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ATLAS AND EPITOME 



Special Pathologic Histology 



DOCENT DR. HERMANN DLJRCk 

\NT IN THE PATHOLOGIC INSTITUTE; PROSECTOR TO THE MUNICIPAL 
HOSPITAL L. I. IN MUNICH 



AUTHORIZED TRANSLATION FROM THE GERMAN 



EDITED BY 

LUDVIG HEKTOEN, M.D. 

PROFESSOR OF PATHOLOGY IN RUSH MEDICAL COLLEGE, CHICAGO 



CIRCULATORY ORGANS; RESPIRATORY ORGANS 
GASTRO-INTESTINAL TRACT 



WITH 62 COLORED PLATES 



PHILADELPHIA 

W. B. SAUNDERS 
925 Wai nut Stri 

1900 

V.. 



TWO COPIES HICEIVID, 

t itfti) of Congrot% 
tktflet df tli« 

MAY S 1 1900 

ItegUter tf Copyright* 

#, 9-32^ 

«tCONO COPY, 



59057 



Copyright, 1900, by W. B. Saunders 



PRESS OF 
W. B, SAUNDERS, PHILADA. 



EDITOR'S PREFACE. 



The objects of this book are well set forth in the 
author's preface, and it has been a pleasure to aid in plac- 
ing the work within the easy reach of the vast army of 
medical students in America. Two more volumes follow 
shortly, one completing special pathologic histology, the 
other dealing with general pathologic histology. The 
few notes I have added are inclosed in brackets. 

Ludvig Hektoex. 



AUTHOR'S PREFACE. 



Since Virchow showed that what we call "disease" 
depends ob disturbances of cell-life, our conception of the 
nature of pathologic processes has conic to rest on the 

knowledge of the changes that occur in the elementary 
constituents of the organism. 

Pathologic histology ahme can make it clear to us why 
the morbid changes in a given case necessarily a^kne 
the appearances presented at the postmortem table ; and in 
many instances pathologic histology is the first to reveal 
the reasons for the suspension or alteration of the func- 
tions of an organ. 

A- pathologic anatomy has become the teacher of 
clinical medicine in general. -<> it also has become insepa- 
rable from the study of the microscopic tissue changes or 
pathologic histology. 

It i- no easy task for the beginner to select among the 
many changes those that are typical of a certain proc< ss, 
and t<> determine the causa] relations between the micro- 
scopic and macroscopic, but. having mastered the essence 
of a disease as shown in it- characteristic changes in the 
elementary constituents of the body, it no longer becomes 

7 



8 



AUTHOR'S PREFACE. 



difficult to understand the changes visible to the naked 
eye. 

To further the knowledge of the microscopic changes 
produced by disease is the object of the present " Atlas 
and Epitome. " This statement at once makes it clear 
that its use will yield good results only when combined 
with the study of preparations under the microscope. 
Never will he who shuns the postmortem room acquire a 
conception of pathologic anatomy ; and it is no less impos- 
sible to master pathologic histology without direct micro- 
scopic study. 

If the work, whose first volume this is, proves a trusty 
guide in this study, as an adjunct to other instruction, 
stimulating and leading the beginner to personal and 
exact microscopic observations, then its object will be 
attained. 

All the illustrations have been drawn by C. Krapf 
from my own preparations. The magnification has been 
calculated by means of the stage micrometer, due regard 
being paid to the level of projection. 

Naturally, I have attempted to secure the most typical 
pictures of the various processes, but in no case has it 
been sought to do this by a schematic representation ; 
even the " combination " of various areas in one or more 
preparations has been avoided in the interests of absolute 
exactness. 

Hermann Dürck. 



LIST OF ILLUSTRATIONS. 



Plate 1. Fig. I. 

Fig. II. 

Plate 2. Fig. I. 

Fig. II, 

Fig. III. 
Plate 3. Fig. I, 

Fig. II.- 

Plate 4. Fig. I, 

Pig. II.- 

PJate 5. Fig. I, 

Fig. II, 
Plate 6. Fig. I, 

Fig. [I.- 
Plate 7. Fig. [.- 

Fig. II.- 

Plate 8. Fig. I.- 

_. II, 

Plate U. Fig. I. 

i 11. 



Fatty Degeneration of the Heart-muscle in Acute 
Pernicious Anemia. A Fresh Teased Prepara- 
tion. X340. 

Frozen Section of a Papillary 
Mitral Valve. Stained with 



Frozen Section, Stained with 



The Same Case 
Muscle of the 
Sudan. X 80. 

Adipositas Cordis. 
Sudan. X 80T— 

Brown Atrophy of the Heart-muscle in Longi- 
tudinal Section. 

The Same in Transverse Section. X 340. 

Infarction of the Heart-muscle Undergoing Organ- 
ization. X 70. 

Embolic Abscess of a Papillary Muscle of the 
Mitral Valve. X?0. 

-Acute Interstitial Myocarditis. X 300. 

chronic Fibrous Myocarditis. X 80. 

-A Normal, So-called Fetal. Gelatinous Nodule 
upon the Line of Closure of the Mitral Valve 
of t lie New-born. 70. 

-From an Acutely Inflamed Heart-valve (Mitral) 
in Mycotic Endocarditis. 80. 

-Acute Verrucose, Mycotic Endocarditis of the 
Mitral Valve. 16. 

-Verrucose Endocarditis of the Mitral Valve Under- 
going ( organization. in. 

Acut«- Fibrinous Pericarditis (Cor Villosum). 
Fibrin Stain. 64. 

-Fibrinous Pericarditis Undergoing Organization. 
127. 

-Subacute Tuberculous Pericarditis. 50. 

•Milk- Spots of the Epicardium. 65. 

-Arteriosclerosis of a Cerebral Artery. ■ 75. 

-Arteriosclerosis of a Coronary Artery. X 70. 



10 



LIST OF ILLUSTRATIONS. 



Plate 10. 


Fig. 

Fig. 


I. 

II. 




Fig. 


Ill 


Plate 10a. Fig. 


L- 


Fig. 
Plate 10b. Fig. 


II.- 
L- 




Fig. 


II.- 


Plate 11. 
Plate 12. 


Fig. 
Fig. 
Fig. 


I. 

II. 

I. 




Fig. 


II. 


Plate 13. 


Fig. 


I. 


Plate 14. 


Fig. 

Fig. 


II. 
I 




Fig. 


II. 


Plate 15. 


Fig. 


I. 




Fig. 


II. 


Plate 16. 


Fig. 


I. 




Fig. 


II. 


Plate 17. 


Fig. 


I 


Plate 18. 
Plate 19. 
Plate 20. 


Fig. 

Fig. 
Fig. 
Fig. 
Fig. 
Fig. 


II. 

I. 
II. 

I. 
II. 

I. 




Fig. 


II. 




Fig. 


Ill 



— Atheroma of the Aorta. X 20. 

— Cholesterin Plates and Free Fat-globules from an 
Atheromatous Patch of the Aorta X 130. 

. — Fatty Degeneration of the Cells of the Intima in 
Atheroma of the Aorta. X 300. 

-Atheroma (Arteriosclerosis) of the Crural Artery. 
X55. 

-Wall of a Small Aneurysm of the Aorta. X 20. 

-Acute Arteritis in Tuberculous Leptomeningitis. 
X 745. 

—Gummatous Arteritis of the Subclavian Artery. 
X16. 

— Arteritis Obliterans. X 37. 

— Arteritis Obliterans in Syphilis. X 80. 

— Tuberculous Arteritis in Subacute Tuberculous 
Leptomeningitis. X 280. 

— Tubercle in the Wall of a Large Stem of the Por- 
tal Vein. X 40. 

— Acute Purulent Phlebitis in Phlegmonous Inflam- 
mation of the Cellular Tissue. X 40. 

— Varix from the Leg. X 26. 

, — Pigment Deposits within an Axillary Lymph- 
gland in Tattooing of the Forearm. X 300. 

— Mesenteric Lymph-gland in Typhoid Fever. 
X 360. 

— Acute Lymphadenitis. A Peripheral Sinus of 
a Peribronchial Lymph-gland in Croupous 
Pneumonia. X 385. 

— Increased Cellular Hyperplasia of a Lymph-gland 
in Acute Pernicious Anemia. X 745. 

— Hyaline Degeneration of the Eeticulum of a 
Lymph -gland. X 280. 

— Chronic Indurative Lymphadenitis with Destruc- 
tion of the Lymph-sinus and Lymph-follicle in 
Leukemia. X 180. 

— Chronic Indurative Lymphadenitis with Destruc- 
tion as a Result of an Increase of the Recticu- 
lum in Leukemia. X 460. 

— Subacute Tuberculosis of a Lymph-gland. X 70. 

— Passive Hyperemia of the Spleen. X 360. 

— Senile Atrophy of the Spleen. X 80. 

— Anemic Infarction of the Spleen. X 22. 

— Hemorrhagic Infarction of the Spleen. X 250. 

— Acute Hyperplastic Splenic Tumor. Fresh teased 
Preparation. X 300. 

— Acute Hyperplastic Splenic Tumor in Sepsis. 
X 300. 

, — Chronic Splenic Tumor Resulting in Induration. 
X 250. 



LIST OF ILLÜSTBATJOltS. 11 

Plate 21. Fig. L — Diffuse Amyloid Degeneration of the Spleen 
Bacon Spleen). \ 250. 
II. — Advanced Diffuse Amyloid Degeneration of the 
Spleen. \ 70, 
Plate 22. Fig, I. — Amyloid Degeneration of the Splenic Follicles 
50 Spleen 1. 2 I. 

II — Amyloid Degeneration of the Spleen (Sago 
Spleen . 260. 

Piatt' 23. Fig. I. — Spleen in Amte Leukemia, x :><><>. 

Fig. IL — Staphylococcal Emboli of the Spleen in Pyemia. 
\ 7d. 
Piatt- -34. Fig. [.—Tuberculosis of the Spleen. \ 92. 

Fig. II. — From the Center of a Spleen-Follicle in Diph- 
theria, x ~ J '>. 
Plate 25. Fig. I. — Bone-marrow in Pernicious Anemia. From the 
Diaphysis of the Humerus. \ 520. 
II. — Bone-marrow in Acute Leukemia. X 6-10. 
I.— Diphtheria of the Trachea. X 18. 
II.— Diphtheria of the Trachea. X 130. 
I. — Fleers of the Larynx in Typhoid Fever. X 35. 
II. — Pachydermia Laryngis. X 00. 

I.— Tuberculosis of the Larynx. X 16. 
II. — Tuberculosis of a Large Bronchus. X 54. 
I.— Ectasia of a Small Bronchus. X 10. 
IL— The Wall of an Eetatie Bronchus. \ 127. 

I.— Colloid Goiter. \ 56. 

II. — Parenchymatous Goiter with Hyaline Degenera- 
tion of the Interstitial Substance. > 70. 
L— Fetal Atelectasis of the Lung. X 70. 
II. — Compression Atelectasis of the Lung in Sero- 
fibrinous Pleuritis. X 70. 
L— Anthracosis of the Lung. X 100. 
II. — Siderosisof the Lung (Red lion Lung). X 300. 
I. — Emphysema of the Lung. 40. 

1 1. Emphysema of the Lung. • :*> 10. 
[IL— Emphysema of the Lung 1 Injected). X 54. 

I. — Brown Induration of the Lung. 130. 

II. — Passive Hyperemia of the Lung. • 250. 
I. — Peripheral Zone of a Hemorrhagic infarction of 

the Lung. 1<>. 

II. — Fit Embolism of the Lung in Fracture of a Long 
Bone 300. 

Plate ema of the Lung. Pi:. 

II. Marantic Splenization of the Lung. 360. 
III. — Beginning Red Hepatization of the Lung in 
Croupous Pneumonia. 340. 
Plat- I. —Croupous Pneumonia ;it the Heighl of Hepatiza- 

tion. 





Fig. 


Plate 26. 






Fig. 




Km. 




Fig. 


Plate 28. 


Liu. 




Lm. 


Plate 29. 






Liu. 


Plate 30. 








Plate 31. 


Fig. 




Fig. 








Liu. 



























12 



LIST OF ILLUSTRATIONS. 



Plate 37. 


Fig. 


II.- 


Plate 38. 


Fig. 


I. 




Fig. 


II. 


Plate 39. 


Fig. 
Fig. 


I. 
II. 


Plate 40. 


Fig. 


I. 


Plate 41. 
Plate 42. 
Plate 43. 


Fig. 
Fig. 
Fig. 
Fig. 
Fig. 
Fig. 
Fig. 


II. 

I. 
II. 

I. 
II. 

I. 
II. 


Plate 44. 


Fig. 


I. 




Fig. 


II. 


Plate 45. 


Fig. 


I. 




Fig. 


II. 


Plate 46. 


Fig. 


I. 




Fig. 


II. 



Plate 47. Fig. I.— 
Fie;. II. 



Plate 48. 


Fig. 


I. 




Fig. 


II. 


Plate 49. 


Fig. 


I. 




Fig. 


II. 


Plate 50. 


Fig. 


I. 




Fig. 


II. 


Plate 51. 


Fig. 


I. 




Fig. 


II. 


Plate 52. 


Fig. 


I. 



