STUDIES 
IN 
PATHOLOGICAL ANATOMY 
BY 
FRANCIS DELAFIELD, M.D. 
adjunct professor of pathology and practical medicine; visiting physician and curator to 
BELLEVUE HOSPITAL; VISITING PHYSICIAN AND PATHOLOGIST TO THE ROOSEVELT HOSPITAL 
VOLUME I. 
PLATES I.-XOIII. 
NEW YORK 
WILLIAM WOOD & COMPANY 
1882 Copyright 
WILLIAM WOOD & COMPANY 
1882 
Prow's 
Printing and Bookbinding Company 
201-213 East 12 tk Street 
NEW YORK PREFACE. 
In presenting to the profession the first volume of my "Studies 
in Pathological Anatomy," it seems proper to say a word concerning 
the scope and object of the work. 
It has not been my intention to write a treatise on Pathological 
Anatomy, nor to give an account of the labors of others in the 
same field. My object has been a much more restricted one:-to 
describe and figure the minute lesions of disease from the material 
which lias fallen under my own observation. 
In doing this I have attempted to follow the purely objective 
method-to see and to describe whatever could be made out in the 
different post-mortem lesions of disease. Such a plan of study in- 
volves following Nature wherever she may lead, and gives rise to 
apparent contradictions, which cannot always be reconciled. 
In such a descriptive work the drawings are of importance. It 
would, of course, be preferable to reproduce all the specimens by 
photography, but this plan seems to be only available for low mag- 
nifying powers. In this way I have employed the process for topo- 
graphical purposes. The photographs have been made by Mr. Mason, 
and by the Artotype Company. 
For high magnifying powers it is necessary to make drawings 
with the camera lucida, and these drawings should be of the actual IV 
PREFACE. 
size of the specimens. They must also be reproduced without the 
intervention of an artist, even at the sacrifice of much beauty. The 
plates must, therefore,' be of large size, and must be drawn directly 
on wood, stone, or copper, or reproduced by one of the photographic 
processes; all these plans have been tried with varying success. No 
one can feel more than I, how imperfect many of the plates are. 
It is 'my intention to continue the work until I have described 
all the lesions with which I am acquainted; but the original plan 
of publishing in monthly parts will be abandoned. The fasciculi will 
be issued of varying size and at different intervals, according to 
the subjects treated of. 
In the second volume the description of the lesions of chronic 
pulmonary phthisis will be completed. 
FRANCIS DELAFIELD, 
12 West Thirty-second Street. STUDIES 
IN 
PATHOLOGICAL ANATOMY. 
CONNECTIVE TISSUE. 
There is a certain convenience in considering the human body as com- 
posed of connective tissue, mucous membranes, epithelial membranes, and 
viscera. Of these the viscera and the mucous membranes are not merely 
living tissues, but are capable of performing certain functions. The epi- 
thelial membranes and connective tissue simply act as a living frame- 
work, by which the viscera and mucous membranes are supported and 
held together. 
To the connective-tissue group belong bone, cartilage, mucous tissue, 
neuroglia, and connective tissue proper; it is of the last of these that we 
have to speak. 
Connective tissue proper covers the bones and holds their articular 
ends together, lines all the cavities of the body, forms a layer beneath 
the skin, separates the muscles from each other, joins them to the bones, 
covers the nerves, forms the walls of the blood-vessels, and makes part 
of the viscera. In these different situations it is called by different 
names, such as periosteum, ligaments, synovial membranes, serous mem- 
branes, subcutaneous connective tissue, fasciae, tendons, neurilemma, 
interstitial tissue. 
Wherever it is situated, connective tissue is composed of a basement 
substance and of cells, and imbedded in it are blood-vessels, lymphatic 
vessels, and nerves. 6 
STUDIES IN PATHOLOGICAL ANATOMY. 
The basement substance, while still alive, is translucent and nearly 
homogeneous. After death it coagulates regularly into small fibres com- 
.posed of still smaller fibrillae. These fibres are arranged side by side so 
as to form lamellae, or they cross and interlace with each other irregu- 
larly ; they are then called fibrillated connective tissue. Or, the fibres 
may be so arranged as to form a network or reticulum; and they are then 
called reticulated connective tissue. In many places the basement sub- 
stance is strengthened by small, smooth fibres, sometimes anastomosing 
with each other. These are called yellow elastic fibres, and seem to be 
of a different chemical composition from the rest of the basement sub- 
stance. 
The cells, excluding the wandering cells or white blood-globules, 
conform to two types: 1st, that of flat cells; 2d, that of cells with 
irregular branching bodies. 
Wherever the basement substance is arranged in lamellae and these 
lamellae are joined together so as to form a membrane with a free sur- 
face, this free surface is covered by the flat cells. These flat cells have 
a large nucleus- surrounded by a large, flat cell-body. The edges of the 
cells are in very close apposition, so that they adhere to each other. On 
the surfaces of the serous membranes, of the blood-vessels and of the lym- 
phaticvessels these cells are called endothelial cells; they are also found, 
however, in the subcutaneous tissue and the fasciae, although in these 
latter situations they have received but little attention. If we inject a 
solution of gelatine beneath the skin and allow it to harden, we find 
the subcutaneous connective tissue is separated into a great number of 
lamellae enclosing irregular spaces. If we take the leg of a small ani- 
mal, strip off the skin, soak it in a solution of nitrate of silver of the 
strength of 1 to 1,000, and then expose it to the light, we find the sur- 
faces of these lamellae covered by black lines enclosing regular spaces. 
These black lines mark the edges of the flat cells. If we prepare another 
leg in the same way, but soak it for a week in a solution of alcohol 100 
parts, water 200 parts, 1 per cent, solution of osmic acid 1 part, then cut 
off small portions of the lamellae and stain them with haematoxylin and 
eosin, we will see large, flat, nucleated cells covering the lamellae; such 
cells are figured in Plate 1. In the upper part of the plate are figured CONNECTIVE TISSUE. 
7 
the cells as shown by nitrate of silver, in the lower part the same cells 
as they appear when isolated. 
The branched cells are found everywhere imbedded in the basement 
substance, or rather perhaps between the fibres of which the basement 
substance is composed. For the knowledge of the importance of these 
cells we are indebted to Virchow. He described them as fusiform or 
stellate cells with anastomosing processes, and gave them the name of 
connective-tissue corpuscles - a name which they have since retained. 
While he recognized their general shape and arrangement, he failed, 
owing to imperfect modes of preparation, to observe their full size and 
contours. 
A few years ago Ranvier and Boll studied these cells more thoroughly, 
especially in tendons, and described them as flat cells. It seemed at first 
as if the older idea of connective-tissue corpuscles must be given up. 
Still further study, however, has shown that they are not flat cells, but 
are large irregular masses of protoplasm, with branching and anastomo- 
sing processes given off in all directions. 
The nuclei of these cells are large, ovoid bodies, easily stained and 
easily seen, preserving their shape under most circumstances. One 
or more such nuclei are found in each cell. The cell-bodies, on the 
contrary, are composed of a very delicate substance, not easily 
stained and not easily seen. This substance coagulates into various 
shapes after death. As we look at the cell-bodies with the microscope, 
our idea of their shapes will vary with the completeness with which 
they are demonstrated. They will look like oval nuclei, or like narrow 
fusiform cells, or like flat, nucleated cells, or like large, irregular masses 
of protoplasm with processes running in every direction. The more com- 
plete the demonstration, so much the larger do the cell-bodies appear, 
and so much the more numerous are their anastomosing processes. 
They form a continuous system of cells imbedded in the basement sub- 
stance. Their processes anastomose not merely in the same plane, but in 
every direction from the nucleus. Their branching shape resembles so 
closely that of the small lymph-spaces that the two have been supposed 
to be identical. But both cells and lymph-spaces can be demonstrated 
in the same specimen as distinct objects. Plate II. shows the branching 8 
STUDIES IN PATHOLOGICAL ANATOMY. 
cells in the tendon of a dog's leg; Plate III. the cells in the omentum 
of the rabbit. 
Connective tissue contains a very abundant system of lympha- 
tics, consisting of canals of different sizes and of stellate spaces com- 
municating with them. In it ramify also the blood-vessels and the 
nerves. 
There are a number of changes which may occur in connective tissue 
called inflammatory changes, but they differ so widely in their anatomy 
that they must be described under separate names. We speak, 
therefore, of 
1. Cellular Inflammation. 
2. Inflammation with the production of Serum, Fibrine, and Pus. 
3. Necrotic Inflammation. 
4. Inflammation with the formation of Abscesses. 
5. Reparative Inflammation. 
6. Hyperplastic Inflammation. 
7. Tubercular Inflammation. 
By cellular inflammation I mean a change involving principally the 
fixed connective-tissue cells, these cells becoming increased in size and 
number. The blood-vessels and the basement substance undergo little 
or no change. 
By inflammation with the production of serum, fibrine, and pus, I 
mean changes involving principally the blood-vessels. The plasma of 
the blood transudes and appears as fibrine and serum; the white glob- 
ules emigrate and appear as pus-cells. 
By necrotic inflammation, I mean changes involving both the blood- 
vessels and the tissue, and resulting in the death of the inflamed parts, 
either with or without putrefaction. 
By inflammation with the formation of abscesses, I mean a complex 
process involving both the blood-vessels and the tissues, and resulting 
in the destruction of tissue, and the formation of pus. 
By reparative inflammation, I mean the changes which result in the 
formation of new tissue, to take the place of tissues destroyed by injury 
or disease. 
By hyperplastic inflammation, I mean an inflammatory growth of 9 
CONNECTIVE TISSUE. 
new connective tissue, both cells and basement substance, not preceded 
necessarily by the production of pus or fibrine, or of cells alone. 
By tubercular inflammation, I mean a form of inflammation resulting 
in the formation of an inflammatory product called tubercle. Tubercle 
is composed of a reticulated basement substance, of flat nucleated cells 
and of giant cells. It seems to be merely a form of connective tissue. 
It is produced either in the form of little rounded masses-tubercle- 
granula, or of a diffuse growth. Tubercle is a permanent inflammatory 
product. When once formed it remains unchanged or is transformed 
into ordinary connective tissue, or undergoes cheesy degeneration. 
Tubercular inflammation seldom, if ever, occurs by itself. It is accom- 
panied by one or other of the varieties of inflammation, so that with 
the tubercle we find pus, fibrine, serum, new connective tissue, or 
necrotic changes. THE PLEURA. 
Concerning the anatomy of the pleura not much has been written. 
The most important contributions to our knowledge of it are by 
Dybkowsky and Klein. 
Dybkowsky has described very fully the lymphatics of the pleura, 
especially those in the parietal portion of that membrane. His conclu- 
sions are in the main identical with my own observations. 
Klein has described the endothelium and the lymphatics of the pul- 
monary and of the mediastinal pleura in a very satisfactory manner. 
My own studies have been directed principally to that portion of 
the pleura which lines the chest-wall. Although in every pleurisy all 
the different parts of the pleura are usually inflamed, yet it is the 
parietal pleura which takes the principal share in the morbid process, 
and in idiopathic pleurisy it is the part first inflamed. The pleura is 
classed by anatomists with the serous membranes. The following 
general description of it is taken from Quain's " Anatomy 
"The pleurae are serous membranes, forming two shut sacs, quite 
distinct from each other, which line the right and left sides of the 
thoracic cavity, form by their approximation in the middle line the 
mediastinal partition, and are reflected each upon the root and over the 
entire free surface of the corresponding lung. Each pleura consists of 
a visceral and a parietal portion. The visceral portion (pleura pulmo- 12 
STUDIES IN PATHOLOGICAL ANATOMY. 
nalis) covers the lung; and the parietal portion lines the ribs and inter- 
costal spaces (pleura costalis), covers the upper convex surface of the 
diaphragm, enters into the formation of the mediastinum, and adheres 
to the sides of the pericardium. At the root of each lung the visceral 
and parietal portions of the corresponding pleura are continuous with 
one another; and, at the lower border of the root, is a triangular fold 
of the serous membrane extending vertically along the inner surface of 
the lung down to the diaphragm, to which it is attached by its extremity; 
this fold is named ligamentum latum pulmonis. 
" The upper part of the pleura rises into the root of the neck, reach- 
ing an inch or an inch and a half above the first rib, and passes up 
under cover of the scaleni muscles. The right pleura is generally 
stated to reach higher in the neck than the left, but this is certainly not 
always the case. Anteriorly the pleural sacs of opposite sides come 
nearly or altogether into contact behind the second piece of the sternum 
and continue so for some distance; but opposite the lower end of the 
sternum the right pleura passes beyond the middle line or remains close 
to it, while the left recedes to a variable distance. Inferiorly the pleurae 
do not pass quite down to the attachments of the diaphragm, but 
leave a portion of its circumference in contact with the costal parietes. 
The right pleural sac is shorter and wider than the left." 
Such is the usual description given of the pleura by general anato- 
mists. For our purposes, however, it seems more convenient to consider 
it in a somewhat different manner. 
The pulmonary pleura is not merely a membrane covering the lungs, 
but it is an essential part of those viscera. The lungs are composed 
principally of connective tissue, and this tissue is arranged on the sur- 
face of each lung in the form of a smooth membrane. It would be 
difficult for the lungs to be constructed at all without some such smooth 
external surface. 
In the same way the inner surface of the thoracic cavity in which 
the lungs are contained is lined with connective tissue. There is not a 
membrane distinct from the tissues beneath, but a layer of connective 
tissue continuous with these tissues. The costal pleura is continuous 
with the periosteum of the ribs and the fasciae of the intercostal THE PLEURA. 
13 
muscles. The diaphragmatic pleura is continuous with the tendons and 
fascirn beneath it. The mediastinal pleura forms a membrane by itself 
of somewhat different structure from the rest of the pleura. 
The minute anatomy of the pleura may be conveniently studied in 
the dog and in man. In both the pleura is of sufficient thickness to be 
easily handled and split up into thin layers. 
If now we cut out two or three ribs with the pleura in place, either 
from a dog or a human being, and allow them to soak for twenty-four 
hours in a mixture of dilute alcohol and osmic acid, we can with the 
forceps and scissors tear off one plane after another of connective tissue 
until we come down to the muscle and bone. The innermost of these 
planes, forming the free surface of the pleura, is covered with a con- 
tinuous layer of flat nucleated cells, usually called endothelial cells. 
These cells, if demonstrated in this way, or with chloride of gold, or if 
looked at fresh in salt and water, look at first almost like a continuous 
nucleated membrane. The edges of the cells are in such close apposi- 
tion that the lines of demarcation between the cell-bodies are not easily 
seen. Close inspection, however, with a high power shows that there 
really are dividing lines between the cells. If we soak the pleura for 
about twenty minutes in a solution of nitrate of silver (1-1000) and 
then expose it to the light, the silver will be oxidized in black lines 
between the ed^es of the cell-bodies. It is still uncertain whether 
these black lines indicate the existence of a cement substance uniting 
the cells, or whether the silver is precipitated between the edges of the 
cells. 
When the endothelium is thus demonstrated with silver it becomes 
evident that all the cells are not of the same size, and that every here 
and there are small spaces where the oxidized silver forms black patches. 
These black patches are probably openings through the layer of endo- 
thelium into the lymphatics. These openings, or stomata, however, are 
not as regularly formed as they are in some other serous membranes. 
In Plates IV. and V. is shown the endothelium of a dog's pleura; 
in Plate VI. the endothelium of the human pleura treated with nitrate 
of silver. 
If now we carefully brush off the layer of endothelium, we find that 14 
STUDIES IN PATHOLOGICAL ANATOMY. 
it was spread out over a smooth surface formed by the apposition of 
fibres of connective tissue reinforced by elastic anastomosing fibres. 
Running in parallel rows at the edges of the fibres are the fixed con- 
nective-tissue cells, which appear as bodies of ovoid or fusiform shape, as 
seen in Plate IV. More careful demonstration and a higher magnifying 
power show that the fixed cells really have a large cell-body with 
branching processes, as is seen in Plate V. 
The deeper layers of the pleura are formed in the same way of 
planes of connective-tissue fibres, of anastomosing elastic fibres, and of 
branching cells, but the cells are most numerous in the layer just 
beneath the endothelium. 
To demonstrate the blood-vessels of the pleura we can inject down- 
wards through the carotid arteries, or upwards through the aorta. The 
capillaries show well after soaking in chloride of gold. The intercostal 
arteries break up into smaller branches terminating in a capillary 
plexus with wide meshes. Some of the capillaries extend into the 
layer of connective tissue immediately beneath the endothelium. The 
vessels are surrounded by a layer of branching connective-tissue cells. 
The lymphatics can be shown either by soaking the pleura in a solu- 
tion of nitrate of silver (1-1000), or by injecting a five per cent, solu- 
tion of Prussian blue into one of the pleural cavities about two hours 
before the animal is killed. 
There are a great number of anastomosing lymphatic vessels of 
large size lined with endothelium, and apparently communicating with 
these vessels are irregular stellate spaces. The lymphatic vessels are 
only found over the intercostal spaces; they do not extend into the 
pleura which covers the ribs. In Plate VII. are seen the lymphatics of 
a dog's pleura, and it will be seen that the lymphatics occupy a 
larger area than does the tissue between them. 
The lymphatic spaces do not correspond to the branching connective- 
tissue cells, but are distinct from them. Both can be demonstrated 
in the same specimens, as is seen in Plate VIII. THE INFLAMMATIONS OF THE PLEURA 
Tile human pleura may become the seat of a variety of inflamma- 
tory processes, which we will describe under the following names: 
(1.) Pleurisy with the production of fibrine alone. Dry pleurisy. 
Pleuritis sicca. Acute pleurisy. 
(2.) Pleurisy with the production of fibrine and serum. Pleurisy 
with effusion. Subacute pleurisy. 
(3.) Pleurisy with the production of pus. Empyema. 
(4.) Dropsical effusions in the pleural cavities. Hydrothorax. 
(5.) Chronic pleurisy with permanent adhesions. 
(6.) Pleurisy of chronic pulmonary phthisis. 
(7.) Tubercular pleurisy. 
1. Pleurisy with the production of fibrine. 
This variety of pleurisy occurs after exposure to cold, after fracture 
of the ribs, with pneumonia, with phthisis, with infarctions of the lungs, 
in the course of pyaemia, of puerperal fever, of peritonitis and of 
Bright's disease. Some individuals have a peculiar predisposition to the 
disease, and will suffer from repeated attacks during successive winters. 
In the idiopathic cases the inflammation usually involves circum- 
scribed portions of the costal, pulmonary, mediastinal, or diaphragmatic 
pleura. Sometimes, however, a larger area of pleura is involved; and, 
as an exceptional thing, the entire pleura of one side is inflamed. 16 
THE INFLAMMATIONS OF THE PLEURA. 
Such cases usually die (if they die at all) after the inflammation is 
fairly established, or else after it has run its course. When the inflam- 
mation is fairly established, we find the affected portions of the pleura 
covered with a thin layer of fibrine, while the pleura beneath is con- 
gested. I have seen one case in which the amount of fibrine was so 
great that the lung was compressed by it against the vertebral column. 
After the inflammation has run its course, we find new connective tissue 
thickening the pleura and forming adhesions between the lobes of the 
lungs, and between the lungs and the chest wall. 
2. Pleurisy with the production of fibrine and serum. 
This form of pleurisy is due to the same causes as the form just 
described. It usually involves the entire pleura of one side, sometimes 
of both sides. If the pleurisy is double, it is often complicated by 
pericarditis. 
While the inflammation is in progress we find most of the pleura 
covered with a thick layer of fibrine. This fibrine varies in color and 
consistence according to the number of pus-globules entangled in it. 
It not only coats the pleura, but it forms adhesions between the pulmo- 
nary and costal pleura. In the pleural cavity is serum in variable 
quantity. This serum is almost clear, or turbid from the admixture of 
pus-cells and flocculi of fibrine. The lung is compressed against the 
vertebral column by the fluid, or the adhesions fasten it to the chest 
wall in different positions. 
The patients may die during this stage of the disease; or the 
inflammation may change its character and become purulent; or the 
patients recover with permanent adhesions and thickenings of the pleura. 
These two forms of pleurisy, although differing widely in their 
clinical history, are yet essentially the same. In both of them we find 
a regular sequence of changes. First, the production of fibrine and a 
few pus-cells either with or without serum. Second, a gradual absorp- 
tion of the serum, and a disappearance of the fibrine. Lastly, as the 
regular termination of the inflammation, the formation of permanent 
new connective tissue in the shape of adhesions or of thickenings of the 
pleura. Variations from the regular course of the inflammation are 
effected by the excessive formation either of the fibrine, the pus, or the 17 
THE INFLAMMATIONS OF THE PLEURA. 
serum, and by the failure of the absorption of these inflammatory 
products. 
If we endeavor to follow out the successive changes by which the 
fibrine, pus, and serum make their appearance and then disappear, and 
the way in which permanent new tissue takes their place, we encounter 
several difficulties. It is impossible, in any ordinary experience, to 
obtain autopsies which will give the lesions belonging to each successive 
day of the disease; the pleura does not really show well if the patient 
has been dead more than two or three hours before the autopsy ; and in 
most cases the inflammation is too energetic, its products are too abundant 
to be easily studied. 
To obviate these difficulties we must resort to the lower animals. 
By injecting a saturated solution of chloride of zinc, with a hypodermic 
syringe, into the pleural cavity of a dog, we can excite a pleurisy exactly 
resembling what we see in the human subject. By varying the amount 
of fluid injected, and by injecting it into one or both pleural cavities, 
we can obtain pleurisies of different degrees of intensity, and with dif- 
ferent amounts of products of inflammation. By using a number of 
animals we can observe the course of the inflammation from hour to 
hour, and from day to day. 
The very first change we observe in such an artificial pleurisy is a 
simple congestion. The parietal pleura is of a uniform rosy red color, 
its surface is shining and moist as in health. There is no serum and no 
fibrine. Minute examination, however, shows that the endothelial cells 
have fallen off in patches, and that where they have thus fallen off the 
superficial connective-tissue cells are swollen and multiplied, and there 
are some pus-cells. This is all that takes place for from half an hour 
to six hours after the injection has been made. 
The next step in the inflammatory process is the appearance of 
serum and fibrine in variable amounts. The serum collects in the 
bottom of the pleural cavity. It is usually slightly turbid from the 
admixture of blood-globules and pus-cells. The fibrine coats the whole 
surface of the pleura. There may be so little of it that it cannot be 
seen with the naked eye, or its amount may be considerable. The sur- 
face of the pleura loses its natural glistening appearance in proportion 18 
THE INFLAMMATIONS OF THE PLEURA. 
to the amount of fibrine coating it. The fibrine appears first in the form 
of little knobs and strings, or of a thin layer of granular matter. Where 
the endothelium still adheres the edges of the cells are separated from 
each other by granular matter. A few pus-cells are seen entangled in 
the fibrine, and imbedded in the pleura. The swelling and new growth 
of the fixed connective-tissue cells is now very marked. The branching 
bodies of the old cells are readily seen. The new cells are of different 
shape from the old ones. They are polygonal cells with a distinct cell 
body and nucleus, and are arranged in rows parallel with the course of 
the fibres. These new cells give the impression of being formed in some 
way from the old fixed cells, but precisely how I am unable to say. 
The time varies from half an hour to seven hours before these changes 
take place. By the end of twenty-four hours they are always fully 
developed. 
Plate IX. shows the swollen connective-tissue cells, and the new cells 
in the superficial layer of the pleura, just beneath the fibrine, the latter 
being stripped off. 
On the second day of the pleurisy the gross and minute appearances 
are unchanged, only the layer of fibrine is thicker and there is more 
serum. Up to this time the lymphatic vessels and spaces can still be 
demonstrated with nitrate of silver, and are apparently empty. 
On the third day in some cases, not until the fourth in others, the 
growth of new cells has become well marked. The layer of fibrine on 
the pleura is more consistent, the serum is still abundant or has begun 
to disappear. The new cells present a great variety of shapes. Some 
are of the shapes seen in Plate IX., others are of the same shape but 
smaller, others are much larger and of polygonal, rounded, fusiform, or 
branching shape. These cells are very abundant in the superficial layers 
of the pleura, but not in the deeper layers. The pleura is not much 
thickened. They are also present in large numbers entangled in the 
layer of fibrine coating the pleura, and in the adhesions of fibrine 
between the pulmonary and costal pleura. 
Plate X. shows such a layer of fibrine stripped off from the pleura 
with large numbers of new cells imbedded in it. 
By the fourth or fifth day, according to the case, new blood-vessels THE INFLAMMATIONS OF THE PLEURA. 
19 
make their appearance in the layer of fibrine and cells. These vessels can 
be injected artificially from the aorta; they are continuous with the old 
vessels of the pleura. They are of large size, numerous, and with thin 
walls. In the pleura itself the vessels are increased in size and number. 
At the same time the fibrine begins to disappear, and the new cells form 
a more continuous layer. 
Plate XI. represents a portion of the layer of new tissue stripped off 
from the pleura. The vessels are distorted by the pressure of the arti- 
ficial injection. The cells form a continuous layer, the fibrine at this 
place having disappeared. 
By the sixth day the layer of fibrine and new tissue on the surface 
of the pleura is more adherent. It begins to form a part of the pleura. 
The serum has by this time usually disappeared; the fibrine also is less 
in amount. The new cells are still numerous, and they are becoming 
arranged into two divisions : a superficial layer resembling the old 
endothelium, and a deeper layer of fusiform and branching cells. Of 
the new endothelial cells some present a curious appearance from the 
distention of the cell-bodies by cavities or vacuoles. 
On the seventh day the condition is much the same. The new endo- 
thelial cells appear first in patches and rows, which afterwards increase 
in area. At this time the adhesions between the costal and pulmonary 
pleura are also partly covered with endothelium. 
After this time the fibrine continues to diminish in amount until by 
the fourteenth day it has usually entirely disappeared. Of the new 
cells, the superficial layer gradually forms a continuous layer of endo- 
thelium. In the deeper layer the rounded and polygonal cells are not 
as numerous, while there are many large and small fusiform and branch- 
ing cells, some of them very long and continuous with each other, as 
seen in Plate XII. Gradually a basement substance makes its appear- 
ance between the cells, at first homogeneous, afterwards fibrillated. 
These changes continue until by the end of three weeks the pleura 
has its normal appearance, except that it is thickened, and that there 
are adhesions between the costal and pulmonary pleura. But if we 
examine the superficial layers of this thickened pleura we will still find 
an excess of cells. 20 
THE INFLAMMATIONS OF THE PLEURA. 
The lesions of human pleurisy are substantially the same as those 
just described. The only difference is that the fibrine, pus, and serum 
are produced in very much larger quantities, and as a result of this the 
absorption of these products and the formation of new tissue follow 
more slowly. It may also happen that the inflammation changes its 
character and becomes purulent. 
We may then draw the following conclusions: 
1. In pleurisy with the production of fibrine alone, or of fibrine 
and serum, two distinct pathological processes regularly take place, 
(a) The blood-vessels become congested and through their walls transude 
the plasma of the blood and a few white blood-globules; part of the 
plasma appears as serum, part of it contains substances which by the 
action of the emigrated white globules are transformed into fibrine. 
(Z>) At the very commencement of the inflammation the superficial fixed 
connective-tissue cells also begin to increase in size and number. 
2. The products of the first of these processes - the fibrine and 
serum-are regularly reabsorbed. In many patients, however, the 
course of the disease is irregular, and these products remain for a long 
time. 
3. The product of the second of these processes regularly increases. 
The new cells formed in the superficial layers of the pleura wander 
into the fibrine coating the pleura and forming adhesions, and there 
grow and multiply. New blood-vessels and a new basement substance 
are formed between these cell 
4. The natural termination of such a pleurisy is the formation of 
new tissue coating the pleura and forming adhesions. 
5. The irregular terminations of such a pleurisy are : the death of 
the patient; the protracted existence of the fibrine and serum; the 
change into empyema; and the formation of an excessive amount of 
new connective tissue. EMPYEMA. 
Pleurisy, with the production of fibrine, serum, and a large amount 
of pus, occurs under several different conditions. 
1. A person may be attacked by a pleurisy in which there is from 
the first an undue amount of pus with the fibrine and serum. In such a 
case the constitutional disturbance is very severe. These cases are 
fortunately not common. 
2. The pleurisy at first is only attended with the production of 
fibrine and serum, and after the lapse of weeks or months gradually 
assumes a purulent character; or, instead of the change in the character 
of the inflammation being gradual, it is sudden, with a corresponding 
change in the constitutional symptoms. 
3. Abscesses in the wall of the thorax, or in the liver, or in the 
abdomen, rupture into a pleural cavity and set up a purulent inflamma- 
tion. 
4. Abscesses of the lung, or phthisical cavities in the lung, rupture 
into the pleural cavities and produce empyema. 
5. In the course of pyaemia the pleura may become the seat of puru- 
lent inflammation. 
6. The inflammation may be not only purulent, but gangrenous. The 
fluid in the pleural cavity, the fibrine and pus coating the pleura, and 
the pleura itself, may putrefy with the production of bacteria and the 
evolution of gases. This may take place either in a closed pleura, or in 
one which has been opened by incision. 
7. If there is a permanent opening either in the lung or in the chest- 
wall, there is air in the pleura in addition to the inflammatory products. 
Such a condition is called pyopneumothorax. 
In all these different cases the pleural cavity is partly or completely 
filled with purulent fluid, and the lung is either compressed against the 
vertebral column, or partly adherent to the chest-wall. Occasionally, 
however, the purulent fluid is shut in by adhesions either between part 
of the lung and the thoracic wall, or between the lung and the dia- 
phragm, or between the lung and the pericardium, or between the lobes 
of the lun£. 
o 22 
THE INFLAMMATIONS OF THE FLEURA. 
The gross appearance of the purulent fluid is not like that of the 
pus of an abscess, but is thinner and has more the character of a puru- 
lent serum. It seems to be composed of serum, such as is produced in 
a pleurisy with effusion, of pus-globules, and of larger cells looking 
like altered endothelium. According to the number of pus-globules in 
proportion to the serum, the fluid is thicker or thinner. The pus- 
globules are some of them well formed, with a spherical body containing 
two or three nuclei; others have a single large nucleus surrounded by 
a narrow polygonal cell-body; others are fatty or partly broken down. 
In these different clinical varieties of empyema it will be observed 
that the inflammation may be from the outset a purulent one, as in the 
sets of cases marked 1, 3, 4, 5; or it may be first a pleurisy with the 
production of fibrine and serum, and the pus appears later. 
I am unable to say what are the first changes in a pleurisy which 
has a purulent character from the outset. Patients do not die until the 
disease has lasted for a number of days. It is difficult to produce 
empyema in dogs, and when produced one cannot be sure that the 
early stages are identical with what occurs in the human subject. 
The best way I have been able to find of producing empyema in the 
dog is to tie a string around one of the ribs. This acts as a seton and 
excites suppurative inflammation along its track; sometimes also the 
sinus thus formed allows air to enter the pleural cavity. 
In such an empyema the first change to be noticed is that the bodies 
of the endothelial cells become shrunken in such a way that they look 
as if processes were given off from them. At the same time pus- 
globules make their appearance in the pleura just beneath the endothe- 
lium. Such a condition is seen in Plate XIII. During the first twenty- 
four hours no other changes were observed. There was no fibrine, no 
serum, no increase of fixed connective-tissue cells. 
By the second day there is al ittle purulent serum in the pleural 
cavity, but no fibrine on the pleura. The endothelium is now still more 
altered. Large vacuoles are formed in the bodies of many of the cells, 
and the other cells are compressed and misshapen. There are more pus- 
cells in the pleura, and the fixed connective-tissue cells are moderately 
increased in size and number. THE INFLAMMATIONS OF THE PLEURA. 
23 
After the second day the amount of purulent serum increases. The 
vacuolated condition of the endothelium is more marked, and the vacu- 
oles contain pus-globules. The pleura becomes thicker and thicker; 
more pus-globules accumulate in it; and the connective-tissue cells 
continue to increase in number. The blood-vessels of the pleura are 
dilated and appear more numerous. 
By the tenth day the surface of the thickened pleura has become 
uneven, looks like granulation tissue, and is covered with pus. The 
superficial layers of the thickened pleura are formed of small polygonal 
cells, with large nuclei, arranged in a reticulated basement substance. 
There are numerous large blood-vessels with thick walls. Plate XIV. 
represents a vertical section of the inner layer of the pleura in the 
empyema of a dog on the tenth day. 
It is not until this stage of the inflammation is reached that the 
gross appearance of the artificial empyema looks like that of the 
empyema of the human subject, so that it is doubtful how far the early 
changes just described correspond with the early stages of human 
empyema. 
If, however, the pleurisy is at first a pleurisy with effusion, and 
afterwards becomes purulent, we have more opportunities of seeing the 
different stages of the inflammation. In the earlier stages the serum is 
still thin, but yellow from the admixture of pus-globules; the surface of 
the pleura is thickly coated with fibrine, and in the fibrine are some pus- 
cells and but few new connective-tissue cells. There is a growth of new 
connective-tissue cells on the surface of and in the superficial layer of the 
pleura. After the empyema has lasted somewhat longer, the layer of 
fibrine remains the same, but the pleura itself is thicker, and this 
thickening is not due to a layer of new tissue on its surface, but to a cell- 
growth through its whole thickness. The new cells resemble the new 
polygonal cells seen in Plate IX., but they are smaller and more numer- 
ous. They split up the basement substance and present such an ap- 
pearance as is seen in Plate XV., which represents a vertical section of 
the human pleura from a case of empyema of some weeks duration. 
When the empyema has lasted for several weeks or months, the con- 
dition of the pleura is the same whether the inflammation was from the 24 
THE INFLAMMATIONS OF THE PLEURA. 
outset purulent, or whether it succeeded a pleurisy with effusion. The 
pleural cavity contains purulent serum. The pleura itself is thickened, 
sometimes as much as half an inch. The surface of the pleura is in 
some cases coated with fibrine, in other cases it is bare of fibrine and 
looks something like the surface of an old ulcer of the leg. If we 
make vertical sections of the pleura we find in its deeper layers such an 
appearance as is seen in Plate XV.; the fibres split up by small poly- 
gonal cells, the number of the cells varying in different cases. In the 
superficial layers of the pleura the cells are very much more numerous 
They are of the same polygonal shape, and are so close together as to 
obscure the basement substance. There are a few pus-cells mixed with 
them. The fibres of the basement substance are not parallel with the 
fibres of the deep layers of the pleura, but run vertically to these and 
may form a fine reticulum. In the most superficial cells the cell-bodies 
may be wanting, and the nuclei may be fatty. There is a very abundant 
supply of large blood-vessels with thin walls. Such a vertical section 
is seen in Plate XIV., which is taken from the artificial empyema of a 
dog on the tenth day. The plate represents equally well the appear- 
ance of any old human empyema. 
In this condition the pleura may remain for months or years, its 
inner layers continuing to be formed of this same arrangement of small 
cells, scanty basement substance, and large blood-vessels, while the 
deeper layers are formed of a dense fibrous tissue with comparatively 
few cells. 
Many of the patients die with the pleura in this condition ; some 
from exhaustion, some from inflammations of the lungs, some from gan- 
grene of the pleura, some suddenly from unknown causes. 
In some old cases the inflammation will extend to the perichondrium 
of the cartilages and the periosteum of the ribs and cause necrosis of 
thes\; or there may be ossifying periostitis with thickening of the ribs. 
In some cases the inflamed pleura reaches an enormous thickness, and 
is infiltrated with the salts of lime, so that calcareous plates are formed 
in it. 
In the cases which recover the formation of pus ceases. The sur- 
face of the pleura becomes clean and of a reddish color, looking like a THE INFLAMMATIONS OF THE PLEURA. 
25 
recent cicatrix. The superficial layer of small cells is no longer seen, 
but is replaced by fusiform, stellate, and polygonal cells imbedded in 
an abundant fibrillated basement substance. If an empyema becomes 
gangrenous, the pleural cavity contains foul gases, the purulent serum 
is dirty and stinking, and swarms with bacteria. The fibrine coating 
the pleura is green or brown, and is infiltrated with bacteria. Some- 
times smaller or larger portions of the pleura itself are destroyed. In 
such cases the destruction of tissue is not effected by suppuration, but 
by a molecular death and disintegration. 
There are cases, however, in which the whole thickness of the pleura 
does suppurate and soften; the same process extends to the fasciae, the 
muscles and the skin, and the pus is discharged externally. By modifi- 
cations of the same process, the pus may be discharged through the 
bronchi, or perforate into the peritoneal cavity or into some of the 
abdominal viscera. 
It is evident, therefore, that the regular course of an empyema is to 
produce very profound changes in the pleura. Its inner layers are con- 
verted into granulation tissue, its deeper layers into thick, dense, fibrous 
tissue. The pleura after such changes can never return to its normal 
condition. The utmost that can be expected is that the granulation 
tissue should be converted into cicatricial connective tissue, and that 
the formation of purulent serum should cease. THE INFLAMMATIONS OF THE PLEURA. 
27 
HYDROTHORAX. 
