possible, and no expense has been 
spared in this or in any other branch of the work to secure the highest order of excellence. 
THE REFERENCE HANDBOOK OF THE MEDICAL SCIENCES, will be limited to a series of Eight 
Splendid Imperial Octavo Volumes. 
The pages are'of large size, in double columns and the type as small as can be read comfortably by a person 
of ordinary good eyesight. Each page carrying as many words as three ordinary full octavo pages. 
It will be seen that the volumes admit of the introduction of an enormous amount of reading matter (equal 
to the contents of twenty or more of the usual size of octavo volumes), which will be of so practical a nature 
that the entire work will be literally a handbook for the daily, constant reference of the Profession,-a book 
which no physiciah, whose time is worth anything at all, can afford to be without. 
Large treatises on the Practice of Medicine and Surgery, and on other branches of medical knowledge have 
their appropriate and necessary place -for long, deliberate and patient study,-but this Reference Hand* 
book is designed to furnish not only Thorough and Exhaustive Information, but to be a Con- 
stant daily companion and ready reference on all branches of Medicine and the Collateral 
Sciences. 
A large part of the material contained in this handbook is original work, and upon some subjects, the1 
information now to be presented has heretofore been inaccessible, by reason of its being scattered through 
governmental and other manuscript records and archives. 
Prices at which this work will be sold: 
In extra English muslin binding, per volume, $6.00 ; in fine leather, raised bands, per volume, 
$7.00 ; in extra Turkey morocco, English cloth sides, per volume, $8.00. 
Send for a complete Circular (jiving list of Contributors (300) and 
Specimen pages from the Work (free). 
Seven volumes have now Been published. Volume eight, completing the work, 
will follow shortly. PRICE, $5.00 
STUDIES 
IN 
pathological Ana I o my 
BY 
FRANCIS DELAFIELD, M.D., LL.D. 
PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
VOLUME II. 
PART 4 
CHRONIC BRIGHT'S DISEASE 
PLATES LXXXIII. - CXXXIII. 
SEPTEMBER, 1891 
NEW YORK 
WM. WOOD & CO. 
56 & 58 Lafayette Place 
1891 REFERENCE HANDBOOK 
OF THE 
MEDICAL SCIENCES 
MESSRS WILLIAM WOOD & COMPANY beg leave to announce to the Medical Profession of the Unite*. 
States and Canada that they have for several years past been organizing and arranging for the preparation 
of a work differing from all others heretofore published in this country, and calculated, as they believe, from its 
character and the nigh reputation of its very large staff of learned contributors, to be the most practically and 
generally useful work to all classes of the Medical Profession of any hitherto presented to their notice. 
It is designed that this superb work shall cover so wide a field, and embrace such a great variety of topics, as 
to make it of the greatest practical utility, not only to the general practitioner font also to those who are interested 
more particularly in special departments of medical knowledge. 
This work will consist of a collection of consisely written essays on all the Important Topics 
belonging- to the Broad Domain of Medicine. Its subject matter will be alphabetically arranged, 
thus admitting of instant and ready reference, with no loss of time in reading over page after page to find the 
precise item desired. 
The number of those physicians who take an interest in the more purely scientific branches of medical know- 
ledge is already quite large, and will undoubtedly increase as time goes on. It has, therefore, been thought 
advisable to devote considerable; space to the more important topics belonging to the domain of Anatomy, 
Embryology, Histology, Physiology, Physiological and Pathological Chentistry, 
Pathological Anatomy, Climatology, and Medical Botany. All these topics, as well as those 
belonging to the more directly practical branches of medical knowledge, such as General Pathology and 
Therapeutics, Surgery, Gynaecology, Neurology, Otology, Ophthalmology, Obstet- 
rics, &C., &C-, have been assigned to writers who are experts in their respective departments. 
Wood-cut illustrations of the best character and full-page lithographic plates will be a decided feature in the 
work, and will be introduced wherever the authors themselves think that they will serve to elucidate the text. 
Special pains have been taken to secure as large a proportion of original cuts as possible, and no expense has been 
spared in this or in any other branch of the work to secure the highest order of excellence. 
THE REFERENCE HANDBOOK OF THE MEDICAL SCIENCES, will be limited to a series of Eight 
Splendid Imperial Octavo Volumes. 
The pages are of large size, in double columns and the type as small as can be read comfortably by a person 
of ordinary good eyesight. Each page carrying as many words as three ordinary full octavo pages. 
It will be seen that the volumes admit of the introduction of an enormous amount of reading matter (equal 
to the contents of twenty or more of the usual size of octavo volumes), which will be of so practical a nature 
that the entire work will be literally a handbook for the daily, constant reference of the Profession,-a book 
which no physician, whose time is worth anything at all, can afford to be without. 
Large treatises on the Practice of Medicine and Surgery, and on other branches of medical knowledge have 
their appropriate and necessary place,-for long, deliberate and patient study,-but this Deference Hand- 
book. is designed to furnish not only Thorough and Exhaustive Information, but to be a con- 
stant daily companion and ready reference on all branches of Medicine and the Collateral 
Sciences. 
A large part of the material contained in this handbook is original work, and upon some subjects, the 
information now to be presented has heretofore been inaccessible, by reason of its being scattered through 
governmental and other manuscript records and archives. 
Prices at which this work will be sold: 
In extra English muslin binding, per volume, $6.00 ; in fine leather, raised bands, per volume, 
$7.00 ; in extra Turkey morocco, English cloth sides, per volume, $8.00. 
Send for a complete Circular giving list of Contributors {300) and 
Specimen pages from the Work {free). 
Seven volumes have now been published. Volume eight, completing the work, 
will follow shortly.