Fig. II 



-Croupous Pneumonia, Stage of Gray Hepatiza- 
tion. X 360. 
-"Carnification" of the Lung, Following Croup- 
ous Pneumonia. X 1*70. 
-Organization of the Exudate in Bronchopneu- 
monia. X 200. 
-Beginning Catarrhal Pneumonia. X 250. 
-Peribronchial Inflammatory Area with Beginning 
Extension to the Surrounding Lung Tissue. 
X80. 
-Lobular (Purulent) Bronchopneumonia Folio w- 

ing Diphtheria. X 250. 
-Postdiphtheric Lobular Pneumonia. X 280. 
-Embolic Abscess of the Lung in Pyemia. X 75. 
-Caseous Bronchitis. X 40. 
-Miliary Tuberculosis of the Lung. X 35. 
-Caseous Pneumonia. X 70. 
-Miliary Tuberculous Pneumonia. X 1*70. 
-Caseation of the Exudate of an Alveolus in Case- 
ous Pneumonia. X 360. 
-Desquamative Pneumonia (Buhl) Surrounding a 

Tuberculous Area of the Lung. X 340. 
-Proliferation and Desquamation of the Alve- 
olar Epithelium in Tuberculous Pneumonia. 
X 520. 
-Wall of a Tuberculous Cavity of the Lung with 

" Apex Cirrhosis. " X 16. 
-Slaty Induration of the Lung in Obsolete Apex 

Tuberculosis. X 55. 
-Syphilitic "White " Pneumonia of the New-born. 

X 250. 
-Indurative Interstitial Pneumonia in Congenital 
Syphilis. X 80. 
Acute Fibrinous Pleuritis in Croupous Pneu- 
monia. X ^- 
— Beginning Organization in Fibrinous Pleuritis. 

X340. 
— Variola Vera of the Tongue. X 75. 
— Tuberculosis of the Pharynx. X *75. 
— Diphtheria of the Pharynx. X 80. 
—Diphtheria of the Tonsils. X 280. 
— Acute (Purulent) Embolic Parotitis. X 70. 
— Thrush Vegetations in Esophagus. X 270. 
— Chronic Granular Gastritis. X 30. 
— Chronic Catarrh of the Stomach. X 160- 
— Hemorrhagic, Necrotic Gastritis in Phosphorus 

Poisoning. X 80. 
— Hemorrhagic Erosion of the Stomach. X 57. 



LIST OF ILLUSTRATIONS. 



13 



Plate 53. Fig. I.— 



Fig. I 
Plato 54. 

Fig. I 



Plate 55. Fig. 

Fig. I 

Plate 56. Fig. 

Fig. 1 

Plate 57. Fig, 

Fig. I 
Plate 58. Fig. 

Fig. I 

Plate 59. Fig. 

Fig. I 
Plate 60. Fig. 

Fig. I 



Pound Ulcer of the Stomach with Erosion of a 
Blood-vessel. \ 16. 

Border of a Round Ulcer of the Stomach. X 54. 

Beginning Carcinoma of the Stomach. \ 5 1. 

Marked Stenosis of the Pyloric Orifice, the Re- 
sult o[ a Scirrhous Carcinoma of the Stomach. 
13. 

■Atrophy of the Large Intestine. \ 85. 

Brown Atrophy of the M oscularis of the Small In- 
testine in the Cachexia of Carcinoma. X 330. 

Diphtheric Colitis in Corrosive Sublimate Poison- 
ing. \ 20. 

Dysentery of the Large Intestine. X 50. 

Marked Swelling of a Lymph-follicle of the Large 
Intestine in Typhoid Fever. > 50. 

Marked Swelling of a Lymph-follicle with Uegin- 
ning Necrosis in Typhoid Fever. X 50. 

Ulcer after Detachment of the Slough in Typhoid 
Fever. X 50. 

Intestinal Lymphangitis. Cellular ''thrombus" 
in a lymph-vessel of the Submucosa of the 
Large Intestine in Dysentery. X 360. 

Beginning Tuberculosis in the Vermiform Ap- 
pendix. X 80. 

Border of a Tuberculous Ulcer of the Intestine. 
X80. 

Beginning Purulent Peritonitis Twenty-four 
hours after Ligating the Tntestine. X 6*25. 

Tuberculous peritonitis. X 72. 



CONTENTS. 



PAGE 

I. The Organs of Circulation 17 

The Heart 1? 

Diseases of Heart-muscle 18 

Circulatory Disturbances of the Myocardium 21 

Endocardium 26 

Pericardium .... 30 

The Vessels :'>:> 

Arteries 34 

Veins 43 

Lymphatic Glands 4."> 

The Spleen 53 

Infarcts 55 

Acute Splenic Tumor 57 

Chronic Splenic Tumor 59 

Degeneration 61 

The Bone-maerow , . . . ... 64 

II. The Respiratory Organs 67 

The Nose 67 

The Larynx, Trachea, and Bronchi 69 

The Lungs 77 

ilatory Disturbances 

Infarction 86 

Pneumoconiosis 

Pneumonia 1)1 

Croupous Pneumonia , 95 

Bronchopneumonia .... ... 100 

Tuberculosis . 104 

Syphilis 115 

The Pleüb \ in 

Tin. Thyroid Gland ... . 1 1 - 

15 



16 CONTENTS. 






PAGE 

III. The Digestive Organs ... 121 

The Oeal Cavity, Pharynx, Esophagus 126 

Croupous aud Diphtheric Inflammation 130 

The Salivary Glands 132 

The Stomach 133 

Gastric Ulcer 135 

The Intestine 138 

Inflammations 140 

Tuberculosis 147 

The Peritoneum 148 

Index 149 






PATHOLOGIC HISTOLOGY. 



I. THE ORGANS OF CIRCULATION. 
HEART. 

The heart-wall consists of three layers : the epieardium, 
myocardium, and endocardium. The epieardium (vis- 
ceral portion of the pericardium) is composed of connec- 
tive-tissue fibers, and is covered on its outer surface by 
Hat, irregular, polygonal epithelium. [Throughout this 
book the word epithelium is used in the morphologic 
sense.] Underneath the epieardium lies, normally, at 
various place- a distinct layer of fat-cells. The elastic 
fibers of the auricular epieardium are lost in the adven- 
titial of the larger venous trunks. 

The myocardium is made up of short, cylindric, trans- 
versely striated muscle-cells. As in the voluntary mus- 
cle-, they consist of isotropic and anisotropic transverse 
hand-, which alternate. The protoplasm is divided into 
a peripheral, longitudinally striated, fibrillar substance 
and a central portion — the sarcoplasm. In the latter 
lies the oval, vesicular nucleus, around which is usually 
seen a -mall deposit of tine, granular, brownish pigment. 
A cell-membrane — the so-called sarcolemma — is absent 
in the heart-muscle of man. Many muscle-cells are 
united with one another through oblique and transverse 
branches. 

The endocardium is composed, like the epieardium, of 

2 17 



18 PATHOLOGIC HISTOLOGY. 

an avascular connective-tissue membrane, containing, espe- 
cially in the auricles, a great number of elastic elements 
with a few smooth muscle-fibers. It is lined on its inner 
surface by a layer of polygonal, flattened epithelium. The 
heart-valves are reduplications of the endocardium with 
strongly developed elastic fibers. Blood-vessels are not 
found normally in the valves of the full grown ; in the 
case of the auriculoventricular valves, blood-vessels reach 
to the bases. 

In the fetus, however, as well as in the new-born, the 
leaflets are richly supplied with blood-vessels up to their 
free borders. Along the lines of closure the connective 
tissue is soft and myxomatous, and is composed of numer- 
ous stellate cells which anastomose with one another. 
Here are formed the fetal, gelatinous nodules which some- 
times are mistaken for endocardial inflammatory processes. 
Later, the blood-vessels disappear, and the gelatinous 
nodules are transformed into fibrous nodules, which are 
never missed at the borders of the tricuspid and mitral 
leaflets. (Plate 5, Fig. I.) 

Diseases of the Heart=muscle. 

In the course of the acute general infectious diseases 
(sepsis, typhoid, diphtheria, scarlatina, variola, etc.) there 
occurs quite frequently in the myocardium an albumin- 
ous degeneration, or so-called cloudy swelling, as is the 
case in the large parenchymatous organs. Microscopically, 
the fresh preparations show enlargement of the individual 
muscle-cells. The cement lines appear more distinctly 
and are broader than normal, while the nuclei and the 
transverse striae are indistinct or entirely obscured. The 
protoplasm contains an enormous number of very fine 
granules, of a dust-like, opaque, grayish appearance. On 
the addition of weak solution of acetic acid this cloudi- 
ness immediately clears up, owing to the transformation 



THE ORG Ays OF CIRCULATION. 19 

of the albuminous granules into acid albumin, which be- 
comes dissolved in the residual acid. The striatums and 
nuclei now become distinctly visible. In stained prepa- 
ration- thi> cloudy swelling is not seen. 

Cloudy swelling is frequently a forerunner, or inter- 
mediate staue, of a more deep-seated degenerative process 
of the heart-muscle — namely, fatty degeneration. This 
may occur independently of cloudy swelling. It may be 
either circumscribed or diffuse. Usually, it is found in 
patches in the form oi* wavy lines, parallel with the longi- 
tudinal axis of the muscle-bundles, giving the muscle an 
appearance similar to that of a timer's skin, the degener- 
ated area- appearing light in color. Fatty degeneration 
may result from local disturbance of nutrition, such as may 
follow narrowing or occlusion of the coronary vessels, or 
from the pressure of pericardial exudate. It may occur 
from acute intoxications : the most important toxic agents 
in this respect are phosphorus and arsenic ; less frequently, 
chloroform, ether, and alcohol ; and it is found quite fre- 
quently also in the course of the acute infections diseases, 
through the action of bacterial toxins ; furthermore, in all 
diseases that lead to a diminution or destruction of the 
blood, such as pernicious anemia and the severer forms 
of leukemia. Microscopic examination of fresh prepa- 
rations will show that the mu>cle-eells are filled with fine, 
round, highly retractile globules, which are arranged 
parallel with the longitudinal fibrils, and which may 
completely cover the nuclei as well as the transverse 
Striae. On the addition of acetic acid or potassium hy- 
drate the granule- do not become dissolved, showing that 
they are fat-globules. Fn Long-standing and severe cases 
the individual droplets run together, forming large drops. 
The fat-globules are easily pressed out of the cells, after 
which are seen only their shadows or outlines in the cell. 
In the latt<T the transverse striae are completely lost ; the 
longitudinal striatums^ however, may >till be present. 



20 PATHOLOGIC HISTOLOGY. 

PLATE 1. 

Fig. I.— Fatty Degeneration of the Heart=muscle in Acute 
Pernicious Anemia. Fresh teased preparation. X 340. In the 
center are seen muscle-fibers totally rilled with fat-globules ; the 
fibers are partly ruptured. Transverse striations are not discernible. 
Above and to the left a fiber is seen, out of which the fat-globules 
are partly extruded; here the longitudinal striation is still noticed. 
Free, large fat drops are seen ; below and to the right, several slightly 
degenerated fibers still containing transverse striae. 

Fig. II. — From the Same Case. Frozen sections of a papillary 
muscle of the mitral valve. Stained with sudan III. X 340. The 
fat-droplets are stained orange-red. Here and there are seen the 
degenerated areas ; above and to the right, almost normal muscle- 
fibers. 

In frozen preparations stained with sudan III the de- 
generated areas are well differentiated from the normal 
striated muscle-fibers. 

Fatty degeneration must not be confounded with increase 
of fat in the normal subepicardial fat-layer — adipositas 
cordis or obesitas, also known as lipomatosis cordis ; here 
the fat does not appear in globules, but as distinct fat-cells 
and as an independent tissue. It infiltrates the heart-wall 
in clusters, extending toward the endocardium. In severe 
cases it appears especially over the right ventricle and 
below the endocardium. The musculature becomes com- 
pressed, pushed aside, is frequently atrophied, and substi- 
tuted by fat. The muscle-fibers may decrease to one-half 
or two-thirds their normal size ; the striations, however, 
being well preserved. At times, especially in corpulent 
individuals, it is very hard to distinguish between physio- 
logic and pathologic infiltration or deposition of fat. 
Usually, the finding of atrophied muscle-bundles between 
rows of fat-cells will differentiate these conditions. 

A quite common, almost physiologic, condition, found 
in advanced age, is brown atrophy of the heart-muscle. 



Tab.L 



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LUh. Anst F. Rcic/thoUl, München . 



THE ORGANS OF CIRCULATION. 21 

It also occurs in young individuals suffering from exhaus- 
tive diseases with general marasmus. The muscle-fibers 
appear more or less diminished in size, oftentimes to a 
considerable degree, and their striations are indistinct or 
have entirely disappeared, while the nuclei may have be- 
come Battened. Around the latter are found masses of 
amorphous, finely granular, yellowish-brown pigment. In 
severe cases the cells are completely filled with this pig- 
ment, or the pigment maybe found free between the fibers, 
owing to the destruction o{ the cells. Tu eases not so far 
advanced transverse sections will not always show pigment 
in each individual cell, for the reason that the groups of 
pigment particles, like the nuclei, are found only at certain 
plane- ; fat-vacuoles are sometimes seen in the sarcoplasm 
at the same time. The pigment gives no iron reaction, 
and it is undoubtedly related to the pigment normally 
found in the heart-muscle. 

In severe cases of general amvloid disease there is 
sometimes found in the myocardium amvloid degeneration 
of the blood-vessels of the intermuscular connective tis- 
sue. Hyaline degeneration may also be observed in the 
intermuscular connective tissue. 

[Among the degenerative changes of the myocardium 
should be mentioned segmentation, or separation of the 
muscle-fibers along the cement lines into the individual 
cells that compose the fiber- ; and fragmentation, or the 
breaking of the fiber- into fragments irrespective of the 
cement lin These changes are terminal or agonal 

«vent- in diseases of various kinds, and are found to a 
fcer or less degree in about two-thirds of all heart- ex- 
amined.] 

Circulatory Disturbances of the Myocardium. 

Embolism, Infarction. — Embolism of the coronary 
arteries of the heart occur- bin infrequently, as the result 



22 PATHOLOGIC mSTOLOGT. 

PLATE 2. 

Fig. I. — Adipositas Cordis. Frozen section. Stained with 
hematoxylin and sudan III. X 80. 1, Transversely striated muscle- 
fibers, pressed together, diminished in size, and continuity inter- 
rupted ; 2, fat-cells in rows between the muscle-fibers. 

Fig. II.— Brown Atrophy of the Heart= muscle in Longi= 
tudinal Section. 