The term hydrothorax is usually applied to dropsical accumulations 
of serum in the pleural cavities, in contradistinction to pleurisy with 
effusion. The ordinary causes of such dropsical effusions are valvular 
disease of the heart, chronic Bright's disease of the kidneys, and cir- 
rhosis of the liver. 
Although this condition of the pleura is not usually considered as 
an inflammatory condition, and although the serum is not of inflamma- 
tory origin, yet there are certain changes in the endothelium which do 
seem to be of an inflammatory nature. 
If we examine the thorax of a patient who has died with general 
dropsy, we And either one or both pleural cavities partly filled with 
serum. This serum is usually clear at first, but, after exposure to the 
air, flocculi of fibrine may coagulate in it. The surface of the costal 
pleura is usually clean and smooth, and of nearly normal appearance. 
Sometimes, however, it is coated with a little fibrine, and sometimes it 
has a somewhat opaque and sodden appearance; or, if the dropsy is due 
to heart disease, the blood-vessels of the pleura may be dilated. The 
endothelium of the pleura, however, is as a rule much altered. The 
alteration consists in a change of the old endothelial cells, and the pro- 
duction of new ones beneath the old. Some of the old cell-bodies become 
irregularly shrunken and more opaque, so that they look like branching 
cells; other cells become hypertrophied and misshapen. If these old 
cells are brushed off, we find beneath them patches of small, polygonal, 
nucleated cells, arranged side by side, and having all the appearance of 
new endothelium. In some places the old endothelium has entirely dis- 
appeared, and the pleura is coated over a considerable area with the new 
cells. The fixed connective-tissue cells beneath the endothelium may 
also be somewhat increased in size and number. 
Plate XVI. shows the appearance of the old and new endothelium- 
the old cells large and misshapen; the new cells small, but of regular 
shape. 
The precise way in which the new endothelium is formed is not evi- 
dent. It would seem that it must be developed either from the old en- 28 
THE INFLAMMATIONS OF THE PLEURA. 
dothelium, or from the superficial connective-tissue cells, or from emi- 
grated white blood-globules. I must confess, however, that I have not 
seen any positive proof of either of these modes of origin. 
CHRONIC PLEURISY WITH ADHESIONS. 
I employ this name, not to designate all those cases in which we find 
after death old pleuritic adhesions, either with or without a previous 
history of pleurisy, but to group together a set of cases which have a 
characteristic clinical history, as well as anatomical lesions. I can per- 
haps give the best idea of my meaning by a short history of a case. 
A gentleman of rather slender physique, and disposed to dyspepsia 
and other smaller ailments, was actively engaged in business till he was 
sixty years old. He then retired from affairs and settled in the country. 
After about eighteen months he began to be troubled with a slight 
cough, with dyspnoea on exertion, and lost flesh and strength. He be- 
came alarmed about himself, and consulted a number of physicians. The 
prevailing opinion was that he was suffering from pulmonary phthisis, 
and he was treated accordingly. He continued, however, to grow worse; 
the dyspnoea increased and was aggravated by irregular action of the 
heart. The cough was very troublesome, and was accompanied with 
scanty muco-purulent sputa. The loss of strength and flesh reached 
such a degree that he was confined to his bed. So he gradually wasted 
and died. At the autopsy there were no lesions found except of the 
thorax. The lungs were adherent to the wall of the thorax over their 
entire surfaces. Neither the pulmonary nor the costal pleurae were 
much thickened. The adhesions were all formed of connective tissue; 
none of them were very dense, and some were extremely thin and deli- 
cate. In the superficial portions of the lungs were a few patches of in- 
terstitial fibrous tissue, but none of any size. The larger bronchi were 
trabeculated and coated with a little muco-pus. Except for a moderate 
degree of senile emphysema, the lungs were otherwise normal. The 
heart was pulled upward and to the right, apparently by the pleuritic 
adhesions. 
Such cases as these come under the notice of every clinical observer. THE INFLAMMATIONS OF THE PLEURA. 
29 
They are all characterized by essentially the same symptoms: gradual 
loss of strength and emaciation, cough and dyspnoea, no acute invasion 
of the disease, but a slow and steady progress. 
It is not easy to determine the exact pathology of these cases; they 
seldom die until the disease has existed a long time and the adhesions 
are already extensive. As a rule, both lungs are involved in about the 
same degree. The complicating bronchitis varies in its degree in differ- 
ent cases; in some being quite slight, in others sufficient to coat the 
bronchi with muco-pus. 
Interstitial pneumonia is also a regular, complicating lesion, but it 
also is found in different degrees in different patients. In some cases 
there are large patches and bands of new fibrous tissue ; in others it is 
only to be.discovered by close examination. In all cases the new fibrous 
tissue begins just beneath the pulmonary pleura, and extends from 
thence inward into the lung. 
Some of the pleuritic adhesions are quite thick, others so thin as 
to form mere films. Some are covered on both sides with a regular 
layer of endothelium, the basement substance is distinctly fibrillated, 
the fixed connective-tissue cells are not large or numerous, the blood- 
vessels are only in moderate numbers; these seem to be the oldest 
adhesions. 
Other adhesions are also covered with endothelium, but the endothe- 
lial cells are of more irregular shape; the fixed connective-tissue cells 
are larger and much more numerous; the blood-vessels are also more 
abundant, and there are groups of pus-cells along their course; these 
adhesions seem to be younger, and still growing. 
The thinnest adhesions are not covered with a continuous layer of 
endothelium, but with irregular patches ; the fixed connective-tissue cells 
are numerous, large, with long, branching processes; the basement sub- 
stance is not fibrillated, but more homogeneous. These seem to be the 
youngest adhesions. 
The costal pleura between the adhesions does not present any marked 
change to the naked eye, except at those places where the adhesions are 
very close together. At such places the costal pleura and the adhesions 
form together a sort of loose, spongy tissue. 30 
THE INFLAMMATIONS OF THE PLEURA. 
The pleura between the adhesions, although it presents no gross 
changes, is nevertheless altered. The endothelial cells are increased in 
size and number. There are giant-cells containing a number of nuclei, 
and in places the cells are heaped one upon another. The fixed connec- 
tive-tissue cells are also increased in size and number. The blood-ves- 
sels are numerous and may project above the surface of the pleura; they 
are accompanied by a thick coating of connective-tissue cells and by 
groups of pus-cells. There are also bands of fibrillated tissue stretch- 
ing across the surface of the pleura, looking like the commencement of 
adhesions. In Plate XVII. some of these changes are seen, especially 
the altered endothelium; the drawing represents the surface of the cos- 
tal pleura between the adhesions. 
We may, therefore, conjecture that in this variety of pleurisy the 
morbid changes begin in the endothelium and connective tissue, without 
any previous production of fibrine, and that the adhesions are formed by 
a direct outgrowth from the costal and pulmonary pleura. 
THE PLEURISY OF CHRONIC PHTHISIS. 
In the course of chronic pulmonary phthisis any one of the different 
varieties of pleurisy may be, and usually one of them is, developed; 
but there is one variety of pleurisy which occurs with chronic phthisis, 
and is never seen except with this disease. 
It is perhaps more apt to occur with that form of phthisis in which 
the air-cells are filled with solid matter, so that the lung is large, does 
not contract and fills the pleural cavity almost completely. 
Both the costal and pulmonary pleura are thickened, but are only 
adherent in places. The free surface of the pleura has a peculiar, 
roughened, lustreless appearance. If we make a vertical section through 
the thickened pleura, we find that its surface is covered with a thick 
layer composed of fibrine and of new tissue. If we tear off successive 
planes of tissue from the surface of the pleura, the same structure is 
evident. The peculiarity of the inflammation is this: that the produc- 
tion of fibrine and of new tissue seem to go on simultaneously. There 
is not, as in ordinary pleurisy, first a production of fibrine and then a THE INELAMMATIONS OF THE PLEURA. 
31 
formation of new tissue and a disappearance of the fibrine. But these 
two processes are repeated over and over again, so that the layer on the 
surface of the pleura gives us an inextricable confusion of fibrine, of 
blood-vessels, and of new connective tissue in different stages of growth. 
I his form of pleurisy has also a clinical interest. The roughened 
surfaces of the pleura are well adapted to give a friction sound, and it 
is a question how many of the subcrepitant rales that we hear in such 
cases of phthisis are produced in this way. 
TUBERCULAR PLEURISY. 
Tubercular inflammation of the pleura occurs in the course of chronic 
pulmonary phthisis, as one of the lesions of acute general tuberculosis 
and as a local inflammation. 
The appearance of the affected pleura varies with the amount and 
arrangement of the tubercles, and with the character of the other in- 
flammatory lesions which accompany the tubercular inflammation. 
The tubercle is usually arranged either in the form of small, circum- 
scribed nodules of white, gray, or yellow color, miliary tubercles; or of 
larger, yellow, flat masses. It may be situated either on the surface of 
the pleura, or deep in its tissue. If we examine more closely the small 
miliary tubercles, we find that in some cases they have undergone cheesy 
degeneration and consist of nothing but granular matter; in other cases 
they are largely composed of small, round cells which cover over and 
obscure the tubercle proper; while in still others the tubercular foci are 
so small as to be hardly visible to the naked eye, but are not degener- 
ated or obscured by other products of inflammation. When this latter 
condition prevails, we find the tubercle in its characteristic forms of 
tnbercle-granula and diffuse tubercle. The granula are formed of 
polygonal, nucleated cells and giant-cells arranged in a reticulated base- 
ment substance, while the diffuse tubercle is composed of the same tis- 
sue spread out diffusely. There is at the same time a multiplication of 
the fixed connective-tissue cells of the pleura. Plate XVIII. represents 
a vertical section of the pleura, including its entire thickness, and show- 
ing the arrangements of the tnbercle-granula and diffuse tubercle. 
O o o 32 
THE INFLAMMATIONS OF THE PLEURA. 
When the tubercle is produced in the form of larger rounded or 
flat masses, these masses retain no distinct structure; they are degener- 
ated, and consist of nothing but granules and fragments of tissue. 
With the tubercular inflammation there is always combined some 
one of the other different forms of inflammation. 
The simplest condition is found with the tubercular pleurisy which 
accompanies acute general tuberculosis. In this case there is no fibrine, 
serum, or pus-only a change in the endothelium. The endothelial cells 
over and around the miliary tubercles are altered; some are large and 
misshapen, some are much smaller than the normal. The fixed connec- 
tive-tissue cells are also moderately increased in size and number. 
Next in order are the local tubercular pleurisies. With these we 
find combined the- production of fibrine and serum; or of fibrine, serum, 
and pus; or, added to these inflammatory products, blood. The fol- 
lowing case is an example of tubercular pleurisy with the production of 
fibrine and serum. 
A man, fifty-five years old, a clerk by occupation, about six months 
before his death began to cough, with muco-purulent expectoration. 
There was also some dyspnoea. I saw him first six weeks before his 
death. At that time he was still well-nourished, his appetite fair; he 
was feeble; temperature 101°, pulse 90; his urine was normal, although 
of rather low specific gravity. He still coughed and complained of 
dyspnoea. Physical examination showed flatness, absence of voice, of 
breathing, and of vocal fremitus over the whole of the right side of the 
chest. The diagnosis of pleurisy with effusion was made. After this 
his general condition gradually improved; he was able to walk about; 
but the chest continued full of fluid, and his temperature ranged from 
96° to 102°. Suddenly one day, without any discoverable cause, at four 
o'clock in the morning, while in bed, he died. The autopsy was made 
the same day. The brain was not examined. The heart was normal; 
its cavities were empty. The liver and kidneys were congested. The 
stomach and intestines were normal. The right lung was coated with 
fibrine, compressed, and unaerated; at its apex was a little fibrous indu- 
ration. The left lung was emphysematous, the bronchi contained muco- 
pus; at the apex was a lobule of hepatization as large as a turkey's egg, 33 
THE INFLAMMATIONS OF THE PLEURA. 
red, mottled, with small cheesy nodules. The left pleura was normal. 
The right pleura had its cavity nearly full of reddish serum. The surface 
of the costal pleura was coated with a thin layer of fibrine. The pleura 
was thickened, of a bright red color, mottled with white spots. Ver- 
tical sections of the pleura showed that it was composed of three layers. 
The middle layer was formed of fibrillated connective tissue, the cells 
and blood-vessels increased in number. The outer and inner layers were 
composed of reticulated connective tissue, with many cells and blood- 
vessels. In these two layers was also a large amount of tubercle, both 
diffuse and in the form of ^ranula. 
In the same way there may be tubercular pleurisy of one side of the 
chest, combined with the ordinary lesions of empyema. 
If tubercular pleurisy is secondary to pulmonary phthisis, it may 
involve either one or both sides of the chest. There may be miliary 
tubercles in the pulmonary and costal pleura, with no other change 
except in the endothelium; or there may be also fibrine and serum; or 
the lesions of empyema; or the combination of fibrine and cell-growth 
that is found in the pleurisy of chronic phthisis. THE PERITONEUM. 
The abdomen, like the thorax, forms a cavity containing viscera. 
The inner surface of this cavity and the surfaces of the viscera are cov- 
ered with connective-tissue membranes, and folds of similar membranes 
hold the viscera in place. All these membranes are considered by anat- 
omists to form together a closed serous sac called the peritoneum. The 
membrane lining the wall of the abdomen is termed the parietal perito- 
neum; and that covering the viscera, the visceral peritoneum. The 
membranes which hold in place the small intestines-the caecum, the 
transverse colon, the sigmoid flexure, and the rectum-are called respec- 
tively the mesentery, the meso-caecum, the transverse and sigmoid meso- 
colon, and the meso-rectum. Certain folds of membrane which are 
spread out over the viscera are called the great omentum, the small 
omentum, and the gastro-splenic omentum. Still other membranes, 
which hold in place the liver, spleen, uterus, and bladder, are called 
ligaments. 
The parietal peritoneum resembles in its structure the costal pleura. 
Its free surface is covered with a single layer of flat, polygonal, nucle- 
ated cells the endothelium. Beneath these cells are successive planes 
of connective tissue extending down to the musclesandfasciae. These 
o 
planes are formed of a fibrillated basement substance, reinforced by 
elastic fibres, and of branching cells like those of the costal pleura. 36 
THE PERITONEUM. 
Imbedded in the connective tissue are lymphatic spaces and vessels; the 
spaces are numerous, but the vessels are not nearly as large or abundant 
as those of the costal pleura. The blood-vessels are very numerous, and 
break up into a capillary plexus with close meshes. See Plate XIX., 
which represents the endothelium, basement substance, connective-tissue 
cells, and lymphatic spaces. 
The mesentery has two free surfaces, each covered by endothelium. 
In it are the large blood-vessels and lymphatic trunks which pass to the 
intestines, besides a system of blood and lymphatic vessels belonging to 
itself. 
The omentum in the human subject and in some animals consists of 
fibrillated connective tissue arranged in a mesh-work. The trabeculae 
of this mesh-work are completely covered by large endothelial cells. In 
the basement substance, beneath the endothelium, are branching cells, 
which in the normal omentum are not readily seen, but become swollen 
and plainer when inflamed. In the larger trabeculae are blood and 
lymphatic vessels and fat. Plate XX. represents part of the normal 
human omentum. 
Klein has called attention to the fact that in the omenta of different 
animals are to be found small nodules, and that these nodules are not 
all of the same structure. Some, he says, are formed of germinating 
endothelium; some of branched cells; some of adenoid tissue; some of 
blood-vessels and branched cells. In the human omentum such nodules 
are also to be seen, especially if the individual has suffered from heart 
disease or cirrhosis of the liver. They are formed of an accumulation of 
cells resembling the endothelium, but smaller and with thicker cell- 
bodies ; or of accumulations of branched cells, with a network of capil- 
lary vessels. It is also not uncommon to find from two to ten nuclei of 
endothelial cells close together. 
THE INFLAMMATIONS OF THE PERITONEUM. 
Although, the peritoneum resembles the pleura very closely in its 
structure, yet the inflammations which invade these two membranes 
differ widely in their anatomy and clinical history. One reason for this THE PERITONEUM. 
37 
difference is that peritonitis is a much more serious lesion than pleurisy, 
and causes death in a much shorter time. Pleurisy is not necessarily a 
fatal, or even a severe disease ; peritonitis produces a very marked 
change in the general condition of the patient, and is very often fatal. 
A well-marked acute peritonitis usually destroys life within from two 
to fourteen days. 
We cannot, therefore, classify peritonitis as we do pleurisy, accord- 
ing to the anatomy of the inflammation, but rather we follow its clinical 
history and speak of acute and chronic peritonitis; or its extent, and 
speak of local and general peritonitis. 
I. Acute Peritonitis. 
We can distinguish two anatomical varieties of acute peritonitis. 
There may be no change except in the endothelium ; or there may be 
changes in the endothelium and fixed connective-tissue cells, with pro- 
duction of fibrine, serum, and pus. This last is the most frequent form 
of acute peritonitis. 
1. The variety of acute peritonitis in which the changes are confined 
to the endothelium we may call, for convenience, Cellular Peritonitis. 
This form of peritonitis may be produced by any irritant which does not 
act too energetically. It can be excited in dogs by injections of very 
small quantities of a solution of chloride of zinc. In the human subject 
we find it with perityphlitis, with abscesses shut in in any part of the 
peritoneum, and in cases of puerperal fever which die within forty-eight 
hours after the development of symptoms. 
If the autopsy is made within a few hours after death, we find the 
entire peritoneum of a bright red color from the congestion of the blood- 
vessels ; but this is all-there is no fibrine, no serum, no pus. If, however, 
we examine the peritoneum with the microscope, we find a well-marked 
change in the endothelium, especially that of the omentum. The cells 
are increased in size and number, and present such an appearance as is 
seen in Plates XXI. and XXII.' Plate XXL shows the human omentum 
in a case of perityphlitis ; Plate XXII. the omentum of the dog on the 
fourth day after an injection of chloride of zinc. 
The following case may serve as an example of this form of peri- 
tonitis : 38 
THE PERITONEUM. 
A boy, seventeen years old, nine days before his death was suddenly 
seized with severe pains in the right lumbar and iliac regions. He went 
home, and in the evening had a chill and felt ill. The next day he had 
two chills, vomited everything he ate, and was delirious. The third day 
he managed to walk to a dispensary, although still suffering and feeling 
very ill. His bowels were moved on that day, and continued to be regu- 
lar until two days before he died. On the fourth day his pulse was 100, 
temperature 104°; there was tenderness and swelling in the right iliac 
fossa. On the fifth day his pulse was 104-112, temperature 101-100° 
On the sixth day the pulse was 106, temperature 99|° ; there was more 
general tenderness and pain over the abdomen, and the boy looked 
worse. On the seventh day his pulse was 124-140, temperature 99-104°; 
he was sweating profusely, and was worse. On the eighth day his 
pulse was 144, temperature 103°; he was delirious, his face drawn and 
anxious, his abdomen tympanitic, his urine was passed involuntarily, and 
on the ninth day he died. At the autopsy there was found general con- 
gestion of the entire peritoneum, but no fibrine, pus, or serum. The 
vermiform appendix was behind and adherent to the posterior wall of the 
caecum. In the appendix was a large fecal concretion, and around this 
the wall of the appendix was infiltrated with pus; around this was a 
small collection of pus completely shut in. 
It seems evident that this form of peritonitis, although not affording 
marked gross lesions, is yet capable of giving clinical symptoms. It is 
wrorthy of special notice as an example of inflammation producing new 
cells without the presence of fibrine, serum, or pus. We will see later 
that it is also of importance in reference to the pathology of tubercle. 
2. The ordinary form of acute peritonitis is attended with changes in 
the endothelium and fixed connective-tissue cells, and with the produc 
tion of serum, fibrine, and pus. 
Such a peritonitis may be produced by wounds or contusions of the 
abdomen ; by ulcers, inflammations, new growths, and incarcerations and 
intussusceptions of the stomach and intestines; by lesions of the uterus, 
ovaries, and Fallopian tubes ; by ruptures, inflammation and new growths 
of the bladder; by abscesses in the kidneys; by abscesses and hydatid 
cysts of the liver; by inflammation of the gall-bladder and biliary pas- THE PERITONEUM. 
39 
sages; by thrombosis of the portal vein; by inflammations and new 
growths of the spleen and pancreas ; by inflammations and new growths 
of the lymphatic glands and retro-peritoneal connective tissue; by 
abscesses in the abdominal wall; by perforation of an empyema; by 
inflammations of the vertebrae, ribs, and pelvic bones. It also occurs 
with septicaemia, with puerperal fever, with the acute exanthemata, 
with scurvy, with Bright's disease, and as an idiopathic lesion. 
In* studying peritonitis we must first observe the changes in the 
mesentery of the frog, following the now famous experiments of Cohn- 
heim. 
If we open the side of the abdomen of a curarized frog, pull out a 
loop of intestine and spread it over a cork ring, we have the mesentery 
so arranged that we can look at it directly with the microscope. The 
contact with the air is sufficient to excite a peritonitis. 
The first change is that the arteries, then the veins, and then the 
capillaries become dilated, the current of blood within them is slower, 
and in some of the capillaries is stationary. Next we observe that there 
is an accumulation of white globules in the peripheral portion of the 
blood-current, and these white globules remain almost stationary, lining 
the walls of the vessels while the central column of red globules flows 
on uninterruptedly; this change is most marked in the veins. Next we 
see, on the outside surface of the walls of the veins, little knobs and pro- 
jections making their appearance. These little knobs send out fine pro- 
cesses in every direction, they become larger and larger, and finally 
there appear on the outside of the veins bodies identical in appearance 
with white blood-gobules and pus-cells. 
In the capillaries these changes are to be seen more distinctly. We 
can see a single white globule moving slowly in the blood-current, 
adhering to some point of the wall of the vessel, then a little promi- 
nence appearing on the outside of the wall of the vessel, then the white 
globules inside becoming smaller and the prominence outside becoming 
larger until the entire globule appears on the outside of the vessel. In 
the same way the red globules may be seen to emigrate. 
After these changes have gone on for several hours, the veins are 
surrounded by a thick layer of white globules, and after a still longer 40 
THE PERITONEUM. 
time the entire mesentery is coated with a layer of white globules en- 
tangled in coagulated fibrine. Such an experiment shows that in the 
peritonitis of frogs the pus-cells are emigrated white blood-globules. 
If we inject a solution of chloride of zinc or of ammonia into the 
peritoneal cavity of a rabbit or dog, we usually find that, by the end of 
one or two hours, inflammatory changes are evident. There is a little 
serum in the peritoneal cavity, and little knobs and threads of fibrine 
can be seen on the surface of the peritoneum. The endothelium shows 
little or no changes, nor do the fixed connective-tissue cells. Pus-cells, 
however, are already present in moderate numbers in the stroma of all 
parts of the peritoneum just beneath the endothelium. In the dog the 
pus-cells have no connection with any other cells; in the rabbit they 
are sometimes so close to the branching cells (as seen in Plate XXIII.), 
that it is difficult to be certain of their relationship. 
After the lapse of twenty-four hours the lesions are more marked : 
there is general congestion of the peritoneum, reddish serum in its 
cavity, and an appreciable coating of fibrine and pus on its surface. 
Minute examination shows that two distinct sets of changes are 
going on at the same time: 1, a production of fibrine, serum, and 
pus; 2, a swelling and multiplication of the endothelial cells. If the 
inflammation is very intense, the pus and fibrine are most abundant; 
if the inflammation is milder, the changes in the endothelium are more 
marked. 
There may be a considerable amount of pus produced and yet the 
layer of endothelium remain in place. But, in silver preparations, 
little black spots are seen along the edges of the cells, and at many 
points there are large, rounded openings between the cells, in some of 
which appear to be pus-globules. The pus-globules are seen in num- 
bers beneath the layer of endothelium, and may infiltrate the entire 
thickness of the peritoneum. They seem to have no connection with 
the fixed connective-tissue cells, and the latter are only a little swollen. 
The blood-vessels contain a very large number of white globules. 
Plate XXIV. represents the parietal peritoneum of a dog, inflamed for 
forty-eight hours; the endothelium is in place, but there are large open- 
ings between some of the cells, and numbers of pus-globules can be THE PERITONEUM. 
41 
seen beneath, the endothelium, while some of the capillaries are filled 
with white globules. 
If, however, the pus and fibrine are produced in large amounts, the 
endothelium falls off and leaves the surface of the peritoneum bare. 
The swelling and multiplication of the endothelium give such pic- 
tures as are seen in Plates XXI. and XXII. 
These two sets of changes go on in the dog up to the third day, the 
serum, fibrine, and pus increasing in amount, and the endothelial cells 
increasing in size and number. But few dogs survive the third day of 
a well-marked acute peritonitis. 
In the human subject, if death takes place before the third day, both 
the gross and minute changes are the same as those seen in the dog. 
There is the same general congestion, the same production of pus, 
fibrine, and serum, the same desquamation and multiplication of the 
endothelium. 
In many cases, however, of peritonitis, death occurs between the 
sixth and fourteenth days of the disease. The appearance of the peri- 
toneum at this period of the inflammation is not always the same. The 
congestion of the vessels may persist, it may be very intense and 
accompanied with extravasations of blood, or it may be entirely absent. 
There may be a thin coating of fibrine and pus gluing together neigh- 
boring surfaces of peritoneum, or this layer may be thick and may shut 
in collections of pus. The lesions may be superficial or may infiltrate 
the subperitoneal tissue. There may be a small or a large quantity of 
purulent serum in the peritoneal cavity, and this serum may contain a 
few or a great many pus-globules, or the serum maybe of a dirty brown, 
fetid character, filled with bacteria. 
The microscopical appearances differ from those seen after forty- 
eight hours, chiefly in the larger amounts of inflammatory products and 
in the changes in the fixed connective-tissue cells. It has been stated 
already that during the first three days of a peritonitis the connective- 
tissue cells beneath the endothelium are but little changed; but by the 
seventh day these cells are markedly increased in size and number in all 
parts of the peritoneum. Plate XXV. shows the condition of the 
human omentum in a peritonitis of eight days' duration. 42 
THE PERITONEUM. 
The rule is for peritonitis to prove fatal by the fourteenth day. 
Sometimes, however, the inflammation becomes chronic and may con- 
tinue for a long time. Sometimes the patients recover and permanent 
adhesions are formed between different parts of the peritoneum; and 
these adhesions may shut in collections of pus. It seems probable that 
these adhesions are formed by the new cells derived from the endothe- 
lial and connective-tissue cells. 
Whether recovery from peritonitis takes place without the formation 
of permanent adhesions, I have no personal knowledge, although it seems 
probable that this may take place. 
Acute local peritonitis is often followed by the formation of perma- 
nent adhesions; this is especially the case in the peritoneum about the 
uterus, the liver, and the spleen. I have not been able to follow all the 
steps of such forms of peritonitis, but, so far as I can tell, the process is 
much the same as in acute pleurisy : first, the production of a layer of 
fibrine and a little pus on the surface of the peritoneum; then a growth 
of the superficial fixed connective-tissue cells to form permanent new 
tissue. 
Acute general peritonitis differs, therefore, from acute pleurisy. In 
acute pleurisy, fibrine and serum are produced in large amounts, but not 
much pus; the endothelium has no active share in the inflammatory 
process; the superficial connective-tissue cells begin to multiply very 
soon, and from them are formed permanent new tissue. As the inflam- 
mation is not a fatal one, weeks and months may elapse before it has 
run its course. 
In acute peritonitis there is usually a good deal of pus with the 
fibrine and serum; the endothelium does undergo marked changes; the 
connective-tissue cells are multiplied, but they do not go on to form 
permanent new tissue. The inflammation is a fatal one, and runs its 
course within a few days. THE PERITONEUM. 
43 
II. Chronic Peritonitis. 
Chronic peritonitis occurs in several anatomical forms, most of which 
can be conveniently grouped under the following heads: 
1. Cellular peritonitis. 
2. Peritonitis with adhesions. 
3. Peritonitis with thickening of the peritoneum. 
4. Peritonitis with adhesions, pus, fibrine, and serum. 
5. Hemorrhagic peritonitis. 
1. Cellular Peritonitis. This variety of peritonitis resembles very 
closely acute cellular peritonitis. There is no fibrine present and no 
pus, but there may be clear serum in the cavity of the peritoneum. To 
the naked eye there may be no changes visible; or we may see on the 
omentum minute semi-translucent granules, and on the parietal perito- 
neum small, rounded elevations. With the microscope, however, we 
find constant changes in the endothelium and fixed connective-tissue cells. 
These cells are everywhere increased in number and altered in shape ; 
or, to speak more guardedly, the surface of the omentum is covered 
with cells which look as if they were derived from the endothelium and 
connective-tissue cells, although they differ from the normal shape of 
these. The new cells are for the most part polygonal cells of different 
sizes, with one or several nuclei, and giant-cells-large granular masses 
filled with nuclei. Although the new cells are produced over the entire 
surface of the peritoneum, yet as a rule they are more numerous in lit- 
tle patches scattered here and there. These little patches may be com- 
posed of only a few cells, or the cells may be heaped together in such 
numbers as to form nodules visible to the naked eye. There is never 
any stroma between the cells. Plate XXVI. represents the omentum 
from a case of chronic pulmonary phthisis, showing the production of 
new cells. 
This form of peritonitis occurs most frequently with organic heart 
disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and 
with acute general tuberculosis. With the two latter diseases the nod- 
ules produced by the accumulation of cells are often called tubercles-- 
as it seems to me very improperly. 44 
THE PERITONEUM. 
2. Peritonitis with Adhesions. There may be a formation of per- 
manent adhesions, without the previous production of fibrine and pus. 
It is often, indeed, not easy to be certain whether old peritoneal adhe- 
sions are the result of an acute peritonitis, or whether they have been 
formed without any such preceding inflammation; in many cases we have 
to rely on the history of the patient to solve the problem. 
There are, however, cases in which the manner of growth of such 
adhesions seems clear. If, either from perityphlitis or from any other 
cause, a collection of pus is shut in, in some part of the peritoneal cavity, 
we may find the rest of the peritoneum smooth and shining; no serum, 
fibrine, or pus, no thickening, but the different free surfaces of the peri- 
toneum are attached to each other by adhesions. These adhesions are 
in the shape of threads or of membranes, often of the most extreme 
tenuity. They are formed of a fibrillated basement substance, the 
fibrils crossing each other in all directions. Imbedded in the basement 
substance are cells, some fusiform and stellate, but most of them repre- 
sented by large nuclei apparently imbedded in the larger fibres of the 
basement substance. They give the impression of being large branching 
cells of which the cell-bodies have become fused into basement sub- 
stance, while the nuclei remains. Plate XXVII. shows part of such an 
adhesion. 
Close to these adhesions the peritoneum may appear normal to the 
naked eye, but, if it is put in water, very fine threads and membranes will 
float upward from its free surface. Minute examination shows that the 
connective-tissue cells are increased in size and number, that the endo- 
thelial cells are replaced by cells of a great variety of shapes, and that 
the thin little threads and membranes on the surface are formed of large 
branching cells. Plate XXVIII. represents the surface of the perito- 
neum in such a condition. The large branching cells, which are drawn 
as if laid flat, really float out from the surface, only adhering by one or 
more of their ends. 
Such a peritonitis with adhesions appears to be a more advanced 
stage of the forms of cellular peritonitis already described. It is pro- 
duced in the same way by some constant, but not very energetic irritant. 
But the inflammation, instead of stopping at the point of a simple new THE PERITONEUM. 
45 
growth of cells, continues, and the new cells are changed into mem- 
branes. 
3. Peritonitis with thickening of the peritoneum. This form of in- 
flammation is not common, and its causation is obscure. The patients 
are sick and gradually waste away without well-defined symptoms. 
There is usually vomiting, often diarrhoea. One can feel that there is 
something wrong about the abdominal cavity, but an exact diagnosis is 
difficult. 
The abdomen usually contains serum, either clear or purulent. The 
coils of intestine are slightly adherent to each other, or are matted to- 
gether so as to form an almost solid mass. But the most striking lesion 
is the thickening of the peritoneum. The parietal peritoneum and that 
covering the liver, stomach and intestines are all thickened. The sur- 
face of the peritoneum is smooth, or is covered with fibrine, or adhe- 
sions. The endothelium is always changed. The peritoneum may be 
as much as an inch thick. It is composed of fibrillated connective tissue, 
with a moderate number of cells, the cells most abundant near the sur- 
face. The change in the peritoneum usually produces changes in the 
viscera. The liver is small, compressed, and its venous circulation ob- 
structed. The cavity of the stomach is diminished and its mucous 
membrane is the seat of chronic inflammation. The lumen of the intes- 
tines is also diminished in size and their mucous membrane inflamed. 
It is necessary to be careful not to confound such cases with diffuse 
carcinoma of the peritoneum, or tubercular peritonitis. It is sometimes 
very difficult to distinguish between these three anatomical conditions. 
4. Peritonitis with fibrine, serum, and pus. This variety of perito- 
nitis may follow acute peritonitis, may be due to lesions of the abdominal 
viscera, or may occur without known cause. The following case will 
serve as an example of the obscure history that belongs to many of 
these patients. A woman, 36 years old, married, was attacked nine 
months before her death by a fever which kept her in bed four weeks. 
At the end of the four weeks she was able to get up and walk about, but 
never felt really well. For seven months before her death there was pain 
m the abdomen and gradual increase in its size. There was also a cough 
With mucous expectoration. I first saw her two months before her death; 46 
THE PERITONEUM. 
She was then feeble and emaciated. Her abdomen was large, but not 
tender. It did not seem to be distended by fluid, but gave the impres- 
sion of there being some large, diffuse growth filling up the deeper 
parts of the abdomen. Her bowels were moved regularly. She re- 
mained in this condition gradually losing strength from day to day. 
Her temperature was sometimes 99 or 101°, but on many days was nor- 
mal during the twenty-four hours. At the autopsy all the viscera were 
examined, but there were no lesions except of the peritoneum. This 
membrane was everywhere moderately thickened and its surface covered 
with fibrine and pus, while the abdominal viscera were firmly matted 
together by organized adhesions, so as to form a single large mass. Be- 
tween the adhesions were shut in numerous collections of purulent 
serum. 
In all the cases permanent adhesions, pus, fibrine and serum are the 
regular lesions; the adhesions either binding up most of the viscera 
together, or dividing the abdomen into a number of cavities containing 
pus and serum. The walls of the intestines are usually soft and easily 
torn. 
The adhesions are formed of bundles of connective tissue crossing 
and interlacing, and of polygonal and branching cells of many shapes. 
The thickened peritoneum is also covered and infiltrated with similar 
cells and with pus-cells. 
5. Hemorrhagic peritonitis. This form of peritonitis is seen most 
frequently as a local inflammation. It affects the peritoneum behind 
and around the uterus in the female, and that covering- the recto-vesical 
excavation in the male. The affected portion of the peritoneum is 
covered with layers of thin membrane infiltrated with more or less 
blood. The membranes are formed of numerous blood-vessels with thin 
walls; of branching cells, often pigmented; and of a scanty basement 
substance. It resembles very much the chronic hemorrhagic inflamma- 
tion of the dura mater, and, as in the latter, the extravasated blood 
may form tumors of large size. 
General hemorrhagic peritonitis I have not seen. Friedreich, how- 
ever, describes two cases occurring in patients with ascites, who had been 
frequently tapped. He says that both the parietal and visceral perito THE PERITONEUM. 
47 
neum were covered with a continuous membrane of a diffuse yellowish 
brown color, mottled with small and large extravasations of blood. 
The membrane was thickest over the anterior abdominal wall. It could 
be separated into a number of layers. These layers were composed of 
blood-vessels, masses of pigment, branching cells, and fibrillated base- 
ment substance. In many places the extravasated blood was coagulated 
in the shape of round, hard, black nodules. The entire new membrane 
could be readily stripped off from the peritoneum, and there were no 
adhesions between the visceral and parietal peritoneum. 
TUBERCULAR PERITONITIS. 
Tubercular peritonitis occurs as one of the lesions of acute general 
tuberculosis, with chronic pulmonary phthisis, with tubercular inflam- 
mation of the genito-urinary tract, and as a local inflammation. When 
it occurs as a local inflammation there is often tubercular pleurisy as a 
complication. 
The gross appearance of the lesions varies with the amount of 
tubercle produced and with the character of the accompanying inflam- 
matory lesions. 
When tubercular peritonitis occurs as one of the lesions of general 
tuberculosis, the tubercle is usually in the form of small nodules, some 
of them hardly visible to the naked eye. The only inflammatory 
changes in addition are an increase of the endothelial and connective- 
tissue cells, with sometimes a little fibrine. The tubercle is in the form 
of tubercle-granula. Some writers describe the accumulations of cells 
on the omentum, such as are figured in Plate XXVI., as tubercle. It 
seems to me, however, that if we compare the omentum in acute cellular 
peritonitis and in the different examples of chronic cellular peritonitis, 
it is evident that the changes are in all the cases essentially the same, 
and when we find the same lesions accompanying the production of 
tubercle, they are merely accompanying inflammatory lesions. Tubercle, 
so far as I know, is never produced alone; there is always at the same 
time, fibrine, or pus, or serum, or a new growth of connective-tissue cells. 48 
THE PERITONEUM. 