Fig. III.— -The Same in Transverse Section. X 340. In the 
muscle-cells are seen masses of brownish, amorphous pigment. In 
the transverse section are seen round vacuoles in the sarcoplasm. 



of detached pieces of thrombi or endocardial vegetations 
being swept into those vessels. Provided sudden death 
by obstruction of a larger stem does not occur, the results 
are anemic infarct ; since the coronary arteries are, in the 
sense of Cohnheim, end arteries — in other words, do not 
form collaterals. The whole infarcted area undergoes 
anemic necrosis. Through coagulation of the albuminous 
substances, the area presents a homogeneous, dry, firm con- 
sistency, while the contours of the cells and transverse 
striae of the muscle-fibers disappear, and the nuclei do not 
stain. Later, the musculature breaks up into a granular 
substance. The infarct, like necrotic tissue in general, 
acts upon the neighboring tissue as an inflammatory irri- 
tant, which causes the accumulation of numerous round 
cells, lymphocytes, and leukocytes around the periphery 
of the infarct, forming a compact wall. At this stage 
softening may take place in the infarct as the result of an 
infiltration of serous fluid throughout the area, the fluid 
being transuded from the surrounding blood-vessels that 
are in a state of stasis (Neelsen). This condition is desig- 
nated as myomalacia cordis. The softened tissue can not, 
when extensive, withstand the blood pressure, a local 
bulging occurs, and an aneurysm of the heart develops. 
It is much more common to observe that shoots of new 



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I 



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THE ORGANS OF CIRCULATION. 23 

blood-vessels and proliferative connective-tissue cells grow 
into the periphery of the infarct, which becomes gradually 

infiltrated with granulation tissue — that is to say, the in- 
farct becomes organized, the necrotic muscle-tissue is sub- 
stituted by a connective tissue at first richly cellular and 
vascular. | Plate 3, Fig. I.) Later, the blood-vessels 
disappear through obliteration, and the large, plasmatic, 
" epithelioid " fibroblasts give way to small spindle-shaped 
cells and long connective-tissue fibers. Minute extravasa- 
tion- of blood lead frequently to a deposit of brownish 
pigment In this way the intarcted area is gradually 
replaced by a connective-tissue scar, which is outlined from 
the surrounding muscle-tissue by an irregular line. Myo- 
cardial scar- may also develop in another way, which will 
be described later. 

Embolism takes the course previously described when the 
embolus acts in a purely mechanical way. Should, how- 
ever, the embolus contain micro-organisms, as in the case 
<>r* pyemia or mycotic ulcerative endocarditis, then acute 
inflammatory changes ensue, and there results an embolic 
abscess. ( Plate 3, Fig. II.) Microscopically, we find in the 
center of the latter staphylococcal or streptococcal masses, as 
well a- fragments of necrotic muscle-tissue, the nuclei and 
striae of which have disappeared. In the early stages the 
il emboli arc -till -ecu inclosed within the blood-ves- 
sels. Naturally, the walls -<><m break down, and the 
bacteria then lie free in the tissue. They are usually sur- 
rounded with numerous leukocytes with lobulated and 

rmented nuclei. The muscle-tissue at this area has 
entirely disappeared. Around the margin of the abscess 
the leukocytes may be seen a- irregular shoots into the 
intermuscular connective tissue. Sometimes the abscess 
undergoes healing ; this takes place when the bacteria do 
n<>t flourish, but undergo destruction. The pus-cells break 
down through fatty degeneration, and the contents of the 
abscess are then entirely absorbed, while from the per- 



24 PATHOLOGIC HISTOLOGY. 



PLATE 3. 



Fig. I. — Infarction of the Heart = muscle, Organizing. 

X 70. 1, Heart-muscle still containing nuclei ; 2, young connective- 
tissue cells growing into the infarcted area, and infiltrated with 
numerous small flakes of brownish pigment ; 3, new shoots of blood- 
vessels ; 4, necrotic heart-muscle. 

Fig. II. — Embolic Abscess in a Papillary Muscle of the 
Mitral Valve in Septicopyemia. Stained by Gram's method. 1, 
Heart-muscle infiltrated with small round cells ; 2, abscess cavity 
filled with leukocytes ; 3, colonies of cocci in the center of the neigh- 
boring abscesses ; 4, remains of necrotic muscle cells. 



iphery granulation tissue grows into the cavity, which 
is finally replaced by scar tissue, as described in sim- 
ple infarction. In this way also myocardial scars are 
formed. 

Besides the previously described form of myocarditis 
which leads to such rapid softening of larger or smaller areas 
of muscle-tissue, there occurs another form, the real inter- 
stitial myocarditis. The latter is not circumscribed, but 
more diffuse in character, and is not accompanied by direct 
necrosis. Apart from the processes in the endocardium 
which may extend directly to the heart-muscle, this form 
is principally observed in connection with the acute gen- 
eral infectious diseases. Through the action of bacterial 
products or toxins, there is produced first nutritional dis- 
turbances and later inflammatory changes. Primarily, we 
find in these forms quite frequently such degenerative 
changes of the muscle-fibers as cloudy swelling, areas of 
fatty degeneration, vaeuolations, and transverse tears of 
the cement lines — the so-called " myocardite segmentaire " 
of Renaut. [Segmentation and fragmentation of the 
heart muscle-fibers are of common occurrence. The ex- 
istence of a distinct form of segmentary myocarditis, as 
claimed by Renaut, has not been established. Segmenta- 






Tab.3. 









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Hg.l. 






— 

* 






...*2 



■•••:• 



Eig.2. 

Lith.Anst /-: ftechhold, München. 



THE ORGANS OF CIRCULATION. 25 

turn appears as a terminal or agonal event in various dis- 
eases not necessarily involving the myocardium primarily.] 
The transverse striations may be absent over largo areas, 
while the nuclei also -how changes. (Plate 4, Fig. I.) 
Ihre and there the nuclei an- found increased in numbers, 
so that in a single muscle-cell several nuclei occur in rows ; 
<>r tlu-y are found enlarged, ballooned, with a loose chro- 
matin network. Through disintegration of the cells part 
of these nuclei become free. The most striking chang 
however, are observed in the intermuscular connective 
tissue. The fixed connective-ti>sue cells proliferate and 
produce fibroblasts — large spindle-shaped or round, plas- 
matic cells with vesicular nuclei. These accumulate es- 
pecially around the blood-vessels, forming numerous foci, 
while the surrounding muscle-tissue disintegrates more 
and more. 

Gradually, these areas are transformed into fibrous 
sear-, which remain after the inflammatory processes have 
subsided. In this manner various sized -ear- are de- 
veloped without necessarily being preceded by infarction 
or necrosis of muscle-tissue, which, as it degenerate-, is 
substituted by fibrous tissue. Myocardial scars, therefore, 
may develop in three ways: After infarction, after heal- 
ing of nn abscess, and a- a termination of acute interstitial 
myocarditis (Plate 4, Fig. II); but their genesis is not 
yel exhausted, inasmuch as focal disappearance of muscle- 
substance, accompanied with chronic proliferative changes 
of tin- interstitial connective tissue, occur- in nil cases of 
narrowing of the coronary arteries in endarteritis and 
arteriosclerosi — eh ionic fibrous myocarditis or arterio- 
sclerotic myocarditis. 

Infectious new growths, ;i- syphilis and tuberculosis, 
are rare in the heart-muscle, but occasionally are ob- 
served« They do oo1 present any special histologic pecu- 
liarities. 



26 PATHOLOGIC HISTOLOGY. 

PLATE 4. 

Fig. I.— Acute Interstitial Myocarditis. X 300. The trans- 
verse strise of the muscle-fibers are obliterated in places, their nuclei 
increased and swollen, and partly rounded in shape. 

Between the muscle-fibers are seen (1) small round cells, lympho- 
cytes and leukocytes, (2) also young connective-tissue cells (fibro- 
blasts) . 

Fig. II.— Chronic Fibrous Myocarditis. X BO. 1, Heart mus- 
culature ; 2, long connective-tissue fibers between the muscle-bundles, 
containing but very few nuclei and blood-vessels. 



Endocardium. 

Inflammation of the endocardium is usually localized 
upon the valves of the heart, and especially upon those of 
the left side, because their exposed position and peculiarity 
of function render them liable to the primary and most 
intense action of the infectious agents. It has, therefore, 
become customary to apply the term endocarditis to an in- 
flammation of the valves of the heart, while the much rarer 
inflammation of the mural endocardium is generally desig- 
nated as mural endocarditis. According to the views now 
current, all forms of acute valvular endocarditis are con- 
sidered as infectious diseases — that is to say, as due to 
the action of micro-organisms — while the slow, chronic, 
and sclerotic forms are due to atheromatous and arterio- 
sclerotic changes in the intima of the larger vessels that 
spread to the valves, especially to the aortic valve and the 
aortic curtain of the mitral valve. 

It is customary to distinguish two varieties of acute 
endocarditis — the verrucose or rheumatic (sometimes des- 
ignated as benign) and the ulcerative or diphtheric (also 
malignant) form. This classification may be retained, 
provided gradual and quantitative, and not essential and 
qualitative, differences are thereby understood. Quite 
frequently, wart-like vegetations and ulcerative changes 



Tab. 4. 



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THE ORG ASS OF CIRCULATION. 27 

occur at the same time ; they cither develop simultaneously, 
or ulceration is established in a valve the seat of warty 
outgrowths. Both tonus occur primarily as the result of 
minute lesions of the endocardium, which, in turn, are due 
to the action o\' micro-organisms. The organisms either 
accumulate directly on thi' valves from the blood, or act 
on the endothelial lining by their toxins, causing minute 
necrosis on the basis of which other inflammatory changes 
develop. 

In all cases of endocarditis two groups of processes 
occur — namely, inflammatory and thrombotic; at first 
distinct, they later cooperate in producing the so-called 
endocardia] vegetations or efflorescences« The inflamma- 
tory process runs its course in the substance of the valve, 
and the thrombi are deposited from the blood upon the 
diseased valve. 

Verrucose endocarditis is characterized by the forma- 
tion upon the valves, at their lines of closure, of either 
.-ingle or rows of wart-like excrescence-, which later in 
their course usually become organized — that is to say, are 
transformed into connective tissue. (Plate 5, Fig. II ; 
Plate 6, Fig. I.) At first there are small defects of the 
endothelium, followed by proliferation and hyperplasia of 
the fixed cells of the underlying connective tissue of the 
valve. Prom the latter develop strings and groups of 
spindle-shaped, polygonal, and round cells, — so-called 
fibroblasts, — among which lie single small round cells. 
Occasionally, micro-organisms accumulate upon the sur- 
face of these cellular nodules, either singly or in small 
masses. At the border of the proliferating zone are seen, 
embedded in the normal connective tissue, Bingle, large, 
star-shaped, richly protoplasmic cells with oval and 
vesicular nuclei, evidently formed by mitosis from small, 
spindle-shaped, connective-tissue cells. Before long 
there is deposited upon the surface of these cellular 
nodules constituents of the blood, because of the endothe- 






28 PATHOLOGIC HISTOLOGY. 

PLATE 5. 

Fig. L— A Normal So = called " Fetal Gelatinous Nodule" 
at the Line of Closure of the Mitral Valve of the New=born. 

X 70. The connective tissue is very cellular ; ground substance 
partly myxomatous in character ; in it are seen (1) a number of thin- 
walled blood-vessels. 

Fig. II.— A Section of an Acutely Inflamed Mitral Leaflet 
in Mycotic Endocarditis. X 80. 1, Necrotic tissue of the leaflet ; 
2, new formed blood-vessels growing into the connective tissue. 
Between the spindle-shaped, connective-tissue cells are seen many 
large protoplasmic epithelioid cells. 

lial defects which incite thrombotic precipitation. Usu- 
ally, a clear, finely granular mass of closely packed con- 
glutinated blood-plates is deposited directly on the cells ; 
over this layer there forms a fibrinous network or clumpy 
masses appear, which inclose leukocytes. Upon the sur- 
face of this irregularly shaped vegetation a thin cluster 
of leukocytes and bacteria in various numbers also accu- 
mulate. 

In the subsequent course of verrucose endocarditis 
organization of the thrombotic deposit, which leads to 
healing, takes place. From the attachment of the valves 
blood-vessels grow between the connective-tissue lamellae 
toward the excrescences ; they send numerous shoots be- 
tween the fibroblasts toward the thrombotic mass. (Plate 
6, Fig. I.) These consist at first of extraordinarily fine, 
solid processes, which later become hollow and filled with 
red blood-corpuscles. Gradually, the thrombotic mass 
becomes completely infiltrated with granulation tissue, 
which is made up of fibroblasts, small round cells, and 
blood-vessels. Later, this richly cellular and vascular 
granulation tissue is transformed into fibrous scar tissue, 
in which single blood-vessels may remain present for some 
time. In this manner are produced nodular and diffuse 
thickenings of the valves. Sometimes these processes of 



Fig.l. 



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Tab. s. 






■ 






■ 



■ 



- . 

... .. 

■ 



Fig. 2. 



Lith.Anst I: Heuhliold München . 



THE ORGANS OF CIRCULATION. 29 

healing lead to various changes in the form of the valves, 
which produce valvular insufficiency ; or the new tissue 
may cause the valves to become adherent to each other 
ami thus produce narrowing or stenosis of the orifice. 
Subsequently, lime salts may be deposited upon the 
sclerosed tissue in the form of irregular and ridge-like 
projections. 

Ulcerative endocarditis in the early stages can not be 
distinguished from the verrucose, except that almost from 
the very first micro-organisms arc present in much greater 
numbers and are demonstrable in the form of dense, dark 
balls or masses of micrococci. The further differences of 
the course depend upon the specific action of the microbes, 
which, o\\ the <>ne hand, is essentially chemotactic, and, 
on the other, necrotic. We find the connective-tissue 
lamella? of the valves infiltrated to a considerable extent 
with leukocytes, which in places are so dense that there 
result minute abscesses in the valvular tissue with soften- 
ing of the fibers. In the neighborhood of the masses of 
cocci the tissue does not stain nor does it contain nuclei 
— it is necrotic. This zone is marked off from the sur- 
rounding tissue by intense aggregations of leukocytes. 

Suppuration and necrosis lead to more or less extensive 
destruction, to ulceration, and to loss of continuity in the 
inflamed valve. The latter may become perforated, and 
after complete necrosis and suppurative softening whole 
fragments may be detached and -wept into the blood- 
stream. Hence, this malignant type of endocarditis usu- 
ally leads to a fatal end. because metastatic abscesses 
develop in various organs of the body through the pro- 
of embolism ; and, moreover, the individual becomes 
profoundly affected by the toxic action of the ever multi- 
plyii ria. 

The micro-organisms observed in verrucose and ulcera- 
tive endocarditis are the staphylococci, streptococci, diplo- 
i pneumoniae, and, in rare cases, the gonococcL 



30 PATHOLOGIC HISTOLOGY. 

PLATE 6. 

Fig. I.— Acute Verrucose Mycotic Endocarditis of the 
Mitral Valve. Section through the valve and vegetation. Stained 
by Gram's method. X 16- Bird's-eye view. 1, Connective tissue of 
the valve ; 2, a vegetation composed of conglutinated blood-cells, 
fibrin, and, at the periphery, aggregations of staphylococcal colonies, 

3, around which leukocytes have accumulated ; 4, disintegrated and 
partly necrotic valve tissue with infiltrated leukocytes. 

Fig. II.— Verrucose Endocarditis of the Mitral Valve, Or= 
ganizing. X40. 1, Connective tissue of the mitral valve with 
increased number of cells ; 2, endocardial efflorescence ; 3, blood-ves- 
sels growing through the valve and penetrating into the excrescence ; 

4, leukocytic accumulations. 



Diseases of the Pericardium. 

Both layers of the pericardium are frequently the seat 
of inflammatory processes, which are accompanied by an 
outpouring of a fluid exudate into the pericardial cavity 
and with a deposit of fibrin upon the opposing serous sur- 
faces. Most frequently, pericarditis results from exten- 
sion of the inflammation from the pleura, the lung, the 
mediastinum, or also from the heart ; or from metastases 
(embolic) in certain infectious diseases (articular rheuma- 
tism, septicopyemia), and from chemic irritants, as in 
uremia. In the last case micro-organisms are not met 
with. 

Microscopically, we find in the early stages intense 
congestion of the pericardial blood-vessels. Sometimes 
the lumen of the vessel is filled with a network of fibrin 
or with leukocytic thrombi. At the same time, there are 
seen cloudiness and loosening of the endothelium, which, 
later, is rapidly destroyed, so that in advanced cases only 
fragments of endothelial cells are found in areas, mostly 
detached from the underlying membrane. Upon the endo- 
thelial lining, as well as below it, appear, at first, single 



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THE ORGANS OF CIRCULATION. 3 1 

threads of fibrin ; later, more as an interwoven network 
forming a thick layer in which are inclosed varying num- 
bers of leukocytes. The deposition of fibrin, which is the 
result of the exudation of plasmatic finid from the dilated 
vessels followed by coagulation, may attain a consider- 
able degree, forming a thick, reticular membrane or long, 
hairy-like projections upon the surface (cor villosum). 
(Plate 7. Figs. I and II. Compare also Plate 60, Fig. 
I. In the underlying connective-tissue layer of the peri- 
cardium various cellular processes also run their course. 
The connective-tissue cells produce, through mitosis, 
short spindle-shaped or polygonal cell-elements with 
laige vesicular nuclei (epithelioid cells, fibroblasts), while 
the endothelial cells of the lymph and blood-vessels also 
undergo proliferation. Between these appear a great 
number of lymphocyte- and Leukocytes. 

Later, the blood-vessels give off sprouts, which, at first 
.-«»lid. become lmllow and pass into the loosened and cellu- 
lar layer of connective tissue and out toward the fibrin, 
which is gradually infiltrated with new cells and eventu- 
ally completely substituted by granulation tissue. And 
now the new vessels gradually disappear, the cells diminish, 
and the granulation tissue changes into connective tissue 
which is at first rieh in spindle-shaped cells, but later be- 
comes more and more fibrillated at the expense of the cells. 

In thi- way the fibrinous deposit is gradually changed 
into cicatricial tissue, which produce- either flat, glisten- 
opaque thickenings in the epicardium (so-called ten- 
dinous spots, u soldier-spots "), or more or less extensive 
adhesions of the pericardial layers up to a complete 
fibrous obliteration of the pericardial cavity. 

In tuberculous pericarditis the processes described — of 
exudation, proliferation, and organization — run their 
course in the same manner ; but, in addition, there appear 
in the granulation tissue, under the fibrinous layer, typical 
tubercles, generally composed of radially arranged epi- 



32 PATHOLOGIC HISTOLOGY. 

PLATE 7. 
Fig. I.— Acute Fibrinous Pericarditis (Cor Villosum). 

Fibrin stain. X 64. 1, Myocardium ; 2, subepicardial fat-tissue ; 3, 
thickened and richly cellular epicardium ; 4, fibrin deposit, in the 
meshes of which leukocytes are seen ; 5, blood-vessels growing toward 
the fibrin and filled with leukocytes. 

Fig. II.— Fibrinous Pericarditis, Organizing. X127. 1, 
Pericardial connective tissue ; 2, young, connective-tissue layer with 
numerous, thin-walled blood-vessels, epithelioid (fibroblasts) and round 
cells ; 3, fibrin layer (stained red with eosin); 4, the fibrin penetrated 
by new blood-vessels and fibroblasts. 

thelioid cells, giant cells, and round cells, the center early 
becoming the seat of caseous necrosis. 

The confluence of nodules and caseous areas leads to 
the formation of extensive necrotic layers, which are sur- 
rounded by granulation tissue or fibrous tissue. New 
tubercles spring up in the young connective tissue exter- 
nally, undergo the same degeneration, and become covered 
by a new layer of fibrin and of granulation tissue ; in this 
way thick masses are formed, which consist of, at times, 
numerous alternating layers of granulation tissue and 
caseous and necrotic material. Usually, this process goes 
on in the same way in both the pericardial layers, which 
become firmly adherent and thus obliterate t^pericardial 
cavity. 

PLATE 8. 

Fig. I.— Subacute Tuberculous Pericarditis. X50. 1, Heart- 
muscle ; 2, subepicardial fat-tissue greatly infiltrated with small 
round cells ; 3, thickened pericardium ; 4, tubercle with cheesy center 
and epithelioid cells arranged in a radiating manner ; 5, giant cells ; 
6, fibrin deposit. 

Fig. II.— Sclerotic or Milk Spots of the Epicardium. X 65. 
1, Transverse section of the heart-muscle ; 2, normal epicardial con- 
nective tissue ; 3, layer of greatly thickened sclerotic connective-tissue 
fibers. 









"**«« . ' 



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Lilh. An.st A' Hcirhhold . Munrhcn 



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THE ORGANS OF CIRCULATION. 33 



VESSELS. 

The arteries present a wall in which throe layers are 
recognizable: the internal, middle, and external coats. 
In all arteries the internal coat, or intima, is covered with 
Hat. polygonal or four-sided, epithelial cells. The other 
layers are composed of fibrous, elastic, and muscular 
tissues, which reach varying thicknesses and are variously 
disposed according as the caliber of arteries varies. Three 
general groups may be distinguished : In the smallest, 
died precapillary, arteries the epithelial lining is 
situated upon a thin, elastic membrane, outside of which 
lies the media, which is composed of a single layer of 
circularly arranged smooth muscle-fibers. The external 
e<»at i- formed of a few longitudinally disposed, eonnective- 
tissue, and elastic fibers. 

In the middle-sized arteries there occurs, outside the 
epithelium, a layer of connective tissue made up of fine 
fibers, scattered among which lie flat, triangular, or stellate 
cells. This reinforced intima is bordered externally by 
the inner elastic layer, or fenestrated membrane, which is 
perforated by numerous round openings. The media con- 
sists of several layer- of circular, muscular fibers, between 
which are distributed line elastic fibers in varying num- 
bers. Externally, also, the media is bordered by a 
thick«-]* elastic membrane, the external elastic. The 
adventitia consists of partly circular, partly longitudinal, 
connective-tissue fibers, between which ran occasional 
elastic fibers. In some arteries isolated bundles of longi- 
tudinally arranged muscular fibers are found in the ad- 
ventitia. Furthermore, the adventitia supports the minute 
vasa vasorum. 

In the large arteries (aorta, pulmonary, carotid, sub- 
clavian) all the three layers receive additional reinforce- 
ments. In the intima several layers of connective-tissue 
fibers, with polygonal, flat cell-, and also circular elastic 
:; 



34 PATHOLOGIC HISTOLOGY. 

fibers occur outside the epithelial lining. The internal 
elastic coat consists generally of several layers. In the 
middle coat the elastic elements are especially well devel- 
oped, and consist of thick, fenestrated, elastic plates 
that are connected with one another by bands of fibers. 
In the interspaces lie the muscular fibers, which here also 
have a circular arrangement. The elastic membrane is 
not so sharply demarcated as in the arteries of medium 
caliber. The adventitia shows the same structure as in 
these, but does not contain any muscular bundles. The 
two inner layers of the walls of arteries consequently 
never contain vessels when normal ; whenever such a 
condition exists, it is pathologic. 

The veins differ from the arteries especially in the 
marked reduction that takes place in the middle coat. 
External to the epithelial lining there are, in the largest 
and medium-sized veins, some fibrillated connective-tissue 
and also, occasionally, longitudinal, muscular bundles. 
The internal elastic coat is distinctly marked, and consists 
often of several layers. The middle coat contains usually 
only a few circular, muscular bundles, but more elastic 
and connective-tissue elements, which often cross one 
another obliquely ; in some veins — e. g. y the meningeal 
and osseous veins — the media may be entirely absent. 
The external tunic contains also much connective tissue, 
as well as many longitudinal bundles of smooth muscle- 
fibers, which in some veins form a continuous muscular 
coat. The valves in veins are formed by a duplicature 
of the intima. 

The walls of capillaries consist only of a single layer of 
flat, many sided, epithelial cells. 

Arteries. 

Atheroma and Arteriosclerosis.— Atheroma is a dis- 
ease of the vessel wall produced by a combination of pro- 
cesses, in part inflammatory, in part degenerative. It 



THE ORGANS OF CIRCULATION. 35 

nearly always begins in the intima, and leads to diffuse or 
circumscribed, often quite marked, thickening of this 
coat ; eventually, the outer tunics also become involved. 
According to the vascular tunic affected, the process may 
be called endarteritis, mesarteritis, or periarteritis. 

By the word atheroma, or atheromatosis, special stress 
is laid upon the retrogressive changes. It should, there- 
fore, be reserved for those cases in which softening gives 
rise to curdy material : while arteriosclerosis is the more 
appropriate designation for the remaining forms. [Inas- 
much as there is no distinction of fundamental import 
between atheroma and arteriosclerosis, and as arterio- 
sclerosis in it- broadest significance includes atheroma, 
there is no good reason why the term atheroma should not 
be discarded in the interests of simplicity and clear- 
When the process involves a medium-sized or smaller 
vessel of about the caliber of the basilar artery, the ex- 
amination of transverse sections of the diseased vessel will 
show, under low magnification, that the lumen is narrow and 
distorted; it no longer has the normal circular form, and 
i- not central, but eccentric; at one point, or several, the 
wall appears thinner; at others, considerably thicker, due 
t<> nodular or oftener to semilunar protuberances, which 
iroach upon the lumen. Closer examination will show 
that the section i- surrounded by an intact adventitia of 
uniform thickness, and also that the media i- continuous 
and of uniform width. Contrariwise, the intima presents 
marked changes, inasmuch a- the halfmoon-shaped bulg- 
are found to be due to a large increase in it- vol- 
ume at th«-»' points. The internal elastic layer and the 
epithelium are retained only over the thin or normal por- 
tions of the wall. Where the intima begins to be thick- 
1. it is seen that a layer of new tissue arises in the sub- 
epithelial <'<»nn<-ctiv<' tissue between the elastic membrane 
and ill»- epithelial lining. The two points of die crescent 



36 PATHOLOGIC HISTOLOGY. 

PLATE 9. 

Fig. I. — Arteriosclerosis of a Cerebral Artery (Sylvian 
Artery) ; Transverse Section. X 75. The lumen is eccentric in 
outline, as a result of irregular thickening of the wall : 1, Adventitia ; 
2, media ; 3, the internal elastic coat ; at 4 the elastic layer becomes 
lost ; 5, slightly thickened side of the intima ; 6, newly formed, richly 
cellular connective tissue from the inner layer of the intima ; 7, outer 
layer of the same, noncellular, containing several slit-like and rounded 
spaces filled with fat. 

Fig. II.— Arteriosclerosis of a Coronary Artery of the 
Heart; Transverse Section. Weigert's elastic fiber stain. X?0. 
1, Adventitia ; 2, media ; 3, internal elastic coat, at 4 becoming fibril- 
lar and sending shoots into the newly formed connective tissue (5). 

start here. (Compare Fig. I, Plate 9.) The new forma- 
tion consists principally of connective tissue. The elastic 
layer may be traced for a distance into the new tissue, 
where it is soon lost ; often the ends become distinctly 
split up into fibrils. The inner layers of the thickened 
area are relatively cellular, and contain numerous, short, 
dense, spindle-shaped, and also some round, nuclei. The 
external layers are less cellular and densely fibrillated, at 
times almost homogeneous ; in places there are small, 
round, and oval openings, which in the fresh state contain 
fat ; in the latter stages this part of the tissue generally 
undergoes retrogressive changes. The fibers coalesce to 
form uniformly glistening, thick beams, and assume a 
hyaline appearance, not unlike the ground substance of 
cartilage ; small areas may become necrotic and break up 
into a granular detritus in which are free fat, crystals of 
fatty acids, and, quite generally, Cholesterin tablets. Cal- 
cification frequently takes place ; small, round, and irregu- 
lar calcareous granules are deposited, or there arise larger 
calcareous scales or concentrically lamellated, roundish 
masses, which may so press upon the muscular coat as to 
cause it to atrophy in places. 