Even the smallest tubercle-granula are not composed of a mere accumu- 
lation of cells, but of a regular arrangement of reticulated basement 
substance with cells imbedded in it, as is seen in Plate XXIX. 
The practice of calling every accumulation of small cells tubercle 
leads to a confusion which is quite unnecessary. It is very easy in 
animals to excite artificial chronic cellular peritonitis, and, as a result .of 
this, little nodules in the omentum formed by the accumulation of endo- 
thelial and connective-tissue cells, but such nodules have nothing to do 
with true tubercle. It is evident that we can make no real advance in 
our knowledge of tubercle unless we adhere strictly to some one ana- 
tomical lesion as being tubercle. Such a distinct lesion we have in the 
regular arrangements of basement substance and cells which make up 
tubercle-granula and diffuse tubercle. All the accompanying inflamma- 
tory products must be recognized as accessories only. 
In local tubercular peritonitis, although there are many varieties, 
we may conveniently follow Wilks and Moxon in distinguishing three 
groups of cases. First, tubercular ascites. The peritoneum is thick- 
ened, it is studded with accumulations of tubercle from the size of half 
a pin's head up to large masses as much as an inch in diameter. Some 
of these nodules are rounded, others are spread out in flat plates. 
There are but few adhesions, but there is a large amount of turbid 
serum. The omentum may be much thickened. Such cases are some- 
times hard to distinguish from diffuse cancer of the peritoneum, espe- 
cially if the tubercle has degenerated. There is of ten tubercular pleurisy 
at the same time, and sometimes tubercle in the spleen and lymphatic 
glands, but the other viscera are usually free. 
The symptoms of such cases are much like those of ascites with 
cirrhosis of the liver. 
Second, tubercular peritonitis with fibrine. The peritoneum is 
studded with tubercular nodules imbedded in the midst of a soft, semi- 
gelatinous matter which covers the whole of the peritoneum and sticks 
together its different surfaces. The soft matter is principally composed 
of fibrine infiltrated with serum. These cases are apt to have very 
obscure clinical histories. There may also be tubercular pneumonia as 
a complication. THE PERITONEUM. 
49 
Third, tubercular peritonitis with adhesions. The peritoneum is 
thickened and there are numerous organized adhesions. All the ab- 
dominal viscera are firmly matted together, and there may be collec- 
tions of pus shut in by the adhesions. The adherent coils of intestine 
may ulcerate and open into each other. The tubercular nodules are 
small or large ; they are found everywhere in the peritoneum, and also 
in the adhesions. 
Such a tubercular inflammation may be confined to the peritoneum, 
or there may be also tubercular pleurisy, or pulmonary phthisis, or 
tubercle in the spleen and liver, or tubercular nephritis, or metritis. 
It is evident that the different characters of these different forms of 
tubercular peritonitis depend not so much upon the different kind of 
tubercle produced as upon the different kind of accessory inflammation. 
The presence of cells, or of serum, or of fibrine, or of adhesions, forms 
the most marked feature in each case. PNEUMONIA. 
The lungs are composed of bronchi, air-vesicles, blood- and lymph- 
vessels, and connective tissue; the latter forming part of the walls of 
the bronchi, the air-vesicles, and the blood-vessels, holding together 
the different parts of the lung, and constituting the pulmonary pleura. 
The anatomy of the lungs has been so often, described that it is 
useless to speak of it here. I must say a word, however, concerning 
the epithelium of the air-vesicles. In fcetal life the air-vesicles are 
lined with cylindrical cells resembling the epithelium of the bronchi. 
As the foetus grows older these cells become broader and flatter, until 
at the time of birth there is a continuous layer of flat, polygonal, nu- 
cleated cells lining each of the air-vesicles. As soon as breathing be- 
gms, the air-vesicles expand and their walls are stretched to corre- 
spond with the increased size of the contained spaces. The epithelial 
cells which line the air-vesicles must, under these circumstances, either 
be separated from each other or else the cell-bodies must become broader 
and flatter, so as to cover more space. The latter seems to be the case. 
As the child grows up to adult life this thinning of the cell-bodies of 
the epithelium seems to continue and to be accompanied by an atrophy 
of some of the nuclei. In adult human lungs, therefore, we find the 
air-vesicles lined with a very thin homogeneous layer, apparently 
formed of the flattened cell-bodies, and with nitrate of silver this layer 52 
PNEUMONIA. 
is shown to be divided up into irregular spaces. In this layer are 
large nuclei scattered at irregular intervals. There are also, however, 
in most of the air-vesicles, cells which resemble the foetal epithelium, 
with a well-marked cell-body and nucleus. Fig. XXX. shows part of 
the wall , of an air-vesicle covered with its epithelium. The prepara- 
tion was from a healthy, adult human lung removed from the body one 
hour after death and treated with osmic acid and hsematoxyline. It 
will be seen that there are a number of large nuclei, irregularly ar- 
ranged, imbedded in a thin layer of finely granular matter. Around 
some of these nuclei the layer of granular matter may be thicker and 
more opaque, but there is no well-defined cell-body. There are, how- 
ever, a few flat cells with a distinct nucleus and cell-body. This is all 
that can be seen of an epithelium in the adult human lung: a very 
few flat, nucleated cells, and a considerable number of nuclei imbedded 
in a thin layer of finely granular matter. If we use nitrate of silver 
we obtain such a picture as is given in Fig. 154 of Stricker's 
Manual. 
This arrangement of nuclei and cells is spread out over the walls of 
the air-vesicles, walls composed of a thin layer of connective tissue re- 
inforced with elastic fibres. Imbedded in this connective-tissue mem- 
brane is a layer of capillary blood-vessels. 
The walls of the air-vesicles are, then, an arrangement of tissues de- 
signed for the performance of a special function. It can serve no good 
purpose to compare them with either mucous or serous membranes. 
They are simply air-vesicles, and nothing else. 
It is customary to class all those inflammatory processes which in- 
volve the air-vesicles and the interstitial tissue of the lung under the 
name of Pneumonia. It is also customary to subdivide pneumonia into 
the anatomical varieties of catarrhal, croupous, and interstitial pneu- 
monia. To the name of interstitial pneumonia there can be no objec- 
tion ; to the names of catarrhal and croupous pneumonia there are very 
serious ones. They are the result of comparing the air-vesicles with 
mucous membranes, structures from which they are entirely distinct. 
These names seem to me so utterly inappropriate that I prefer to de- 
scribe the different forms of pneumonia as follows : PNEUMONIA. 
53 
1. The pneumonia of heart disease. 
2. The lobar pneumonia of adults and children. 
3. The lobular pneumonia of adults and children. 
4. Interstitial pneumonia. 
5. The pneumonia produced by pressure on the trachea or bronchi. 
6. The lesions of acute tuberculosis, and of acute and chronic pul- 
monary phthisis. 
I. The Pneumonia of Heart Disease. 
Lesions of the valves of the heart and dilatation of its ventricles are 
regularly followed by chronic congestion of the brain, lungs, liver, 
spleen, alimentary canal, kidneys and subcutaneous connective tissue. 
In some cases all these viscera suffer; more frequently one viscus will 
be affected more than the others. Such a chronic congestion is as a 
rule followed by certain regular changes in the tissues of the affected 
viscera, so that not only chronic congestion, but also chronic inflamma- 
tion exist. In old cases the changes due to the chronic inflammation 
may eventually become more marked than the congestion. 
In the lungs such chronic congestion is very frequently followed by 
marked structural lesions. These lesions have never attracted the 
attention of clinical observers which their importance demands. One 
reason, perhaps, for this is that it is very difficult to make out this con- 
dition during the patient's life. There are indeed usually cough and 
an expectoration of mucus and blood, but these may only indicate bron- 
chitis. Dyspnoea exists, but we expect to find it with organic heart dis- 
ease under any circumstances. The physical signs also are not charac- 
teristic. There may be dulness on percussion, but not always, and the 
hydrothorax, which so often exists, may mask it. If there are any 
rales, they belong to an accompanying bronchitis. Bronchial breathing 
and bronchophony are not usually heard, even when the lung is fairly 
solidified. 
And yet the lesion may have the principal share in causing the 
patient's death. Indeed, if these changes in the lung are once fairly es- 
tablished, the prognosis of the case is hopeless, for the lung can never 
return to a natural condition, but becomes constantly more unfit for its 54 
PNEUMONIA. 
work. The pathological recognition of this condition dates back to its 
description by Virchow in 1847. 
"There is a process," he writes, "which, in spite of its frequency 
and characteristic appearance, has attracted but little attention. It 
occurs in patients who have suffered for a long time from asthma or 
chronic bronchitis, dependent upon disease of the left heart and accom- 
panied by haemoptysis. Insufficiency and still more frequently stenosis 
of the mitral valve most frequently produce it. When the thorax is 
opened, the lungs appear prominent, do not collapse, are compact, 
heavy, inelastic, crepitate but little, and have frequently a peculiar 
yellow, brown, or reddish-brown color. On section the tissue is denser, 
and at many points are red spots, dark colored at their centres, lighter 
at their edges, also other spots of a brown, rusty, or black color. The 
parenchyma between these spots is seldom of its normal color, but is 
yellow, orange, or rust-colored. A yellow or brown, slightly frothy 
fluid, in many cases, escapes on section abundantly. Microscopical ex- 
amination of such lungs shows only the normal tissue, with extravasated 
blood in different stages of transformation into pigment. In the 
neighborhood of the points of extravasation the epithelial cells of the 
alveoli are stained yellow, and it is easy to see that these cells are 
identical and continuous with the colorless pavement epithelium. 
There are also other cells retained in the same way, but containing in 
addition granules of pigment. These granules show all gradations of 
color from yellow to black. Finally the cells may be destroyed and 
the pigment left free. In addition, extravasations of blood take 
place in the interstices of the tissue, and these become changed into 
pigment. 
" This lesion of the lungs is produced by a chronic hyperaemia. There 
is at the same time chronic bronchitis with hyperaemia and thickening 
of the mucous membrane of the bronchi, and dilatation of their calibre. 
Any thickening of the walls of the air-cells is hypothetical. I consider 
the most appropriate name for this condition of the lungs to be brown 
or pigment induration." 
These names of brown or pigment induration have since been gen- 
erally adopted. PNEUMONIA. 
55 
The attention of Virchow seems to have been directed especially to 
the hypersemia and the formation of new pigment. 
Of late years several observers have called attention to the dilata- 
tion of the capillaries of the air-vesicles, and to the hypertrophy of the 
walls of the air-vesicles. The thickening of their walls is due to a new 
growth, partly of connective tissue and partly of smooth muscle. 
A single case is described by Orth in which there was also pig- 
ment in the capillaries and some of the smaller vessels. 
The lesion is a common enough one in New York, occurring in a 
large number of the cases of organic heart disease, especially with 
mitral stenosis. 
The lungs are usually small, not large and prominent as in Vir- 
chow's cases. There are often old pleuritic adhesions connecting the 
pulmonary and costal pleura and binding together the different lobes 
of the lungs. In the pleural cavities is a moderate amount of clear 
serum. When the lungs are removed from the thoracic cavity their 
small size is still more apparent. The pulmonary pleura is thick and 
opaque, and gives the surface of the lung a grayish color, mottled by 
the pigment in the lung-substance beneath it. When the lungs are cut 
open, the color and texture are very characteristic. The texture is 
dense and leathery; it does not have the elastic feeling of a normal 
lung, nor does it contain as much 'air,. On section very little blood or 
serum escape, and the cut surface is almost dry. The color of the lung 
is peculiar-a sort of yellow-pink, quite different from the color of a 
normal lung. This pink is mottled with spots of-brown or black pig- 
ment, varying in amount in different cases. These changes embrace all 
the lobes of both lungs. 
The leathery consistence of these lungs is often somewhat changed 
by an hepatization of parts of the lung. This hepatization may involve 
portions of the different lobes or an entire lobe. The solidification may 
be partial or complete, and the texture of the lung will be accordingly 
less or more firm. It is a perfectly smooth hepatization, not resem- 
bling that of acute lobar pneumonia. I have never seen it in any stage 
except that of red hepatization. 
There may be hemorrhagic infarctions scattered through the lungs, 56 
PNEUMONIA. 
and sometimes these are surrounded by a zone of pneumonia; but this 
pneumonia is different from the red hepatization of which I have just 
spoken. 
The gross appearance of the lungs may be modified by the coexist- 
ence of emphysema or oedema. 
If the lungs are emphysematous they will be large, instead of small, 
and they will contain more air and be of a less leathery texture, al- 
though their general appearance will be as described above. 
If the lungs are oedematous, they will be infiltrated with serum, and 
consequently large and heavy. 
Microscopical examination of lungs which exhibit the gross appear- 
ances mentioned shows that there are four separate pathological condi- 
tions existing: 
(1.) Hypertrophy of the capillaries. This change exists in very 
different degrees in different cases. In some lungs the capillaries are 
both dilated and increased in length, so that they appear tortuous and 
project in loops into the air-vesicles. If they are injected artificially 
they occupy so much space as to obscure all the other tissues. In other 
cases the capillaries can hardly be said to be dilated at all; even when 
injected artificially, they are not large. Between these two extremes of 
great dilatation and no dilatation at all we find every gradation. In 
all cases, however, if we inject these lungs artificially, the injection re- 
quires more pressure than in a normal lung and the vessels are not as 
uniformly filled. Although, therefore, the mechanical cause-the ob- 
struction to the passage of blood into the left auricle-would seem 
likely simply to cause an accumulation of blood in the pulmonary veins 
and their capillaries, and then a dilation of these vessels, yet the mech- 
anism does not seem to be quite so simple as this. There does not 
seem to be necessarily any real accumulation of blood in the lungs, but 
rather a retardation of the circulation. The lungs do not at any one 
time contain more blood than do normal lungs-if we can judge from 
post-mortem appearances, they may contain less-but the blood passes 
through them more slowly than it should. If this view be correct, then 
the large size of the capillaries depends, not upon their dilatation by 
the pressure of the blood, but upon an hypertrophy of their walls. PNEUMONIA. 
57 
The increased size of the capillaries, as well as the other lesions yet to 
be described, are due to a change in the nutrition of the lungs produced 
by the slow circulation of the blood through them, and these changes 
may fairly be classed with other chronic inflammations. 
(2.) Hypertrophy of the walls of the air-vesicles. This lesion also 
varies in extent. The walls of the air-vesicles may not be thicker than 
those of a normal lung, or they may be moderately thickened, or very 
much thickened. When hypertrophy of the walls of the air-vesicles 
does exist, it is due partly to the increased size of the capillaries, partly 
to a new growth of smooth muscle, and partly to a new growth of con- 
nective tissue. 
(3.) Formation of pigment. The pigment is usually of black or 
brown color, in the form of granules and small masses, or of a diffuse 
staining. It is deposited in the walls of the air-vesicles, in the inter- 
stitial tissue, and in the cells found within the air-vesicles. Orth 
describes a case in which there was pigment within the capillaries. It 
seems probable that this pigment is derived from the blood circulating 
slowly in the capillaries and from that extravasated in the air-vesicles 
and the interstitial tissue. It is very likely that some of the red blood- 
globules are taken inside of other cells, and their pigment then trans- 
formed, and that others give up their coloring matter more directly. 
I he whole amount of pigment varies in diff erent cases. 
(4.) Filling up of the air-vesicles with polygonal nucleated cells 
and red blood-globules. 
It has been already stated that in the normal lung the epithelium is 
represented by a continuous thin layer of granular matter in which 
nuclei are imbedded at irregular intervals, and by a small number of 
polygonal nucleated cells. In pigment induration of the lung these 
polygonal nucleated cells increase enormously in number, and take the 
place of the nucleated membrane. We find, then, the entire walls of air- 
vesicles covered with a continuous layer of flat nucleated cells, either 
transparent or stained yellow, or containing granules of pigment. 
There are also similar cells free in the cavities of the air-vesicles and 
even in sufficient numbers to fill them. These free cells, however, are 
larger, often more rounded and coarsely granular, and frequently con 58 
PNEUMONIA. 
tain more pigment than do the more regular cells which line the air- 
vesicles. 
Plate XXXI. is from a case in which the thickening of the walls of 
the air-vesicles and the production of new epithelium were the most 
marked lesions. The capillaries were not dilated, nor was there much 
new pigment. The drawing is made out of proportion, the air-vesicles 
being magnified 300 diameters and the epithelium 700 diameters. 
Plate XXXII. is from a case in which the increase in the size of 
the capillaries was marked. It represents a single air-vesicle, not in- 
jected, magnified 750 diameters. PNEUMONIA. 
59 
II The Lobar Pneumoilia of Adults and Children. 
Tins disease prevails regularly in New York and furnishes from 
about three to four per cent, of the yearly mortality. Since 1873 the 
mortality has not been less than four per cent. This is the number 
after deducting the deaths from pneumonia in children under five years, 
in most of whom the disease is not lobar but lobular. What proportion 
of children under five years old have lobar pneumonia, I am unable to 
ascertain. 
The larger number of the deaths occur in the three spring months- 
March, April and May-and the three winter months-December, Janu- 
ary, and February-corresponding to the period of cold and wet weather. 
Still in the hottest months-June, July, and August-there are from 
fifteen to forty deaths a month. 
Persons between the ages of ten and twenty furnish the smallest, 
and those between forty and fifty the largest number of deaths. 
Lobar pneumonia affects large portions of the lung tissue, either the 
whole of one lobe, or of one lung, or portions of both lungs. It often 
begins in one lobe and then extends to the rest of the same lung. In 
rare cases nearly the whole of both lungs is involved at the very outset 
of the disease. 
It is customary to divide the lesions into the stages of Congestion, 
Hed Hepatization, Gray Hepatization, and Resolution. 
(1.) Congestion. Of this stage we have but little knowledge de- 
rived from actual observation. It seems probable, however, that there 
is such a stage characterized by an increase of the blood circulating in 
the vessels. 
(2.) Red Hepatization. The lung loses its natural consistence and 
becomes solid. Firm pressure causes it to break down. Its color is red, 
sometimes mottled with hemorrhagic spots of a deeper hue. A section 
looks as if the lung was composed of a multitude of small granules 
closely packed together, each granule corresponding to an air-vesicle. 
If the lung is seen soon after death, the section is dry; in a short time, 
however, part of the inflammatory products liquefies and the section is 60 
PNEUMONIA. 
covered with a thick, grumous, reddish fluid. The larger bronchi are 
congested and coated with mucus, or dry, or filled with firm, yellow, 
fibrinous cords. The pulmonary pleura is coated with fibrine. 
In the earlier stages of red hepatization, before the air-vesicles are 
fairly filled, we find in them fibrine, epithelial cells, pus-cells and red 
blood-globules. The vessels of the lungs are full of blood, the walls 
of the air-vesicles are unchanged. Although the blood-vessels are full 
of blood, it is not coagulated, and the vessels are easily filled with an 
artificial injection after death. The fibrine is present in variable 
amount, sometimes forming a large part of the inflammatory products, 
sometimes hardly visible. It has seemed to me that large amounts of 
fibrine are usually associated with severe constitutional symptoms. It 
usually coagulates in the form of a net-work. The epithelial cells also 
are found in variable proportion. They are more numerous in children, 
in persons already suffering from emphysema and bronchitis, and in 
those who have chronic phthisis. They are often swollen and coarsely, 
granular. The pus-cells are always numerous, often obscuring both 
fibrine and epithelium. The red globules may only be found in small 
numbers, or they may completely fill some of the air-vesicles. When 
the stage of red hepatization is complete, the air-vesicles are completely 
filled with these products of inflammation. Plate XXXIII. represents 
a single air-vesicle, only partly filled with the products of inflammation. 
The specimen was from a person who died forty-eight hours after the 
initial chill. The blood-vessels are injected artificially. 
The smallest bronchi are filled with the same products of inflamma- 
tion as are the air-vesicles-fibrine, pus, and epithelium. The same pro- 
ducts may fill the medium-sized and even the largest bronchi. Plate 
XXXIV. represents a vertical section of the wall of a smaller bronchus; 
there is a layer of fibrine and pus coating its inner surface and a similar 
layer lifts up and separates the epithelium from the stroma beneath. 
I have seen one case of lobar red hepatization characterized by the 
presence of large masses of bacteria within the air-vesicles. The 
patient was a woman thirty-two years old, a laundress by occupation. 
She was perfectly well until five months before her death. At that 
time she began to have a slight cough with expectoration, which con- PNEUMONIA. 
61 
tinned until her present attack. Eleven days before her death, after 
being exposed to cold and wet, she had several rigors followed by high 
fever. The next day she began to have pain in the left side of 
the chest. On the fifth day she began to vomit, and after that time 
vomited everything she ate. I saw her first on the eighth day of her 
disease. Her temperature was then 106°, pulse 122, respiration 42; 
there was a good deal of pain and dyspnoea; the woman looked very 
sick. Over the left upper lobe there was dulness, bronchial breathing, 
and coarse and subcrepitant rMes; over the rest of both lungs coarse 
rfiles. She became rapidly worse, with high temperature, delirium, 
brown and dry tongue, and died on the eleventh day of the disease. 
At the autopsy there were no lesions except of the lungs. The bronchi 
of both lungs were congested and coated with muco-pus. The left 
upper lobe was in the condition of red hepatization, the pleura coated 
with fibrine. The lung did not look exactly like most specimens of red 
hepatization, being moister and less firm. The air-vesicles were found 
to be filled with large masses of micrococci, not affected by acetic acid 
or chloroform. Mixed with these was a moderate amount of pus, epi- 
thelium, and fibrine. See Plate XXXV. 
The duration of the stage of red hepatization seems to be quite vari- 
able. About one-fourth of the autopsies of pneumonia which I have 
made have shown red hepatization existing at the time of death. In 
these cases the duration of the disease has varied from twenty-four 
hours to eleven days, dating from the initial chill. 
(3.) Gray Hepatization. The stage of red hepatization passes into 
the gray gradually, the lung being first mottled red and gray and then 
completely gray. Except for the difference in color, a difference which 
seems to depend partly on the diminished congestion, and partly on 
the loss of color of the red globules already extravasated, the condition 
of the lung remains almost the same. The products of inflammation-- 
the pus, fibrine, and epithelium - have much the same appearance. 
Some granular degeneration of them, however, is usually apparent. 
Tlie epithelium and pus-cells become swollen and filled with coarse 
granules, and there may be coarse granules in the fibrine. The air- 
vesicles are more completely filled and packed with the inflammatory 62 
PNEUMONIA. 
products. Plate XXXVI. shows one air-vesicle and parts of others 
from a lung in the condition of gray hepatization. The lungs have 
been in the mottled condition of partly red and partly gray hepati- 
zation in nearly half of my autopsies of pneumonia, so that in New 
York at least the end of the period of red hepatization is a favor- 
ite time for death. The time of the disease, however, at which the 
lung is found mottled red and gray is very variable. I have found it 
from the second to the eighteenth day of the disease. The lung was 
completely gray at the time of death in only about one-fourth of my 
cases. It was found in this condition from the fourth to the twenty- 
fifth day of the disease. 
(4.) Resolution. I have very little actual knowledge of this stage. 
It is evident that in persons who recover from pneumonia, the solid 
products which fill the air-vesicles must in some way become liquefied 
so that they can be absorbed or coughed out. There are also a moderate 
number of autopsies in which the lungs look like gray hepatization, 
but are softer, and covered with grumous fluid when cut. Of course 
this condition must not be mistaken for the post-mortem softening 
which may affect any gray hepatization. 
In such soft lungs the air-vesicles still contain the products of in- 
flammation, but are not so closely packed with them. There is not 
nearly as much fibrine, but a great deal of coarse granular matter ; 
the pus-cells and epithelial cells are large and filled with coarse gran- 
ules, or broken and fragmentary. One receives the impression that all 
the inflammatory products are degenerating and breaking down; and 
it seems probable that this is the way in which resolution is effected 
during the life of the patient. 
There are some exceptions to this ordinary course of lobar pneu- 
monia. 
(1.) The lung after reaching the stage of gray hepatization may 
remain in that condition for weeks, without any attempt at resolution. 
When this is the case, the lung presents a peculiar appearance after 
death. It is very firm and dry; its color is rather white than gray. 
The air-vesicles are found completely filled with fibrine, pus, and epithe- 
lium. These retain their shape and can be recognized in some air-vesi- PNEUMONIA. 
63 
cles, while in others they are changed into a mass of granules. This is 
the nearest approach to cheesy hepatization that I have seen in lobar 
pneumonia. 
(2.) Portions of the hepatized lung may die and become separated 
from the surrounding lung tissue, so as to form irregular cavities con- 
taining portions of necrotic lung tissue. Tn the earlier stages of this 
change, which I have seen, I have been struck by the large amount of 
fibrine present. All through the hepatized lung the air-vesicles are 
filled with coagulated fibrine, while pus and epithelium are scanty. 
There seems to be a necrosis of portions of the hepatized lung, either 
from complete stasis of the blood, or from the presence of the large 
amount of fibrine on the vessels. In the later stages the cavities con- 
tain pus in addition to the necrotic lung tissue and look more like ordi- 
nary abscesses. 
(3.) Portions of the hepatized lung may become not only necrotic, 
but gangrenous, and such portions may be either small or large. Their 
causation is very obscure. PNEUMONIA. 
65 
III. The Pneumonia which occurs after Surgical Operations and 
Injuries. 
The etiology of this variety of pneumonia is very obscure. The 
disease is developed either a few days after the operation or injury, or 
not until the patient has been confined to bed for some time. The 
Existence of the inflammation may be indicated by well-marked consti- 
tutional symptoms, or such symptoms may be entirely absent. There 
may be severe rigors followed by a well-marked febrile movement, 
rapid breathing, dulness on percussion, crepitant rMes, and bronchial 
breathing; or all these symptoms will be wanting, and the lesion is only 
discovered at the autopsy. 
The amount of lung inflamed may be small or large; but the central 
portions of the lung are those usually involved. The rest of the lung 
is apt to be congested and oedematous. No matter how small the 
hepatized portions of lung, they have the characters of a diffuse inflam- 
mation. They do not look as if the inflammation began in the bronchi 
or in the blood-vessels. The suspicion arises, of course, that such a 
pneumonia may be produced by irritating matters inhaled through the 
bronchi, or lodged in the vessels as emboli. But the lungs do not look 
so ; there is no appearance of foci; the hepatization has the same diffuse 
character, the same color and general appearance that it has in idio- 
pathic lobar pneumonia. There is, however, very often catarrhal inflam- 
mation of the larger bronchi with the pneumonia. 
When we examine the hepatized lung, we find the air-vesicles are 
filled principally with fibrine and pus; with these are a few epithelial 
cells and red blood-globules. There is no essential difference between the 
lesions and those found in idiopathic lobar pneumonia. Plate XXXVII. 
represents a single air-vesicle full of fibrine and pus. The specimen was 
taken from a woman who died on the fourth day after receiving a 
severe blow on the head, which produced laceration of the brain. 
IV. The Lobular Pneumonia of Children and Adults. 
Most of the examples of lobular pneumonia in adults which I have 
seen have occurred in persons suffering from chronic bronchitis. 66 
PNEUMONIA. 
Chronic bronchitis, either with or without emphysema, is usually 
attended with an increase in the number of the epithelial cells of the 
air-vesicles. Some of these cells are found in position, others are 
detached and free within the cavities of the vesicles. . The production 
of new cells is not, however, sufficient to fill the air-vesicles or produce 
red hepatization. But sometimes a patient, already suffering from such 
a chronic bronchitis, becomes worse. There is an exacerbation of the 
bronchitis, and the inflammation extends to the lungs. We then find a 
number of hepatized lobules scattered through one or both lungs. 
These lobules are not very sharply outlined; they are usually in the 
condition of red hepatization, resembling the same condition in lobar 
pneumonia, but giving a smoother surface on section. Minute exami- 
nation shows that the air-vesicles contain epithelium, pus, fibrine and red 
blood-globules.. The epithelium is always abundant, many of the cells 
are well formed, others swollen and granular. The pus-globules are 
present in considerable numbers, and are usually round and well formed. 
The fibrine varies in amount in different lungs and in different air-vesi- 
cles in the same lung. It is not as abundant as in lobar pneumonia. 
The red blood-globules also vary in number in different cases. See 
Plate XXXVIII. The larger bronchi are usually trabeculated, and con- 
tain muco-pus; the smaller bronchi contain pus and detached epithe- 
lium. 
Acute inflammation of the lungs in children is either lobar or lobu- 
lar. The lobar pneumonia of children resembles in all respects that of 
adults, both in its gross and minute anatomy. There are, usually, how- 
ever, a larger number of epithelial cells, and the interstitial connective 
tissue is more infiltrated with pus and fibrine. 
The lobular pneumonia of children, however, is something quite dif- 
ferent. It is essentially a broncho-pneumonia, not merely in the sense 
that the bronchi are inflamed as well as the lung tissue, but that the 
pneumonia is dependent on the bronchitis. In lobar pneumonia it 
seems as if a large part of the lung, including both air-vesicles and 
bronchi, become inflamed at the same time. But in lobular pneumonia 
the inflammation appears to begin in the bronchi and then extends to 
the groups of air-vesicles belonging to the inflamed bronchi, and the PNEUMONIA. 
67 
bronchitis continues to be an important factor in the inflammatory 
process. 
A large number of the cases of lobular pneumonia occur in the 
course of whooping-cough, measles, and scarlatina, diseases which are 
regularly complicated by bronchitis. Other cases occur with bronchitis 
due to exposure'to cold, and in children who are badly nourished from 
any cause. 
The course of the disease, also, is very different from that of lobar 
pneumonia. It does not run a regular course, terminating in a few 
days in death or resolution, but may be protracted for weeks or months 
before the patient dies, or before the products of inflammation are ab- 
sorbed. Cheesy degeneration of the hepatized portions of lung and 
interstitial pneumonia are also much more common with lobular than 
with lobar pneumonia. 
If we look at the lungs of a child in whom lobular pneumonia has 
existed for only a few days, we find the pulmonary pleura either nor- 
mal, or coated here and there with a little fibrine. 
The large bronchi are congested and coated with mucus; the smaller 
bronchi are congested, their walls are often thickened, and they may 
contain pus. 
Scattered through one or both lungs are hepatized globules, which 
may be large or small, few or numerous, scattered or crowded close 
together. These hepatized lobules may be of a light or deep red 
color, or pinkish-gray, or of a livid, bluish color. They may be so 
solid as to stand out sharply defined from the surrounding lung 
tissue, or only partly hepatized and blending gradually with the 
adjacent lung. On section they are not granular like lobar pneu- 
monia, but smooth. Sometimes the hepatized lobules have their red 
color mottled with white spots or lines marking the position of the 
bronchi. 
Such hepatization is not to be confounded with the condition of 
atelectasis, when groups of air-vesicles are simply collapsed. But some- 
times there appears to be an inflammatory process complicating this 
condition of collapse. 
The rest of the lung around the hepatized lobules may appear 68 
PNEUMONIA. 
normal, or be congested, or be of firmer and denser consistence, of be 
emphysematous. 
Minute examination of the hepatized lobules shows that their condi- 
tion is not always the same. In some cases the air-vesicles are filled 
principally with pus; in other cases, almost entirely with epithelial 
cells; in other cases, with both pus and epithelium; in others, with pus, 
epithelium, and fibrine. The capillaries in the walls of the air-vesicles 
are usually large and prominent, and there are red. blood-globules in the 
air-vesicles. The degree in which the air-vesicles are filled also varies ; 
they may be only partly occupied by the inflammatory products, or 
they may be so closely packed with them that the walls of the vesicles 
cannot be distinguished. The rest of the lung tissue, although it is 
not hepatized, shows some change, for the epithelial cells appear larger 
and. more distinct than they do in the healthy lungs of children of the 
same age. Plate XXXIX. shows part of a hepatized lobule from a 
case of scarlatina. The air-vesicles contain pus, epithelium, fibrine, and 
red blood-globules. 
Plate XL. shows part of' a hepatized lobule from a case of whoop- 
ing-cough. The air-vesicles are partly filled with epithelium, and the 
epithelial cells are especially prominent on the edges of the walls of 
the air-vesicles. 
In many cases of lobular pneumonia there are well-marked changes 
in the walls of the bronchi. Not only are the larger bronchi congested 
and coated, with mucus and the smaller filled with pus and epithelium, 
but their walls are thickened and. infiltrated with cells. Sometimes the 
thickening is so great that the bronchi appear like white lines and dots 
to the naked eye when the lung is cut. This thickening of the bronchi 
seems to be due merely to an infiltration of pus, or, in other cases, to a 
growth of connective-tissue cells in addition to the pus. 
Plate XLI. represents a vertical section of part of the wall of a 
small bronchus thus thickened. The epithelium lining the bronchus is 
swollen and deformed, and the wall of the bronchus beneath is thickly 
infiltrated with cells. The connective tissue between the lobules may 
be in the same way infiltrated with cells. 
Many of the patients die while the lungs are still in the condition of PNEUMONIA. 
69 
red hepatization. If they live longer the red hepatization changes to 
gray, the change in color beginning in the centres of the lobules. In 
this condition of gray hepatization the pus and the epithelial cells are 
found swollen, granular, and fatty. 
If resolution does not take place, the granular and fatty degeneration 
go on and the lobules pass into the condition of cheesy hepatization. They 
are then hard and yellow, the air-vesicles filled with granular matter. 
It seems probable that resolution may take place even after cheesy 
hepatization is fully established. If it does not, however, after a time 
the cheesy lobules soften and cavities are formed, or there is interstitial 
pneumonia with production of new connective tissue, or both these pro- 
cesses go on together. 
The condition of collapse of the lungs, or atelectasis, is one of a 
good deal of importance, particularly that variety which occurs as a 
complication of bronchitis. Larger or smaller bronchi become occluded, 
and the groups of air-vesicles which empty into them collapse. There 
can be no question of the frequency and importance of this condition, 
but I think that there is at present a tendency to call much atelectasis 
that is really pneumonia. 
If we examine a portion of lung which is in the condition of 
atelectasis, without distending the air-vesicles, we find that the walls of 
the undilated vesicles give quite an irregular picture. They project 
inwards so that we no longer get the regular outline of the vesicles. 
The capillary vessels are large and may be distended with blood. The 
epithelium is more distinct, and there are a few large, granular epithelial 
cells in the cavities of the vesicles, with perhaps a few pus-globules and 
a little granular matter. That is all; there is no large number of either 
pus or epithelial cells. Sometimes, however, we find lobules of the lung 
in a condition which suggests the idea that there has been first collapse 
and afterwards inflammation. 
The old test of inflating the lung to determine between atelectasis 
and pneumonia does not seem to be of very much value, for there are 
many degrees of pneumonia short of complete hepatization. There may 
be enough pneumonia to cause a partial Alling up of the air-vesicles, but 
not sufficient to prevent their inflation. 70 
PNEUMONIA. 
The lobular pneumonia with the characters described above belongs 
properly to children under five years old. It is sometimes met with in 
older children, however, and I have seen it in persons between nineteen 
and twenty years old. It is said also that adults in whom bronchitis 
complicates measles may suffer from a lobular pneumonia like that of 
children. 
V. Interstitial Pneumonia. 
This term is applied to a chronic form of inflammation involving the 
fibrous framework of the lung and resulting in the production of per- 
manent new connective tissue. The new tissue thus produced is dense, 
contains comparatively few cells, and is often pigmented. It is usually 
arranged in the form of nodules, of bands, or of irregular patches. 
The walls of the air-vesicles, of the bronchi, and of the blood-vesicles 
may all be involved in such an inflammatory process. 
The examples of the disease, which have come under my observa- 
tion, have been in connection with emphysema and chronic bronchitis, 
with anthracosis, with pleurisy, and with chronic phthisis. 
In emphysematous lungs there are sometimes numerous small, hard 
nodules, sometimes bands and patches of fibrous tissue, which seem to 
have no relationship with phthisis or tuberculosis, but to be simply the 
results of an interstitial inflammation. 
The inhalation of coal dust and stone dust may excite an interstitial 
pneumonia, but I have not seen enough cases of these lesions to speak 
of them with confidence. 
Extensive old pleuritic adhesions with thickening of the pulmonary 
pleura are often accompanied by the production of bands of fibrous tis- 
sue extending from the pleura inwards into the lungs. The extreme 
examples of this lesion, when the entire lung is converted into fibrous 
tissue and the bronchi dilated, have not fallen under my observation. 
The interstitial pneumonia of phthisis will be described farther on. 
VI The Pneumonia produced by pressure on the Trachea and 
Bronchi. 
If an aneurism presses upon the trachea or upon the right or left 
bronchus it usually gives rise to a catarrhal inflammation of the trachea PNEUMONIA. 
71 
and bronchi. In a certain number of cases there are also characteristic 
changes in the lungs. If the trachea is compressed by the aneurism, both 
lungs may be affected ; if one bronchus is compressed, then the lung 
belonging to that bronchus will be alone affected. 