Tab. Ä 



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Eiff.2. 



Ltth. Ans/ /■: Heichhohi '. München . 



THE ORGANS OF CIRCULATION. 37 

Rapture of degenerated areas into the lumen rarely 
occurs in the smaller arteries. The processes of connec- 
tive-tissue growth and of calcification may gradually 
spread so as to encircle the entire lumen, and then the wall 

of the artery becomes changed, over a greater or less ex- 
tent, into a rigid calcareous cylinder. 

In the larger arteries the process differs, in so far as here 
the degeneration in the intima frequently appears in the 
ground, while the other walls presenl changes of an 
otially inflammatory nature. Here, also, proliferation 
and thickening of the normally well-developed tissue of 
the intima constitute the primary changes; circumscribed 
fibrous areas are formed, which may extend into the media 
and project into the lumen as nodular elevations. Over 
such districts the epithelium is losi early ; the elastic ele- 
ment- are separated and split up; frequently they disin- 
tegrate throughout large area-, forming' small, irregular 
pieces ; and in the midst of the fibrous areas single frag- 
ment- may he demonstrable by means of special staining 
method-. The part of the fibrous tissue adjacent to the 
lumen frequently presents a yellowish appearance. In 
such place- thin, continuous lamellae can he peeled oil', 
which, it' examined when fresh, distinctly -how fatty de- 
ration of the large, Hat cells they contain. Elongated, 
triangular, and stellate groups of closely aggregated, line, 
glistening fat-drops are -ecu, a- well as large connective- 
tissue cells, which become especially distinct on accounl 
of the fat in their interior. ( Plate 10, Fig. III.) 

Lreas of necrosis are common in the fibrous and cica- 
tricial tissue; at firs! oval, or round, inclosed on all Bides 
by connective tissue, they may in time break through 
into the lumen ami thus produce sinuous ulcers with 
undermined edges, the floor being covered with a curdy 
material composed of detritus and crystals of fatty acid-, 
and frequently large accumulations of Cholesterin tablets 
also found". ( Plat.- 10, Fig. II.; 



38 PATHOLOGIC HISTOLOGY. 

PLATE 10. 
Fig. I. — Atheroma of the Aorta (Arteriosclerosis). X20. 

1, Intima, greatly thickened through sclerotic, slightly cellular, con- 
nective tissue ; 2, media, also thickened with patches of new connec- 
tive tissue (at 3) ; 3, shoots of new blood-vessels, surrounded by small, 
round cells, growing from the adventitia toward the intima. 

Fig. II.— Cholesterin Plates and Free Fat=droplets from an 
Atheromatous Patch of Wall of Aorta. X 130. A fresh preparation. 

Fig. III.— Fatty Degeneration of the Cells of the Intima in 
Artheroma of the Aorta. X 300. Fresh preparation, which was 
obtained by stripping a fine lamella from the thickened and yellow 
intima of the aorta. 

The star-shaped cells normally present in the intimal connective 
tissue are clearly shown, since they are filled with a large number of 
variously sized fat-droplets. 

The frequent occurrence of very extensive calcification 
in such cases is well known. The calcareous deposits 
may be situated at various levels ; they occur either in 
the innermost layers of the connective tissue, while the 
necrosis progresses underneath ; or they may reach down 
into the media in the form of broad and thick plates and 
scales with irregular projections toward the lumen. 

The external layers of the arterial wall may also 
show abnormal conditions. Cellular accumulations in 
the adventitia pass in between the muscular bundles and 
elastic plates of the media. These generally correspond 
to the newly formed vessels, originating from the vasa 
vasorum, and running in various directions, sometimes 
reaching into the intima. In their course are seen large, 
polygonal, and spindle-shaped cells, as well as lympho- 
cytes. The elastic elements of the media may be sepa- 
rated by the cell accumulations, and their continuity 
interrupted. Often evidences of degeneration are noticed. 
In the adventitia groups of leukocytes resembling lymph- 
follicles may occur. 



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THE ORGANS OF CIRCULATION. 39 

Arteritis. — Inflammations occur in the walls of all 
arteries that lie in tissue the seat of inflammatory pro- 
cesses : involvement of the arterial walls is especially 
marked in tuberculous and syphilitic granulation tissue, 
hut the arterial changes do not, of necessity, present 
specific characteristics. The acute stages of these pro- 
cesses :uc seen especially well in tuberculous leptomenin- 
gitis. In the beginning the adventitia is richly infiltrated 
with leukocytes, which form broad, deeply stained, cellu- 
lar circle- about the innermost arterial walls. Gradually, 
wandering cells pass into the muscular layers of the 
media. Under high magnification the cells are seen 
plainly making their way between the circularly arranged 
muscular cells ; the wandering cells assume long-drawn- 
out form- ; the nucleus, at first shaped like a pear, be- 
comes long and filamentous, so that narrow passages are 
traversed ; frequently, the emh of the nucleus are swollen 
while the connecting central piece is creeping through a 
tight place. The cells also seem to pass through the pre- 
formed -pace- in the internal elastic coat, and accumu- 
late in small heaps under the epithelium, which is raised 
up fr«»m its normal substratum ; later, the epithelium is 
broken through in place-, and leukocytes reach the lumen 
of the vessel, where they aggregate in the form of small, 
parietal, cellular masses. 

In thi- process exactly the reverse occurs of the leuko- 
cytic emigration as is seen in Cohnheim's well-known ex- 
periment. (Se< General Part, Inflammation.) Here it 
concerns immigration. In the further course the internal 
elastic layer becomes more and more separated from the 
endothelium, which i- lifted up: usually, this condition 
i- not uniformly present at the entire periphery of the 
arterial lumen, <>n<- side of which generally shows the 
normal relations of the elastica and the epithelium. 

Commonly, the continuity of the elastic coal becomes 
destroyed at the point of the greatest accumulation of 



40 PATHOLOGIC HISTOLOGY. 

PLATE 10 a. 

Fig. I.— Arteriosclerosis of the Crural Artery. X 55. Stain- 
ing of the elastic fibers according to Weigert : 1, Adventitia ; 2, com- 
pressed and atrophied media ; 3, greatly thickened intima ; at 4 scle- 
rotic, fibrous tissue, noncellular ; at 5 scales of lime salts containing 
spaces filled with a fatty detritus. 

Fig. II. — Wall of a Small Aneurysm of the Aorta. X 20. 

Weigert's elastic fiber stain. The intima is somewhat diffusely thick- 
ened, and surrounds the lumen of the aneurysm completely (1) ; the 
media (with numerous elastic fibers) is greatly atrophied and nearly 
torn (2) ; 3, thickened adventitia, infiltrated with spindle-shaped and 
round-cell accumulations. 

leukocytes, among which are now found other cells, such 
as large, spindle-shaped cells with much protoplasm and 
a vesicular nucleus ; these cells are plainly fibroblasts 
and descendants of the normal, subepithelial connective 
tissue. 

[In tuberculous leptomeningitis and probably also in 
tuberculous processes elsewhere, there quite constantly 
occurs a subepithelial proliferation of connective-tissue 

PLATE 10 b. 

Fig. I.— Acute Arteritis in Tuberculous Leptomeningitis. 

(From the wall of a small meningeal artery.) X 745. 1, Adven- 
titia ; 2, media ; 3, el astica interna ; 4, detached epithelium ; 5, in the 
muscularis, emigrating leukocytes, showing various stages of deformity; 
6, leukocytes which have passed through the internal elastic coat and 
reached the epithelium. 

Fig. II.— Gummatous Arteritis of the Subclavian Artery. 

X 16. Weigert's elastic fiber stain. The lumen is almost occluded 
as the result of the proliferation of the intima, the elastic fibers of 
which are greatly increased. In the media numerous gummata with 
cheesy centers (1) and giant cells (2) reaching to the intima. Vasa 
vasorum of the adventitia infiltrated with small, round cells. 



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THE OBGANS OF CIRCULATION. 41 

cells, resulting in the formation of a layer of epithelioid 
cells among which giant cells are sometimes found ; this 
form of tuberculous endoarteritis is not due to extension 
from without.] 

Similar changes are observed in tuberculous areas in the 
lungs, especially in the vessels which pass like hands 
through the caverns. In such the increase in the thick- 
ness of the walls leads to great narrowing and even 
closure of the lumen, whereby the entrance into the blood 
of the infectious agent is prevented. Later, the small, 
round cells and leukocytes disappear, and a fibrillated con- 
nective tissue forms in the former vascular channel. 
( I icasionally, in the midst of this connective tissue a new 
elastic membrane appears, thinner than the original elas- 
tic membrane whose general course it imitates ; it forms 
the inner hounds of the new, greatly narrowed, lumen. 
But the process is not necessarily at a standstill as yet. 
Inside of the new elastic layer connective tissue may 
again form, which then lead- to complete obliteration of 
the lumen and occludes the vessels permanently (endarter- 
itis obliterans). Obliterating endarteritis of this kind 
must not be confounded with the process of organization 
which occurs in occluding thrombi and which also event- 
ually may «»Miniate the lumen by new fibrous ti-<ue. 
This process is described in the General Part in connec- 
tion with the consideration <>f Thrombosis. 

In addition to this indifferent form of arteritis, which, 
it is true, is observed principally in tuberculous and syph- 
ilitic granulation tissue, there arc also true, specific forms, 
in which syphilitic or tuberculous nodules arise in the 
rial walls. In gummous arteritis the adventitia es- 
pecially is the seal of the nodules thai more rarely 
develop in the media or reach to the intima, which be- 
comes thick "ii account of newly formed fibrous and elastic 
tissue. At first, the areas are rounded aggregations of 
lymphocytes and epithelioid cells ; soon a caseous necrosis 



42 PATHOLOGIC HISTOLOGY. 

PLATE 11. 

Fig. I.— Arteritis Obliterans (Orcein Stain). X 37. 1, Ad- 

veutitia ; 2, media ; 3, internal elastic coat, which at some places is 
flbrillated ; 4, newly formed connective tissue, nearly filling the lumen; 
at 5 it contains several blood-vessels ; 6, part of lumen limited by a 
fine, new-formed elastica. 

Fig. II.— Arteritis Obliterans (Sylvian Artery) in Syphilis. 

X 80. 1, Adventitia ; 2, muscularis ; 3, normally preserved old 
elastica interna ; 4, proliferated connective tissue ; 5, newly formed 
tunica elastica, imitating the course of the old ; G, newly proliferated 
connective tissue growing into the lumen, which it has fully occluded. 

occurs in the center, while at the periphery there is a ten- 
dency to fibrous encapsulation. Occasionally, a single 
cross-section of large vessels may show in the wall a series 
of such nodules. (Compare Fig. I, Plate 10 b.) 

Tubercle usually extends to the walls of vessels from 
the neighborhood. The thin walls of veins are not rarely 
infiltrated by tuberculous foci, from the rupture of which 
into the lumen the circulating blood may become con- 
taminated with infectious material, leading to a multiple 
embolic tuberculosis in the corresponding capillary terri- 
tory. In case of invasion through a pulmonary vein 
the general circulation becomes involved ; in case of 
a vein elsewhere, a miliary distribution in the lungs would 
follow, and in an artery in its capillaries. 

Aneurysm. — Only those aneurysms are of histologic 
value in which the arterial walls remain intact. In the 
dissecting aneurysms there occurs a simple rupture of the 
intima, and also of the media, through the base of a 
defect of arteriosclerotic or other nature. The entering 
blood stretches the adventitia and forces it outward. 

In the true aneurysm the intima is retained and clothes 
the inner surface of the aneurysm throughout its whole 
extent. The usual changes of the intima are those of 
arteriosclerosis ; the elastic fibers are replaced over exten- 



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TUE OkGANS OF CIRCULATION. 43 

sive areas by a sclerotic fibrous tissue; often the intima 
shows recent vascular foci of infiltration, and its thickness 
is increased. The media presents constant and character- 
istic changes, which must be regarded as essential and of 
fundamental import in the development of the aneurysm. 
It- muscular and elastic layers arc greatly reduced in 
thickness, amounting to complete absence at the point of 

itest dilatation. This is especially well shown in 
aneurysms of the aorta, where the media consists mostly 

lastic fibers, which are now seen to end abruptly in the 
margin of the dilatation, or to become greatly attenuated. 
quently, there are seen interruptions in the contin- 
uity of the muscular and elastic fibers, the fragments hav- 
ing been pushed aside irregularly so that they have lost their 

finally circular arrangement. At the bottom of large 
aneurysms the media isoften wholly absent, the intima be- 
ing in direct contact with the adventitia ; frequently, granu- 
lar blood pigment is found in such places. The adventitia 
also is nearly always altered, especially in the way of 

ssive thickness, on account of increase in the connec- 
tive-tissue fibers ; there are also areas of cell infiltration, 
- r marked about the vasa vasorum, which commonly 
show more or less narrowing and often complete endarter- 
itis obliterans. 

Amyloid degeneration of arteries is considered in the 
i in connect ion with A uivloidosis. 



Veins. 

mmations of the walls of veins are either due to 
nsion from the neighborhood, as in erysipelas of the skin 
and in phlegmons, and successively attack the adventitia, 
media, and intima (periphlebitis, mesophlebitis, endophleb- 
iti — V^irchow), or they arise from infectious thrombi. — 
that is, from within. — in which case the intima is first 
involved. The second form is designated as thrombo- 



44 PATHOLOGIC HISTOLOGY. 

PLATE 12. 

Fig. I. — Tuberculous Arteritis from a Subacute Tubercu= 
lous Meningitis. X 280. 1, Lumen eccentric in outline and greatly 
narrowed ; 2, internal elastic coat, which is torn at 3 ; 3, between it 
and the endothelial lining a number of cells have proliferated, con- 
sisting of leukocytes, lyrnphocy tes, and epithelioid cells ; the muscu- 
lar coat is present only to a slight extent above and to the left ; 4, 
large sized tubercle with caseous center at 5. 

Fig. IL— Tubercle in the Wall of a Larger Branch of the 
Portal Vein. Rupture iuto the lumen ; subacute disseminated tuber- 
culosis of the liver. X 40. 1, 1, Liver tissue ; 2, centrally caseated 
tubercle ; 3, lumen of branch of the portal vein ; at 4 the vessel 
wall is ruptured on account of the richly cellular infiltrations of the 
periphery of the tubercle, Avhich is projecting into the lumen of the 
vein. 



phlebitis, and is more fully considered under Thrombosis, 
as are also the processes in the walls of the veins asso- 
ciated with the organization of thrombi. 

Pure phlebitic processes run a course similar to acute 
arteritis. The vasa vasorum of the adventitia are con- 
gested, leukocytes migrate into the inner layer of the vein 
w r alls and reach the lumen, into which they occasionally 
penetrate and induce a secondary thrombosis, so that here 
also a thrombophlebitis is established. In phlegmonous 
processes a formal suppuration of the venous walls may 
occur. In addition to the pus-cells there are found, how- 
ever, also large polygonal and spindle-shaped cells with 
vesicular nuclei — derivatives of the connective-tissue cells 
normally present in the wall. The muscular coat is 
pressed asunder, its fibers are disarranged, and often the 
muscle nuclei can not be found throughout large areas. 
Severe purulent forms of phlebitis are caused mostly by 
streptococci, and lead, in the majority of cases, to multiple, 
purulent metastases and death, under the clinical picture 
of pyemia. Chronic inflammations of the wralls of veins 




Fifj.L 



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LUfu Anst 'Heiciiholil Simulien 



THE ORGANS OF CIRCULATION. 45 

cause a diminution (»1* their elasticity, followed by dilata- 
tion of the lumen, which assumes a markedly irregular 
form (varix, phlebectasia). In old varices the intima 
consists mostly of a coarse connective tissue of varying 
thickness in different places, often producing nodular pro- 
jections into the lumen. The muscular elements of the 
media are generally wholly destroyed, while the elastic 
fibers usually do not suffer in such marked degree. 'The 
adventitia is usually much thickened, and passes without 
any distinct boundary into the surrounding connective 
tissue, which, especially in the case of subcutaneous 
varices, generally shows a diffuse hyperplasia. 

Occasionally, calcification of the walls of veins occurs ; 
large, calcareous masses of this kind are called phlebo- 
liths, especially those which result from infiltration of 
thrombi. 

The extension to the venous wall of tuberculous and 
syphilitic area- in the adjacent tissue has been referred to. 



LYMPHATIC GLANDS. 

The lymphatic glands are organs in which lymphocytes 
develop, intercalated in the system of lymphatic vessels. 
They consist of a framework of connective tissue in which 
lymphatic cells are accumulated into regular groups. The 
glands, which are more or less reniform, are surrounded 
by a capsule of several layers of connective-tissue fibrill«, 
among which lie a few smooth muscle-fibers. The inner 
surface of the capsule sends off connective-tissue septa, or 
trabecule, which converge toward the hilus, and are con- 
nected with an extremely fine reticular tissue, which is 
tehed across the spaces between the septa. At the 
intersection of the fine fibrillae lie fiat cells with small, 
round^ dense nuclei. The reticulum contains accumula- 
tions of lymphoid cells arranged in the form of rounded 
nodules situated at the periphery of the convexity of the 



46 PATHOLOGIC HISTOLOGY. 

PLATE 13. 

Fig. I. — Acute Suppurative Phlebitis in Phlegmonous In= 
flammation of the Cellular Tissues of the Skin. X 40. The 

lumen of the vein has become narrowed to a slit-like opening (1). in 
which are seen cloudy coccal masses ; the wall is hardly recognizable, 
due to the great infiltration of leukocytes ; the vessels of the adventitia 
are greatly dilated and filled with blood (2) ; some of their shoots have 
proliferated toward the lumen (3) : at 4, remains of tunica media. 

Fig. IL— Varix from the Leg. X 26. Elastic stain. 1, Epi- 
dermis ; 2, cutis ; 3, sweat-glands ; the adventitia of the dilated vein 
with the numerous elastic fibers can not be separated from the sur- 
rounding connective tissue ; the media has disappeared ; 4, thickened 
intima ; the lumen is more or less affected as the result of the great 
irregularity and tortuosity of the vessel. 

glands. These are called secondary nodules or follicles ; 
they lie between the trabecule, and present a dense and 
dark outer zone of concentric layers, and a lighter center 
— the germinal center — in which the lymphocytes are 
produced and in which numerous mitoses are normally 
found. The zone in which the follicles lie is called the 
cortex of the lymph-glands. The follicles send off into the 
central parts cord-like, lymphocytic accumulations, which 
anastomose freely. These form the medullary substance 
or follicular cords. Between the follicles themselves, be- 
tween the follicles and the capsule and the trabecule, and 
between the follicular cords run cleft-like spaces traversed 
by reticulum. These spaces are called lymph-sinuses ; 
they are in direct communication with the lymph-vessels, 
which enter the convexity of the glands as vasa afferentia, 
and emerge at the hilus as vasa efferentia. The sinuses 
that lie between the capsule and the cortex are called mar- 
ginal, those near the hilus and in continuity with the 
efferent vessels are called terminal sinuses. All sinuses 
are lined with flat, polygonal, epithelial cells, as are also 
the fibers of the reticulum which pass through the sinuses. 



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THE ORGANS OF CIRCULATION. 47 

The lymph flows through the sinuses and receives cells 
from the germinal renter-. The larger blood-vessels run, 
for the most part, within the trabecular 

By virtue of their peculiar structure and et* their 
situation as way-stations in the lymph-stream, the lymph- 
glands are capable of retaining chemic substances and 
term«'.] elements of all kinds which reach them from 
the periphery. I [ence, they nearly always are involved by 
inflammatory processes which run their course in the terri- 
tory drained by their respective radicle-. Not <>niy irri- 
tating substances, hut also substances of indifferent nature 
are brought to and deposited in the lymph-gland — a-, for 
instance, blood from hemorrhagic extravasations accom- 
panied with rupture or opening of the lymph-channel-. 
The red corpuscles reach the glands, either tree or in- 
closed in cells, and are here changed to pigment masses. 
Granular and flaky blood pigment may later be carried 
to the sinuses by lymphocytes. 

The peribronchial and other intrathoracic glands are 
extensively involved in the various forms ^l' pneumoconi- 
osis; and after tattooing, exogenous pigments of various 
kind- may reach the regional lymph-glands. 

The distribution of corpuscular elements in the lymph- 
glands follows a certain regularity, depending on the phy- 
sical peculiarities. The line particles are carried by the 
lymph-stream through the vasa efferentia into the lymph- 
sinuses, and are deposited in the perifollicular lymph- 
spaces, either free or inclosed in large, round cells« The 
circumstance that in the early stages the granules usually 
found free, hut later intracellular, indicates that they 
taken up by the cells after they have reached the 
lymph-glands. From the perifollicular lymph-spaces the 
- 3 pass into the follicles and the follicular cords. 
In the earlier periods they are found only at the periphery 
the follicles, the germinal centers remaining free ; at 
first the granules are found mostly in .-mall, round cell-; 



48 PATHOLOGIC HISTOLOGY. 

PLATE 14. 
Fig. I. — Deposition of Pigment in an Axillary Lymph=gland 
as a Result of Tattooing on the Forearm. X 300. The lymph- 
sinuses and peripheral portions of the follicle are filled with large, 
dark masses of pigment which is partly intracellular. 

Fig. IL— Mesenteric Lymph = gland in Typhoid Fever. 

X 360. 1, Small artery with partly detached epithelium ; in the 
adjacent lymph-sinus are numerous large, round cells, some containing 
two nuclei. Their protoplasmic bodies are infiltrated with fat-droplets 
[digestive vacuoles ?] (2); furthermore, lymphocytes (3), red blood- 
corpuscles, and a granular detritus ; 4, clumps of typhoid bacilli. 

later, also in spindle- and star-shaped cells, which un- 
doubtedly belong to the reticulum, as well as in the flat 
cells, which cover the trabeculse. The nuclei of the cells 
are sometimes recognizable among the granules, but often 
the granules cover them, in which case the occurrence of 
masses with regular outlines indicates the intracellular situ- 
ation of the foreign particles. Up to this stage it con- 
cerns a simple deposition of particles in the glands ; later, 
the follicles and follicular cords may atrophy at the same 
time as the connective tissue undergoes hyperplasia, and 
thus obliterate the lymph-spaces. The capsule becomes 
materially thicker than when it is normal ; from its inner 
surface arise the broadened trabecule, which pass as mas- 
sive connective-tissue bands into the gland, and at the 
same time the reticulum is increased by the proliferation 
of spindle-shaped and stellate cells, while the lymphoid 
cells disappear ; the reticular tissue becomes more and 
more fibrous, and eventually it presents a wavy, fibril- 
lated structure. In time the connective-tissue bands 
which are formed in this way change into broad, glis- 
tening, anuclear, hyaline beams, similar to those seen in 
other chronic inflammatory conditions of the lymph- 
glands. 

Occasionally, the particles in an overladen lymph-gland 



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THE ORGANS OF CIRCULATION. 49 

are transferred to the blood ; this is especially due to ero- 
sion of the walls of adjacent blood-vessels by the indur- 
ated and enlarged glands. 

Pathologic pigments originating in the skin and else- 
where may be carried to the lymph-glands, and, under 
certain circumstances, the normal cutaneous pigment may 
likewise be taken to the glands — as, for instance, in syph- 
ilitic leukoderma. 

When phlogistic substances, especially bacteria, are 
brought to the lymph-glands from the territory drained 
by these, then secondary inflammatory foci are produced. 
The course of these processes varies, depending on the 
kind and specific mode of action of the micro-organisms 
in question. Thus, in suppurative inflammations in the 
peripheral parts, in erysipelas, and in pneumonic pro- 
he corresponding regional lymph-glands severally 
present inflammations of the suppurative type. The cap- 
Bule is loosened and richly cellular, and its lymph-vessels 
are distended with leukocytes; the trabecule may also be 
infiltrated with cells ; the vessels are congested : and it is 
especially noticeable that the lymph-sinuses are widened 
at the expense of the follicles and follicular cords. The 
sinuses also contain masses of leukocytes with fragmented 
nuclei, as well as red corpuscles in varying numbers, and 
a finely granular, molecular mass, which consists of de- 
tritus imported from the periphery. The cells of the 
r< ticulum and also the epithelial cells of the glands always 
undergo marked proliferation in processes of this kind. 
\\ hen the pyogenic microbes are present in great num- 
bers, purulent disintegration and abscess formation may 
take place in the glands, in which cases the follicles and 
the medullary parts become infiltrated with leukocytes 
which crowd out the lymphocyte-. In croupous and 
diphtheric inflammations of the mucous membranes the 
onal lymph-glands are also the seal of exudative pro- 
!i the sinuses and at the peripheries of the follicles 



50 PATHOLOGIC HISTOLOGY. 

PLATE 15. 

Fig. I.— Acute Lymphadenitis. Peripheral sinus of a peri- 
bronchial lymph-gland in croupous pneumonia. X 386. 1, Capsule 
of the lymph-gland, the fibers loosened and spread apart ; 2, marginal 
sinus, containing 3, lymphocytes, 4, leukocytes, 5, enlarged and pro- 
liferating epithelium, 6, shadows of red blood-corpuscles, 7, granular 
detritus. 

Fig. II.— Large Cellular Hyperplasia of a Lymph=gland in 
Acute Pernicious Anemia. X 745. The lymph-sinuses are filled 
with large, elongated, fusiform, and round cells, which are looked 
upon as springing from the reticular epithelium. Amoug them are 
single (1) lymphocytes. 



fibrin is deposited ; the blood-vessels of the glands may 
be occluded by fibrinous plugs. 

Characteristic changes occur in the mesenteric and retro- 
peritoneal lymph-glands in typhoidal disease of the intes- 
tines : Typhoid bacilli are found in large, close, aggre- 
gated heaps in the greatly swollen and softened glands 
(medullary infiltration) ; the blood-vessels are greatly 
dilated and filled with red and white corpuscles ; the 
lymph-sinuses are many times wider than normally, the 
follicles correspondingly small and compressed, and at 
times almost unrecognizable ; in the sinuses are found 
numerous, large, protoplasmic cells that often are some- 
what flattened by mutual pressure ; their nuclei are deeply 
stained and granular, resembling those of the lympho- 
cytes ; frequently a cell contains two or three or more 
nuclei ; in the protoplasm are numerous fat-vacuoles. [As 
shown by Mallory, these cells have marked phagocytic 
properties, and the vacuoles may be digestive vacuoles. 
The large cells are often seen to contain red blood-corpus- 
cles, lymphocytes, etc.] These cells appear to originate 
not from the fixed cells, but from the lymphocytes whose 
cytoplasm has greatly enlarged under the influence of the 
infection. [Undoubtedly the epithelium of the blood- and 



Tab. to. 









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THE ORGANS or CIRCULATION. : > 1 

lymph-vessels also may give rise to these cells.] In 
the lat; k tensive but circumscribed ureas o\ 

necrosis develop in the accumulations of these cells ; at 
first the nuclei stain less deeply, followed by their gradual 
but complete fading away ; the cell-body crumbles into a 
granular mass in which the typhoid bacilli remain demon- 
strable lor a Ion-- time. [Capillary thrombosis is a 
prominent cause of the necrosis, j 

In acute inflammations of lymph-glands there some- 
times occur- a hyperplasia of large cells. The sinuses 

»me widened and filled with large, polygonal, spindle- 
shaped, epithelioid cells with one or more vesicular nuclei. 
These cells originate principally from the epithelial cells 
of the glands, and also in part from the branching, fixed 

- of the reticulum. 