The appearance of the lungs is something like that of the lungs in 
phthisis. The lung is thickly studded with hepatized lobules from the 
size of a pea to that of a chestnut. Some of the lobules look like red 
hepatization, more are gray or cheesy, some are softened and converted 
into cavities containing pruriform fluid. If the aneurism has partly 
opened into the trachea or bronchus so that small quantities of blood 
are inspired, then some of the hepatized lobules are partly filled with 
blood. 
Minute examination, however, shows the lesions to be different from 
those of phthisis. There seems to be a combination of three different 
processes: (1) an intra-alveolar pneumonia; (2) collapse of groups of 
air-vesicles; (3) an interstitial pneumonia. I have not yet seen enough 
cases of this lesion to speak of it with certainty, but my belief is that 
the process is first a bronchitis, then a plugging of the bronchi with 
pus and mucus, then a collapse of groups of air-vesicles, after this an 
interstitial pneumonia involving the walls of the collapsed vesicles and 
an intra-alveolar pneumonia involving the interior of the air-vesicles 
which surround the collapsed lobules, and resulting in the filling of 
these vesicles with epithelium and pus. ACUTE MILIARY TUBERCULOSIS. 
Although all are not agreed as to the causes and nature of miliary 
tubercles, yet it must be allowed that important advances have been 
made in our knowledge of their anatomy. 
From the time that Virchow described them as organized tissue, 
composed of cells, and not as amorphous masses with shrivelled nuclei, 
the study of their minute anatomy has been steadily pursued. Virchow 
compared them to lymphatic glands, laying especial stress on the cells, 
which he described as small round cells with a small cell body, and 
large nucleus. Wagner and others have called attention to the exist- 
ence of a basement substance in 'which the cells are imbedded, and 
which resembles the basement substance of connective tissue, and have 
spoken of tubercles as composed of adenoid tissue. 
Schuppel and others have shown that giant-cells are frequently 
present, and that many of the apparently round cells really have a 
polygonal cell body of some size, and resemble connective-tissue cells 
rather than the cells of lymphatic glands. 
Charcot and others have shown that it is possible that the giant cells 
and other cells may be developed from the epithelium of the air-vesicles, 
and that the giant-cells are concerned in forming the basement substance 
of the tubercle. 
The tendency has been more and more to establish a definite anat- 74 
* ACUTE MILIARY TUBERCULOSIS. 
omy for tubercle, although many still call any little nodule formed of 
round cells and partly cheesy, a miliary tubercle. There is also a good 
deal of confusion as to whether miliary tubercles should be regarded as 
new growths, or as products of inflammation. 
So far as the gross appearance of miliary tubercles is concerned, 
almost every one has followed the description of Laennec. 
" The tubercles," says Laennec, " resemble small grains; they are 
of a gray color, and semi-transparent, sometimes even transparent and 
colorless, and of a consistence somewhat less than that of cartilage. 
Their size varies from that of a millet to that of a hemp seed. Their 
shape, roundish at first sight, is found on inspection with a lens to be 
less regular. They adhere intimately to the pulmonary substance, and 
a number of them may be united so as to form a group. After a 
certain time a yellowish, opaque speck appears in the centre of each 
tubercle." 
Miliary tubercles of this character have been observed in almost 
every part of the body. They may be developed in the course of a few 
days and be accompanied by acute constitutional symptoms; or they 
are formed slowly and remain during months and years. We speak, 
therefore, of acute tuberculosis and of chronic tuberculosis. We will 
consider, first, the miliary tubercles, which are produced in a short space 
of time. 
In the lungs miliary tubercles are usually numerous, and are found 
both in the parenchyma of the lung and the pulmonary pleura. 
The lung tissue between the tubercles may appear to the naked eye 
normal. Very frequently it is congested, or partly hepatized. Minute 
examination always, so far as I know, shows some changes in the air- 
vesicles, even when the lung tissue appears normal to the naked eye. 
The change in the air-vesicles consists in a production, within their cavi- 
ties, of large, polygonal (epithelial) cells, of pus-cells, of fibrine, and of 
red blood-globules. The amount and proportion of these inflammatory 
products vary in the different cases. 
The bronchi also usually show changes; their mucous membrane is 
congested and coated with mucus. 
The miliary tubercles are scattered singly through the lungs, or are ACUTE MILIARY TUBERCULOSIS. 
75 
aggregated in groups, or situated close to each other and joined together 
by more diffuse infiltrations of similar tissue. They may be separated 
from each other by considerable intervals of lung tissue, or be so close 
together that the lung is rendered almost solid by them. There is much 
variety in the size of the tubercles; most of them are about the size of 
a pin's head, but some are so small they can hardly be seen with the 
naked eye, and occasionally they are as large as peas. Their consistence 
may be as hard as cartilage, or as soft as coagulated fibrine, and 
between these extremes are all gradations. In color some are gray and 
semi-translucent, some are white, some are gray or white with yellow 
centres, some are entirely yellow. They all have a tendency to pass 
into the condition of cheesy degeneration, but the degree in which this 
tendency is developed varies in different lungs. In some cases a large 
number of the tubercles escape degeneration altogether ; in some only 
their centres are cheesy; in some the larger number are completely 
cheesy. The cheesy matter may be hard and dense, or soft and friable. 
The extent of cheesy degeneration has generally a relation to the age of 
the tubercles : the older the tubercles, the more cheesy degeneration. 
This rule, however, is not without exceptions. 
If we look at the tubercles with a low magnifying power we see that 
some are of spheroidal shape, some look like irregular infiltrations, and 
some are joined together so as to form masses of some size. The 
appearances vary with the number of the tubercles, their arrangement, 
and the amount of consolidation that has taken place in the intervening 
lung. Plate XLII. represents a section of lung magnified twenty-two 
diameters. The tubercles are numerous and close together, many are 
united to neighboring tubercles by consolidated lung, all have under- 
gone cheesy degeneration at their centres. 
When we look at the individual miliary tubercles with higher mag- 
nifying powers, and compare them as they exist in different lungs, it 
soon becomes evident that they are not all of the same structure, and 
that it is necessary to distinguish four principal varieties of miliary 
tubercles in the lungs. 
(1.) Miliary tubercles composed entirely of amorphous granular 
matter, with a few shrunken cells, and an external zone of pus-cells. 76 
ACUTE MILIARY TUBERCULOSIS. 
These tuberclexS cannot be said to have a definite anatomical structure. 
Many of them look as if they were the results of cheesy degeneration 
of pre-existing anatomical elements, the walls of the air-vesicles sharing 
in the degenerative process. In others, however, the walls of the air- 
vesicles are intact, while their cavities are filled with amorphous granu- 
lar matter. At the first glance it may be thought that this variety of 
miliary tubercles hardly needs any separate mention ; that it is merely 
a question of the extent of the degenerative process; that these tuber- 
cles have the same structure as others, but arc further advanced in de- 
generation. In the larger number of all miliary tubercles it is indeed 
the rule for the centre of the tubercle to undergo cheesy degeneration 
and be converted into amorphous granular matter, and in many lungs 
we can see the different steps of the degenerative process and the con- 
version of more and more of the original anatomical elements into gran- 
ular matter. But the miliary tubercles of which I am now speaking 
present no such gradations. In the entire lung all the tubercles are 
simply masses of granular matter with pus-cells at their peripheries. 
The only difference between the smaller and larger tubercles is that in 
the smaller ones the walls of the air-vesicles are still visible, and their 
blood-vessels can be injected ; in the larger, the walls of the vesicles 
are destroyed. I am very far from saying that in these tubercles there 
have not been anatomical elements first produced, which have after- 
ward degenerated. But I think that the earliness and completeness of 
the transformation of these tubercles and the absence of any visible in- 
termediate stages of degeneration entitle them to separate consideration. 
A possible explanation seems to be that in these cases there is no for- 
mation of regular anatomical elements, but that from the very first 
amorphous inflammatory products are formed which rapidly degenerate 
and involve with them in their destruction the walls of the air-vesicles. 
Miliary tubercles of this same indeterminate character are also not un- 
common in the peritoneum. 
(2.) Miliary tubercles composed principally of new tissue, which 
apparently replaces the parenchyma of the lung, while at the periphery 
of this nodule of new tissue are air-vesicles filled with cells. Plate 
XLV. represents a miliary tubercle of this kind. In the right of the field ACUTE MILIARY TUBERCULOSIS. 
77 
is a blood-vessel, to the left of this is a mass of solid tissue occupying 
most of the field, while at the ed^es of this mass are air-vesicles, of 
which the walls are covered with large (epithelial) cells. In one air- 
vesicle an invasion of the solid tissue into the cavity of the vesicle 
seems to have taken place, although the outline of the wall of the vesi- 
cle is preserved. The solid tissue is composed of elements, having the 
same general appearance but arranged in two different ways. Part of 
the tissue is arranged so as to form two irregularly spherical bodies, 
and the rest as a diffuse infiltration around and between these two 
bodies. The spherical bodies we may call, for convenience, " tuber- 
cle granula;" the diffuse tissue, "diffuse tubercle." When we exam- 
ine the tubercle granula more carefully, we see that the centre of each 
is occupied by a large mass of protoplasm filled w'ith nuclei. If we 
isolate one of these masses of protoplasm, or giant cells, we see that it 
is of such a form as is represented in Plate XLVIIL, and that its 
branching processes are apparently continuous with the basement sub- 
stance situated between the surrounding cells. The rest of each 
tubercle granulum is composed of cells of irregularly polygonal shape 
imbedded in a basement substance as in Plates XLIV., XXIX., and 
XLIX. The bodies of the cells are very delicate and easily escape 
observation unless carefully prepared; the nuclei, on the contrary, are 
readily seen. Besides these polygonal cells, there may be round cells 
looking like pus globules. The basement substance between the cells 
varies in its character in different tubercles; it may look like the base- 
ment substance of reticulated connective tissue, or it may be a delicate, 
finely granular material requiring careful demonstration, and between 
these two extremes we see many gradations. The basement substance 
sometimes, but not always, appears to be continuous with the processes 
of the central giant-cell. The giant-cells are indeed often entirely 
absent from the tubercle granula, and these latter are then composed 
only of the basement substance, polygonal cells and round cells. When 
the giant-cells are present, they may be situated in any part of the 
tubercle granulum, not necessarily in its centre ; there may be two or 
three such giant-cells in a single granulum. The diffuse tubercle has 
the same structure as the tubercle granula-polygonal cells and small 78 
ACUTE MILIARY TUBERCULOSIS. 
round cells imbedded in a basement substance. See Plate XLVI. The 
basement substance, however, is better marked than in the tubercle 
granula, the bodies of the polygonal cells are less delicate, the round 
cells are more numerous, and the giant-cells are less constantly present. 
This variety of miliary tubercle may become the seat of cheesy de- 
generation. I think, however, that the extent and constancy of cheesy 
degeneration of all miliary tubercles has been somewhat exaggerated 
by authors. Such degeneration is common enough, but there are very 
many miliary tubercles of which all the anatomical elements are well 
preserved. Even in those tubercles, which look opaque at their cen- 
tres, there may be no destruction of tissue. 
It is very difficult to be certain of the earlier stages of this form of 
tubercle. Some authors are disposed to believe that the process begins 
in the cavities of the air-vesicles with a subsequent growth of new tis- 
sue in their walls. It is said that there is first a growth of cells within 
the air-vesicle, a transformation of some of these cells into one or more 
giant-cells, a formation of basement substance from the body of the 
giant-cell, and then an infiltration and thickening of the wall of the 
air-vesicle. If this explanation were true, then each tubercle granulum 
is a single air-vesicle, or bronchiole, with thickened walls and filled 
cavity. This explanation is plausible enough, but it is difficult to 
really demonstrate the different steps of the process. The mere shape 
of the tubercle granula does not at all show that they are altered air- 
vesicles, for they are of the same shape in whatever part of the body 
they occur. See Plate XVIII. 
(3.) Miliary tubercles composed partly of solid tissue, partly of 
air-vesicles filled with tubercle tissue, partly of air-vesicles filled with 
epithelium, pus, and fibrine. Plate XLIII. represents a section of a 
single miliary tubercle of this kind. It will be seen that in the upper 
and left hand portion of the plate, and extending to its centre, is a group 
of five tubercle granula surrounded by diffuse tubercle. In these 
granula the cells are larger than in those in Plate XLV., and there are 
no giant-cells. In the granulum in the centre of the drawins' the tissue 
is broken down and softened, otherwise the structure of the granula 
and of the diffuse tubercle is the same as of those in Plate XLV. In ACUTE MILIARY TUBERCULOSIS. 
79 
the lower and right hand portion of the plate are four large irregular 
spaces looking as if they were formed of the fusion of one or more air- 
vesicles and full of cells. On looking at these spaces more closely, it 
will be seen that one of them is filled with tissue identical with that 
composing the tubercle granula and diffuse tubercle; while the three 
others are only partly filled with such tissue, the rest of their cavities 
being filled with large epithelial cells, granular matter, and blood 
globules. In other parts of the field are air-vesicles filled with epithe- 
lial cells, and all the surrounding air-vesicles are lined with similar- 
large epithelial cells. In these composite tubercles there are often air- 
cells of which the contents are somewhat puzzling. The walls of these 
air-vesicles are not thickened, their blood-vessels can be injected, the 
elements which fill the air-cell do not seem to be continuous with its 
wall. The cells contained within the air-vesicle looks more like those 
of tubercle tissue than like epithelial cells; they are imbedded in a 
finely granular basement substance. See Plate XLVII. 
In this kind of miliary tubercles also cheesy degeneration may begin 
at the centre, and involve a large part of the tubercle. 
It will be seen that these tubercles differ from the second variety, 
in that they are composed not merely of solid tissue replacing the air- 
vesicles, but that a large part of the tubercle is composed of filled air- 
vesicles. The tubercle tissue is essentially the same in both varieties- 
polygonal cells imbedded in a basement substance, and giant-cells, 
either present or absent. But in this third variety the production of 
epithelial cells, the filling of the air-vesicles with tubercle tissue, with 
epithelial cells, and with a tissue intermediate between these two, is 
much more marked. It is very difficult in either variety to see any- 
thing which looks like an early stage of infiltration of the wall of an 
air-vesicle. 
These two varieties of tubercle do not usually occur in the same 
lung; but in different cases of acute tuberculosis the lungs are filled 
with one or the other variety, and it is hardly proper to look on them 
as different stages of the same process. 
(4.) Miliary tubercles which consist simply of infiltrations of the 
walls of air-vesicles, of bronchi, of blood-vessels, and of lymphatics. 80 
ACUTE MIL [ARY TUBERCULOSIS. 
These tubercles are usually small and of irregular shape. Many of 
them are composed of diffuse tubercle, not of tubercle granula; they 
rarely contain giant-cells. Some of them seem to consist of nothing but 
small round cells imbedded in a basement substance. 
These tubercles do not occur by themselves, but are found in larger 
or smaller numbers in the same lungs which contain the second and third 
varieties. 
It has become the fashion to lay great stress on the absence of blood- 
vessels in miliary tubercles, and to ascribe the cheesy degeneration to the 
scantiness of the vascular supply. I think that there is some exaggera- 
tion in this. If we inject, artificially,lungs which are the seat of miliary 
tubercles, the injection does not indeed penetrate the tubercle granula, 
but it runs freely into the walls of the air-vesicles which form part of 
the miliary tubercle, and even into the diffuse tubercle. It is only the 
first variety of soft cheesy tubercles which cannot be thus injected. 
If we look at the miliary tubercles which occur in other parts of the 
body, we find a repetition of what we have seen in the lungs. 
(1.) Miliary tubercles, composed of nothing but amorphous granular 
matter, with pus-cells at their edges. Such tubercles are found especially 
in the pleura, peritoneum, liver, spleen, and kidneys. 
(2.) Miliary tubercles, composed of one or more tubercle granula and 
of diffuse tubercle; around such tubercles are pus-cells and new con- 
nective-tissue cells in variable numbers. Such tubercles are found espe- 
cially in the pleura, peritoneum, liver, spleen, bladder, lymphatic glands, 
medulla of bones, muscles, in syphilitic ulcers, in lupus, in granulation 
tissue, in the synovial membranes of the joints, in sarcomatous tumors. 
(3.) Miliary tubercles formed of an accumulation of large and small 
polygonal cells and of small round cells. These polygonal cells are 
much more distinct than the cells in tubercle granula; they seem to be 
held together by some kind of basement substance which I have never 
been able to demonstrate. These tubercles are found in the pia mater 
and omentum, and I have seen them once in the liver. They remind one 
of some of the air-vesicles in the third variety of the miliary tubercles 
of the lungs. See Plates XXVI. and L. In these tubercles there may 
be, large multinucleated cells, which look something, but not exactly, ACUTE MILIARY TUBERCULOSIS. 
81 
like the giant-cells found in tubercle granula. There is a well-marked 
growth of endothelial and connective-tissue cells in the pia mater and 
omentum in the neighborhood of such tubercles. 
(4.) Miliary tubercles formed by an accumulation of small round 
cells around blood-vessels, between the peri vascular sheath of the vessel 
and its wall. These tubercles are only found in the pia mater, unless 
some of the very small tubercles in the lungs are of the same nature. 
(5.) Miliary tubercles apparently formed of nothing but an aggre- 
gration of small round cells, not to be distinguished from what is seen 
in ordinary inflammation, except by their being arranged so as to form 
little nodules. 
We find, then, that the bodies, commonly known by the name of 
miliary tubercles, do not all have the same structure, so that this name 
does not designate any definite anatomical tissue, and in this sense it is 
proper to say that there is no regular structure belonging to tubercle. 
In the larger number of miliary tubercles, however, we do find a tissue 
of a particular kind which is found nowhere else, a tissue composed of 
polygonal and giant-cells imbedded in a basement substance. This 
tissue, as being the only anatomical characteristic of tubercle, we may 
call tubercle tissue; and according to the arrangement of its elements 
we may divide it into tubercle granula and diffuse tubercle. This, how- 
ever, brings us to the somewhat curious conclusion that some tubercles 
are formed only of tubercle tissue, some of tubercle tissue and ordinary 
products of inflammation, some of cells resembling those of tubercle 
tissue, but not regularly arranged in a basement substance, while some 
contain no tubercle tissue at all. The temptation is great to deny the 
name of miliary tubercle to all the nodules which do not contain tubercle 
tissue, and it is to be hoped that further studies may enable us to do 
this, but for the present we have to abide by the conclusion stated 
above. 
Thus far we have been concerned with the study of the structure of 
miliary tubercles ; we must next inquire under what circumstances such 
tubercles are formed. We must distinguish, first, the cases in which 
miliary tubercles are found in large numbers scattered through different 
parts of the body-general tuberculosis ; and the cases in which the 82 
ACUTE MILIARY TUBERCULOSIS. 
tubercles are confined to a particular part of the body-local tuber- 
culosis. 
The cases of general tuberculosis again must be divided into two 
sets, cases of chronic phthisis complicated by general tuberculosis, and 
cases of idiopathic general tuberculosis. 
(1.) Idiopathic, acute, general, miliary tuberculosis. This disease 
occurs at all ages and in both sexes. Its duration varies between one 
and six weeks. It probably always terminates fatally. The tempera- 
ture is usually between 99° and 103°, sometimes as high as 107°, occa- 
sionally never over 99°. 
As a rule, cerebral symptoms-delirium, muscular twitchings, con- 
vulsions, and coma, exist during the course of the disease. The pa- 
tients emaciate, their tongues become dry and brown, and they look 
like persons suffering from a continued fever. In addition to the gen- 
eral symptoms, there may be local symptoms corresponding to the 
organ in which the largest number of tubercles are developed. If 
there are many tubercles in the pia mater, there will be convulsive 
movements of the muscles of the face, general convulsions, difficulty in 
swallowing; the delirium and coma come on earlier. If the lungs are 
extensively involved, there may be pain in the chest, rapid breathing, 
cough, cyanosis, and subcrepitant rales. If the peritoneum is princi- 
pally affected, there may be pain and tenderness over the abdomen and 
tympanites. In a large number of these cases, however, the symptoms 
are obscure and indefinite. The diagnosis must be made partly by 
exclusion, partly by familiarity with similar cases. 
The opinion has prevailed that the cause of the disease in these 
cases is a focus of pus, in the condition of cheesy degeneration, in some 
part of the body. So many cases, however, occur in which no such 
focus exists, that such an opinion is no longer tenable. We certainly 
cannot account for all cases of general tuberculosis in this way, al- 
though it is quite possible that some cases may be thus produced. 
(2.) Acute, general, miliary tuberculosis, occurring in persons al- 
ready suffering from chronic pulmonary phthisis. In these cases the 
lesions and the symptoms are much the same as in the preceding set of 
cases, except so far as they are modified by the chronic phthisis. It ACUTE MILIARY TUBERCULOSIS. 
83 
has been customary in these cases to regard, the production of miliary 
tubercles as in some way secondary to the chronic phthisis, either from 
absorption of cheesy matters, or in some other way. 
(3.) Acute, local, miliary tuberculosis occurring in persons already 
suffering from chronic phthisis. In these cases the miliary tubercles are 
usually confined to the lungs, the pleura, and the pia mater, but may 
also occur in other parts of the body. 
(4.) Acute, local, miliary tuberculosis in persons not suffering from 
chronic phthisis. The miliary tubercles have been observed in the pia 
mater, the lungs, the costal pleura, the peritoneum, the bones, the syno- 
vial membranes of joints, in granulation tissue, in the walls and floors 
of old ulcers, of syphilitic ulcers, and of ulcers due to lupus. It is as- 
serted that they have been seen in gummy tumors and in sarcomatous 
tumors of bone. 
From the consideration of the anatomy of miliary tubercles, and of 
the circumstances under which they occur, it seems to me that we are 
driven to one of two conclusions. 
(1.) We may believe that certain persons, either from the absorp- 
tion of cheesy matter, from natural constitution, or from unknown 
causes, become tuberculous. They become the subjects of some general 
vital changes which produce symptoms and lesions, the lesions being 
miliary tubercles. The tubercles, however, have no essential anatomi- 
cal characters, but vary in different cases. We do not say that a per- 
son is tubercular from the consideration of the minute anatomy of the 
lesions; but if we make up our minds, from the clinical history and the 
gross post-mortem appearances, that a person is tubercular, then we call 
all the little nodules that we find in that person miliary tubercles. 
(2.) We may believe that there is a definite and essential anatomy 
belonging to miliary tubercles, which can be always recognized. Then 
we must admit that tubercle is composed of a tissue, like granulation 
tissue, on the border line between the new growths and the inflamma- 
tory products. This tissue is developed under a variety of circum- 
stances, and is not confined to persons suffering from general tubercu- 
losis, but occurs as a strictly local lesion. We must also admit that, in 
persons suffering from acute general tuberculosis, all the nodules found 84 
ACUTE MILIARY TUBERCULOSIS. 
after death are not composed of such tissue. In other words, tubercle 
is not a specific tissue necessarily implying the existence of a diathesis, 
but is a tissue of indifferent character, produced under a variety of 
circumstances. It may be the lesion of a general disease; or the lesion 
of a local, progressive inflammation; or an accidental lesion forming a 
non-essential part of local inflammations and new growths. 
We may then continue to use the word miliary tubercle to designate 
all the little nodules which occur in tuberculous persons, irrespective 
of their structure, employing the terms tubercle granula and diffuse 
tubercle to the special tissue found in some of the nodules. Or we 
may hold that the nodules, although of different structure, are exam- 
ples of the same tissue in different stages of development. Or we may 
deny the name of miliary tubercle to all the nodules which are not 
composed of characteristic tubercle tissue. CHRONIC PULMONARY PHTHISIS. 
There is hardly any disease which occurs as frequently as does pul- 
monary phthisis. Not onlyis it a common disease, but a fatal one. Year 
after year every hospital autopsy-room is filled with the bodies of persons 
whoh ave died of phthisis. But despite of this large material for examina- 
tion, not even the morphology of the lesions is thoroughly understood. 
Just at the present time there are current three principal theories 
as to the nature of pulmonary phthisis. 
First there is the older German school, which teaches that we can 
distinguish between an inflammatory phthisis and a tubercular phthisis; 
that, in many cases of phthisis, tubercle does not exist at all, or is devel- 
oped secondarily to the inflammatory products; that most of the larger 
cheesy masses met with in the lung are ordinary inflammatory products. 
This theory has led to the use of such names as catarrhal, caseous, and 
interstitial pneumonia; peribronchitis nodosa; catarrhal and fibrous 
phthisis, to designate the different lesions. 
Secondly there is the modern French school, which teaches that the 
essential and primary lesion of all phthisis is tubercle; that the accom- 
panying inflammatory lesions are comparatively unimportant; that an 
inflammatory phthisis without tubercle does not exist. Some even go 
so far as to deny that simple inflammatory products ever undergo 
cheesy degeneration. 86 
CHRONIC PULMONARY PHTHISIS. 
Lastly, there is the younger German school, which denies that there 
is any characteristic lesion at all belonging to phthisis, and holds that 
the only test is their inoculability. Whatever lesions can be inoculated 
in animals and produce in them miliary tubercles, are to be regarded 
as tubercle, no matter what their anatomy may be. Added to this 
theory is the belief that a specific form of bacteria is the exciting cause 
of the productions of tubercles. 
Besides these principal theories there are innumerable modifications 
of them. 
My particular object is not to advocate any one of these theories, 
nor to advance a new one. It is simply to describe and figure what I 
have been able to see in the lungs of persons who have died with 
chronic phthisis. 
When we look at the lungs of such persons, we observe a number of 
lesions. Some of these lesions look as if they were not related to each 
other; others look as if they represented different stages of the same 
process. The clinical histories of these patients also enable us to judge 
that some of the lesions are recent and that others have existed for a 
long time. 
In the ordinary forms of the disease we find: 
1. Lungs studded with small nodules like the nodules which we see 
in acute miliary tuberculosis, but the nodules are larger, harder, and 
look older. 
2. Lungs studded with similar nodules, but the nodules are joined 
together or aggregated into masses by a dense tissue. At the same 
time more or less of the lung is converted into a dense, fibrous-looking 
mass. 
3. Lungs studded with white or yellow lobules, surrounded by red 
or gray hepatization. 
4. Lungs in which are large, dense, cheesy masses. 
5. Lungs which look as if they consisted entirely of fibrous tissue 
and cheesy nodules. 
6. Lungs in which these different lesions are associated. 
Besides we find cavities of different sizes and in different conditions 
associated with these different lesions. CHRONIC PULMONARY PHTHISIS. 
87 
The cases characterized by the presence of small nodules, either with 
or without diffuse fibrous-looking tissue, form a group by themselves. 
The cases characterized by the presence of white or yellow lobules, 
form another different group. 
The first group we will, for convenience, describe under the name of 
" Chronic Miliary Tuberculosis." 
CHRONIC MILIARY TUBERCULOSIS. 
This form of chronic phthisis has hardly received the attention 
which it deserves. At the present time, while the strife is going on 
between the partisans of an inflammatory phthisis on the one hand, and 
those of a tubercular phthisis on the other, study has been principally 
directed to the lobular infiltrations which we shall have to describe 
later. Chronic miliary tuberculosis has been rather summarily classed 
as a sequence of pneumonic phthisis; as representing tubercles which 
have become obsolete; or as a form of fibrous phthisis. And yet, in 
New York, at least, it is a very common form of chronic phthisis, and 
is seen in patients of many different nationalities. 
The cases, however, are not all alike, and it is convenient to distin- 
guish, 
1. Miliary tubercles scattered singly through the lungs. 
2. Miliary tubercles scattered through the lungs, but joined together 
by diffuse fibrous-looking tissue, or aggregated into masses by the same 
J O' OO Q J 
tissue, and often accompanied by the presence of large masses of the 
same fibrous-looking tissue. 
I. Miliary tubercles scattered singly through the lungs. 
The patients who suffer from this form of phthisis exhibit symp- 
toms very much like those of patients who are the subjects of emphy- 
sema and chronic bronchitis. There is the same dyspnoea; the same 
cough with mucous, or muco-purulent expectoration ; the same gradual 
emaciation ; the same physical signs. But the loss of general health is 
more marked, and haemoptyses, hectic fever, and night-sweats are 88 
CHRONIC PULMONARY PHTHISIS. 
added to the other symptoms. The lesion seems to be a progressive 
one, but the progress is not always continuous. The history is often 
one of repeated attacks separated by considerable intervals, and after 
death the lesions in the lungs look as if they were not of the same 
date, but had been developed at different periods. Sometimes a pa- 
tient will die of apoplexy or some other disease, while the tubercles are 
in an early stage of formation. 
These cases are often very obscure and difficult of diagnosis. The 
absence of any physical signs except those of emphysema, bronchitis, 
and pleurisy, adds to the difficulty. Most of the patients die, not from 
the tuberculosis, but from some intercurrent disease. 
If we can credit the testimony of some patients, the disease may 
exist without producing any symptoms. 
After death we find old adhesions between the pulmonary and cos- 
tal pleura; the lungs large, emphysematous and pale, unless pneumonia, 
congestion, or oedema exist as complications. The bronchi contain 
muco-pus; their mucous membrane is often congested and trabeculated; 
their entire walls may be thickened. 
The whole or parts of the lungs are studded with small, white or 
grayish, hard, fibrous, or cheesy nodules, from the size of a pin's head 
to that of half a pea. These nodules are single, not joined together 
by diffuse tissue, not aggregated in patches. At the apices of the 
lungs, however, there may be older tubercles and a little diffuse 
fibrous tissue. Sometimes the tubercles are unusually close together, 
and there may then be a little diffuse tissue joining them together in a 
sort of network. 
Not infrequently there is a growth of fibrillated connective tissue 
around the bronchi and blood-vessels, in the walls of the air-vesicles, 
and in the interlobular septa. On section these growths may give 
irregular figures somewhat resembling those of the miliary tubercles. 
There may be also miliary tubercles in the pleura, the peritoneum, 
the liver, the spleen, and the kidneys. 
It is somewhat curious that, even in the cases in which the tubercu- 
losis is general, there are no such marked and fatal symptoms as exist 
in acute miliary tuberculosis. CHRONIC PULMONARY PHTHISIS. 
89 
II Miliary tubercles accompanied by the growth of a diffuse fibrous- 
looking tissue. 
This form of phthisis is very common. It is often spoken of as 
"fibrous phthisis." It must be remembered, however, that dense tis- 
sue, looking like fibrous tissue, is produced in the lungs in large amount 
simply as the result of an interstitial pneumonia, without the produc- 
tion of tubercle. In old lobular pneumonic phthisis, also, where cavi- 
ties have been formed, the tissue between the cavities may look like 
fibrous tissue. It is usually not possible to determine by the naked eye 
the real nature of the fibrous-looking tisssue which we see in such 
lungs. Whether it is fibrillated connective tissue alone, whether it is 
tubercle-tissue, or whether air-vesicles can still be seen in it, is only to 
be made out with the microscope. 
The cases of this kind of phthisis run a slow course. The disease 
may be arrested after involving a small part of the lung, or it may go 
on until the larger part of both lungs is rendered unfit for use. When 
only a small part of the lung is involved there may be no rational 
symptoms (if we can believe the patients) and no physical signs. 
The disease may begin insidiously, or it may be ushered in by one 
or more attacks of haemoptysis. For a considerable time the symptoms 
are apt to be very obscure. The patient's general health suffers, but 
there may be no cough, no febrile movement, very little dyspnoea, no 
physical signs. 
When, however, more of the lungs is involved by the lesions, the 
patients lose flesh and strength; cough, dyspnoea, and a febrile move- 
ment are developed; the pleuritic adhesions, the bronchitis, and the 
consolidation of the lungs give their appropriate physical signs. 
The pleurisy, the laryngitis, the bronchitis, or the ulceration of the 
small intestines, which often exist as complications, may give rise to 
symptoms more prominent than those which belong to the lung lesion. 
The fatal cases finally die in a condition of extreme emaciation. 
The whole course of the disease is such as to give the impression of 
its being a chronic local inflammation of the lungs. The entire recovery 
of some patients and the regular proportion between the development 90 
CHRONIC PULMONARY PHTHISIS. 
of the lesions and the intensity of the symptoms favor such a view. 
On the other hand, the formation of similar lesions in other parts of the 
body seems to stamp it with the character of a general disease. 
After death we find the characteristic lesions developed to a greater 
or less extent. 
Organized pleuritic adhesions are the rule, and with these there may 
be thickening of the pulmonary and costal pleura. Miliary tubercles 
also are not infrequently found in the pleura. 
The bronchi show the changes common to chronic bronchitis, or 
there may be tubercle-tissue formed in their walls, or there may be 
ulcers. Less frequently they are the seat of croupous inflammation. 
If the disease is not of long standing, we find at the apex of one of 
the lungs a few small, hard nodules joined together by a little solid 
tissue, or imbedded in a larger mass of fibrous-looking tissues. The 
adjacent air-vesicles are irregularly dilated, and bands of fibrous tissue 
run off from the central mass. 
If the disease has existed for a longer time, the nodules are present 
in greater numbers, are distributed over a larger portion of the lungs, 
and look as if they had been developed at different periods. Some are 
of about the size of a pin's head, hard, grayish; others are larger, 
harder, and look more like fibrous tissue; others are large and cheesy, 
and may be softened at their centres. These nodules are joined to- 
gether by solid tissue so as to form a sort of network, or they are im- 
bedded in masses of solid tissue. This solid tissue is sometimes pig- 
mented and the masses are then often called "patches of slate-colored 
induration." 
In other cases there is developed a diffuse growth of fibrous-looking 
tissue, more or less pigmented, which replaces a considerable part of the 
parenchyma of the lung. 
In the old cases a large part of the lung-tissue may be thus replaced 
by the miliary tubercles and diffuse solid tissue. Not infrequently, 
cavities of large size are also formed, especially at the apices of the 
lungs. 
There are also changes in the lung-tissue between the tubercles. 
General emphysema may exist, or irregular dilatation of the air-vesicles CHRONIC PULMONARY PHTHISIS. 
91 
adjoining the tubercles. Interstitial pneumonia, with a production of 
fibrillated connective tissue in the walls of the air-vesicles, the bronchi 
and the blood-vessels, is a frequent complication. There may be a 
growth of polygonal nucleated cells on the walls of the air-vesicles, 
and the cells may be numerous enough even to fill the vesicles. 
The patients may be attacked by ordinary lobar pneumonia, as an 
intercurrent disease. 
Tubercular lesions are often present in other parts of the body, es- 
pecially in the larynx and trachea, the small intestine, and the perito- 
neum. 
The anatomy of the miliary tubercles is the same in the two sets of 
cases of which we have been speaking. The difference between the 
two sets of cases consists in the presence or absence of the diffuse, 
fibrous-looking tissue. 
It is convenient to describe separately the diffuse tissue and the 
miliary tubercles. 
Of the nodules which have the gross appearance of miliary tuber- 
cles we can distinguish: 
1. Nodules formed of fibrous tissue. 
2. Nodules formed of tubercle-tissue. 
3. Nodules formed of tubercle-tissue in different stages of decenera- 
tion. 
(1). The nodules formed of fibrous tissue are composed of a dense, 
fibrillated basement substance in which are imbedded a few cells. The 
nodules are of irregular shape and are situated around the bronchi and 
blood-vessels, or in the walls of the air-vesicles. These nodules seem to 
be only part of a process of interstitial pneumonia which is in some lungs 
associated with the production of the true tubercles. Such an intersti- 
tial pneumonia not only forms the nodules spoken of, but also such a 
diffuse thickening of the walls of the vesicles as is seen in Plate LXIII. 
There is at the same time a change in the size of the air-vesicles: some 
are dilated, others are small and deformed. New cells are formed on 
the walls of the vesicles. Some of these are the large, polygonal, nu- 
cleated cells which we see in many forms of pneumonia. Others are 
smaller, are arranged in rows, and look like the new cells in inflamed 92 
CHRONIC PULMONARY PHTHISIS. 
connective tissue. Plate LVIIL represents part of the wall of such an 
air-vesicle. The blood-vessels have been artificially injected. All the 
cells seen in the drawing were adherent to the wall of the vesicle, not 
free in its cavity. 
(2). Nodules formed of tubercle-tissue. These nodules are of two 
varieties: 
(a). The simplest nodules, which have such a structure as is repre- 
sented in Plate LI. Such a nodule, to the naked eye, is of a globular 
shape, but wdien magnified is seen to be of the irregular form represented 
in the plate. It will be seen that the nodule is composed of tubercle- 
granula surrounded by a dense tissue-partly tubercle-tissue, partly 
connective tissue. The shape and arrangement of the granula is such 
as to make it probable that they have been formed within the air-vesi- 
cles. This method of formation is much plainer in chronic than in 
acute miliary tuberculosis. The granula have the same structure as 
those found in acute miliary tuberculosis, but their basement substance 
is denser and more abundant, the cells are less numerous and often 
smaller. The basement substance may be much in excess and homo- 
geneous, as seen in Plate LXIL, or it may be fibrillated. The cells pre- 
serve their regular polygonal shape, or appear as round and oval nuclei 
The giant cells may be present or absent. 
The diffuse tissue between the granula also has the same structure 
as in acute tuberculosis, but here again the basement substance is more 
abundant and in places is replaced by ordinary connective tissue. 