The majority of the forms of inflammation mentioned 
may pa— into a chronic stage : interstitial inflammation 
of lymph-glands is at times primaiyand chronic from the 
start. In these cases there is connective-tissue hyper- 
plasia of the reticulum at the expense of the lymphatic 
passages, the follicles, and the medullary substance. In 
place of the extraordinarily fine and fibrillated network 
thick, anastomosing, fibrous bands are formed, the spaces 
between which become -mailer and -mallei* until they are 
wholly obliterated. The epithelioid cells change to small, 
spindle-shaped cells with long fibrillar prolongations. 
The folli sist the connective-tissue increase the longest, 

but finally they also become so small and so deficient in 
cells that they are hard to locate in the dense fibrous tissue. 
Hyaline degeneration of the thickened reticulum, which 
frequently tak< - pi. - rise to glassy, anuclear scales, 

such as are also seen in the dust diseases of lymph-glands. 

Tuberculosis of lymph-gland — an exceedingly common 

nearly always in the follicles, where the 

cha tic nodules develop from the accumulation of 

epithelioid and giant cells formed by the descendants of 



52 PATHOLOGIC HISTOLOGY. 

PLATE 16. 
Fig. I.— Hyaline Degeneration of the Reticulum of a Lymph» 
gland in Tuberculosis. X 280. Among the lymphocytes are seen 
single reticular fibers, which are greatly thickened and transformed 
into shining, homogeneous, nonnucleated bars (1). 

Fig. II.— Chronic Indurative Lymphadenitis with Destruc= 
tion of the Lymph=sinuses and Follicles in Leukemia. X 180. 
1, Thickened capsule ; 2, Lymphaclenoid tissue compressed as a result 
of the new growth of wavy bundles of short fibers of connective tissue. 

connective-tissue elements of the reticulum. At the 
periphery there is a massing of leukocytes (Baumgarten). 
The center of the nodules undergoes caseation, and the 
confluence of several caseous areas may give rise to casea- 
tion involving whole glands or gland packets — " scrof- 
ula/' because so often observed in swine (skropha). In 
the vicinity of the nodules proliferation of the sinus epi- 
thelium occurs and dilatation of the spaces ; occasionally, 
caseation takes place in such districts of proliferation 
without there having first formed distinct nodules or tuber- 
cles. The caseous necrosis may extend to the capsule, 
whence it may extend to the neighborhood, and lead, per- 
chance, to perforation of adjacent hollow organs, such as 
the trachea, bronchi, and vessels. 

PLATE 17. 

Fig. I.— Chronic Indurative Lymphadenitis with Destruc= 
tion as a Result of Increase of the Reticulum in Leukemia. 

X 460. (A part of the preceding section.) The lymphocytes (1) as 
well as the epithelium are greatly diminished on account of the enor- 
mously thickened reticulum. 

Fig. II.— Subacute Tuberculosis of a Lymph=gland. X~0. 

1, Thickened capsule ; 2, caseous centers of the tubercles. At the 
periphery of the gland the tubercles are still discrete, and between 
them lies lymphadenoid tissue. In the center of the gland the 
nodules have formed larger confluent areas. Numerous giant cells. 






Tab. 16. 




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THE una ASs OF CIRCULATION. 53 



THE SPLEEN. 

The hi-, structure of the Spleen presents certain 

similarities to that of the lymph-glands. The capsule, 
coalesced with the external peritoneal covering, is com- 

3ed of rigid, connective-tissue fibers, among which are 
scattered muscular and elastic elements. In the spleen, 
also, the trabecule give rise to an exceedingly delicate, 
e-like, reticular, connective tissue, which is stretched 
across the intertrabecular -pare-, and constitutes the 
framework of the splenic parenchyma. The trabecule 
and the reticulum are clothed with large, flat, and peculiar 
b-shaped epithelial cells. The splenic artery enters 
the organ at the hilus, and divide- into branches whose 
adventitial -heath- at regular intervals are surrounded 
by oval, nodular accumulations of lymphocytes, called 
splenic follicles or Malpighian bodies. The splenic 
follicles are built up exactly according to the plan of the 
lymphatic follicle, like which they also contain germ- 
inal centers in which lymphocytes are continuously pro- 
duced. 

The arteries rapidly break np into arterial capillaries, 
which, contrary to those of other organs, do aol go over 
into - capillaries but end in the so-called intermed- 

iate lacunae, which are wide, vascular spaces, hounded by 
perforated, sieve-like walls, which coalesce to form vein-. 

The remaining space in the spleen is occupied by the 
died pulp. This i- a place of origin as well as de- 
struction o\ red blood-corpuscles. In addition to normal 
erythrocytes the pnlp contain- also nucleated or em- 
bryonal red corpuscles, lymphocytes, and other cells in- 
red blood-discs, ami the various >f trans- 
formation of the blood coloring-matter, and aU<> a varying 

Miliar blood-pigmenl a- well a- lyniph- 

eukocytes, and the epithelial cells situated upon 
the stroma« 



54 PATHOLOGIC HISTOLOGY. 

PLATE 18. 

Fig. I.— Passive Hyperemia of the Spleen. X 360. Pulp- 
spaces overfilled with red blood-corpuscles (1) ; the capillaries also 
greatly dilated (2), their walls traceable for a short distance only. 

Fig. II —Senile Atrophy of the Spleen. X 80. The splenic 
pulp is infiltrated with numerous brownish masses of blood-pigment 
and occasional lines of spindle-shaped cells. The trabeculae are con- 
siderably thinned. 



Variations in the blood contents of the spleen are ex- 
ceedingly common and, up to a certain degree, physiologic. 
Permanent delay of the outflow of the blood from the 
spleen on account of obstruction in the portal circulation 
gives rise to passive congestion of the spleen. 

The peculiar structure of the intermediate lacunae of 
the spleen and their close relation to the spaces in the pulp 
make it evident that in all congestions of the splenic ves- 
sels cellular elements from the blood pass out into the 
pulp tissue. In acute passive congestion not only are the 
capillaries dilated and filled with red corpuscles, but the 
red cells pass into the pulp and press its cells apart, so 
that they appear to have undergone diminution ; the 
trabecule are also pressed together, and the outer layers 
of the follicles infiltrated with red cells. Generally, it is 
extremely difficult, if not impossible, to recognize the walls 
of the smaller blood-vessels. Microscopically, a spleen 
in this condition is enlarged and of soft consistency, the 
cut surface of the pulp is deep red and swollen, so that 
the follicles and trabecule are covered over. In passive 
hyperemia of longer duration reactive changes occur on 
part of the walls of the vessels and of the stromal frame- 
work. The trabecule and the adventitia of the arterial 
vessels are thickened, and the Avails of the smaller vessels 
also become more distinct ; frequently, the endothelial 
cells are swollen, rounded, or nearly cubic, and project 



Tab. 18. 









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« S>® <3> .0« . * 















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v5 f Jtf 

LUfuAnst /■•' KpicIükiIiI München 



THE ORGANS or CIRCULATION. 55 

into the lumen. The reticulum appears increased on ac- 
count of the procure of fibrillated tissue. There occurs 
constantly a deposition of blood-pigment in the form of 
brownish-red, scaly heaps between the connective-tissue 
fibers, and the large, rounded pulp-cells also contain pig- 
ment granules. 

Pigmentation occurs, further, in old age and also in the 
course of severe cachectic diseases, especially carcinoma, 
when the spleen is usually atrophied. The reticulum is 
increased and thickened, and connective-tissue elements 
predominate. In the adventitial -heath of the vessels 
and in the pulp abundant, brownish, and granular pig- 
ment occurs in large and small masses, at first intracellu- 
lar ; later, almost entirely free. In chronic malaria there 
is marked pigmentation of the spleen due to the extensive 
disintegration of the red blood-corpuscles and the trans- 
formation of the hemoglobin into a black pigment, some- 
time- called melanin. In this condition the spleen is 
often thickly beset with black masses, at the same time 
showing the usual changes due to chronic inflammation. 

Exogenous pigments also occur in the spleen ; a genu- 
ine anthracosis is-observed, especially in coal-miners, due 
either to the slow entrance into the blood of pigment- 
laden cells or to the rupture of enlarged, anthracotic 
lymph-glands into the lumen of a vein. 



Infarcts. 

[nfarcts in the spleen are frequent, and result from the 
embolic occlusion of arterial branches by fragments of 
thrombi, endocardial excrescence s, etc. The splenic arteries 
end-arteries in ( iohnheim's sense — that is, do Dot anas- 
tomose with each other — and consequently the white or 
anemic infarct is the most frequent Retrograde currents 
in the veins and extravasations from the capillaries may, 
however, had to a fairly uniform and early infiltration 



56 PATHOLOGIC HISTOLOGY. 

PLATE 19. 

Fig. L— Anemic Infarction of the Spleen. X22. 1, Capsule 
of the spleen ; 2, completely necrotic and anuclear center of the wedge- 
shaped infarct ; 3, dark peripheral zone, which, under the high power, 
shows numerous small nuclear fragments ; the infarct has receded 
somewhat from the surrounding tissue, and is being encapsulated by 
fibrous tissue (4). 

Fig. II.— Hemorrhagic Infarct of the Spleen. 1, Normal 
zone ; 2, the infarcted area ; the spleen-tissue is here necrotic, and the 
nuclei do not take the stain. The area is filled throughout with red 
blood-corpuscles ; 3, transverse sections of blood-vessels ; their walls 
are necrotic. 



with red blood-corpuscles of the infarct, which then be- 
comes red or hemorrhagic. In the subsequent stages the 
anemic infarcts nearly always present a hemorrhagic 
border, due to hemorrhages into the vicinity. 

Splenic infarcts constantly have a wedge-shaped or 
pyramidal form, the base corresponding to the capsule and 
the apex pointing toward the hilus. A fresh anemic in- 
farct is a yellowish-white area that projects above the 
level of the healthy tissue, than which it is of greater 
consistency. Microscopically, the necrosis, as shown by 
the absence of nuclear stain, is sharply defined from the 
healthy tissue. The follicles are still recognizable in the 
infarct, being somewhat darker in color, without, however, 
presenting any nuclear structure. These appearances are 
soon changed. On account of the loss of fluids the 
anemic and necrotic area shrinks and appears more or less 
collapsed ; simultaneously, numerous leukocytes accumu- 
late about the necrotic area, into which they gradually 
wander ; in stained preparations the leukocytic accumula- 
tion appears as a dark ring. In the mean time prolifera- 
tion of the preexisting connective tissue about the infarct 
gives rise to a capsule, which surrounds the dead tissue on 
all sides and cuts into it. The connective-tissue fibers are 



Tab. 19. 




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Fig. 11. 



i.iih An.si I '■: Heicliliolti München 



THE OBQANS OF CIRCULATION. 57 

at first short, mixed with large, spindle-shaped, and 
rounded cells, and they run parallel with the margins of 
the necrotic zone; tor a long time they inclose in their 
meshes long rows of lymphocytes; frequently, pigment 
is present as a resull of the hemorrhage about the mar- 
gin of the infarct While the connective-tissue capsule 
increases in thickness, becoming more and more fibrous, 
the inclosed necrotic area dwindles and shrinks and con- 
nective-tissue processes pass into its substance. Ulti- 
mately, there remains a hard, contracted sear, in the center 
of which there may be found a caseocalcareous or calca- 
reous remnant of the infarct. 

Multiple embolic scars are frequently observed. In 
the case of the hemorrhagic infarct it is to be noted, in 
addition, that the red corpuscles on disintegration give 
rise to pigment masses, remains of which are long to be 
seen in the scar. 

Micro-organisms, when present in the blood in large 
numbers, as may be the case in malignant endocarditis, 
are filtered especially out by the spleen, whose vessels are 
n<»t rarely closed up by heap- or emboli of microbes. The 
effects of such emboli are mechanical and inflammatory : 
the arterial closure produces an anemic necrosis, while the 
bacteria rapidly swarm through the arterial wall and in- 
duce ;i circumscribed, purulent inflammation, which may 
<iid in an embolic abscess. Occasionally, purulent foci 
reach tin- capsule of the spleen and the peritoneum, and 
acute purulent peritonitis may develop in consequence of 
the rupture ol an abscess into the peritoneal cavity. 

Acute Splenic Tumor. 

By virtue of it- peculiarly constructed, wide blood- 
spaces, the spleen constitutes a sponge-like filter, and 
in consequence it becomes extensively involved in all 
inflammatory processes in which microbes, or their pro- 



58 PATHOLOGIC HISTOLOGT. 

PLATE 20. 

Fig. I.— Acute Hyperplastic Splenic Tumor. A teased, fresh 
preparation. X 300. There are many crescent- and sickle-shaped 
cells (epithelial), some containing two nuclei (1); also lymphocytes 
(2), leukocytes (3), and red blood- corpuscles (4). 

Fig. II.— Acute Hyperplastic Splenic Tumor in Sepsis (ln= 

fectious Splenic Tumor). Embedded section. X 300. The same 
elements are seen as in the previous section. The epithelium appears 
now as long, spindle-shaped cells (1), or shorter when cut obliquely (2). 