(b.) Nodules of more complex structure. The central portions of 
such nodules have the same structure of tubercle-granula and diffuse 
tubercle as those just described, but in addition to this they are sur- 
rounded by a zone of new tissue. Plate LVIIL represents a single 
tubercle of this kind, of which the blood-vessels have been artificially 
injected. The central portion of the tubercle is composed of tubercle- 
granula and tubercle-tissue, but there is a zone of small-celled tissue 
surrounding this. Plate LVI. represents a group of tubercles of which 
the peripheries are formed of the same small-celled tissue, and this same 
tissue joins some of the tubercles together. 
This zone of new tissue forming the periphery of this variety of CHRONIC PULMONARY PHTHISIS. 
93 
tubercles appears, with a low magnifying power, like granulation tissue. 
Higher powers, however, show that its structure is more complex. It 
may really resemble granulation tissue as in Plate LIX.; or it may be 
a more complicated tissue, such as is represented in Plates LV. and LX. 
In Plate LV. are a number of air-vesicles of which the outlines can 
be seen. Some of these are empty, while their edges are covered with 
large epithelial cells. Other air-vesicles are filled partly with epithelial 
cells, partly with smaller polygonal cells imbedded in a basement sub- 
stance. Other air-vesicles are more or less completely filled by poly- 
poid growths which project into them. These polypoid growths are 
formed of polygonal cells, and oval and round nuclei imbedded in a deli- 
cate basement substance. The portion of the air-vesicles which is not 
filled with such polypoid growths may contain epithelial cells. 
Plate LX. represents portions of two air-vesicles more highly mag- 
nified. The walls of the vesicles are overlaid with large cells. At one 
point the wall splits up and its outlines are lost. One of the vesicles 
is filled with polygonal cells imbedded in a basement substance. The 
other vesicle is partly filled with similar tissue, partly with a denser, 
polypoid growth, partly with free epithelial cells and granular matter. 
(3.) Nodules formed of tubercle-tissue in a condition of degener- 
ation. The degeneration is of such a character that a larger or smaller 
part of the tubercles is converted into fibrous tissue, or granular matter, 
or both these changes may involve different parts of the same tubercle. 
If the tubercle is changed into fibrous tissue, the centre of the nod- 
ule is formed of connective tissue arranged in a concentric shape, and 
imbedded in this are tubercle-granula also changed into connective tis- 
sue, or the granula may be changed into granular matter. Around 
this central portion is a zone of fibro-cellular tissue. Such tubercles 
may be very large, some of them are pigmented. Plate LXI. represents 
such a large miliary tubercle converted into fibrous tissue. Such tuber- 
cles as these are not sections of bronchi with thickened walls. 
If the tubercles undergo cheesy degeneration, the portions first in- 
volved are the tubercle-granula. From these the degenerative process 
may extend and involve the diffuse tubercle in which the granula are 
imbedded. These tubercles are usually possessed of a peripheric zone 94 
CHRONIC PULMONARY PHTHISIS. 
of fibro-cellular tissue composed of granulation tissue and altered air- 
vesicles, such as have already been described. Plate LIV. represents 
several miliary tubercles of which the tubercle-granula have undergone 
cheesy degeneration. 
In a considerable number of cases of chronic miliary tuberculosis an 
important part of the pathological process consists in the development 
of the diffuse, solid tissue which forms the peripheric zone of some 
tubercles, which joins others together, which aggregates others into 
masses, and which may replace a considerable part of the parenchyma 
of the lung by a dense, solid, unaerated structure. In some cases, in- 
deed, this diffuse tissue constitutes a more important part of the lesion 
than do the miliary tubercles, for it replaces and renders useless a larger 
part of the lung. 
This diffuse tissue presents itself to us with a structure varying ac- 
cording to the length of time during which it has existed, and to under- 
stand it we must study both its earlier and later stages. 
Even in the earlier stages the process is not a simple one, and we have 
to distinguish between a production of interstitial connective tissue with 
obliteration of the air-vesicles by pressure, and a growth of a peculiar 
new tissue within the cavities of the air-vesicles and in their walls. 
The interstitial connective tissue is produced in the walls of the vesi- 
cles, the bronchi, and the blood-vessels, in the interlobular septa and 
the pulmonary pleura. Much of it is a dense, fibrillated tissue with 
but few cells, but well supplied with large, irregular blood-vessels. In 
other places the cells are more abundant, and in still others it looks like 
granulation tissue. It is often pigmented. The air-vesicles are de- 
formed : some are small and misshapen, some are so compressed that 
they look like tubes; some are dilated. The epithelial cells which 
line the vesicles are increased in size and number. The whole process 
is essentially an extra-alveolar one, the vesicles suffering principally 
from pressure. 
The growth of the tubercle-tissue is different. The process is both 
an extra- and intra-alveolar one. The solidification of the luno;-tissue is 
accomplished by the formation of new tissue, both in the walls of the 
air-vesicles and within their cavities. CHRONIC PULMONARY PHTHISIS. 
95 
In the walls of the air-vesicles there is a growth of round and poly- 
gonal cells and of intercellular basement substance, or the cells are 
formed in excess and the basement substance is split up so that the nat- 
ural outlines of the wall of the vesicle are lost (Plate LX.). 
The cavities of the vesicles are filled in two ways. Some are partly 
or completely filled with polypoid outgrowths from their walls, com- 
posed of round and polygonal cells imbedded in a basement substance ; 
in others there is a mass of round and polygonal cells, with or without 
giant cells imbedded in a basement substance formed in the cavities of 
the vesicles, but at first not continuous with their walls. If the vesi- 
cles in either of these ways are not completely filled the remaining 
space may be occupied by epithelial cells. When an air-vesicle is com- 
pletely filled with cell growth, it looks like a tubercle-granulum. 
Plate LV. shows the filling up of air-vesicles by polypoid outgrowths 
from their walls. Plate LXIV. shows a number of air-vesicles so filled 
as to look like tubercle-granula; in some places the vesicles have run 
together so that their outlines are lost. There is also an abundant in- 
terstitial growth of tubercle-tissue and connective tissue. 
These two processes-the growth of interstitial connective tissue, 
and the growth of tubercle-tissue in the walls and in the cavities of the 
air-vesicles-are usually associated. When both have existed for some 
time the picture becomes a complicated one. 
We can no longer make out the air-vesicles, nor the relations of the 
new tissue to them. There is nothing but a solid mass, composed of 
miliary tubercles surrounded by tubercle-granula, diffuse tubercle, con- 
nective tissue, and a few deformed air-vesicles. Plate LIL represents 
such a condition, the blood vessels having been artificially injected with 
blue. There are in the field three old, cheesy miliary tubercles and 
part of a fourth. Between these is a solid mass composed of connec- 
tive tissue, diffuse tubercle and tubercle-granula. The blood-vessels are 
large and irregular, and some of them penetrate into the granula. Plate 
LVII. represents a single tubercle-granulum surrounded by diffuse 
tubercle from such a mass of old solid tissue. It seems probable that 
in these old formations tubercle-granula are formed not only in the 
cavities of the vesicles, but in the interstitial tissue. 96 
CHRONIC PULMONARY PHTHISIS. 
When the disease is of still longer duration, the growth of new con- 
nective tissue becomes more marked, and a considerable part of the 
tubercle-tissue is changed into connective tissue. The affected portions 
of the lung then become very hard and dense, and we have the con- 
dition so often called fibrous phthisis. But such a fibrous phthisis is 
nothing but an old tubercular phthisis. 
CONCLUSIONS. 
1. There is a form of chronic pulmonary phthisis of which the char- 
acteristic lesion is the production of a new tissue in the parenchyma of 
the lungs. 
2. This new tissue is not an ordinary inflammatory product, but re- 
sembles the tissue which composes most of the miliary tubercles in acute 
miliary tuberculosis. 
3. This new tissue is arranged in the form of nodules-miliary tuber- 
cles, and in the form of a diffuse infiltration which surrounds the tuber- 
cles, joins them together, and may occupy considerable portions of the 
lung. 
4. The tubercle-granula seem to be formed, for the most part, within 
the cavities of the air-vesicles. 
5. Associated with the production of tubercle-tissue there is often 
interstitial pneumonia, bronchitis and pleurisy, with their characteristic 
inflammatory products. 
6. The tubercle-tissue is often changed into granular matter, or into 
connective tissue. In old cases of the disease the development of the 
different elements of the lesion can no longer be made out. There is 
simply a mass of tubercle-tissue, more or less degenerated, and of con- 
nective tissue. 
7. The disease runs a chronic and progressive course, gradually in- 
volving more and more of the lung-tissue. But it may be arrested and 
the patient may recover permanently. 
8. Tubercle-tissue may also be formed in other parts of the body, 
especially in the larynx, small intestine and peritoneum. ACUTE PHTHISIS. 
The clinical characters 'of acute phthisis are sufficiently well 
known. A person who has previously been in good health, or who has 
already suffered from chronic phthisis, either suddenly, or after a few 
days of indisposition, becomes seriously ill. There is a well-marked 
febrile movement and a rapid pulse, cough, expectoration, the physical 
signs of consolidation of the lung, and sometimes haemoptysis. Rapid 
loss of flesh and of strength follow. Most of the patients die at the 
end of a few weeks or months; a few recover from the immediate 
attack and go on to have the history of chronic phthisis. 
After death we find a considerable portion of one or both lungs 
consolidated, but this consolidation is not of a uniform appearance. 
The larger part of the consolidation looks like ordinary red hepatiza- 
tion, or else it is of a peculiar grayish color, different from the gray 
hepatization of lobar pneumonia. In this diffuse hepatization are other 
portions of solidified lung of different appearance. They are of a 
white or yellow color, much denser than the surrounding hepatization, 
or they may be softened at their centres. These white solidifications 
are of many different sizes and shapes. The smallest are hardly larger 
than an air-vesicle, the largest may include a considerable part of a 
lobe. Their size and shape are made more evident if the blood-vessels 
are artificially injected, for into these nodules the injection does not run. 98 
ACUTE PHTHISIS. 
Many of the smallest of these whitish masses are scattered irregu- 
larly through the lung-tissue like miliary tubercles. As will be seen 
later, they really are miliary tubercles. 
Other similar masses, also of small size, are situated regularly 
around small bronchi. When this is the case, the cavities of the bron- 
chi may be filled with inflammatory products, and their walls infil- 
trated. 
Still other masses will correspond to a single air-passage, or to a 
group of air-passages, looking as if they were produced by some cause 
which affected definite and isolated portions of the lung. 
Other masses again are so large that they have the appearance of a 
diffuse infiltration of a considerable portion of the lung. But these 
large infiltrations seem to be made up of a number of smaller masses. 
If the patient lives long enough after the development of the disease, 
many of these masses, both large and small, will be found degenerated 
and softened. 
The bronchi of the affected lung are regularly the seat of morbid 
changes. They may be congested and coated with mucus ; they may 
be filled with pus, epithelium, and fibrine, and these inflammatory 
products may undergo cheesy degeneration ; they may be irregularly 
dilated, so as to form cavities of some size ; or a great number of the 
smaller bronchi may be symmetrically dilated, so that on section the 
lung looks honeycombed. 
Such a condition of the lung has been interpreted in very different 
ways. 
Some look upon the whole process as one of ordinary inflammation. 
Bronchitis, peri-bronchitis, ulceration of the bronchi, and pneumo- 
nia with subsequent degeneration of the products of inflammation are 
supposed to produce all the lesions. 
Others believe all the white or yellow masses to be of essentially 
the same nature as miliary tubercles, that they are tubercles on a large 
scale-" tubercules massifs; " and are surrounded by ordinary pneu- 
monic hepatization. Others again regard the whole conditions as a 
combination of pneumonia and miliary tubercles. 
Neither of these views seem to me to account for all the lesions. ACUTE PHTHISIS. 
99 
The pathological condition is really a complex one, and we gain nothing 
by trying to make it appear more simple than it really is. 
It is necessary to examine each of the different parts of the lesion 
in detail and see what their real structure is. 
I The diffuse hepatization. 
It must be remembered that we are considering the diffuse hepa- 
tization of acute phthisis, not that of chronic phthisis, and especially 
the conditions found in the lungs of adults. This hepatization presents 
the gross appearance of the red hepatization of lobar pneumonia, ex- 
cept that it is smoother; or it is of a peculiar gray color, sometimes 
almost gelatinous looking. It does not seem to degenerate or to soften 
except immediately around some of the nodules of which we shall 
speak presently. 
The blood-vessels in the walls of the air-vesicles can be easily filled 
with an artificial injection. The walls of the air-vesicles show no 
marked changes in their substance, although their surfaces are overlaid 
with new cells. 
The cavities of the air-vesicles are filled with inflammatory products, 
but this filling is not uniform. Some vesicles are filled and even dis- 
tended, while others only contain a small amount of such new sub- 
stances. These inflammatory products are: pus-cells, fibrillated fibrine, 
large, polygonal, nucleated cells resembling epithelium, minute, shin- 
ing granules and a peculiar transparent matter. The pus-cells have the 
ordinary appearance of these bodies, varying in their size and in the 
character of their cell-substance, some being finely, some coarsely 
granular, and some fatty. The fibrine has the same appearance of a 
network of fibrils as is seen in acute, lobar pneumonia. The large poly- 
gonal cells resemble, in shape and appearance, epithelial cells, but some 
of them undergo degenerative changes, becoming larger, globular, 
coarsely granular or fatty, or very large and transparent. The granules 
are small, shining particles, not dissolved by acetic acid, liquor 
potassse or chloroform, and are stained either with methyl violet or 
haematoxylin. Their nature is uncertain. These different products are 
found in variable relative proportion in different lungs and in different 100 
ACUTE PHTHISIS. 
parts of the same lung. Some vesicles will be entirely filled with the 
granules, others with fibrine, others with epithelial cells; while others 
will contain granules and epithelium, or epithelium and fibrine, with an 
admixture of pus-cells. 
Plate LXV. represents a single air-vesicle, its cavity filled with 
large epithelial cells and a few pus-cells, the vessels in its walls in- 
jected. Plate LXVI. represents a single vesicle filled with coagulated 
fibrine, in which are entangled a few pus-cells and epithelial cells ; the 
blood-vessels are injected. Plate LXVII. represents a group of vesicles 
filled with granules and a few epithelial cells; the blood-vessels are 
injected. 
This diffuse hepatization seems to have no tendency to cheesy de- 
generation or necrosis. The products of inflammation within the 
vesicles may undergo fatty degeneration, but the walls of the vesicles 
remain intact, and the blood-vessels pervious. If we can judge from 
clinical experience and physical signs, this diffuse hepatization is 
capable of resolution and may entirely disappear. If, however, the 
patient goes on to have chronic phthisis then the diffuse hepatization 
undergoes marked changes. 
II The white or yellow nodules. 
These nodules vary in their size, their shape, and their structure. 
They may be close together, or widely separated. Some are surrounded 
by diffuse hepatization, others by nearly normal lung. Even those 
which present the same appearance to the naked eye are not all of 
the same nature. 
. Before attempting to describe these nodules it is necessary to have a 
definite idea of the arrangement of the small bronchi and air-vesicles. 
Quain's Anatomy gives the following description: " The small 
bronchial tube entering a lobule divides and subdivides a variable num- 
ber of times, according to the size of the lobule; its divisions losing 
their cylindrical form, and being converted into irregular lobular pass- 
ages, are beset, at first sparingly, but afterward closely and on all 
sides, with numerous little recesses or dilatations, and ultimately ter- 
minate near the surface of the lobule in a group of similar recesses- ACUTE PHTHISIS. 
101 
These small recesses are the air-cells; and each group of alveoli, with 
the comparatively large passage between them, constitutes an ultimate 
lobule or infundibulum." 
Rindfleisch says: " The lobules are made up of a number of 
acini. Each acinus has the form of a cone-shaped berry. The stem 
of the berry is a single ultimate, terminal bronchiole, which ends ab- 
ruptly at the point where it enters the acinus. From this point the 
walls and the lumen of the bronchiole become continuous with the 
walls and lumina of three diverging alveolar passages, of which the 
shorter side branches may be called infundibula. On all sides of 
the alveolar passages, and opening into them, are the air-vesicles." 
Kolliker, in his recent monograph on the structure of the lung, 
describes the bronchi as dividing and subdividing. The smallest 
bronchi he calls " bronchioli respiratorii." These respiratory bronch- 
ioles are of two forms. Some are tubes lined with cylindrical epithe- 
lium ; others are lined partly with cylindrical, partly with pavement- 
epithelium. Air-vesicles open directly into the cavities of these 
bronchi through openings in their walls. Each of these smallest 
bronchioles terminates in several alveolar passages. 
None of these descriptions seem to me to correspond exactly with 
what we see in normal and diseased lungs. They all imply the ex- 
istence of a set of tubes, which branch, become smaller and more 
numerous, and finally terminate in several smaller tubes, into which 
open the air-vesicles. 
If we fill the bronchi and air-vesicles 'with a mixture of paraffin and 
rosin, and then corrode the parenchyma with hydrochloric acid, we ob- 
tain casts of the air-cavities of the lung. Such casts will break up reg- 
ularly into a great number of little blocks-the lobules of the lung. 
These little blocks have six or seven sides, their long axes are vertical 
to the surface of the lung, their sides measure from 5 to 15 millimetres; 
some of the blocks are made up of several smaller blocks. When the 
blocks are separated from each other some of their sides are smooth, 
other sides are rough and broken from their intimate connection with 
the sides of the adjacent lobules. 
If we make a section of a hardened lung we see in the same way 102 
ACUTE PHTHISIS. 
that the lung is made up of lobules; but that while on some of their 
sides the lobules are separated from each other by fibrous septa, on 
other sides they are continuous with each other. 
When the corroded lung is broken up into lobules it is seen that the 
bronchi enters the lobules irregularly. Some bronchi enter the lob- 
ules at their ends nearest the root of the lune:; others at the side of 
the lobules; others run along the side of a lobule and send branches 
into it at right angles. 
When the lobules are broken up into fragments, we see such 
figures as are represented in Plate LXVIII. Here are fragments of 
a bronchiole, and of several air-passages, as seen by reflected light. 
The air-passages seem to be made up of a succession of large vesicles 
opening into each other, or of an irregular, larger canal, made up of 
vesicles, into which other vesicles open from all sides. These air- 
passages branch and anastomose as seen in the drawing. They are given 
off from the ends of terminal bronchioles or from the sides of small 
bronchi. The structure of the walls of the air-passages is the same 
as that of the air-vesicles. Each lobule seems to consist principally 
of such air-passages; the bronchi and air-vesicles proper do not con- 
stitute as large a part of the parenchyma as do the air-passages. If 
we look at the air-passages shown in the plate, and imagine them to 
be cut in different directions, it will be seen what a variety of figures 
the cut surfaces will srive. If we make rather a thick section of an 
o 
injected lung, and photograph this section with a low power, as seen 
in Plate LXIX., we can get an idea of the shapes of the air-passages 
on section, and of the amount of space they occupy in proportion 
to that occupied by the bronchi and air-vesicles proper. It must be 
understood that these air-passages are really part of the vesicular 
system of the lung and not of the bronchial system. 
The white of yellow nodules of phthisis seem to be formed in air- 
vesicles, in single air-passages, or in groups of air-passages, and in and 
around bronchi. 
(1.) The smallest nodules.-These are not larger than a single air- 
vesicle or part of an air-passage. In the fresh lung it is not easy to 
distinguish them from the diffuse hepatization by which they are sur- ACUTE PHTHISIS. 
103 
rounded. When the blood-vessels have been artificially injected, the 
nodules are more readily recognized. These little nodules consist of a 
single air-vesicle or part of an air-passage filled with tubercle tissue, 
or filled partly with tubercle tissue, partly with epithelium, fibrine, 
and pus. The walls of the air-vesicle or air-passage remain intact, 
and its vessels permeable. Plate LXX. represents a cross section of an 
air-passage and of the air-vesicles surrounding it. The blood-vessels 
are injected. The larger part of the air-passage is filled with tubercle 
tissue, but the peripheric portions and the surrounding air-vesicles are 
filled with epithelial cells and fibrine. Such little nodules may be nu- 
merous and close together.. When surrounded by air-vesicles filled with 
products of inflammation, they constitute a peculiar hepatization, partly 
tubercular, partly inflammatory. Plate LXXI. 
(2.) Nodules a little larger than these, but of the same character are 
composed of several air-vesicles, or of part of an air-passage and air- 
vesicles. The cavities of the vesicles are filled in the same way with 
tubercle tissue, but in addition the walls of the vesicles are affected. 
They become split up and changed into tubercle tissue. As this pro- 
cess goes on, the outline of the vesicles are lost and the blood-vessels 
in their walls can no longer be injected. Such nodules are identical 
in their structure with the miliary tubercles seen in acute miliary 
tuberculosis. Plate LXXII. represents such a miliary tubercle. It 
sometimes happens that a section will show the whole of an air-passage 
filled with tubercle tissue in this way. The centres of these miliary 
tubercles may undergo cheesy degeneration in the ordinary way. 
(3.) The peri-lyronchitic nodules.-These nodules surround either 
partly or completely a bronchus or an air-passage. Their size and 
shape vary with the size of the bronchus, the direction in which it 
is cut, and the number of surrounding air-vesicles involved. Plate 
LXXIII. shows a number of peri-bronchitic nodules, some isolated, 
some surrounded by hepatization. Plate LXXIV., from the same 
lung, shows a section of a single lobule containing a number of peri- 
bronchitic nodules, without any hepatization between them. In 
Plate LXXV. some of the nodules are of the same peri-bronchitic 
character. 104 
ACUTE PHTHISIS. 
When we examine these peri-bronchitic nodules more closely, it be- 
comes evident that they do not all have the same structure. 
(a.) Some of the nodules consist simply of a bronchus filled with 
pus and epithelium, its walls infiltrated with cells, and of a number of 
air-vesicles filled with epithelium, fibrine, and pus. Such nodules are 
identical in their structure with the peri-bronchitic nodules which are 
formed in the ordinary broncho-pneumonia of children and adults. The 
advocates of a purely inflammatory phthisis always lay great stress on 
the character of these nodules. 
(A) Other nodules are composed of a bronchus filled with pus and 
epithelium. The wall of the bronchus is infiltrated with small cells or 
with tubercle tissue. Around the bronchus is a zone of air-vesicles 
filled with tubercle, the walls of the vesicles split up and only visible 
with high magnifying powers. Around this tubercular zone is another 
outer zone of vesicles filled with epithelium, fibrine, and pus. Plate 
LXXVI. 
(c.) Other nodules are composed as before of a bronchus with in- 
filtrated walls, and filled with inflammatory products. Around the 
bronchus is a continuous zone of tubercle tissue, in which the walls of 
the vesicles cannot be seen. Artificial injections of the blood-vessels 
penetrate only very imperfectly into this tubercular zone. Outside 
of this tubercular zone will be a zone of vesicles filled with epithe- 
lium, fibrine, and pus, or with tubercle tissue. Very often the contents 
of the bronchus, the walls of the bronchus, and even some of the tu- 
bercle tissue will undergo cheesy degeneration. Plates LXXVII. and 
LXXVIII. 
(A) In other peri-bronchitic nodules, although the cavity of the 
bronchus contains inflammatory products, yet its wall will remain un- 
changed, and around the bronchus will be air-vesicles filled with tuber- 
cle tissue. Such nodules seem to be peri-bronchitic miliary tubercles. 
Plate LXXIX. It will be observed that in all these peri-bronchitic 
nodules a large part of the consolidation is due to changes in the air- 
vesicles. 
In connection with peri-bronchitis it is convenient to speak of two 
lesions which affect the bronchi directly in some cases of acute phthisis. ACUTE PHTHISIS. 
105 
1. The walls of some of the larger bronchi are infiltrated with 
tubercle tissue which undergoes cheesy degeneration. The cavity of the 
bronchus is dilated, and contains inflammatory products also in a condi- 
tion of cheesy degeneration. The adjacent air-vesicles may be un- 
changed, or may contain tubercle tissue, or pus, fibrine, and epithelium. 
This change affects especially the larger and medium-sized bronchi, 
sometimes a large bronchus and its branches. The dilatation may be 
sufficient to form a cavity of some size, which may be further en- 
larged by the disintegration of the cheesy bronchial wall. Plate 
LXXX. For the most part in these bronchi the cheesy degenera- 
tion of the wall is so advanced that no structure can be made out, 
but sometimes one can find a place which seems to show the previous 
infiltration of tubercle tissue. 
2. There may be a general dilatation of most of the bronchi in a 
considerable portion of the lung without any marked change in their 
walls, and with only a moderate amount of inflammatory products in 
their cavities. This change is especially apt to affect the medium-sized 
and small bronchi. The lung tissue between the dilated bronchi is 
usually consolidated. When such a lung is cut it looks as if it were 
honey-combed with small cavities, but these cavities are only sections 
of the dilated bronchi. Plate LXXXI. 
The larger nodules found in acute phthisis seem to be of three 
kinds. 
1. Peri-bronchitic nodules, such as have been already described. 
2. Bodies resembling miliary tubercles in their structure, but much 
larger-the "tubercules massifs" of French writers. These nodules 
have just the same structure as many of the ordinary miliary tubercles 
already described, but they are on a larger scale, and the centre is regu- 
larly the seat of cheesy degeneration. 
3. Nodules formed by a number of air-vesicles in the condition of 
coagulation necrosis. 
It is necessary here to have precise notions as to what is meant by 
the terms " cheesy degeneration " and " coagulation necrosis." 
Cheesy degeneration, or metamorphosis, is a term made popular by 
Virchow. " It is," he says, " the second stage, or the necrobiotic result 106 
ACUTE PHTHISIS. 
of an originally hyperplastic growth-process, and the cheesy substance is 
nothing but the dead remains of broken down tissue. In this necro- 
biosis both the newly formed and the old parts die; the circulation 
stops, and the vessels disappear; the cells degenerate partly by an in- 
complete fatty metamorphosis, partly by a shrinkage from the loss of 
water. Thus is formed the totally anaemic, dry, dense, and almost 
amorphous mass." Such a change may take place in inflammatory 
products or in new growths. The term then expresses a perfectly 
well-defined condition, namely, the degenerative changes which take 
place in inflammatory products, new growths, and old tissues, and 
result in the transformation of these different elements into an amor- 
phous mass composed of granular matter, fat, and shrivelled tissue. 
The process is one of death, disintegration, fatty degeneration and 
desiccation. 
Coagulation necrosis is a term introduced by Cohnheim to desig- 
nate a condition to which attention has been called by Weigert. It 
is found-if the vascular supply is shut off from a portion of tissue, 
which remains surrounded by other tissue in which the blood circu- 
lates-that this anaemic portion of tissue undergoes certain changes, 
which are of the nature of a coagulation. This is best seen in the 
kidneys and spleen. If, for example, in the spleen one of the arterial 
branches is stopped by an embolus, a corresponding portion of the 
spleen will become anaemic, and will appear as a white, wedge-shape 
mass, sharply defined from the surrounding red normal spleen. If 
such a white infarction has existed but a short time, there is hardly any 
difference between the appearance of its anatomical elements and those 
of the surrounding spleen, except that it will be differently affected by 
staining fluids. If the infarction is older, then the cells become smaller, 
the nuclei disappear, the cell-bodies assume a peculiar shining appear- 
ance. In this condition the infarction may remain for a long time, but 
in the meanwhile changes take place at its periphery. There is a new 
growth of connective tissue so that the infarction may be surrounded 
by a zone of new connective tissue. Finally, cheesy degeneration may 
set in at the centre of the infarction, and extend so as to involve the 
greater part of it. ACUTE PHTHISIS. 
107 
Cheesy degeneration and coagulation necrosis are, therefore, totally 
different conditions. But tissues which are first the seat of coagulation 
necrosis may afterward undergo cheesy degeneration. Although the 
two processes are so distinct, yet the gross appearances produced by 
them may be very similar. Portions of tissue, the seat of coagulation 
necrosis may resemble very closely portions of tissue which have 
undergone cheesy degeneration. It is in the study of phthisis par- 
ticularly, that this similarity has led to confusion. 
In acute phthisis the nodules due to such a process of coagulation 
necrosis are regularly present and form a very important part of the 
lesion. 
The simplest form of such a coagulation necrosis nodule is seen in 
Plate LXXXH. Here is a portion of a small bronchus and a single 
air-passage in the condition of coagulation necrosis surrounded by a zone 
of ordinary hepatization. Plate LXXXIII. shows the same condition 
more extensively developed. Here the areas of coagulation necrosis 
are so large and so close together as to form a nearly continuous 
hepatization. 
A more complex form of nodule is represented in Plates LXXXIV., 
LXXXV., and LXXV. Here are nodules with dark centres and light 
peripheries, the larger nodules being made up of several smaller ones. 
In these nodules the dark centres are areas of coagulation necrosis, 
the light peripheries are made up of tubercle tissue. 
These are the two forms of coagulation necrosis nodules. In each 
form there is a centre of air-vesicles filled with inflammatory products in 
a condition of coagulation necrosis; but around such a centre there may 
be merely a zone of ordinary hepatization, or a zone of tubercle tissue. 
If we look more closely at these areas of coagulation necrosis we 
see that their vascular supply is entirely cut off, and that artificial 
injections do not penetrate them. The outlines of the walls of the 
vesicles are visible, but the walls are thin, transparent, recognizable 
principally by their elastic fibres. The cavities are filled with poly- 
gonal cells and shrivelled nuclei. The cells are pale, shining, devoid 
of nuclei, and have the characteristic appearance of cells in the state 
of coagulation necrosis. Plate LXXXVI. In some vesicles, however, 108 
ACUTE PHTHISIS. 
there is nothing but coagulated fibrine. These vesicles filled with 
fibrine are not as opaque as the others, so that a mottled effect is pro- 
duced, as seen in Plate LXXXIII. 
There is nothing especial to be noticed in the zone of ordinary hep- 
atization which surrounds the necrotic centres. The cavities of the 
vesicles are filled with epithelium, pus, fibrine, and granular matter in 
varying proportions. The walls of the vesicles are unchanged, their 
vessels are pervious. It is to be noticed that there is no appearance 
of a gradual transition between the necrotic centres and the hepatized 
peripheries. There are no vesicles giving pictures of coagulation 
necrosis in different stages. All the necrotic portion is in the same 
condition, and is separated abruptly from the surrounding hepatization. 
In those nodules which have a peripheric zone of tubercle tissue, we 
get, with a higher magnifying power, such a picture as is seen in Plate 
LXXXVIL, which represents a section through a small nodule. The 
necrotic centre is sharply separated from the tubercular zone, and this 
tubercular zone gives an indistinct appearance of being made up of 
altered air-vesicles. 
If we examine this tubercular zone more closely, we find that there 
are changes in the walls of the air-vesicles and in their cavities. The 
walls are changed into tubercle tissue. At first the blood-vessels in the 
walls remain pervious, but as the transformation of the walls becomes 
more complete, the vessels disappear. The cavities of the vesicles are 
partly or completely filled with tubercle tissue, epithelium and pus. 
The tubercle tissue grows inward from the walls of the vesicles, or 
is formed in their cavities; it has the- regular structure of a delicate 
basement-substance, more or less reticulated, provided with nuclei, and 
enclosing spaces containing large polygonal nucleated cells. Giant 
cells are sometimes present, but are not constant. Plates LXXXVIIL, 
LXXXIX., XC. The process seems to be of the same character as the 
formation of diffuse tubercle tissue already described in connection 
with chronic miliary tuberculosis. 
These nodules may remain in the condition just described up to the 
time of the patient's death. But in some cases they undergo further 
changes. Cheesy degeneration begins at the centre of the necrotic ACUTE PHTHISIS. 
109 
portion of the nodule, involves the whole of this portion, and may 
extend to the surrounding zone of hepatization or of tubercle tissue. 
The nodules will then present quite a different appearance. There is a 
centre composed of an amorphous cheesy mass, in which no structure 
can be made out, and around this is a zone of tubercle tissue, or of 
hepatization. In this condition it is often difficult to distinguish these 
nodules from the peri-bronchitic nodules, and the " tubercules massifs." 
In such a condition of dry cheesy degeneration a certain number of 
the nodules may remain indefinitely ; but in others the degenerated 
portions will soften, and in this way cavities will be formed of sizes 
corresponding to the original nodules; or, if the nodules are close to- 
gether, several small cavities will join to form larger ones. Plates XCI., 
XCII. In this way we sometimes find a large part of a lung honey- 
combed with small cavities having ragged walls ; the number of cavities 
corresponding with the number of the areas of coagulation necrosis. 
It is difficult to be certain of the exact way in which these areas of 
coagulation necrosis are produced. 
It has been supposed that they are due to the production of so 
much inflammatory material that the blood-vessels are compressed, and 
the parts lose their nutritive supply. This supposition, however, does 
not account for the extreme definiteness of these areas. In an area of 
coagulation necrosis all the different vesicles are affected equally. 
More than this, in some cases of the lobar pneumonia of adults, and of 
the lobular pneumonia of children, we do have undoubted examples of 
death of portions of the lung from over-production of inflammatory 
products, and in these cases the appearances are quite different. There 
is no formation of areas of coagulation necrosis, but either simple death 
of portions of tissue or cheesy degeneration. 
French writers, on the other hand, seem to confound the coagulation 
necrosis nodules with the " tubercules massifs." But these two forms of 
nodules are really quite different. After the condition of coagulation 
necrosis has been succeeded by cheesy degeneration and softening, then 
indeed coagulation necrosis nodules, large tubercles, and peri-bronchitic 
nodules all look alike, but from the beginning this is not so. In the 
real large tubercles the necrotic process is from the first a true cheesy 110 
ACUTE PHTHISIS. 
degeneration. It does not involve at once the whole of the centre of the 
tubercle, but begins first in a few of the elements at the centre and then 
extends irregularly outward, involving more and more of the nodules. 
It seems to me that the only way to account for the formation of 
these centres of coagulation necrosis is by supposing an occlusion of the 
branches of the pulmonary artery. The changes are exactly similar to 
those seen in the white infarctions of the kidneys and spleen; it is 
generally admitted that the small as well as the large branches of the 
pulmonary artery are terminal arteries; it has been demonstrated by 
different writers that the inner coat of the arteries is often changed in 
phthisis; the different sizes of the areas of coagulation necrosis would 
correspond with the blocking up of smaller or larger arteries. On the 
other hand, I have not been able to demonstrate that the arteries 
are regularly plugged. In some cases indeed I have found a well- 
marked obliterative arteriitis of the larger arteries such as is seen 
in Plate XCIIL, but that is all. 
It seems evident then that in acute phthisis we have a lesion of 
peculiar characters. It is very far from being a simple broncho-pneu- 
monia with degenerative changes, or an acute miliary tuberculosis com- 
bined with pneumonia. The lesions are much more complex. Both the 
bronchi and the parenchyma of the lung take a share in the morbid 
process. The lesion seems to be an inflammatory one, the products of 
inflammation being pus, epithelium, fibrine, and tubercle tissue ; but it 
is complicated by the formation of areas of coagulation necrosis. The 
tubercle tissue is arranged partly so as to form miliary tubercles and 
large tubercles, partly as peri-bronchitic nodules, partly as tubercular 
zones around areas of coagulation necrosis. The prognosis seems to de- 
pend mainly upon the number and size of the areas of coagulation 
necrosis, and it seems probable that most of these are formed at the 
very outset of the disease. The diffuse pneumonia may undergo reso- 
lution, the miliary tubercles and peri-bronchitic nodules do not occupy 
much of the lung and may be transformed into cheesy material or 
fibrous tissue; but the areas of coagulation necrosis destroy a consider- 
able part of the parenchyma of the lung and have a natural tendency to 
soften and form cavities. EXPLANATION OF THE PLATES. 
Many of the plates should be looked at with a magnifying glass. 
PLATE I. x 750. 
(Autographic process.) 
Flat connective-tissue cells from the surface of the fascia of a dog's 
leg. In the upper part of the drawing the outlines of the cells are 
demonstrated with nitrate of silver; in the lower part of the drawing 
the same cells are stained with haematoxylin and eosin, and isolated. 
PLATE IT. x 1500. 
(Photo-lithograph of a drawing.) 
Branching connective-tissue cells from the tendon of a dog's leg. 
Haematoxylin and eosin. 
PLATE III. x 750. 
(Photo-lithograph of a drawing.) 
Branching connective-tissue cells in the omentum of the rabbit. 
Nitrate of silver preparation. 
PLATE IV. x 750. 
(Heliotype of a drawing.) 
The inner surface of the costal pleura of the dog. The endothelial 
cells have been brushed off from the upper part of the specimen, 
showing the connective tissue, elastic fibres, and capillary blood-vessels 
beneath. 112 
EXPLANATION OF THE PLATES. 
PLATE V. x 1500. 
(Photo-lithograph of a drawing.) 
In the upper part of the plate, the endothelial cells; in the lower 
part, the fixed connective-tissue cells of the dog's pleura. Haema- 
toxylin and eosin. 
PLATE VI. x 90. 
(Photo-lithograph of a drawing.) 
Endothelium of the human costal pleura, demonstrated with nitrate 
of silver. 
PLATE VII. x 90. 
(Drawn on wood.) 
The lymphatics of the costal pleura of the dog, demonstrated with 
nitrate of silver. 
PLATE VIII. x 750. 
(Heliotype of a drawing.) 
The costal pleura of the dog, the lymphatic spaces and fixed 
connective-tissue cells. Nitrate of silver and haematoxylin. 
PLATE IX. x 750. 
(Drawn on wood.) 
Pleurisy of the dog, produced by chloride of zinc, of twenty-four 
hours' duration. The cell-growth in the connective tissue just beneath 
the endothelium; swelling of the old cells and production of new ones. 
Haematoxylin and eosin preparation. 
PLATE X. x 750. 
(Heliotype of a drawing.) 
Chloride of zinc pleurisy of the dog on the third day. A layer of 
fibrine, and of new cells stripped off from the surface of the costal 
pleura. Haematoxylin and eosin preparation. EXPLANATION OF THE PLATES. 
113 
PLATE XL x 750. 
(Drawn on wood.) 
Chloride of zinc pleurisy of the dog on the fifth day; the blood- 
vessels have been artificially injected from the aorta. A layer of new 
cells and new blood-vessels stripped off from the surface of the costal 
pleura. Haematoxylin and eosin. 
PLATE XII. x 750. 
(Photo-lithograph of a drawing.) 
Chloride of zinc pleurisy of the dog, seventh to ninth day. Isolated 
endothelial and connective-tissue cells from the layer of new tissue on 
the surface of the costal pleura. Haematoxylin and eosin. 
PLATE XIII. x 750.. 
(Photo-lithograph of a drawing.) 
Empyema of the dog, produced by a seton, of twenty-four hours' 
duration. Changes in the endothelial cells of the costal pleura and pro- 
duction of pus-globules beneath them. Haematoxylin and eosin. 
PLATE XIV. x 750. 
(Photo-lithograph of a drawing.) 
Empyema of the dog, of ten days1 duration. Vertical section of the 
costal pleura; showing new cells, basement-substance and blood-vessels. 
Haematoxylin and eosin. 
PLATE XV. x 750. 
(Etched on copper.) 
Human empyema. Vertical section of the costal pleura, showing 
the splitting up of the basement-substance by new cells. Haematoxylin 
and eosin. 
PLATE XVI. x 750. 
(Etched on copper.) 
Human hydrothorax. Endothelial cells on the surface of the costal 
pleura. 114 
EXPLANATION OF THE PLATES. 
PLATE XVII. x 750. 
(Photo-lithograph of a drawing.) 
Chronic pleurisy with adhesions, human. The surface of the costal 
pleura, covered with changed endothelium and giant-cells; beneath 
these the connective-tissue layer of the pleura, with capillary blood- 
vessels and large connective-tissue cells. Haematoxylin and eosin. 
PLATE XVIII. x 90. 
(Photo-lithograph of a drawing.) 
Tubercular pleurisy. A vertical section of the costal pleura, show- 
ing the infiltration of the substance of the pleura with tubercle granula 
and diffuse tubercle. Haematoxylin and eosin. 
PLATE XIX. x 750. 
(Photo-lithograph of a drawing.) 
The parietal peritoneum of the dog, showing the free surface of the 
peritoneum, partly covered by endothelium, beneath this the connective 
tissue with its lymphatic spaces. Nitrate of silver, haematoxylin and 
eosin. 
PLATE XX. x 750. 
(Etched on copper.) 
The normal human omentum, covered with endothelium, fusiform 
and branching cells in the connective tissue. Nitrate of silver, haema- 
toxylin and eosin. 
PLATE XXI. x 750. 
(Photo-lithograph of a drawing.) 
Cellular peritonitis, human. Production of new cells on the surface 
and in the substance of the omentum. Haematoxylin and eosin. 
PLATE XXII. x 750. 
(Photo-lithograph of a drawing.) 
Cellular peritonitis of the dog on the fourth day after an injection 
of chloride of zinc into the peritoneal cavity. Cell-growth on the sur- 
face of the omentum. Haematoxylin and eosin. EXPLANATION OF THE PLATES. 
115 
PLATE XXIII. x 750. 
(Photo-lithograph of a drawing.) 
The omentum of the rabbit, one hour after an injection of chloride of 
zinc. Fixed connective-tissue cells and pus cells. Nitrate of silver 
and haematoxylin. 
PLATE XXIV. x 750. 
(Photo-lithograph of a drawing.) 
Peritonitis in a dog, forty-eight hours after the injection of chloride 
of zinc. The surface of the parietal peritoneum, showing the endo- 
thelium in place, pus-cells beneath it, and others emerging to the sur- 
face between the corners of the endothelial cells. Nitrate of silver, 
haematoxylin and eosin. 
PLATE XXV. x 750. 
(Photo-lithograph of a drawing.) 
Acute peritonitis, human. The omentum covered with fibrine and 
pus, and with new cells of different shapes. Haematoxylin and eosin. 
PLATE XXVI. x 750. 
(Etched on copper.) 
Chronic cellular peritonitis, human. .Cell-growth on the surface and 
in the substance of the omentum, formation of giant-cells. Haematoxy- 
lin and eosin. 
PLATE XXVII. x 750. 
(Drawn on stone.) 
Chronic peritonitis with adhesions; part of a very thin adhesion 
composed of basement-substance and cells. Haematoxylin and eosin. 
PLATE XXVIII. x 750. 
(Drawn on stone.) 
Chronic peritonitis with adhesions, human. The surface of the pa- 
rietal peritoneum; cell-growth in the peritoneum and on its surface. 
Haematoxylin and eosin. 116 
EXPLANATION OF THE PLATES. 
PLATE XXIX. x 150. 
(Drawn on stone.) 
Tubercular peritonitis, human. Section of a tubercle granulum. 
Haematoxylin and eosin. 
PLATE XXX. x 1300. 
(Drawn on stone.) 
Part of the wall of an air-vesicle of an adult human lung, showing 
O' o 
all the cells that could be seen in a haematoxylin and eosin preparation. 
PLATE XXXI. x 300. 
(Drawn on stone.) 
The pneumonia of heart disease (brown, or pigment induration). 
The walls of the vesicles are thickened, their cavities partly filled with 
epithelial cells. Haematoxylin and eosin. 
PLATE XXXII. x 750. 
(Drawn on stone.) 
The pneumonia of heart disease. A single air-vesicle. Dilatation 
of the capillaries, thickening of the walls, production of epithelium. 
PLATE XXXIII. x 750. 
(Drawn on stone.) 
Acute lobar pneumonia, commencing red hepatization. A single air- 
vesicle, the vessels artificially injected; the cavity of the vesicle is 
partly filled with fibrine, pus, and epithelium. 
PLATE XXXIV. x 500. 
(Photo-lithograph of a drawing.) 
Croupous bronchitis with lobar pneumonia. Vertical section of the 
wall of a bronchus. A layer of fibrine and pus on the inner surface of 
the mucous membrane, and another layer of fibrine and pus between 
the epithelial cells and the basement-membrane. EXPLANATION OF THE PLATES. 
117 
PLATE XXXV. x 300. 
(Drawn on stone.) 
Air-vesicles filled with granules of uncertain nature, possibly bac- 
teria, from a case of acute lobar pneumonia with a peculiar history. 
PLATE XXXVI. x 750. 
(Drawn on stone.) 
Acute lobar pneumonia, gray hepatization. Air-vesicles filled with 
pus, epithelium, and granular matter. Many of the pus and epithelial 
cells are swollen and fatty. 
PLATE XXXVII. x 750. 
(Drawn on stone.) 
Pneumonia in a surgical case, red hepatization; a single air-vesicle 
filled with fibrine and pus. 
PLATE XXXVIII. 750. 
(Drawn on stone.) 
Lobular, red hepatization in an adult with chronic bronchitis. A 
single air-vesicle filled with epithelium, fibrine, and pus. 
PLATE XXXIX. x 750. 
(Drawn on stone.) 
Lobular pneumonia in a child, complicating scarlatina. Air-vesicles 
filled with pus, fibrine, epithelium, and red blood- globules. 
PLATE XL. x 750. 
(Drawn on stone.) 
Lobular pneumonia in a child, complicating whooping-cough. Air- 
vesicles partly filled with epithelium and pus. 
PLATE XLI. x 850. 
(Drawn on stone.) 
Broncho-pneumonia of children. Vertical section of the wall of a 118 
EXPLANATION OF THE PLATES. 
bronchus. The epithelial cells are swollen and altered; the connective 
tissue beneath is infiltrated with cells. 
PLATE XLII. x 22. 
(Drawn on stone.) 
Acute miliary tuberculosis. Section of a number of miliary 
tubercles. 
PLATE XLIII. x 300. 
(Drawn on stone.) 
Section of a single miliary tubercle composed of a group of air- 
vesicles. The walls of the air-vesicles are infiltrated with tubercle 
tissue, and their cavities are filled with the same tissue. It is that 
variety of tubercle tissues in which the cells are large, numerous, and 
close together in the meshes of the basement-substance. In the sur- 
rounding vesicles are an increased number of epithelial cells. 
PLATE XLIII. No. 2. x 300. 
(Artotype of a drawing.) 
Section of a single miliary tubercle composed of a group of air- 
vesicles. The walls of the vesicles are split up into tubercle tissue, 
their cavities are filled with the same tissue. It is that variety of 
tubercle tissue in which the basement-substance is in excess, and the 
meshes, for the most part, empty of cells. Giant-cells are present. 
The entire group of vesicles is surrounded by a zone of connective 
tissue infiltrated with small round cells. 
PLATE XLIV. x 1500. 
(Drawn on stone.) 
Tubercle tissue from a tubercle granulum. The meshes of the 
basement-substance are filled with polygonal nucleated cells. 
PLATE XLV. X 300. 
(Drawn on stone.) 
Section of a single miliary tubercle, composed of two large tubercle EXPLANATION OF THE PLATES. 
119 
granula, surrounded by diffuse tubercle. No outlines of air-vesicles 
can be seen in this tubercle. 
PLATE XLVI. x 1500. 
(Photo-lithograph of a drawing.) 
Tubercle tissue between the tubercle granula of a miliary tubercle. 
Cells and basement-substance. 
PLATE XLVII. x 850. 
(Photo-lithograph of a drawing.) 
A single air-vesicle forming part of a miliary tubercle. The vesi- 
cle is filled with large cells imbedded in a finely granular basement- 
substance. 
PLATE XLVIII. x 1500. 
(Drawn on stone.) 
A single giant-cell from a tubercle granulum in a miliary tubercle. 
PLATE XLIX. x 750. 
(Photo-lithograph of a drawing.) 
Section of a tubercle granulum from a specimen of lupus of the skin 
of the face. 
PLATE L. x 850. 
(Drawn on stone.) 
Acute miliary tuberculosis. A miliary tubercle from the pia mater. 
PLATE LI. 300. 
(Drawn on stone.) 
Chronic miliary tuberculosis. Section of a miliary tubercle made up 
of tubercle granula, diffuse tubercle, and connective tissue. Numerous 
giant-cells. 
PLATE LIL x 90. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. A group of miliary tubercles of differ- 
ent ages, joined together by diffuse tubercle tissue and fibrous tissue. 120 
EXPLANATION OF THE PLATES. 
The blood-vessels have been artificially injected, showing blood-vessels 
in some of the tubercles. 
PLATE LIIL x 850. 
(Drawn on stone.) 
Chronic miliary tuberculosis. Part of the wall of an air-vesicle, 
showing the growth of cells on its surface. 
PLATE LIV. x 90. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. Several miliary tubercles composed 
of tubercle granula and diffuse tubercle. 
PLATE LV. x 300. 
(Drawn on stone.) 
Chronic miliary tuberculosis. Diffuse growth of tubercle tissue 
filling and compressing the air-vesicles. 
PLATE LVI. x 90. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. Oki tubercles changed into granular 
matter and fibrous tissue. 
PLATE LV1L x 850. 
• 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. Tubercle tissue between the miliary 
tubercles. 
PLATE LVIII. x 90. 
(Drawn on stone.) 
Chronic miliary tuberculosis. A single miliary tubercle, the blood- 
vessels injected. EXPLANATION OF THE PLATES.J 
121 
PLATE LIX. x 850. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. The tissue which forms the periphery 
of some of the miliary tubercles. 
PLATE LX. x 850. 
(Drawn on stone.) 
Chronic miliary tuberculosis. Air-vesicles filled with tubercle tissue, 
from the periphery of a miliary tubercle. 
PLATE LXI. x 90. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. A large tubercle changed into fibrous 
tissue. 
PLATE LXII. x 850. 
(Drawn on stone.) 
Chronic miliary tuberculosis. A single tubercle granulum. 
PLATE LXIII. x 90. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. Interstitial pneumonia in the lung 
between the tubercles. 
PLATE LXIV. x 300. 
(Photo-lithograph of a drawing.) 
Chronic miliary tuberculosis. The diffuse growth of tubercle tissue, 
which may render solid a considerable part of the lung. 
PLATE LXV. x 850. 
(Artotype of a drawing.) 
The red hepatization of acute phthisis. A single air-vesicle filled 
with epithelium and pus, the blood-vessels artificially injected. 122 
EXPLANATION OF THE PLATES. 
PLATE LXVI. x 850. 
(Artotype of a drawing.) 
The red hepatization of acute phthisis. A single air-vesicle filled 
principally with fibrine, the blood-vessels artificially injected. 
PLATE LXVII. x 200. 
(Artotype of a drawing.) 
The red hepatization of acute phthisis. A group of air-vesicles 
filled with granules, the blood-vessels artificially injected. 
PLATE LXVIII. x 16. 
(Artotype of a drawing.) 
Human lung, corrosion preparation. Fragments of several air- 
passages, and part of a small bronchus. 
PLATE LXIX. x 5. 
(Photograph of a specimen.) 
Section of a normal human lung, showing the lobules, air-passages, 
and air-vesicles. 
PLATE LXX. x 300. 
(Artotype of a drawing.) 
Acute phthisis. A section of an air-passage with air-vesicles. 
The centre of the air-passage is filled with tubercle tissue, the peri- 
pheral portions and the surrounding vesicles with epithelium and 
fibrine. The blood-vessels are injected. 
PLATE LXXI. x 4. 
(Photograph of a specimen.) 
Acute phthisis. Diffuse hepatization produced by single air-vesicles 
and air-passages filled with tubercle tissue, small areas of coagulation 
necrosis, some of them corresponding to air-passages, and ordinary 
pneumonia. The plate should be looked at with a magnifying glass. EXPLANATION OF THE PLATES. 
123 
PLATE LXXIL x 120. 
(Artotype of a drawing.) 
Acute phthisis. Section of a miliary tubercle. 
PLATE LXXIII. x (?) 
(Photograph of a specimen.) 
Acute phthisis. Peri-bronchitic nodules and diffuse pneumonia. 
PLATE LXXIV. x 15. 
(Artotype of a drawing.) 
Acute phthisis. Section of a single lobule containing isolated peri- 
bronchitic nodules. The blood-vessels are injected. 
PLATE LXXV. x 4. 
(Photograph of a specimen.) 
Acute phthisis. Peri-bronchitic nodules, areas of coagulation ne- 
crosis, miliary tubercles, and diffuse pneumonia. 
PLATE LXXVL x 120. 
(Artotype of a drawing.) 
Acute phthisis. A peri-bronchitic nodule formed principally by a 
change of the surrounding air-vesicles into tubercle tissue. The walls 
of the bronchus are infiltrated and its cavity contains inflammatory 
products. The large blood-vessels are injected. 
PLATE LXXVIL x 120. 
(Artotype of a drawing.) 
Acute phthisis. A peri-bronchitic nodule formed of tubercle tissue. 
Cheesy degeneration has commenced around the bronchus. 
PLATE LXXVIII. x 120. 
(Artotype of a drawing.) 
Acute phthisis. A peri-bronchi tic nodule formed of tubercle tissue. 124 
EXPLANATION OF THE PLATES. 
The wall of the bronchus is infiltrated and has undergone cheesy de- 
generation. The blood-vessels are injected. 
PLATE LXXIX. x 850. 
(Artotype of a drawing.) 
Acute phthisis. Part of a peri-bronchitic nodule. The wall of the 
bronchus is unchanged, but it is surrounded by air-vesicles filled with 
tubercle tissue. The blood-vessels are injected. 
PLATE LXXX. x 5. 
(Photograph of a specimen.) 
Acute phthisis. Large bronchi with infiltrated and cheesy walls 
and dilated cavities. 
PLATE LXXXI. x 8. 
(Photograph of a specimen.) 
Acute phthisis. General dilation of the bronchi with diffuse hepa- 
tization. 
PLATE LXXXIL x 40. 
(Artotype of a drawing.) 
Acute phthisis. A single air-passage in the condition of coagulation 
necrosis, surrounded by pneumonia. 
PLATE LXXXIII. x 4. 
(Photograph of a specimen.) 
Acute phthisis. Large areas of coagulation necrosis. 
PLATE LXXXIV. x 8. 
(Photograph of a specimen.) 
Acute phthisis. Small areas of coagulation necrosis surrounded by 
tubercle tissue. EXPLANATION OF THE PLATES. 
125 
PLATE LXXXV. x 11. 
(Photograph of a specimen.) 
Acute phthisis. Section of a single lobule. Areas of coagulation 
necrosis surrounded by tubercle tissue. 
PLATE LXXXVI. x 850. 
(Artotype of a drawing.) 
Acute phthisis. A single air-vesicle filled with the products of in- 
flammation in tlie condition of coagulation necrosis. 
PLATE LXXXVIL x 300. 
(Artotype of a drawing.) 
Acute phthisis. A small area of coagulation necrosis surrounded 
by tubercle tissue. 
PLATE LXXXVIII. x 850. 
(Artotype of a drawing.) 
Acute phthisis. Air-vesicles from the tubercular zone surrounding 
an area of coagulation necrosis, showing the manner in which the 
vesicles are replaced by tubercle tissue. 
PLATE LXXXIX. x 850. 
(Artotype of a drawing.) 
Acute phthisis. An air-vesicle from the tubercular zone surround- 
ing an area of coagulation necrosis, showing the manner in which the 
air-vesicles are replaced by tubercle tissue. 
PLATE XC. x 1500. 
(Artotype of a drawing.) 
Acute phthisis. Tubercle tissue from the tubercular zone surround- 
ing an area of coagulation necrosis. 126 
EXPLANATION OF THE PLATES. 
PLATE XCI. x 7. 
(Photograph of a specimen.) 
Acute phthisis. Cheesy degeneration and softening of areas of 
coagulation necrosis. 
PLATE XCII. x 10. 
(Photograph of a specimen.) 
Acute phthisis. Cheesy degeneration and softening of areas of 
coagulation necrosis. At the centre of a lobule is a cavity with ragged 
edges formed by the softening of several coagulation necrosis areas. 
The surrounding vesicles are filled with inflammatory products. 
PLATE XCIIL x 480. 
(Artotype of a drawing.) 
Acute phthisis. Cross section of an artery situated in the midst of 
large areas of coagulation necrosis. The lumen of the artery is nearly 
obliterated by a growth of new tissue. INDEX. 
PAGE 
Bronchi in Acute Phthisis, 105 
Cheesy Degeneration, 105 
Coagulation Necrosis, 106 
Connective Tissue, Normal, 6 
Connective Tissue, Inflammation of, 8 
Empyema, 21 
Hydrothorax, ' .27 
Peritoneum, Normal, .......... 35 
Peritonitis, Acute, . . . . . . . . . . .37 
Peritonitis, with Adhesions, ......... 44 
Peritonitis, Chronic, 43 
Peritonitis, Hjemorrhagic, ......... 46 
Peritonitis, Tubercular, 47 
Phthisis, Acute, ........... 97 
Phthisis, Chronic, 84 
Plates, Explanation of, . . . . . . . . . .Ill 
Pleura, 11 
Pleurisy, with Adhesions, ......... 28 
Pleurisy, with Fibrine, 15 
Pleurisy, with Fibrine and Serum, ....... 16 
Pleurisy, with Fibrine, Serum, and Pus, . . . . . . .21 
Pleurisy of Phthisis, . . 30 
Pleurisy, Tubercular, 31 
Pneumonia, 51 
Pneumonia of Heart Disease, . . . . . . . . .53 
Pneumonia, Interstitial, .......... 70 
Pneumonia, Lobar, . . . . . . . . . . .59 
Pneumonia, Lobular, . 65 
Pneumonia from Pressure, 70 
Pneumonia, Surgical, .......... 65 
Tuberculosis, Acute Miliary, . . . . . . . . .73 
Tuberculosis, Chronic Miliary, 87 IPJLATjE i ,i*.» a < 
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OA^oPma/ offlwma/n TIL AT IE XXII. 
(&tn a ^/)ay; c/ay. 
Q'//a^nt^e(/ / 50 (/^ameteli 3L3CMK. 
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■///ay ////r// 7hh /,////mc/ch. JPJLAT1E XXVI. 
Zmenlum, ZZe/ZuZav 
Q'/Zaanf^ec/ 73 O (Zameteu. I ' (। L' ,1'j i I « 
zz/zz^zz/^zX . 
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/^((y//7^rc/ 7,7(7 Tym w . tyr/ty/t r/ ty/r/r/c y '(s/sm ty //f ■ 
//zay r</ 77 f/f^/jns'/s'^. MATE XXX. 
^Z aZtZ& //////////'. Z/f/"/^ 
waan^/feZ 7ZZZ Zf'(f^//(''/e/J ■ MLA3T3E ZXXXIL. 
< z^z z- < zzz z-zz zzz zvzzzz Z^ <z^z zz// ,^/z-ZZVZ.ZZ'- 
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i 
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s/wy //sV/ry/ f//// //////'7J. FILATS XXXIX, 
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7/ 7)^ ,7////<'7f,/. PLAT H 
_ 7,//7 //, ■ 4/77777/77/77777 // 7///</r/t ■ 
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</ ///r //>/// a 
//try/,//< ' '^a,,,. 
>////</// y//r f/,/m ///r/n'j. 'IP3LATE XML ^moq. ® Plate X LI II. No 2. x300 
ACUTE MILIARY TUBERCULOSIS. [ MrAI1, 
zz/z/z/z/z/zz/X IFiATE Xl<v ( , 
dawie/^- d^/t at/ 
s/aayat/^/ea at a^/^e^. re///  pla'ch r,, 
' /v / r/f //(' r^ (7 f //^//r^ 
//(7dM/s/e/etJ. & LIL 
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maaMM^^^aiawfa. 
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' 
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CyZZ/zV^Z^/Z/z/ <J^ZZZ'ZZZZZZV//Z<- way runted'. Plate L X V . x 8 5 0 
ACUTE PHTHISIS Plate LX V I . x850 
ACUTE PHTHISIS Plate L XV I I. x 2 0 
ACUTE PHTHISI S P I a i e LX VIII. x 1 6 
HUMAN LUNG. MR PASSAGES Plate LXIX. x4 
NORMAL HUMAN LUNG. Plate L XX■ x 3 0 0 
ACUTE PHTH I S I s Plate LXXI. x 11 
ACUTE PHTHISIS. Plate LXXI । • x 1 20 
ACUTE PHTH|sis Plate LXXIII. x 5 
ACUTE PHTHISIS. PIaie LX X IV. x ] 5 
ACUTE PHTHISIS Plate LXXV x 4 
ACUTE PHTHISIS Plate L X X V I , x1 2 0 
TUBERCULAR PERIBRONCHITIS Plate L X X V I I . x 1 20 
TUBERCULAR PERIBRONCHITIS. Plate LXXV I I | . x 1 2 0 
TUBERCULAR PERIBRONCHITIS. Plate LXXIX. x850 
TUBERCULAR PERIBRONCHITIS Plate LXXX. x 5 
ACUTE PHTHISIS Plate LXXXI. x8 
ACUTE PHTHISIS. Plate L XXXI I . x 4 0 
ACUTE PHTHISIS Plate LXXXIII. x4 
ACUTE PHTHISIS. Plate LXXXIV. x 8 
ACUTE PHTHISIS. Plate LXXXV. x11 
ACUTE PHTHISIS Plate LX X XV I *850 
ACUTE PHTHISIS Plate *300 
acute pHth 1 sIs. Plate L*^7* 1 । x 85 0 
acute p H S f s Plate LXXXIX. x 850 
ACUTE P^Th ISIS. Plate X C. x 1 5 0 0 
A.CUTE PHTHISIS. Plate XCI. x 7 
ACUTE PHTHISIS. Plate XCII. x 10 
ACUTE PHTHISIS Plaie XC'" '480 
OBLITERATE ARTERlITIs The author must apologize for the delay of the present number. 
It was impossible to get the plates ready any sooner. 
In order to avoid a similar delay in the future, the first number of 
the second year, No. 13 of the entire series, will not be published until 
November, 1879. The subjects to be treated of in the second year will 
be: Acute Tuberculosis, Chronic Pulmonary Phthisis, and the different 
forms of Nephritis. PREFATORY NOTE. 
In this paper, and in those to succeed it, the attempt will be made to give 
an account of some of the changes produced by disease. The particular subjects 
of study will be the inflammations of connective tissue, of the mucous mem- 
branes and of the viscera, and the structure of tumors. 
The fragmentary and contradictory character of our knowledge on these 
subjects is a sufficient excuse for this attempt to add another piece to the existing 
patchwork. 
These papers will give the results of investigations carried on for a number 
of years, and still far from complete. They have, however, been carried far 
enough in some directions to warrant their publication at the present time. 
My intention is that these studies shall be published monthly. Each paper 
will consist of from two to four full-page drawings and the accompanying text. 
The drawings have been made by myself from actual specimens, with the aid of 
the camera lucida. All the elements are represented of the same relative size 
as they exist in the specimens. Some of the drawings have been made directly 
on the block and then cut; others were drawn on paper and then reproduced by 
different photographic processes. 
The first twelve papers will include the pathological anatomy of pleurisy, 
of peritonitis, and of meningitis. 
FRANCIS DELAFIELD, 
12 West Thirty-second Street. 
This page to be cancelled by binder. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
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STUDIES 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine, in the College of Physicians and Stir geons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCTAYO FARTS, 
Each containing from two to four full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts will be published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
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INVARIABLY IN ADVANCE. 
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S T U DI E S 
IN 
^pathological Anatomy 
RY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
INTo. 2. 
MARCH, 1878. 
NEW YORK 
"WZ^C. WOOD & CO. 
27 Great Jones Street 
1878 ^ANNOUNCEMENT.^* 
Over 200 pages additional Beading Matter in a year, 
with no change in price, making two royal 
§ octavo volumes of 520 pages each, 
'The Medical Record. 
A Weekly Journal of Medicine and Surgery. 
& -. - 
g Edited by GEORGE F. SHRADY, A.M., M.D. 
j The publishers have the pleasure of announcing- that, beginning with the first number for January, 1878, 
The. Medical Record will be enlarged by the addition of four pages each week, amounting to 
Q OVER 200 PAGES ADDITIONAL READING MATTER 
0 In a year-with no change in price. This very great increase in the size of the journal has been rendered 
possible by the large advertising patronage enjoyed by it, and is a direct benefit to subscribers from this source. 
g An increased number of advertising pages never costs subscribers any thing, never encroaches upon the reading 
S matter, which is invariably the same each week, and should always be viewed by readers with satisfaction, as an 
g evidence of the prosperity of the journal, and its greater ab lity to provide for them. 
& "THE MEDICAL RECORD" 
For 1878 will, therefore, consist of Two Royal Octavo Volumes of 520 pages each. Subscription price, 
04 $5.00 per year, invariably inadvance. 
® Tlie Volume commences January 1st. 
This Journal, now in its thirteenth volume, is published oh Saturday of each week ; each number consists of 
twenty super-royal octavo pages, double columns, and contains Original Articles from the first men of the country 
p in their respective departments, Reports of Lectures, Societies, and Hospital: an account of the Progress of 
£ Medical Science throughout the world ; Editorial Articles oh Current Topics of Interest, Reviews and Notices of 
Books, Correspondence New Instruments, Medical News and Items, &c., &c. 
tfi It is the only WEEKLY MEDICAL JOURNAL published in New York. 
The Medical Record is intended to be thoroughly Cosmopolitan in its character, representing the interests of 
g the profession in all parts of the country. It is entirely independent of all parties or cliques. Its object is to 
S present to the profession a faithful record of the existing state of medical science, in all its departments; and, as 
K it is more especialy intended to meet the wants of the general practitioner, the articles published in its columns 
are thoroughly practical in their character. 
SPECIMEN COPY SENT FREE. 
♦a . ' .... 
An increase of 200 pages additional Beading Matter 
in a year will be made in 
I The American Journal of Obstetrics 
" And Diseases of Women and Children. 
m 
£ PAUL F. MUNDE, M.D., Editor. 
" ---- --- 
In consequence of the great increase in the number of subscribers to the American Journal of Obstetrics 
© the past year or two, the Publishers take pleasure in announcing that, beginning with January, 1878 (Vol. XI., 
No. 1.), they will permanently increase each number by fifty additional pages, thus giving its subscribers annually 
** about 
ONE-THIRD MORE READING MATTER 
than heretofore, or, a volume of 896 large octavo pages with no change in the subscription price. 
An increased number of illustrations, both wood engravings and lithographed plates, may also be expected in 
M future volumes. 
While the prosperity of the American Journal of Obstetrics, and this consequent'Substantial evidence 
y of it, cannot fail to be gratifying to all its subscribers and other friends, the Publishers trust the Medical 
tL Profession will take this voluntary action on their part as an earnest of their desire and intention, so far as in their 
power, to make all their publications merit the liberal support which is given them. 
Subscription Price, $5.00 per year, invariably in advance. 
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WM. WOOD & CO., Publishers, 27 Great Jones St., New York. New Books Now Beady. 
SIXTH EDITION GREATLY ENLARGED. 
A HANDBOOKOFTHERAPEUTICS 
By SIDNEY RINGER, M.D., 
Prof. of Therapeutics in University College; Physician to University College Hospital. 
In one 8vo volume, handsomely bound in extra muslin. Price, - - - - $4.50 
V The author has selected everything of substantial value among the but we are also sure that, from the mass of valuable, readable, and 
recent advances in Therapeutics. , It is a practical work, replete with welt-arranged information it contains, and the numberless minor prac- 
interesting and reliable information, and will be found to be,one which tical hints scattered throughout its pages, the work will be almost 
can be consulted by the practitioner with much, benefit We would equally useful to the busy practitioner; and that it will receive from 
advise every young physician to procure and read the book. It fills all the profession generally the warm welcome which j it deserves."- 
the author claims for it in letter and spirit, and is written in such a British Med. now. 
clear and simple style that all who read it will do so with pleasure."- , , ... ... . ', 
Western Lancet ' • We can scarcely doubt that the present edition will be quickly sold." 
"The author, as we have said, designed the book simply as an in- 
troduction to Therapeutics for the' use of students and young practi- " A very suggestive and useful work on Therapeutics."-St. Louis 
tioners. That to such it will be found most useful there is no doubt; Med. and Surg. Journal. 
SENT BY MAID, POSTPAID, ON RECEIPT OE PRICE. 
THE ELEMENTS OF THERAPEUTICS. 
A Clinical Guide to the Action of Medicines. 
By DR. C. BINZ, 
Professor of Pharmacology in the University of Bonn. 
Translated from, the Rifth German Edition, and, edited,, with additions, in conformity with the 
British and American Pharmacopoeias. 
By EDWARD I. SPARKS, M.A., M.B., Oxon., 
Member of the Royal College of Physicians of London, Officicr de Sant6 (Alpes Maritimes),. France, formerly Radcliffe Travelling Fellow. 
NOTICES OF THE PRESS. 
The Detroit Lancet says- it is "more trustworthy than the average The Virginia Med. Monthly says: " It is a most valuable work to 
text-book." every teacher; it is no less valuable to the student and to the general 
The Medical Record says: " We rise from a careful perusal of this practitioner ; it will give definite information, and often afford sugges- 
work with feelings of extreme satisfaction. It has not been our tions of practical value not found elsewhere.' 
fortune for a longtime to study a work in which it was evident that New Remedies says: "We are much mistaken if the work in its 
the author was so completely conversant with his subject, and had so prescnt; shape does not become a general favorite with both students 
thoroughly sifted the materials of which he was to make use. We do ,and practitioners. The reputation which Dr. Binz has acquired as an 
not hesitate to recommend it in the strongest manner. observer and writer on therapeutics should prevent any doubt regarding 
The American Practitioner says: "A book in every respect excellent." the valuable character of this work." 
In one handsome 12mo volume, bound in.extra muslin, price $2.00. Sent by mail, free of 
postage, on receipt of price. 
QU -A.I IT'S 
ELEMENTS OF ANATOMY. 
THE EIGHTH EDITION. 
Re-edited by WILLIAM SHARPEY, M.D., LL.D., F.R.S., L. & E., Emeritus Professor of Anatomy and 
Physiology in University College, London; ALLEN THOMSON, M.D., LL.D., F.R. S., L. & E., 
Professor of Anatomy in the University of Glasgow; and EDWARD ALBERT 
SCHAFER, Assistant Professor of Physiology in University College, London. 
ILLUSTRATED BY UPWARDS OF 950 ENGRAVINGS ON WOOD. 
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NOW PUBLISHING IN MONTHLY PARTS, 
AT A SUBSCRIPTION P RIC R OF $3.00 PER Y E A U . 
STUDIES 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professdr of Pathology and Practice of Medicine in the College of Physicians and Snrgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital I 
Visiting Physician and Curator of Bellevue Hospital, j 
I NT ROYAL OCTAVO FARTS., 
Each contains from two to five full-page Lithographic Plates in tint, ^and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. I. contained- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the fascia of a dog's leg; magnified 
750 diameters. 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg; 
magnified 1,500 diameters. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; 
magnified 750 diameters. 
Subscription Price, $5.00 a Year. 
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Single Numbers, 50 cents. 
S T U D I E S 
IN 
pathological 2k na hi nip 
BY 
FBANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
Ko. 3. 
APRIL, 1878. 
NEW YORK 
w:mi. woop & co. 
27 Great Jones Street 
1878 ANNOUNCEMENT. 
Over 200 pages additional Heading Matter in a year, 
with no change in price, making two royal 
* octavo volumes of 520 pages each. 
"The Medical Record. 
A Weekly Journal of Medicine and Surgery. 
: '-- 
g Edited by GEORGE F. SHRADY, A.M., M.D. 
The publishers have the pleasure of announcing that, beginning with the first number for January, 1878, 
The Medical Record will be enlarged by the addition of four pages each week, amounting to 
§ OVER 200 PAGES ADDITIONAL READING MATTER 
Q In a year-with NO change in price. This very great increase in the size of the journal has been rendered 
possible by the large advertising patronage enjoyed by it, and is a direct benefit to subscribe s from this source. 
gj An increased number of advertising pages never costs subscribers any thing, never encroaches upon the reading 
TJ matter, which is invariably the same each week, and should always be viewed by readers with satisfaction, as an 
evidence of the prosperity of the journal, and its greater ability to provide for them. 
S "THE MEDICAL RECORD" 
For 1878 will, therefore, consist of Two Royal Octavo Volumes of 520 pages each. Subscription price, 
23 $5.00 per year, invariably in advance. 
© The Volume commences January 1st. 
This Journal, now in its thirteenth volume, is published on Saturday of each week ; each number consists of 
twenty super-royal octavo pages, double columns, and contains Original Articles from the first men of the country 
" in their respective departments, Reports of Lectures, Societies, and Hospital; an account; of the Progress of 
Medical Science throughout the world ; Editorial Articles on Current Topics of Interest, Reviews and Notices of 
Q Books, Correspondence. New Instruments, Medical News and Items, &c., &c. < 
It is the only WEEKLY MEDICAL JOURNAL published in New York. 
The Medical Record is intended to be thoroughly Cosmopolitan in its character, representing the interests of 
the profession in all parts of the country. It is entirely independent of all parties or cliques. Its object is to 
■J present to the profession a faithful record of the existing state of medical science in all its departments; and, as 
H it is more especialy intended to meet the wants of the general practitioner, the articles published in its columns 
are thoroughly practical in their character. 
SPECIMEN COPY SENT FREE. 
^2 _____ ___________________._______♦ ___ 
£ An increase of 200 pages additional Reading Matter 
in a year will be made in 
-The American Journal of Obstetrics 
« And Diseases of Women and Children. 
& --- ,-- • • ' 
© PAUL F. MUNDE, M.D., Editor. 
A • , 
In consequence of the great increase in the number of subscribers to the American Journal of Obstetrics 
q the past year or two, the Publishers take pleasure in announcing that, beginning with January, 1878 (Vol. NT , 
No. 1.), they will permanently increase each number by fifty additional pages, thus giving its subscribers annually 
f al'°Ut ONE-THIRD MORE READING MATTER 
w 
than heretofore, or, a volume of 896 large octavo pages with no change in the subscription price. 
An increased number of illustrations, both wood engravings and lithographed plates, may also be expected in 
H future volumes. 
SB While the prosperity of the American Journal of Obstetrics, and this consequent substantial evidence 
of it, cannot fail to be gratifying to all its subscribers and other friends, the Publishers trust the Medical 
b Profession will take this voluntary action on their part as an earnest of their desire and intention, so far as in their 
power, to make all their publications merit the liberal support which is given them. 
Subscription Price, $5.00 per year, invariably in advance. 
|[[^If any subscriber has a friend to whose notice he would like to commend the Journal, the Publishers will 
be pleased to mail a Specimen Copy to any address furnished them. 
WM. WOOD & CO., Publishers, 27 Great Jones St., New York. Works of Prof. Alfred L. Loomis, M.D., 
Professor of Pathology and Practical Medicine in the Medical Department of the University of the City of New York; consulting 
Physician to the Charity Hospital, to the Bureau of Out-Door Relief, to the North-Western Dispensary, to the 
Central Dispensary; Late Visiting Physician to the Blackwell's Island Peyer Hospital; 
Visiting Physician toBellevuc Hospital, to the Mount Sinai Hospital, &c., &c. 
LESSONS IN 
Physical Diagnosis. 
THIRD EDITION. REVISED AND ENLARGED. 
In one handsome octavo volume, cloth, $3.00. 
NOTICES OF THE PRESS. 
" The previous editions of this volume have been very well received, "This is a work already well and favorably known to the profession, 
and, from their ready sale, appear to meet a well-recognized want. In the present edition the original text has been entirely revised and 
. . . We find the plan of the work excellent, and, within the limits enlarged by the addition of five new lessons,"-Chicago Medical 
proposed by the author, very well carried out. It would be easy to Examiner. 
point out many omissions; completeness and conciseness to a certain 
degree exclude each other; but in the space assumed, it would be difti- " Students of medicine and practitioners will find this just the work 
cult to include a greater variety and amount of sound teaching. The to meet their wants on the subjects of which it treats. Its instructions 
style is compact, clear, positive, and exact. It is free from all irrelevant are full and very plain."-Cincinnati Medical News. 
discussions ; nothing is allowed to disturb or confuse the distinct image 
of clinical facts. . . . The book is very creditable to its acute and "The previous editions of the work, confined to an exposition of the 
industrious author; and whoever shall practically master its contents subject of physical exploration of the chest and abdomen, we have 
cannot fail to be a discriminating and well-furnished diagnostician."- regarded as among the very best works on the subject extant, and hence 
The Medical Record. recommended 'Loomis on Physical Diagnosis' to our classes; and it 
"For students it is the best work on physical diagnosis that is gives us pleasure to repeat, in this form, our hearty commendation of 
published."-Detroit Review of Medicine. the book."-Mich. University Medical Journal. 
LECTURES ON 
Diseases of the Respiratory Organs, 
HEART AND KIDNEYS. 
In one handsome octavo volume of over 550 pages. Price, in extra muslin, $5.00; or, in leather, $6.00. 
NOTICES OF THE PRESS. 
" It is clear in style, convential in arrangement, very definite and here committed to the press is the result of much learning, sound 
practical in its teachings."-Philadelphia Medical times. judgment, and thorough experience "-American Practitioner. 
" We like the systematic method in which these lectures are arranged, ' '^e.have no hesitation in pronouncing it one of much value to the 
and regard them as excellent in every way."-Cincinnati Lancet and profession, and highly creditable to the author. New York. Medical 
Observer ' Journal. 
T .. , "While the views presented are fully up to what is actually known 
'By all means buy Loomis work and study it. Ohio Medical and on the subjects treated, the doctrines are judicious and safe. At the 
Surgical Reporter. same time they are presented with unusual clearness, and with sufficient 
" In the one before us the reader may look confidently for the last positiveness to command confidence."-New Orleans Medical and 
words on the subject, and may rest assured that what the author has Surgical Journal. 
LECTUBE8 OjN 
Fh h"b "TT 1Epi "M ' > CZ 
J_JI Jiri J rJL Wtar M 
In one handsome octavo volume. Cloth, $4.00; Sheep, $4.75. 
NOTICES OF THE PRESS. 
"We have before us, therefore, a book containing statements of prac- will well repay careful study."- Western Lancet, January, 1878. 
tical facts relating to certain diseases, and the theories regarding their "The work is clearly and concisely written, and will be useful and 
nature, mode of origin and propagation, and arranged so as to be easily acceptable to both student and practitioner."-N. Y. Medical Journal 
comprehended by the medical student. We also believe they will be March, 1878. ' 
read without weariness by the daily practitioner. . . , It contains "In this interesting volume, which contains the lectures on fevers 
much practical knowledge, and cannot fail to be read by a very large delivered by Professor Loomis to his class during the last year we 
proportion of the medical profession; for a concise statement of facts- have a concise and impartial review of the literature concerning fevers 
with only such qualifications as can be safely indulged in without which has been published since 1850 with reference to a few older 
endangering perspicuity-is always acceptable."-The Medical Record, books, 'because they contain many of the so-called new theories and 
Nov. 24, 1877. modes of treating fevers.' In this are embodied the results of the. 
" This last work of Professor Loomis' is a valuable contribution to author's own extensive clinical experience, w'hich has led him to form 
medical literature. His treatment of the subject is mainly.practical, opinions in certain respects at variance with these of some other 
and is in strict conformity with what the author has himself observed observers; and the weak points of theories and modes of practice which 
at the bedside. The general management of fever is justly regarded of have not stood the test of time, are clearly set forth." Boston Medical 
greater importance than the administration of drags. It is a book that and Surgical Jdwnal, Dec. 22, 1877. 
Sent by mail, post-paid, on receipt of price. '' ' 
WM. WOOD & CO,, Publishers, 27 Great Jones St., New York. ANNO_ UNCEMENY 
NOW PUBLISHING IN MONTHLY PARTS, 
AT A SUBSCRIPTION PRICE OF $0.00 FER YEAR. 
STUDIES 
I n" 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospitalg 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCT AYO FARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. I. contains- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the fascia of a dog's leg; magnified 
750 diameters. 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg; 
magnified 1,500 diameters. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; 
magnified 750 diameters. 
No. 2 contains- 
THE PLEURA. 
Plate 4. Pleura of Dog. 
Plate 5- Endothelium and Branching Connective Tissue Cells from Pleura of Dog. 
Plate 6. Endothelium of Human Pleura. 
Plate 7. Lymphatics of the Parietal Pleura of the Dog. 
Plate 8. Lymphatic Spaces and Connective Tissue Cells, from the Pleura of 
the Dog. 
Sub scription Price, $5,00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. ^"Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
S T U D I E S 
IN 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE, OF PHYSICIANS AND SURGEONS 
No. 4. 
MAY, 1878. 
NEW YORK 
WM. W O O ID & CO. 
27 Great Jones Street 
1878 ANNOUNCEMENT.^* 
Over 200 pages additional Beading Matter in a year, 
with no change in price, making two royal 
K octavo volumes of 520 pages each. 
I The Medical Record. 
A Weekly Journal of Medicine and Surgery. 
J Edited by GEORGE F. SHRADY, A.M., M.D. 
55 - ~ - 
The publishers have the pleasure of announcing that, beginning with the first number for January, 1878, 
g The Medical Record will be enlarged by the addition of four pages each week, amounting to 
ri OVER 200 PAGES ADDITIONAL READING MATTER 
2 In a year-with NO change in price. This very great increase in the size of the journal has been rendered 
B possible by the large advertising patronage enjoyed by it, and is a direct benefit to subscribers from this source. 
An increased number of advertising pages never costs subscribers any thing, never encroaches upon the reading 
g matter, which is invariably the same each week, and should always be viewed by readers with satisfaction, as an 
evidence of the prosperity of the journal, and its greater ability to provide for them . 
* "THE MEDICAL RECORD" 
For 1878 will, therefore, consist of Two Royal Octavo Volumes of 520 pages each. Subscription price, 
$5.00 per year, invariably in advance. 
q Tlie Volume commences January 1st. 
ri This Journal, now in its thirteenth volume, is published on Saturday of each week ; each number consists of 
twenty super-royal octavo pages, double columns, and contains Original Articles from the first men of the country 
g in their respective departments, Reports of Lectures, Societies, and Hospital; an account of the Progress of 
Medical Science throughout the world ; Editorial Articles on Current Topics of Interest, Rwiews and Notices of 
Book«, Correspondence. New Instruments, Medical News and Items, &c., &c. 
B It is the only WEEKLY MEDICAL JOURNAL published in New York. 
ill The Medical Record is intended to be thoroughly Cosmopolitan in its character, representing the interests of 
the profession in all parts of the country. It is entirely independent of all parties or cliques. Its object is to 
g present to the profession a faithful record of the existing state of medical science in all its departments; and, as 
m it is more especialy intended to meet the wants of the general practitioner, the articles published in its columns 
™ are thoroughly practical in their character. 
SPECIMEN COPY SENT FREE. 
ri : u u. . 
> An increase of 200 pages additional Beading Matter 
in a year will be made in 
3The American Journal of Obstetrics 
m And Diseases of Women and Children. 
| PAUL F. MUNDE, M.D., Editor. 
In consequence of the great increase in the number of subscribers to the American Journal of Obstetrics 
the past year or two, the Publishers take pleasure in announcing that, beginning with January, 1878 (Vol. XI., 
Q No. 1.), they will permanently increase each number by fifty additional pages, thus giving its subscribers annually 
ab0Ut ONE-THIRD MORE READING MATTER 
ri than heretofore, or, a volume of 896 large octavo pages with no change in the subscription price. 
An increased number of illustrations, both wood engravings and lithographed plates, may also be expected in 
g future volumes. 
aWhile the prosperity of the American Journal OF Obstetrics, and this consequent substantial evidence 
of it, cannot fail to be gratifying to all its subscribers and other friends, the Publishers trust the Medical 
ri Profession will take this voluntary action on their part as an earnest of their desire and intention, so far as in their 
b power, to make all their publications merit the liberal support which is given them. 
Subscription Price, $5.00 per year, invariably in advance. 
[gplf any subscriber has a friend to whose notice he would like to commend the Journal, the Publishers will 
be pleased to mail a Specimen Copy to any address furnished them. 
WM. WOOD & CO., Publishers, 27 Great Jones St., New York. Works on Materia Medica and Therapeutics. 
THE ESSENTIALS OF MATERIA MEDICA AND THERAPEUTICS. 
By ALFRED BARING GARROD, M.D., F.R.S., Fellow of the Royal College of Physicians, etc., etc. 
Second edition, revised and much enlarged. One handsome volume, extra muslin. Price $4.00. 
"The work of Dr. Garrod supplies a want that has long been felt on peutics, leaving it to larger works to enter into details."-Medical and 
this side of the Atlantic. The editor has confined himself to supplying Surgical Reporter. 
a few of the omissions of Dr. Garrod, and to indicating where a differ- 
ence exists in the preparations of the Pharmacopoeia of the United "We have here a brief resume of Materia Medica, all non-essential 
States. His aim has been to make such additions only as are strictly, parts being omitted. It might be called a commentary on the Pharma- 
necessary for the American student. copoeia, as it somewhat resembles Phillips' commentary on the London 
"The author of this book has succeeded admirably in placing in con- Pharmacopoeia, though more extended in its descriptions of the action 
else form what is necessary to be known of Materia Medica and Thera- and uses of remedies."-Eclectic Medical Journal. 
A YEAR-BOOK OF THERAPEUTICS, PHARMACY, AND ALLIED SCIENCES. 1872 & 1873. 
By H. C. WOOD, Jr., M.D. 
In handsome octavo volumes, hound in extra muslin. Price $2.50 each. 
This "Year-Book" is made up from the pages of " New Remedies," and contains all the more important 
articles which have appeared in that journal during the past year, together with a few new ones. It will be pub- 
lished annually for the benefit of those who prefer to purchase the very valuable material it contains in this form 
rather than in unbound numbers as a periodical. A complete index has been added. 
SIXTH EDITION-GREATLY ENLARGED. 
A HANDBOOK OF THERAPEUTICS. 
By SIDNEY RINGER, M.D., Prof, of Therapeutics in University College ; Physician to University College Hospital.' 
In one Svo volume, ' handsomely hound in extra muslin. Price $4.50. 
■' The author has selected everything of substantial value among the but we are also sure that, from the mass of Valuable, readable, and 
recent advances in Therapeutics. It is a practical work, replete with well-arranged information it contains, and the numberless minor prac- 
interesting and reliable information, and will be found to be one which tical hints scattered throughout its pages, the work will be almost 
can be consulted by the practitioner with much benefit. We would equally useful to the busy practitioner; and that it will receive from 
advise every young physician to procure and read the book. It fills all the profession generally the warm welcome which it deserves."-, 
the author claims for it in letter and spirit, and is written in such a British Med. Jour. 
clear and simple style that all who read it will do so with pleasure."- (l We scarcely doubt that the present edition will be quickly sold? 
11 estern Lancet. 
"The author, as we have said, designed the book simply as an in- 
troduction to Therapeutics for the use of students and young practi- "Avery suggestive and useful work on therapeutics." St. Louin 
tioners. That to such it will be found most useful there is no doubt; Med. and Surg. Journal. 
THE ELEMENTS OF THERAPEUTICS. 
A CLINICAL. GUIDE TO THE ACTION OF MEDICINES. 
By Dr. O. BINZ, Professor of Pharmacology in the University of Bonn. 
Translated from the Fifth German Edition, and edited, with additions, in conformity with the British and American Pharmacopoeias. 
By EDWARD I. SPARKS, M.A., M.B., Oxon. 
Member of the Royal College of Physicians of London, Offlcier de Saute (Alpes Maritimes), France, formerly Radcliffe Travelling Fellow. 
In one handsome X2mo volume, bound in extra muslin, price $2.00. Sent by mail, free of postage, on receipt of price. 
" This work contains much valuable information, especially in regard " The book is in every respect excellent. It is a judicious condensa- 
te those remedies which exert an influence on the nervous system,"- tion of practical, useful facts, educed from physiological experiment 
St. Louis Med. de. Surg. Journal, Feb., 1878. and clinical observation."-Am. Practitioner, Feb., 1878. 
"The desire to know how a medicine acts is just beginning to attract "The most striking features of the work are the conciseness with 
the attention it deserves. This work gives a clear description of the which the author expresses what is known on each subject, and a style 
therapeutical action of medicines in a way that is sure to command which gives the subjects a freshness not commonly found in text-books 
attention and cause a more thorough investigation in this branch."- on therapeutics, or in lectures on this topic."-A ew Remedies, Jan.,1878. 
Cincinnati Lancet and Observer, Feb., 1878. " It is, on the whole, more trustworthy than the average text-book. 
"The work appears to have been written with great care, and bears In fact there is little in it that should be neglected by the medical 
the impress of reliability ; and is a volume that we do not hesitate to re- student. We regret that such a work was not available during our own 
commend in the strongest manner."-The Medical Record, J an. 12,1878. student days."-Detroit Lancet, Feb., 1878. 
STUDIES IN PATHOLOGY AND THERAPEUTICS. 
By SAMUEL HENRY DICKINSON, M.D , LL.D., Professor of Practice of Physic in Jefferson Medical College, Philadelphia, etc,, etc. 
In one handsome 12»zo volume, neatly hound in extra muslin. Price $1.50. 
"Mr. Dickson may be styled a medical philosopher, in the best sense bigoted affection for the old, nor any shallow, pedantic passion for the 
of the term. He thinks independently, and has done a vast amount of new. We give his book a hearty recommendation to our medical 
good thinking in the 200 pages composing the ' Studies? There are brethern. They will rise from its perusal informed and refreshed."- 
few writers who find the middle way so successfully. He, shows no Pacific Medical and^Surgical Journal. 
ESSAYS ON INFANT THERAPEUTICS. 
To which are added Observations on Ergot; History of Ute Origin of the Use of Mercury in Inflammatory 
Complaints ; with the Statistics of the Heaths from Poisoning in Hew York, in the Years 1841-2-3. 
By JOHN B. BECK, M.D. 
Ihird Edition. One very neat duodecimo volume, muslin. Price $1.00. 
"A perfect gem. We regard it as one of the most useful books in I "An excellent little work, from the very highest authority. 
our library."--Neio Jersey Medical Reporter. I Western Lancet. 
Sent by mail, post-paid, on /receipt of price. 
WM. WOOD & CO., Publishers, 27 Great Jones Street, New York, ANNOUNCEMENT. 
NOW PUBLISHING IN MONTHLY PARTS, 
ATA SUBSCRIPTION PRICE OF $5.00 X» E It YEAH. 
STUDIES 
pathological anatomy. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IM ROYAL OCTAVO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. i. contains- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the facia of a dog's leg; magnified 750 diameters 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg ; magnified 1,500 
diametres. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; magnified 750 
diameters. 
No. 2 contains- 
THE PLEURA. 
Plate 4. Pleura of Dog. 
Plate 5. Endothelium and Branching Connective Tissue Cells from Pleura of Dog. 
Plate 6. Endothelium of Human Pleura. 
Plate 7. Lymphatics of the Parietal Pleura of the Dog. 
Plate 8. Lymphatic Spaces and Connective Tissue Cells, from the Pleura of the Dog. 
No. 3 contains- 
THE INFLAMMATIONS OF THE PLEURA. 
Plate 9. Pleurisy of the Dog, 24 hours, New Cells. 
Plate 10. Pleurisy of the Dog, 3d day, Layer of Cells and Fibrine. 
Plate 11. Pleurisy of the Dog, 5th day, Layers of New Tissue. 
Plate 12. Pleurisy of the Dog, 7-9 days, New Endothelial and Connective Tissue Cells. 
Subscription Price, $5.00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. 2^ Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
STUDIES 
IN 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE. 
COLLEGE OF PHYSICIANS AND SURGEONS - 
No. 5. 
JUNE, 1878. 
NEW YORK 
■W^ZC. WOOD & CO. 
27 Great Jones Street 
1878 ^ANNOUNCEMENT.^ 
Over 200 pages additional Heading Matter in a year, 
with no change in price, making two royal 
$ octavo volumes of 520 pages each. 
" The Medical Record. 
A Weekly Journal of Medicine and Surgery. 
g Edited by GEORGE F. SHRADY, A.M., M.D. 
The publishers have, the pleasure of announcing that, beginning with the first number for January, 1878, 
The Medical Record will be enlarged by the addition of four pages each week, amounting to 
J OVER 200 PAGES ADDITIONAL READING MATTER 
Q In a year-with NO CHANGE IN price. This very great increase in the size of the journal has been rendered 
possible by the large advertising patronage enjoyed by it, and is a direct benefit to subscribers from this source. 
An increased number of advertising pages never costs subscribers any thing, never encroaches upon the reading 
ri matter, which is invariably the same each week, and should always be viewed by readers yith satisfaction, as an 
evidence of the prosperity of the journal, and its greater ability to provide for them. 
§ "THE MEDICAL RECORD" 
For 1878 will, therefore, consist of Two Royal Octavo Volumes of 520 pages each. Subscription price, 
J2 $5.00 per year, invariably in advance. 
© The Volume commences January 1st. 
This Journal, now in its thirteenth volume, is published on Saturday of each week ; each number consists of 
_ twenty super-royal octavo pages, double columns, and contains Original Articles from the first men of the country 
ri in their respective departments, Reports of Lectures, Societies, and Hospital; an account of the Progress of 
Medical Science throughout the world ; Editorial Articles on Current Topics of Interest, Reviews and Notices of 
g Book«, Correspondence. New Instruments, Medical News and Items, &c., &c. 
J It is the only WEEKLY MEDICAL JOURNAL published in New York. 
The Medical Record is intended to be thoroughly Cosmopolitan in its character, representing the interests of 
the profession in all parts of the country. It is entirely independent of all parties or cliques. Its object is to 
ri present to the profession a faithful record of the existing state of medical science in all its departments; and, as 
■£ it is more especialy intended to meet the wants of the general practitioner, the articles published in its columns 
are thoroughly practical in their character. 
ri SPECIMEN COPY SENT FREE. 
ri . 
£ An increase of 200 pages additional Reading Matter 
in a year will be made in 
(The American Journal of Obstetrics 
- And Diseases of Women and Children, 
ri 
© PAUL F. MUNDE, M.D., Editor. 
ri ---•--- , 
In consequence of the great increase in the number of subscribers to the American Journal of Obstetrics 
a the past year or two, the Publishers take pleasure in announcing that, beginning with January, 1878 (Vol. XI., 
ri No. 1.), they will permanently increase each number by fifty additional pages, thus giving its subscribers annually 
? ab0Ut ONE-THIRD MORE READING MATTER 
ri 
than heretofore, or, a volume of 896 large octavo pages with no change in the subscription price. 
__ An increased number of illustrations, both wood engravings and lithographed plates, may also be expected in 
ri future volumes. 
© While the prosperity of the American Journal of Obstetrics, and this consequent substantial evidence 
of it, cannot fail to be gratifying to all its subscribers and other friends, the Publishers trust the Medical 
b Profession will take this voluntary action on their part as an earnest of their desire and intention, so far as in their 
power, to make all their publications merit the liberal support which is given them. 
Subscription Price, $5.00 per year, invariably in advance. 
i(W°If any subscriber has a friend to whose notice he would like to commend the Journal, the Publishers will 
be pleased to mail a Specimen Copy to any address furnished them. 
WM. WOOD & CO., Publishers, 27 Great Jones St., New York. Works on Materia Medica and Therapeutics. 
THE ESSENTIALS OF MATERIA MEDICA AND THERAPEUTICS. 
- «\ . * By ALFRED BARING GARROD, M.D., F.R.S., Fellow of the Royal College of Physicians, etc., etc. 
Second edition, revised and much enlarged. One handsome 8vo volume, extra muslin. Price $4.00. 
" The work of Dr. Garrod supplies a want that has long been felt on peutics, leaving it to larger works to enter into details."-Medical and 
this side of the Atlantic. The editor has confined himself to supplying Surgical Reporter. 
a few of the omissions of Dr. Garrod, and to indicating where a differ- 
ence exists in the preparations of the Pharmacopceia of the United "We have here a brief resume of Materia Medica, all non-essential 
States. His aim has been to make such additions only as are strictly parts being omitted. It, might be called a commentary on the Pharma- 
necessary for the American student. cOpoeia, as it somewhat resembles Phillips' commentary on the London 
" The author of this book has succeeded admirably in placing in con- Pharmacopoeia, though more extended in its descriptions of the action 
cise form what is necessary to be known bf Materia Medica and Thera- and uses of remedies."-Eclectic Medical Journal. 
A YEAR-BOOK OF THERAPEUTICS, PHARMACY, AND ALLIED SCIENCES. 1872 4 1873. 
By H. C. WOOD, Ju., M.D. 
In handsome octavo volumes, bound in extra muslin. Price ^2.50 each. 
This "Year-Book" is made up from the pages of " New Remedies," and contains all the more important 
articles which have appeared in that journal during the past year, together with a few new ones. It will be pub- 
lished annually for the benefit of those who prefer to purchase the very valuable material it contains in this form 
rather than in unbound numbers as a periodical. A complete index has been added. 
SIXTH EDITION- GREATLY ENLARGED. 
A HANDBOOK OF THERAPEUTICS. 
By SIDNEY RINGER, M.D., Prof, of Therapeutics in University College; Physician to University College Hospital. 
In one 8vo volume, handsomely bound in extra muslin. Price $4.50. 
" The author has selected everything of substantial value among the but we are also sure that. fron<the mass of valuable, readable, and 
recent advances in Therapeutics. It is a practical work, replete with well-arranged information it Contains) and the numberless minor prac- 
interesting and reliable information, and will be found to be one which tical hints scattered throughout its pages, the work will be almost 
can be consulted by the. practitioner with much benefit. We would equally useful to the busy practitioner; and that it will receive from 
advise every young physician to procure and read the book. It fills all the profession generally the warm welcome which it deserves."- 
the author claims for it in letter and spirit, and is written in. such a British Med. Jour. 
Western L^wa. aU d0 R° Wkh ~ "We can scarcely doubt that the present edition will be quickly sold." 
"The author, as we have said, designed the book simply as an in- Pi detitioner. 
troduction to Therapeutics for the use of students and young practi- "A very suggestive and useful work on therapeutics."-St. Louis 
tioners. That to such it will be found most useful there is no doubt; Med. and Surg. Journal, 
THE ELEMENTS OF THERAPEUTICS. 
A CLINICAL GUIDE TO THE ACTION OF MEDICINES. 
By Du. 0. BINZ, Professor of Pharmacology in the University of Bonn. 
Translated from the Fifth German Edition, and edited, with additions, in conformity with the British and American Pharmacopoeias. 
By EDWARD I. SPARKS, M.A., M.B., Oxon. 
Member of the Royal College of Physicians of London, Officier de Sant6 (Alpes Maritimes), France, formerly Radcliffe Travelling Fellow. 
In one handsome 12mo volume, bound in extra muslin, price $2.00. Sent by mail, free of postage, on receipt of price. 
" This work contains much valuable information, especially in regard " The book is in every respect excellent. It is a judicious condensa- 
te those remedies which exert an influence on the nervous system."- tion of practical, useful facts, educed from physiological experiment 
St. Louis Med. ch Surg. Journal, Feb., 1878. and clinical observation."-Am. Practitioner, Feb., 1878. 
"The desire to know how a medicine acts is just beginning to attract "The most striking features of the work are the conciseness with 
the attention it deserves. This work gives a clear description of the which the author expresses what is known on each subject, and a style 
therapeutical action of medicines in a way that is sure to command which gives the subjects a freshness not commonly found in text-books 
attention and cause a more thorough investigation in this branch."- on therapeutics, or in lectures on this topic."-New Remedies, Jan..,1878. 
Cincinnati Lancet and Observer, Feb., 1878. "It is, on the whole, more trustworthy than the average text-book. 
"The work appears to have been written with great care, and bears In fact there is little in it that should be neglected by the medical 
the impress of reliability ; and is a volume that we do not hesitate to re- student. We regret that such a work was not available duripg our own 
commend in the strongest manner."-The Medical Record, Jan. 12,1878. student days."-Detroit Lancet, Feb., 1878. 
STUDIES IN PATHOLOGY AND THERAPEUTICS. 
By SAMUEL HENRY DICKINSON, M.D., LL.D., Professor of Practice of Physic in Jefferson Medical College, Philadelphia, etc., etc. 
In one handsome \%mo volume, neatly bound in extra muslin. Price $1.50. 
"Mr. Dickson may be styled a medical philosopher, in the best sense bigoted affection for the old, nor any shallow, pedantic passion for the 
of the term. Ho thinks independently, and has done a vast amount of new. We give his book a hearty recommendation to our medical 
good thinking in the 200 pages composing the 'Studies.' There are brethren. They will rise from its perusal informed and refreshed."- 
few writers who find the middle way so successfully. He shows no Pacific Medical and Surgical Journal. 
ESSAYS ON INFANT THERAPEUTICS. 
To Which are added Observations on Ergot; History of the Origin of the Use of Mercury in Inflammatory 
Complaints; wfth the Statistics of the heaths from Poisoning in New York, in the Years 1841-2-3. 
By JOHN B. BECK, M.D. . 
Third Edition. One very neat duodecimo volume, muslin. Price $1.00. 
"A perfect gem. We regard it as one of the most useful books in I "An excellent little work, from the very highest authority."- 
our library."-Neio Jersey Medical Reporter. I Western Lancet. 
Sent by mail, post-paid, on receipt of price. 
WM. WOOD & CO., Publishers, 27 Great Jones Street, New York. ANNO UNCEMENT. 
NOW PUBLISHING IN MONTHLY PARTS, 
AT A SUBSCRIPTION RR1 C E OF $5.00 PER YEAR. 
STUDIES 
PATHOLOGICAL ANATOMY. 
Bv FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCTAVO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will dorm, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. i. contains- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the facia of a dog's leg; magnified 750 diametr s 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg ; magnified 1,500 
diametres. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; magnified '750 
diameters. 
No. 2 contains- 
THE PLEURA. 
Plate 4. Pleura of Dog. 
Plate 5. Endothelium and Branching Connective Tissue Cells from Pleura of Dog. 
Plate 6. Endothelium of Human Pleura. 
Plate f Lymphatics of the Parietal Pleura of the Dog. 
Plate 8. Lymphatic Spaces and Connective Tissue Cells, from the Pleura of the Dog. 
No. 3 contains- 
THE INFLAMMATIONS OF THE PLEURA. 
Plate 9. Pleurisy of the Dog, 24 hours, New Cells. 
Plate 10. Pleurisy of the Dog, 3d day, Layer of Cells and Fibrine. 
Plate 11. Pleurisy of the Dog, 5th day, Layers of New Tissue. 
Plate 12. Pleurisy of the Dog, 7-9 days, New Endothelial and Connective Tissue Cells. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema. 
Sub scription Price, $5.00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. ^"Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
STUDIES 
I 
IN 
palhological Inatomi) 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
ISFos. 6 & 7. 
JULY & AUGUST, 1878. 
NEW YORK 
WM. WOOD & CO. 
27 Great Jones Street 
1878 B®* ANNOUNCEMENT.^® 
Over 200 pages additional Heading Matter in a year, 
with no change in price, making two royal 
* octavo volumes of 520 pc^ges each. 
" The Medical Record. 
A Weekly Journal of Medicine and Surgery. 
g Edited by GEORGE F. SHRADY, A.M., M.D. 
The publishers have the pleasure of announcing that, beginning with the first number for January, 1878, 
*■ The Medical Record will be enlarged by the addition of four pages each week, amounting to 
q OVER 200 PAGES ADDITIONAL READING MATTER 
Q In a year-with NO change in price. This very great increase in the- size of the journal has been rendered 
possible by the large advertising patronage enjoyed by it, and is a direct benefit to subscribe, s from this source. 
« An increased number of advertising pages never costs subscribers any thing, never encroaches upon the reading 
j* matter, which is invariably the same each week, and should always be viewed by readers with sa.isfaction, as an 
evidence of the prosperity of the ournal, and its greater ability to provide for them. 
§ "THE MEDICAL RECORD" 
For 1878 will, therefore, consist of Two Royal Octavo Volumes of 520 pages each. Subscription price, 
$5.00 per year, invariably in advance. 
© The Volume commences January 1st. 
This Journal, now in it^ thirteenth volume, is published on Saturday of each week ; each number consists of 
_ twenty super-royal octavo pages, double columns, and co tains Original Articles from the first men of the country 
H in their respective departments, Repjrts of Lectures, Societies, and Hospital ; an account of the Progress of 
Medical Science throughout the world ; Edito ial Articles on Current Topics of Interest, Reviews and Notices of 
Em Book-, Correspondence. New Instruments, Medical News and Items, &c., &c. 
It is the only WEEKLY MEDICAL JOURNAL published in New York. 
The Medical Record is intended to be thoroughly Cosmopolitan in its character, representing the interests of 
__ the profession in all parts of the country. It is entirely independent of all parties or cliques. Its object is to 
■■ present to the profession a faithful record of the existing state of medical science in all its departments; and, as 
PS it is more especialy intended to meet the wants of the general practitioner, the articles published in its columns 
are thoroughly practical in their character. 
SPECIMEN COPY SENT FREE. 
£ An increase of 200 pages additional Heading Matten 
in a year will be made in 
'The American Journal of Obstetrics 
£ And Diseases of Women and Children. 
& ■ ■ ~ 
© PAUL F. MUNDE, M.D., Editor. 
In consequence of the great increase in the number of subscribers to the American Journal of Obstetrics 
a the past year or two, the Publishers take pleasure in announcing that, beginning with January, 1878 (Vol. NT , 
No. 1.), they will permanently increase each number by fifty additional pages, thus giving its subscribers annually 
? ab0Ut ONE-THIRD MORE READING MATTER 
fa 
than heretofore, or, a volume of 896 large octavo pages with no change in the subscription price. 
„ An increased number of illustrations, both wood engravings and lithographed plates, may also be expected in 
2 future volumes. 
While the prosperity of the American Journal of Obstetrics, and this consequent substantial evidence 
fa of it, cannot fail to be gratifying to all its subscribers and other friends, the Publishers trust the Medical 
a Profession will take this voluntary action on their part as an earnest of their desire and intention, so far as in their 
power, to make all their publications merit the liberal support which is given them. 
Subscription Price, $5.00 per year, invariably in advance. 
gt^°If any subscriber has a friend to whose notice he would like to commend the Journal, the Publishers will 
be pleased to mail a Specimen Copy to any address furnished them. 
WM. WOOD & CO., Publishers, 27 Great Jones St., New York. Works on Materia Medica and Therapeutics. 
THE ESSENTIALS OF MATERIA MEDICA AND THERAPEUTICS. 
By ALFRED BARING- GARROD, M.D., F.R.S., Fellow of the Royal College of Physicians, etc., etc. 
Second edition, revised and much enlarged. One handsome 8vo volume, extra muslin. Price $4.00. 
" The work of Dr. Garrod supplies a want that has long been felt on peutics, leaving it to larger works to enter into details."-Medical and 
this side of the Atlantic. The editor has confined himself to supplying Surgical Reporter. 
a few of the omissions of Dr. Garrod, and to indicating where a differ- 
ence exists in the preparations of the Pharmacopoeia of the United "We have here a brief resume of Materia Medica, all non-essential 
States. His aim has been to make such additions only as are strictly parts being omitted. It might be called a commentary on the Pharma- 
necessary for the American student, copoeia, as it somewhat resembles Phillips'commentary on the London 
" The author of this book has succeeded admirably in placing in con- Pharmacopoeia, though more extended in its descriptions of the action 
cise form what is necessary to be known of Materia Medica and Thera- and uses of remedies"--Eclectic Medical Journal. 
A YEAR-BOOK OF THERAPEUTICS, PHARMACY, AND ALLIED SCIENCES. 1872 i 1873. 
By H. C. WOOD, Jr., M.D. 
In handsome octavo volumes, bound in extra muslin. - Price $2.50 each. 
This "Year-Book" is made up from the pages of "New Remedies," and contains all the more important 
articles which have appeared in that journal during the past year, together with a few new ones. It will be pub- 
lished annually for the benefit of those who prefer to purchase the very valuable material it contains in this form 
rather than in unbound numbers as a periodical. A complete index has been added. 
SIXTH EDITION- GREATLY ENLARGED. 
A HANDBOOK OF THERAPEUTICS. 
By SIDNEY RINGER, M.D., Prof, of Therapeutics in University College; Physician to University College Hospital. 
In one 8vo volume, handsomely bound in extra muslin. Prive $4.50. 
" The author has selected everything of substantial value among the but we are also sure that, from the mass of valuable, readable, and 
recent advances in Therapeutics. It is a practical work, replete with well-arranged information it contains, and the numberless minor prac- 
interesting and reliable information, and will be found to be one which tical hints scattered throughout its pages, the work will be almost 
can be consulted by the practitioner with much benefit. We would equally useful to the busy practitioner; and that it will receive from 
advise every young physician to procure and read the book. It fills all the profession generally the warm welcome which it deserves."- 
the author claims for it in letter and spirit, and is written in such a British Med. Jour. 
^esttrnSa. - "Wb can scarcely doubt that the presentedition will be quickly sold." 
"The author, as we have said, designed the book simply as an in- ^lie I''ariitionei • 
troduction to Therapeutics for the use of students and young practi- "A very suggestive and useful work on therapeutics."-St. Louie 
tioners. That to such it will be found most useful there is no doubt; Med. and Surg. Journal. 
THE ELEMENTS OF THERAPEUTICS. 
A CLINICAL GUIDE TO THE ACTION OF MEDICINES. 
By Dr. C. BINZ, Professor of Pharmacology in the University of Bonn. 
Translated from the Fifth German Edition, and. edited, with additions, in conformity with the British and American Pharmacopoeias. 
By EDWARD I. SPARKS, M.A., M.B., Oxon. 
Member of the Royal College of Physicians of London, Offlcier de Sant6 (Alpes Maritimes), France, formerly Radcliffe Travelling Fellow. 
in one handsome VZmo volume, bound in extra muslin, 'price $2.00. Sent by mail, free of postage, on receipt of price. 
" This work contains much valuable'infonnation, especially in regard " The book is in every respect excellent. It is a judicious condensa- 
to those remedies which exert an influence on the nervous system."- tion of practical, useful facts, educed from physiological experiment 
St. Louis Med. dk Surg. Journal, Feb., 1878. and clinical observation."-Am. Practitioner, Feb., 1878. 
"The desire to know how a medicine acts is just beginning to attract "The most striking features of the work are the conciseness with 
the attention it deserves. This work gives a clear description of the which the author expresses what is known on each subject, and a style 
therapeutical action of medicines in a way that is sure to command which gives the subjects a freshness not commonly found in text-books 
at'ention and cause a more thorough investigation in thjs branch."- on therapeutics, or in lectures on this topic."-New Remedies, Jan.,1878. 
Cincinnati Lancet and Observer, Feb., 1878. " It is, on the whole, more trustworthy than the average text-book. 
■ "The work appears to have been written with great care, and bears In fact there is little in it that should be neglected by the medical 
the impress of reliability; and is a volume that we do not hesitate to re- student. We regret that such a work -was not available during our own 
commend in the strongest mariner.":-The Medical Record, Jan. 12,1878. student days."-Detroit Lancet, Feb., 1878. 
STUDIES IN PATHOLOGY AND THERAPEUTICS. 
By SAMUEL HENRY DICKINSON, M.D., LL.D., Professor of Practice of Physic in Jefferson Medical College, Philadelphia, etc., etc. 
Iii one handsome \2mo volume, neatly bound in extra muslin. Price $1.50. 
" Mr. Dickson may be styled a riiedical philosopher, in the best sense bigoted affection for the old, nor any shallow, pedantic passion for the 
of the term. He thinks independently, and has done a vast amount of new. We give his book a heart/ recommendation to our medical 
good thinking in the 200 pages composing the* Studies.' There are brethren. They will rise from its perusal informed and refreshed."- 
few writers who find the middle way so successfully. He shows no Pacific Medical and Surgical Journal. 
ESSAYS ON INFANT THERAPEUTICS. 
To which are added Observations on Ergot; History of the Origin of the Use of Mercury in Inflammatory 
Complaints ; with the Statistics of the Deaths from Poisoning in New York, in the Years 1841-2-3. 
By JOHN B. BECK, M.D. 
Third Edition. One very neat duodecimo volume, muslin. Price $1.00. 
"A perfect gem. We regard it as one of the most useful books in I "An excellent little work, from the very highest authority."- 
our library."-New Jersey Medical Reporter. | Western Lancet. 
Sent by mail, post-paid, on receipt of price. 
WM. WOOD & CO., Publishers, 27 Great Jones Street, New York. ANNOUNCEMENT^ 
NOW PUBLISHING IN MONTHLY PART'S, 
AT A STJBSCRIT'TIOJV P R I C B O 1? S 5 . OIO T> Id R V TP. A R 
STUDIES 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
I JN ROYAL OCTAVO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy df exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. i. contains- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the facia of a dog's leg ; magnified 750 diameters 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg ; magnified 1,500 
diametres. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; magnified 750 
■ diameters. 
No. 2 contains- 
THE PLEURA. 
Plate 4. Pleura of Dog. 
Plate 5. Endothelium and Branching Connective Tissue Cells from Pleura of Dog. 
Plate 6. Endothelium of Human Pleura. 
Plate 7. Lymphatics of the Parietal Pleura of the Dog. 
Plate 8. Lymphatic Spaces and Connective Tissue Cells, from the Pleura of the Dog. 
No. 3 con tain s-- 
THE INFLAMMATIONS OF THE PLEURA. 
Plate 9. Pleurisy of the Dog, 24 hours, New Cells. 
Plate 10. Pleurisy of the Dog, 3d day, Layer of Cells and Fibrine. 
Plate 11. Pleurisy of the Dog, 5th day, Layers of New Tissue. 
Plate 12. Pleurisy of the Dog, 7-9 days, New Endothelial and Connective Tissue Cells. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema. 
No. 5 contains- 
INFLAMMATIONS OF THE PLEURA. 
Plate 16. Endothelial Cells in Hydrothorax. 
Plate if Chronic Pleurisy with Adhesions. 
Plate 18. Verticle Section of the Pleura. Tubercular Pleurisy. 
Subscription Price, $5.00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. Up-Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
STUDIES 
, ' IN 
^pathological Jnatumg 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
No. 8. 
SEPTEMBER, 1878. 
NEW YORK 
WM. WOOD & CO. 
27 Great Jones Street 
1878 IMPORTANT ANNOUNCEMENT. 
For many years past Messrs. Wm. Wood & Co. have had under consideration the 
feasibility of reproducing books, especially of foreign authors, in good style, and yet at 
prices greatly less than heretofore attempted. The high cost of labor, and of all the 
materials used in the manufacture of books, has been an insuperable obstacle. Even now 
it would be impossible to carry out systematically any such idea if the ordinary methods of 
trade were depended upon. 
It is believed that the medical profession will welcome and generously sustain any 
well-directed effort of such character, and, consequently, the following scheme has been 
prepared with much care, and is respectfully submitted for their approval and support: 
WOOD'S LIBRARY 
OF 
Standard Medical Authors. 
Messrs. Wm. Wood & Co. have the pleasure of announcing that in January, 1879, 
they will begin the publication of Medical Books by the most distinguished modern and 
standard authors, in monthly volumes of from 200 to 300 pages and upwards, handsomely 
and strongly bound, at the merely nominal price of One Dollar each. 
Estimating from the regular prices of the books so far selected for publication in 1879, 
subscribers to this Library will obtain about 
FIFTY DOLLARS' WORTH OF MEDICAL BOOKS 
FOR 
TWELVE DOI EARS. 
These books will be printed on handsome cream-laid paper, with broad-faced long 
primer type. Wood engravings and plates will be freely used whenever required. 
With the type and size of page adopted, it will frequently be possible to reproduce 
in one of these monthly volumes, an ordinary book of 400 to 500 pages, and costing from 
$4.00 to $6.00. 
^TERMS OF SALE: ' 
As can readily be understood, it would be impossible to publish books upon this plan 
without a very large assured sale for each volume. Wood's Library of Standard Medical 
Authors will, therefore, be sold 
BY SUBSCRIPTION ONLY ATLTWELVE DOLLARS A YEAR. 
^PAYABLE INVARIABLY .IN ADVANCE. 
Subscriptions must be ^r a complete year. The volumes of this Library will not 
be sold separately. 
■jy See third page of cover. THE FOLLOWING WILL BE PUBLISHED IN 1879: 
ojxt 
REST AND PAIN. 
A COURSE OF LECTURES 
ON THE INFLUENCE OF MECHANICAL AND PHYSIOLOGICAL REST IN THE TREATMENT OF 
ACCIDENTS AND SURGICAL DISEASES AND THE DIAGNOSTIC VALUE OF PAIN. 
By JOHN HILTON, F.R.S., F.R.C.S. 
Edited by W. H. A. JACOBSON, F.R.C.S. 
This valuable work will make a volume in this Library of over 300 pages. It is profusely illustrated by 
ONE HUNDRED AND NINE FINE WOOD ENGRAVINGS. 
DISEASES OF THE INTESTINES AND PERITONEUM. 
COMPRISING ARTICLES ON 
Enteralgia, by JOHN RICHARD WARDELL, M.D.; Enteritis, Obstruction of the Bowels, Ulceration of the 
Bowels, Cancerous and other Growths of the Intestines, Diseases of the C^cum and Appendix Vermi- 
formis, by JOHN SYER BRISTOWE, M.D.; Colic, Colitis and Dysentery, by J. WARBURTON BEGBIE, 
M.D.; Diseases of the Rectum and Anus, by THOMAS BLIZZARD CURLING, F.R.S.; Intestinal 
Worms, by W. H. RANSOM, M.D.; Peritonitis, by JOHN RICHARD WARDELL, M.D.; 
Tubercle of the Peritoneum, Carcinoma of the Peritoneum, Affections of the 
Abdominal Lymphatic Glands and Ascites, by JOHN SYER BRISTOWE, M.D. 
f Taken from Reynolds' System of Medicine.) 
These articles will make a volume in this Library of about 250 pages, with numerous illustrations. 
A PRACTICAL MANUAL 
OF the 
DISEASES OF CHILDREN. 
MITII A FORMULARY. 
By EDWARD ELLIS, M.D. 
THIRD EDITION. 
This book will make a volume in this Library of about 270 pages. 
DISEASES OF WOMEN. 
By LAWSON TAIT, F.R.C.S. 
OF" This work will make a volume in this Library of over 200 pages. 
A CLINICAL treatise 
ON 
DISEASES OF THE LIVER. 
By DR. FRIED. THEOD. FRERICHS. 
Translated by C H A R L EiS MURCHISON, M.D. 
Hgp This classical work-the most valuable ever written upon this subject-will make three volumes of this 
Library of about 300 pages each. They will contain three full-page plates and numerous fine illustrations on wood. 
INFANT FEEDING AND ITS INFLUENCE ON LIFE; 
OR, 
THE CAUSES AND PREVENTION OF INFANT MORTALITY. 
By C, H. F. ROUTH, M.D. 
THIRD EDITION. 
OF" This very practical book will make a volume in this Library of about 280 pages. 
The titles of the remaining four volumes for 1879 will not be announced until later in the season, in order- 
to avail ourselves of whatever may appear in the announcements of books, to be published next year, which are 
usually made in October. 
&"See second page of cover. ANNO UNCEMENT. 
NOW PUBLISHING IN MONTHLY PARTS, 
A.T A S UR S C RIPTI O N I' RICE OF $5.00 F E R Y E A. R . 
STUDIES 
PATHOLOGICAL ANATOMY. 
Bv FRANCIS' DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Ctirator of Bellevue Hospital. 
IN ROYA.L OCTAVO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. i. contains- 
CONNECTIVE TISSUE. Three Plates : 
Plate i. Flat Connective Tissue Cells, from the facia of a dog's leg; magnified 750 diameters 
Plate 2. Branching Connective Tissue Cells, from the tendons of a dog's leg ; magnified 1,500 
diametres. 
Plate 3. Branching Connective Tissue Cells, from the omentum of the rabbit; magnified*750 
diameters. 
No. 2 contains- 
THE PLEURA. 
Plate 4. Pleura of Dog. 
Plate 5. Endothelium and Branching Connective Tissue Cells from Pleura of Dog. 
Plate 6. Endothelium of Human Pleura. 
Plate 7. Lymphatics of the Parietal Pleura of the Dog. 
Plate 8. y Lymphatic Spaces and Connective Tissue Cells, from the Pleura of the Dog. 
No. 3 contains- 
THE INFLAMMATIONS OF THE PLEURA. 
Plate 9. Pleurisy of the Dog, 24 hours, New Cells. 
Plate 10. Pleurisy of the Dog, 3d day, Layer of Cells and Fibrine. 
Plate 11. Pleurisy of the Dog, 5th day, Layers of New Tissue. 
Plate 12. Pleurisy of the Dog, 7-9 days, New Endothelial and Connective Tissue Cells. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema. 
No. 5 contains- 
INFLAMMATIONS OF THE PLEURA. 
Plate 16. Endothelial Cells in Hydrothorax. 
Plate 17. Chronic Pleurisy with Adhesions. 
Plate 18. Verticle Section of the Pleura. Tubercular Pleurisy. 
Subscription Price, $5.00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. ^"Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
STUDIES 
IN 
1 a I h o I o o t eal Anatomy 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
No. 9. 
OCTOBER, 1878. 
NEW YORK 
wzm:. wood & co. 
27 Great Jones Street 
1878 IMPORTANT ANNOUNCEMENT. 
For many years past Messrs. Wm. Wood & Co. have had under consideration the 
feasibility of reproducing books, especially of foreign authors, in good style, and yet at 
prices greatly less than heretofore attempted. The high cost of labor, and of all the 
materials used in the manufacture of books, has been an insuperable obstacle. Even now 
it would be impossible to carry out systematically any such idea'if the ordinary methods of 
trade were depended upon. 
It is believed that the medical profession will welcome and generously sustain any 
well-directed effort of such character, and, consequently, the following scheme has been 
prepared with much care, and is respectfully submitted for their approval and support: 
WOOD'S LIBRARY 
OF 
Standard Medical Authors. 
Messrs. Wm. Wood & Co. have the pleasure of announcing that in January, 1879, 
they will begin the publication of Medical Books by the most distinguished modern and 
standard authors, in monthly volumes of from 200 to 300 pages and upwards, handsomely 
and strongly bound, at the merely nominal price of One Dollar each. 
Estimating from the regular price's of the books so far selected for publication in 1879, 
subscribers to this Library will obtain about 
FIFTY DOLLARS' WORTH OF MEDICAL BOOKS 
FOR 
TWELVE DOLLARS. 
These books will be printed on handsome cream-laid paper, with broad-faced long 
primer type. Wood engravings and plates will be freely used whenever required. 
With the type and size of page adopted, it will frequently be possible to reproduce 
in one of these monthly volumes, an ordinary book of 400 to 500 pages, and costing from 
$4.00 to $6.00. 
TERMS OF SALE: 
As can readily be understood, it would be impossible to publish books upon this plan 
without a very large assured sale for each volume. Wood's Library of Standard Medical 
Authors will, therefore, be sold 
BY SUBSCRIPTION ONLY AT TWELVE DOLLARS A YEAR. 
^PAYABLE INVARIABLY IN ADVANCE. 
Subscriptions must be for a complete year. The volumes of this Library will not 
be sold separately. 
OF" See third page of cover. THE FOLLOWING WILL BE PUBLISHED IN 1879: 
ON 
REST AND PAIN. 
A COURSE OF LECTURES 
ON THE INFLUENCE OF MECHANICAL AND PHYSIOLOGICAL REST IN THE TREATMENT OF 
ACCIDENTS AND SURGICAL DISEASES AND THE DIAGNOSTIC VALUE OF PAIN. 
By JOHN HILTON, F.R.S., F.R.C.S. 
Edited by W. H. A. JACOBSON, F.R.C.S. 
(|^° This valuable work will make a volume in this Library of over 300 pages. It is profusely illustrated by 
ONE HUNDRED AND NINE FINE WOOD ENGRAVINGS. 
DISEASES OF THE INTESTINES AND PERITONEUM, 
COMPRISING ARTICLES ON 
Enteralgia, by JOHN RICHARD WARDELL, M.D.; Enteritis, Obstruction of the Bowels, Ulceration of the 
Bowels, Cancerous and other Growths of the Intestines, Diseases of the CecUm and Appendix Vermi- 
formis, by JOHN SYER BRISTOWE, M.D.; Colic, Colitis and Dysentery, by J. WARBURTON BEGBIE, 
M.D.; Diseases of the Rectum and Anus, by THOMAS BLIZZARD CURLING. F.R.S.; Intestinal 
Worms, by W. H. RANSOM, M.D.; Peritonitis, by JOHN RICHARD WARDELL, M.D.; 
Tubercle of the Peritoneum, Carcinoma of the Peritoneum, Affections of the 
Abdominal Lymphatic Glands and Ascites, by JOHN SYER BRISTOWE, M.D. 
(Taken from Reynolds' System of Medicine.) 
These articles will make a volume in this Library of about 250 pages, with numerous illustrations. 
-A. PRACTICAL MANUAL 
OF THE 
DISEASES OF CHILDREN. 
WITH A FORMULARY. 
By EDWARD ELLIS, M.D. 
THIRD EDITION. 
JEgp This book will make a volume in this Library of about 270 pages. 
DISEASES OF WOMEN. 
By LAWSON TAIT, F.R.C.S. 
This work will make a volume in this Library of oyer 200 pages. 
A. CI/INICLXIj trjkatise 
on . 
DISEASES OF THE LIVER. 
By DR. FRIED. THEOD. FRERICHS. 
Translated by CHARLES MURCHISON, M.D. 
This classical work-the most valuable ever written upon this subject-will make three volumes of this 
Library of about 300 pages each. They will contain three full-page plates and numerous fine illustrations on wood. 
. ' ' " s. ■ ■ . ----------I- ?■-- . . • . ■ 
INFANT FEEDING AND ITS INFLUENCE ON LIFE; 
r or, 
THE CAUSES AND PREVENTION OF INFANT MORTALITY. 
By C. H. F. ROUTH, M.D. 7 
THIRD EDITION. 
|jtW° This very practical book will make a volume in this Library of about 280 pages. 
The titles of the remaining four volumes for 1879 will not be announced until later in the season, in order 
to avail ourselves of whatever may appear in the announcements of books, to be published next year, which are 
usually made in October. 
second page of cover. ANNO UNCEMENT. 
NOW PUBLISHING IN MONTHLY PARTS, 
A. T A S IB M ( U I I'TI ON 1*111 C E O E $ 5 . O O P E B YEAR- 
ST UDIES 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCTAYO RARTS, 
Each contains from two to five full-page. Lithographic Plates in tint, and 
in color; with accompanying explanatory text, These studies will form,, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema. 
No.« 5 contains- 
INFLAMMATIONS OF THE PLEURA. 
Plate 16. Endothelial Cells in Hydrothorax. 
Plate 17. Chronic Pleurisy with Adhesions. 
Plate 18. Verticle Section of the Pleura. Tubercular Pleurisy. 
Part No. 6 and 7, Double Number, contains- 
THE PERITONEUM. 
Plate 19. Parietal Peritoneum of a Dog. 
Plate 20. Normal Human Omentum. 
Plate 21. Cellular Peritonitis, Human. 
Plate 22. Cellular Peritonitis in a Dog; 4th day. 
Plate 23. Chnentum of Rabbit, inflamed for one hour, connective tissue cells and pus cells. 
Plate 24. Peritonitis in a Dog for 48 hours. 
Plate 25. Human Omentum, Acute Peritonitis. 
Part No. 8 contains- 
THE PERITONEUM-continued. 
Plate 26. Human Omentum, Chronic Cellular Peritonitis. 
Plate 27. A Peritoneal Adhesion. 
Plate 28. Peritonitis with Adhesions, Surface of the Peritoneum. 
Plate 29. Tubercular Peritonitis, Section of a Tubercle Granulum. 
Subscription Price, $3.00 a Year. 
INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. S3?- Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great Jones Street, New York. Subscription, S5.G0 a Year. 
Single Numbers, 50 cents. 
STUDIES 
IN 
pathological Anatomy 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
No. IO. 
NOVEMBER, 1878. 
NEW YORK 
WOOD & GO. 
27 Great Jones Street 
1878 ■ IMPORTANT ANNOUNCEMENT. 
For many years past Messrs. Wm. Wood & Co. have had under consideration the 
feasibility of reproducing books, especially of foreign authors, in good style, and yet at 
prices greatly less than heretofore attempted. The high cost of labor, and of all the 
materials used in the manufacture of books, has been an insuperable obstacle. Even now 
it would be impossible to carry out systematically any such idea if the ordinary methods of 
trade were depended upon. 
It is believed that the medical profession will welcome and generously sustain any 
well-directed effort of such character, and, consequently, the following scheme has been 
prepared with much care, and is respectfully submitted for their approval and support: 
WOOD'S LIBRARY 
OF 
Standard Medical Authors. 
Messrs. Wm. Wood & Co. have the pleasure of announcing that in January, 1879, 
they will begin the publication of Medical Books by the most distinguished modern and 
standard authors, in monthly volumes of from 200 to 300 pages and upwards, handsomely 
and strongly bound, at the merely nominal price of One Dollar each. 
Estimating from the regular prices of the books so far selected for publication in 1879, 
subscribers to this Library will obtain about 
FIFTY DOLLARS' WORTH OF MEDICAL BOOKS 
FOK 
TWELVE DOLLARS. 
These books will be printed on handsome cream-laid paper, with broad-faced long 
primer type. Wood engravings and plates will be freely used whenever required. 
With the type and size of page adopted, it will frequently be possible to reproduce 
in one'of these monthly volumes, an ordinary book of 400 to 500 pages, and costing from 
$4.00 to $6.00. 
TEEMS OF SALE: 
As can readily be understood, it would be impossible to publish books upon this plan 
without a very large assured sale for each volume. Wood's Library of Standard Medical 
Authors will, therefore, be sold 
BY SUBSCRIPTION ONLY AT TWELVE DOLLARS A YEAR. 
^PAYABLE INVARIABLY IN ADVANCE. 
Subscriptions must be for a complete year. The volumes of this Library will not 
be sold separately. 
See third page of eover. THE FOLLOWING WILL BE PUBLISHED IN 1879: 
ON 
REST AND PAIN. 
A COURSE OF LECTURES 
ON THE INFLUENCE OF MECHANICAL AND PHYSIOLOGICAL REST IN THE TREATMENT OF 
ACCIDENTS AND SURGICAL DISEASES AND THE DIAGNOSTIC VALUE OF PAIN. 
By JOHN HILTON, F.R.S., F.R.C.S. 
Edited by W. H. A. JACOBSON, F.R.C.S. 
fl®" This valuable work will make a volume in this Library of over 300 pages. It is profusely illustrated by 
ONE HUNDRED AND NINE FINE WOOD ENGRAVINGS. 
DISEASES OF THE INTESTINES AND PERITONEUM, 
COMPRISING ARTICLES ON 
Enteralgia, by JOHN RICHARD WARDELL, M.D.; Enteritis, Obstruction of the Bowels, Ulceration of the 
Bowels, Cancerous and other Growths of the Intestines, Diseases of the Caecum and Appendix Vermi- 
formis, by JOHN SYER BRISTOWE, M.D.; Colic, Colitis and Dysentery, by J. WARBURTON BEGBIE, 
M.D.; Diseases of the Rectum and Anus, by THOMAS BLIZZARD CURLING, F.R.S.; Intestinal 
Worms, by W. H. RANSOM, M.D.; Peritonitis, by JOHN RICHARD WARDELL, M.D.; 
Tubercle of the Peritoneum, Carcinoma of the Peritoneum, Affections of the 
Abdominal Lymphatic Glands and Ascites, by JOHN SYER BRISTOWE, M.D. 
(Taken from Reynolds' System of Medicine.) 
fl®" These articles will make a volume in this Library of about 250 pages, with numerous illustrations. 
A. PRACTICAL MANUAL 
OF THE 
DISEASES OF CHILDREN. 
WITH A FORMULARY. 
By EDWARD ELLIS, M.D. 
THIRD EDITION. 
fl®" This book will make a volume in this Library of about 270 pages. 
DISEASES OF WOMEN. 
By LAWSON TAIT, F.R.C.S. 
fl®" This work will make a volume in this Library of over 200 pages. 
A. CLINICAL treatise 
ON 
DISEASES OF THE LIVER. 
By DR. FRIED. THEOD. FRERICHS. 
Translated by CHARLES MURCHISON, M.D. 
fl®" This classical work-the most valuable ever written upon this subject-will make three volumes of this 
Library of about 300 pages each. They will contain three full-page plates and numerous fine illustrations on wood. 
INFANT FEEDING AND ITS INFLUENCE ON LIFE: 
OR, ' ' 
, THE CAUSES AND PREVENTION OF INFANT MORTALITY. 
By C. H. F. ROUTH, M.D. 
THIRD EDITION. 
fl®" This very practical book will make a volume in this Library of about 280 pages. 
fl®" The titles of the remaining four volumes for 1879 will not be announced until later in the season, in order 
to avail ourselves of whatever may appear in the announcements of books, to be published next year, which are 
usually made in October. 
See second page of cover. ANNO UNCEMENT. 
NOW PUBLISHING IN MONTHLY PARTS, 
AT A S U 15 S C R I F T I O IX PBICB OF $5.00 PPK YEAR 
STUDIES 
PATHOLOGICAL ANATOMY. 
By FRANCIS-DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCTAYO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint,* and 
in color, with accompanying explanatory text, pgr3 These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema-. 
No. 5 contains- 
INFLAMMATIONS OF THE PLEURA. 
Plate 16. Endothelial Cells in Hydrothorax. 
Plate 17. Chronic Pleurisy with Adhesions. 
Plate 18. Verticle Section of the Pleura. Tubercular Pleurisy. 
Part No. 6 and 7, Double Number, contains- 
THE PERITONEUM. 
Plate 19. Parietal Peritoneum of a Dog. 
Plate 20. Normal Human Omentum. 
Plate 21. Cellular Peritonitis, Human. 
Plate 22. Cellular Peritonitis in a Dog; 4th day. 
Plate 23. Omentum of Rabbit, inflamed for one hour, connective tissue cells and pus cells. 
Plate 24. Peritonitis in a Dog for 48 hours. 
Plate 25. Human Omentum, Acute Peritonitis. 
Part No. 8 contains- 
THE PERITONEUM-continued. 
Plate 26. Human Omentum, Chronic Cellular Peritonitis. 
Plate 27. A Peritoneal Adhesion. . 
Plate 28. Peritonitis with Adhesions, Surface of the Peritoneum. 
Plate 29. Tubercular Peritonitis, Section of a Tubercle Granulum. 
Sub scription Pr ice, $5,00 a Year. 
(INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. £3^ Specimen Copies will be sent on receipt'of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
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Single Numbers, 50 cents. 
S I U D I E S 
IN 
latlnrbjjiW Anatomy 
BY 
FRANCIS DELAFIELD, M.D. 
ADJUNCT PROFESSOR OF PATHOLOGY AND PKACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
Nos. 11 & 12. 
DECEMBER, 1878, and JANUARY, 1879. 
NEW YORK 
WM. WOOD & CO. 
27 Great Jones Street 
1879 
NOTE The second volume of this work will be commenced in the 
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WOOD'S LIBRARY 
OF 
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I®* See third page of cover. THE FOLLOWING WILL BE PUBLISHED IN 1879: 
ON 
REST AND PAIN. 
A COURSE OF LECTURES 
ON THE INFLUENCE OF MECHANICAL AND PHYSIOLOGICAL REST IN THE TREATMENT OF 
ACCIDENTS AND SURGICAL DISEASES AND THE DIAGNOSTIC VALUE OF PAIN. 
By JOHN HILTON, F.R.S., F.R.C.S. 
Edited by W. H. A. JACOBSON, F.R.C.S. 
OF" This valuable work will make a volume in this Library of over 300 pages. It is profusely illustrated by 
ONE HUNDRED AND NINE EINE WOOD ENGRAVINGS. 
DISEASES OF THE INTESTINES AND PERITONEUM, 
COMPRISING ARTICLES ON 
Enteralgia, by JOHN RICHARD WARDELL, M.D.; Enteritis, Obstruction of the Bowels, Ulceration of the 
Bowels, Cancerous and other Growths of the Intestines, Diseases of the Ctecum and Appendix Vermi- 
formis, by JOHN SYER BRISTOWE, M.D.; Colic, Colitis and Dysentery, by J. WARBURTON BEGBIE, 
M.D.; Diseases of the Rectum and Anus, by THOMAS BLIZZARD CURLING, F.R.S.; Intestinal 
Worms, by W. H. RANSOM, M.D.; Peritonitis, by JOHN RICHARD WARDELL, M.D.; 
Tubercle of the Peritoneum, Carcinoma of the Peritoneum, Affections of the 
Abdominal Lymphatic Glands and Ascites, by JOHN SYER BRISTOWE, M.D. 
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7k PRACTICAL MTkNTTTkL 
OF THE 
DISEASES OF CHILDREN. 
WITH A FORMULARY. 
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DISEASES OF WOMEN. 
By LAWSON TAIT, F.R.C.S. 
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7k' CLINICAL TREATISE 
ON 
DISEASES OF THE LIVER. 
By DR. FRIED. THEOD. FRERICHS. 
Translated by CHARLES MURCHISON, M.D. 
This classical work-the most valuable ever written upon this subject-will make three volumes of this 
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INFANT FEEDING AND ITS INFLUENCE ON LIFE; 
OR, 
THE CAUSES AND PREVENTION OF INFANT MORTALITY. 
By C. H. F. ROUTH, M.D. 
THIRD EDITION. 
OF" This very practical book will make a volume in this Library of about 280 pages. 
OF" The titles of the remaining four volumes for 1879 will not be announced until later in the season, in order 
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See second page of cover. ANNO_ UNCEMENT_ 
NOW PUBLISHING IN MONTHLY PARTS, 
A. T A s U IJ S C R T I ' T I O IV PRICE OF $ S . O O P i: B Y E A R . 
STUDIES 
IN 
PATHOLOGICAL ANATOMY. 
By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL OCTAVO FARTS, 
Each contains from two to five fulLpage Lithographic Plates in tint, and 
in color, with accompanying explanatory text. pT These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their minute and 
elaborate detail. The Parts are published regularly, the first of each month, 
and sent to subscribers carefully rolled to protect the Plates from injury. 
No. 4 contains- 
EMPYEMA. 
Plate 13. Empyema in a Dog. 
Plate 14. Empyema of ten days' duration in a Dog. 
Plate 15. Vertical Section of Human Pleura, Empyema. 
No. 5 contains- 
INFLAMMATIONS OF THE PLEURA. 
Plate 16. Endothelial Cells in Hydrothorax. 
Plate if Chronic Pleurisy with Adhesions. 
Plate 18. .Verticle Section of the Pleura. Tubercular Pleurisy. 
Part No. 6 and 7, Double Number, contains- 
THE PERITONEUM. 
Plate 19. Parietal Peritoneum of a Dog. 
Plate 20. Normal Human Omentum. 
Plate 21. Cellular Peritonitis, Human. 
Plate 22. Cellular Peritonitis in a Dog; 4th day. 
Plate 23. Omentum of Rabbit, inflamed for one hour, connective tissue cells and pus cells. 
Plate 24. Peritonitis in a Dog for 48 hours. 
Piate 25. Human Omentum, Acute Peritonitis. 
Part No. 8 contains- 
THE PERITONEUM-continued. 
Plate 26. Human Omentum, Chronic Cellular Peritonitis. 
Plate 27. A Peritoneal Adhesion. 
Plate 28. Peritonitis with Adhesions, Surface of the Peritoneum. 
Plate 29. Tubercular Peritonitis, Section of a Tubercle Granulum. 
Sub scription Price. $5.00 a Year. 
(INVARIABLY IN ADVANCE. 
Single Parts, 50 cents each. Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers, WILLIAM WOOD & CO., 
27 Great "Jones Street, INew York. Subscription, $5.00 a Year. 
Single Numbers, 50 cents. 
STUDIES 
IN 
| athnl o g i ca I 1 nato mg 
BY 
FRANCIS DELAFIELD, M.D, 
ADJUNCT PROFESSOR OF PATHOLOOY AND PRACTICAL MEDICINE, 
COLLEGE OF PHYSICIANS AND SURGEONS 
Nos. 16, 17, 18 & 1©. 
JANUARY. FEB'Y, MARCH & APRIL, 1880. 
NEW YORK 
■wim:. WOOD co. 
27 Great Jones Street 
1880 A TREATISE 
) ON (-- 
HYGIENE 
---) AND ( 
PUBLIC HEALTH. 
EDITED BY 
ALBERT H. BUCK, M.D. 
PUBLISHERS' ANNOUNCEMENT. 
The study of Hygiene and Public Health has, more particularly of late years, become an absolute 
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possible. Intelligent people everywhere are alive to its importance, national and State legislatures are 
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The necessity of diminishing, as much as possible, and ultimately, except through criminal neglect, 
wholly eradicating the class of diseases clearly known to be preventable, is generally conceded,, arid such 
professional foresigj.it and knowledge, such general and local enactments as will soonest bring about this end, 
are urgently demanded by the people. 
It is-safe to predict that, during the n^yt few years, vigorous efforts will be made throughout the 
length and breadth of the United States to eradicate or diminish such prolific sources of illness and death 
as yello_w fever, the different malarial diseases, typhoid fever, small-pox, scarlet fever, measles, etc.; 
It appears strange that, with so much active interest in this subject, _ there, has mot hitherto been 
published any American work upon it. Those who have given special study to sanitary matters in this 
country have only published now and then an article in some journal, or quite rarely a brief monograph 
on some one branch of hygiene. It seems, therefore, to be not only a fitting time, but also absolutely 
necessary that both the people at large and the medical profession should be provided with a trustworthy 
and coiifprehensive text-book that will not merely lay down in detail the gtneral principles of individual 
and public hygiene, but will take cognizance of the peculiar conditions of soil,, climate, social customs, laws, 
relations to , ther nations, etc , which exist in the United States. The publishers believe that the present 
treatise fulfils all these requirement-'. The different writers are men who are well known as authorities in 
the several branches of which they treat, and their teachings will therefore carry with them a weight which 
could not possibly attach to any similar treatise written by a single person. No expense has been spared 
to illustrate the book as fully as the demands of clearness and ease in understanding the text seemed 
to require. . 
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secure an immediate service. 
P K I ( E S : 
Back's Hygiene, 2 vols., Illustrated, Muslin binding, per vol., . .... $5.00 
" " " " Leather " " . . 6.00 
" « n ^Morocco " " . . 7.50 
Air TO SUBSCRIBERS TO ZIEJISSE^S CYCLOPAEDIA.^ 
ks there is no. volume in Ziemssen's Cyclopedia devoted to Hygiene and Public Health, the Publishers 
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WM. WOOD & CO., Publishers, 27 Great Jones St., New York. 
See third page of cover. CONTE1VTS 
-) OF(- 
BUCK'S TREATISE ON HYGIENE. 
VOLUME I. 
INTRODUCTION.-Including: I. Prefatory Remarks. II, Causes of Disease. III. Jurisprudence 
of Hygiene. By John S. Billings, M.D., Surgeon U. S. Army. 
PART I. 
INDIVIDUAL HYGIENE. 
HYGIENE OF INFANCY.-By Abraham Jacobi, M.D., Clinical Professor of Diseases of Children in 
the College of Physicians and Surgeons, New York. 
FOOD AND DRI^IK.-By James Tyson, M.D., Professor of General Pathology and Morbid Anatomy in the 
University of Pennsylvania. 
DRINKING WATER AND PUBLIC WATER SUPPLIES.-By William Ripley Nichols, Boston, 
Mass., Professor in the Massachusetts Institute of Technology. 
PHYSICAL EXERCISE By A. Brayton Ball, M.D., New York City. 
THE CARE OF THE PERSON.-By Arthur Van Harlingen, M.D., Chief of the Clinic, Department of 
Skin Diseases in the University of Pennsylvania. 
u Art ii. 
HABITATIONS. 
THE ATMOSIncluding Climate, Ventilation, and Heating. By D. F. Lincoln, M.D., 
Boston, Ma.-s. ' ' 
DRAINAGE, SEWERAGE, ETC.-By William- H. Ford. M.D., President of the Board of Health, 
Philadelphia, Pa. ' - 
PRINCIPLES OF HOSPITAL CONSTRUCTION.-By Francis H. Brown, M.D., Boston, Mass. 
VOLUME IL 
f A r. t i. 
OCCUPATIONS. 
HYGIENE OF OCCUPATION.-By Roger S. Tracy, M.D., Sanitary Inspector of the Board of Health, 
New. York. ' . ' ' ' 1 . 
HYGIENE OF CAMPS.-By Charles Smabt, M.B., C.M., Assistant Surgeon U. S. Anny. 
HYGIENE OF THS MERCHANT AND NAVAL MARINE.-By Tuomas J. Turner, M.D., Medical 
Director U. S. Navy. , 
HYGIENE OF COAL MINES.-By Henry C. SheafER, Pottsville, Pa., Coal Editor of the " Miners' Journal." 
HYGIENE OF METAL MINES.-By Rossiter W. Raymond, Pii.D., Editor of the '"Engineering and 
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F Al R T I I. 
PUBLIC HEALTH. 
INFANT MORTALITY.-VITAL STATISTICS.-By Tiios. B .Curtis, M.D., Surgeon to the out-patients 
Department, Massachusetts General Hospital; Boston, Mass 
ADULTERATION OF FOOD By Stephen P. Sharples, Boston, Mass., State Assayer. 
PUBLIC NUISANCES.-By Roger Si Tracy, M.D., Sanitary Inspector of the Board of Health, New York. 
EXTERNAL QUARANTINE.-By S. Oakley Vander Poel, M.D,, Health Officer of the Port of New York. 
INLAND QUARANTINE.-By S. S. Herrick,, M.D., New Orleans, La., Secretary of the State Board of 
Health. . ■ • 
SMALL POX, SCARLET FEVER- ETC.-By Al. LAN McL. Hamilton, M. D., Sanitary Inspector of the 
Board of Health, New York, and Bache McE. Emmet, M.D., New York City. 
SYPHILIS.-By Frederic R. Sturgis, M.D., New York, Visiting Surgeon to Charity Hospital. 
DISINFECTANTS-By Elwyn Waller, Ph.D., Chemist to the Board of Health, New York. 
VILLAGE SANITARY ASSOCIATIONS.-By Roger S. Tracy, M.D., Sanitary Inspector of the Board 
of Health, New York. 
SCHOOL HYGIENE.-By D. F. Lincoln, M.D., Boston, Mass. ANNO UNCEMENT_ 
NOW PUBLISHING IN MONTHLY PARTS, 
AT A SRRSCRIPTIOIV PRICE OF 9 5.00 I'ER YEAR 
STUDIES 
I N . . 
PATHOLOGICAL ANATOMY. 
' By FRANCIS DELAFIELD, M.D., 
Adjunct Professor of Pathology and Practice of Medicine in the College of Physicians and Surgeons ; 
Visiting Physician and Pathologist of the Roosevelt Hospital; 
Visiting Physician and Curator of Bellevue Hospital. 
IN ROYAL O C TA VO PARTS, 
Each contains from two to five full-page Lithographic Plates in tint, and 
in color, with accompanying explanatory text. These studies will form, 
when completed, a treatise on Pathological Anatomy of exceptional value, 
especially for the remarkable fidelity of the illustrations, their mimjte and 
elaborate detail. The Parts are published monthly, and sent to subscribers 
carefully rolled to protect the Plates from injury. 
Single Parts, 50 cents each. Specimen Copies will be sent on receipt of 50 cents. 
Address the Publishers^ WILLIAM WOOD & CO., 
27 Great Jones Street, Neiv York.