Fig. III.— Chronic Splenic Tumor Ending in Induration ; 
from Leukemic Spleen in Chronic Leukemia. X 250. Reticu- 
lum greatly thickened ; poorly cellular, fibrillar connective tissue is 
taking the place of the richly cellular pulp. In the connective tissue 
the remains of the pulp, epithelial cells, lymphocytes, and red blood- 
corpuscles are present. At 1 there is a deposit of amorphous masses 
of blood -pigment. 

ducts, enter the circulating blood, just as the lymphatic 
glands constitute a filtering apparatus for the lymph- 
stream. The enlargement of the spleen under such cir- 
cumstances depends on an increased amount of blood in 
the capillaries, — especially the venous, — the exit of red 
blood-discs into the spaces of the pulp, the swelling and 
increase of the cells of the pulp, and on an importation of 
new cells (acute hyperplastic splenic tumor or swelling). 
General septic processes are usually accompanied with a 
marked increase in the volume of the spleen. A fresh 
smear preparation of the soft, swollen pulp of a splenic 
tumor of this kind will be found to contain numerous red 
corpuscles ; large, round, granular, mononuclear cells, 
which often contain whole erythrocytes or fragments of 
such ; also leukocytes with peculiar and horseshoe-shaped 
nuclei ; and especially noteworthy are numerous large, 
sickle- and crescent-shaped cells drawn out into two fine 
processes. Corresponding to the site of the nucleus 
the protoplasmic body is swollen, and often such cells 



Tab. 20. 






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THE ORGANS OF CIRCULATION. 59 

contain two nuclei. These last-mentioned cells evi- 
dently correspond to the fiat cells which normally 
clothe the -picnic framework ; probably the epithelium 
of the capillaries also partake in the formation. At all 
events, the fixed cells are greatly increased ; in sections 
their arched form is, of course, only exceptionally visible ; 
isionally, they arc -ecu in short rows, but generally 
they are cut across at all possible levels. At times the 
cell- and nuclei in the splenic pulp undergo disintegration, 
and large mononuclear lymphatic oells( phagocytes [are seen, 
laden with fat-droplets and granular, cellular detritus ; 
often large area- appear necrotic and tail to take the 
-tain. Frequently, micro-organisms can be demonstrated 
in microscopic sections of the spleen, and, as in lymphatic 
glands, typhoid bacilli are found in characteristic heap-. 
(Plate 14, Fig. II.) 

Accumulations of pyogenic bacteria may cause circum- 
scribed suppurations or -picnic abscesses. In many in- 
fection- diseases, as diphtheria, scarlet fever, and measles, 
the follicles undergo characteristic changes, when they 
appear much enlarged, stellate, and frequently coalesced. 
Microscopically, the follicles are found to contain numer- 
ous, large, polygonal cells, provided with processes, 
vesicular, and at times misshapen, nuclei, a- well a- fat- 
vacuoles. Many of these cells are crowded with -mall, 
deeply stained, nuclear fragments, which also occur free 
in the spaces between the cell-. Such appearances evi- 
dently represent degenerative processes with nuclear dis- 
integration. 

Chronic Splenic Tumor. 
Tin-,. nie infectious diseases, especially malaria and 
syphilis, and occasionally aU<> tuberculosis, may produce 
forms "t* splenic swelling that differ markedly from thai 
just described. In this case indurative changes pre- 
dominate. The reticulum becomes thickened and i- 



60 PATHOLOGIC HISTOLOGY. 

PLATE 21. 

Fig. I.— Diffuse Amyloid Degeneration of the Spleen (Bacon 
Spleen). X 250. The process has as yet not advanced very far. The 
walls of all the blood-vessels are uniformly thickened, and the capil- 
lary and pulp-spaces narrowed. 1, Transverse section of a small 
artery with a greatly thickened and amyloid wall ; at the periphery 
are still seen a few muscle nuclei ; 2, oblique section of a similar 
vessel ; 3, longitudinal section of a small artery ; 4, capillaries. 

Fig. II. — Advanced Diffuse Amyloid Degeneration of the 
Spleen (Bacon Spleen). Spontaneous amyloidosis in a woman, age 
eighty. X "70. Almost complete destruction of the pulp. The amy- 
loid bands (1) are not confined to the blood-vessels, but the reticulum 
is also uniformly affected. The pulp-cells are largely destroyed. The 
remaining cells are the epithelium of the capillaries and a small num- 
ber of lymphocytes. At 2 there are remains of an atrophied Malpig- 
hian corpuscle. 

changed into a densely fibrillated tissue, which is distin- 
guished with difficulty from the trabecule. The lym- 
phatic cells are crowded out, and the capillary spaces are 
narrowed and contain but few blood-corpuscles. The 
follicles are small and widely separated, containing but few 
lymphocytes. Brownish blood-pigment is found quite con- 
stantly between the connective-tissue fibers. A spleen like 
this is naturally hard, firm, pale in color, and dry ; often 
the pigment gives the tissue a distinctly brownish tinge. 

PLATE 22. 
Fig. I.— Amyloid Degeneration of the Spleen (Sago Spleen). 

X24. 1, An amyloid follicle, in which are seen only a few nuclei ; 
the blood-vessels, in transverse section, have also undergone amyloid 
degeneration ; 2, compressed pulp-spaces ; 3, trabecule. 

Fig. II. — Amyloid Degeneration of the Spleen (Sago 
Spleen). X260. 1, Follicle that has undergone amyloid degenera- 
tion, only few islands of cells remaining ; 2, transverse sections of 
blood-vessels with broad, glistening (amyloid) walls ; 3, normal pulp. 






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THE ORG ASS OF CIRCULATION. 1)1 



Defeneration. 

Amyloid degeneration of the spleen is frequent; usu- 
ally, it occurs in connection with amyloidosis of other 
organs, such as the kidney, liver, and intestine : rarely, 
the change is confined to the spleen. As elsewhere, the 
change begins in the walls of the smaller arteries ; later, 
the capillary walls arc involved, and then the other struc- 
tures. It is <[uite peculiar that in the spleen amyloid 
degeneration occurs in two macroscopically differenl forms, 
according to the localization of the process. The degen- 
eration is either diffuse, when it lead- to a uniform in- 
crease in the size and the consistence of the spleen, which 
ha- a characteristic, lardaceous, and glistening appearance, 
or it is confined to the Malpighian bodies, which are 
alv enlarged, glistening, and prominent, appearing on 
the cut surface as swollen grains of sago (sago spleen). 
In the former instance the early stages -how characteristic 
changes: the arterial wall- are greatly thickened and ap- 
pear as homogeneous, glistening rings surrounded by the 
cell- of the adventitia. Oblique section- of such vessels 
appear a- -olid piece- of amyloid substance. The capil- 
laries are unusually plain and sharply outlined, forming 
uniformly colored hand-, or ribbons, when stained with 
diffusely staining anilin dye.-. In the early stages the 
epithelium i- -till present, but tin- is soon h»t here and 
there. The Bpaces of the pulp become -mailer, and the 
number of cells i- reduced ; soon the degeneration spreads 
t«> the reticulum, whose fibers become broader and finally 
coalesce in places ; the reticular -pace- become lined with 
flat and spindle-shaped cells, and the amount of blood 
present i- reduced ; tin- follicles also become smaller, hut 
remnants persist into the latest stages. 

8 _ • spleen i- different ; in this case the degeneration 
begins in the arteries, which bore their way through the 
follicles the so-called arterise penicillate) j their wall 



62 PATHOLOGIC HISTOLOGY. 

PLATE 23. 

Fig. I.— Spleen in Acute Leukemia. X 300. The pulp is 
loaded with mononuclear, small round cells (lymphocytes), and larger 
cells (myelocytes). 1, Capillary epithelium. 

Fig. II. — Staphylococcal Embolism of the Spleen in Pyemia. 

X 70. Two follicles are seen in the field with their arteries in trans- 
verse section, filled with colonies or clumps of cocci (stained by Gram's 
method) (1); between the follicles is the pulp (4); at 2 a clear zone is 
seen surrounding blood-vessels in transverse section. The follicular 
tissue consists largely of lymphocytes. The thickened, darker, outer 
zone is due to the presence of large numbers of leukocytes (pus-cells) 
— early stages of the embolic abscess. 

becomes broadened, and the media is changed into a broad, 
glistening band. The degeneration next extends to the 
adjacent structures, being at first limited to the follicles, 
the lymphoid cells of which rapidly disappear, their place 
being taken by a homogeneous material, which evidently 
arises from the follicular reticulum. Viewed under 
higher magnification, the follicles show coalescing cords, 
which still inclose small groups of lymphoid cells, while 
the degenerated vascular walls remain clearly defined. 
Gradually, the follicles become larger and larger, and 
crowd out the intervening pulp and capillaries, but in 
pure forms of sago spleen the generally homogeneous and 
glistening appearance of the pulp is not produced. Occa- 
sionally, however, the two forms are combined, the amy- 
loid change taking place in the follicles as well as in the 
pulp. 

The histologic changes in the spleen in leukemia and 
pseudoleukemia are quite characteristic. These two dis- 
eases differ in this respect, that in acute leukemia the pro- 
portion between the red and white blood-corpuscles changes 
greatly in favor of the leukocytes, while in pseudoleuke- 
mia there is no such marked increase of the leukocytes, 
the swelling of the lymphatic organs being, however, 



Tab.23. 








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THE ORGANS OF CIRCULATION. do 

similar to that in leukemia. In both diseases the Volume 
of the spleen increases to many times above 1 the normal. 
Acute and chronic changes are recognizable. In the first 
the space- in the pulp and the capillaries are widened and 
tilled with mononuclear cells, while the red corpuscles tall 
into the background and the epithelial cells are only occa- 
sionally visible. The Malpighian bodiesare greatly hyper- 
plastic, and their limit- from the surrounding tissue indis- 
tinct. At time- the follicles only are enlarged, being 
readily distinguishable from the darker pulp as grayish- 
white nodules. In the pure, -picnic form of leukemia 
the -mall, mononuclear lymphocytes principally predomi- 
nate. In addition may occur large colorless cells with 
oval or round nuclei and a granular, eosinophilic proto- 
plasm ; such cells are found especially in the so-called 
myelogenic leukemia. 

Later, the lymphatic hyperplasia of the spleen dis- 
appear- ; frequently, larger areas undergo a uniform necro- 
sis, such as is seen in infarcts. There develops a thick- 
ened stroma, the reticulum becomes fibrillated, as in the 
chronic infectious swellings of the spleen, and brownish 
blood-pigment accumulates about the follicles ; finally, the 
spaces in the pulp become obliterated on account of the 
increasing amount of connective-tissue formation ; only 
the narrowed capillaries persist. The consistency of the 
spleen i- greatly increased, being often almost wooden. 
Tubercles in the spleen are frequently encountered in 

eral miliary tuberculosis. The nodules occur thickly 
in the pulp underneath the capsule, the follicle- generally 
remaining intact. Larger, conglomerate tubercles in the 
spleen are observed frequently in children, a- well as in 
many animals, especially swine, guinea-pigs, and monkeys. 
'I'll'- histologic structure of the tubercles is the same as that 
<>f other organs. 



64 PATHOLOGIC HISTOLOGY, 

PLATE 24. 

Fig. I.— Tuberculosis of the Spleen. X 92. Two tubercles 
are seen situated beneath the capsule : 1, Thickened fibrous capsule ; 
2, trabecular ; 3, caseated centers of the tubercles ; 4, giant cells. 

Fig. IL— Central Portion of a Spleen -follicle in Diphtheria. 

X 745. There are seen numerous, large, polygonal cells with vesic- 
ular, swollen nuclei (1), some are filled with small, dark, nuclear 
fragments (2), also free chromatin granules (3). 

THE BONE=MARROW. 

In the adult the bone-marrow is the principal seat 
of production of red corpuscles. The shafts and the dis- 
tal epiphyses of the long bones contain the yellow, fatty 
marrow ; all other bones, the red marrow. The red 
marrow consists of an extremely fine reticulum, in which 
the cellular elements and the vessels are suspended. 
Here are found, first of all, the so-called myelocytes, or 
marrow-cells, which are ameboid cells of the type of lym- 
phocytes, but with larger, though less chromatic, nuclei ; 
lymphocytes, such as are found in the blood ; large proto- 
plasmic cells with regularly fragmented, lobulated nuclei, 
or many nuclei, — the giant cells of the marrow, or mye- 

PLATE 25. 

Fig. I.— Bone=marrow from the Diaphysis of the Humerus 
in Pernicious Anemia. X 520. The normal fat of the marrow has 
almost disappeared. At 1 only a few fat-cells or fat-vacuoles are seen; 
the number of cells in the marrow is greatly increased ; 2, white mar- 
row-cells, myelocytes ; 3, the same with several nuclei ; 4, nucleated, 
red blood-corpuscles ; 5, cells containing red blood-corpuscles ; 6, 
eosinophilic cells ; between the cells a fine fibrillar reticulum. 

Fig. IL— Bone=marrow in Acute Leukemia from the Di= 
aphysis of the Femur. X 640. The fat of the marrow has disap- 
peared here also. 1, Erythrocytes ; 2, myelocytes, greatly increased 
in number ; 3, lymphocytes ; between the cells is the reticulum. 



Tab. 24. 






■t 



F,g.l. 



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&> 









•fe 



^ • ^ <%> £* ,v >^ 

*«' O. 

© • • • 



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««P CID 



v-i. 



••/v 



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/,////. .i//.s7 /-: Reichhold, München. 



Tab. 17. 



6 4 



•«•4 






















/> ;/. i. 



i % 



P* «®@ ,C «& 



V 7- Jpg* (B 






€> 









1 Vifj. II. 

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W 



THE ORGANS OF CIBCÜLATIOK 65 

loplaxes : nucleated red blood-cells, the forerunners of 
the erythrocytes ; rounded cells, whose protoplasm con- 
tains hemoglobin, the nuclei being small and dense : 
eosinophile cells and ml blood-corpuscles. 

The venous capillaries of the hone-marrow are wide, 
and have sieve-like openings in the walls, like the splenic 
lacume. 

The yellow marrow consists only of connective tissue 
and fat; it develops by fatty changes in the red marrow 
in postfetal life. 

The so-called gelatinous marrow is found in emaciated 
and cachectic individual-, and is the result of fat atrophy 
in the yellow marrow. 

Focal necrosis of the bone-marrow occur- in certain in- 
fectious diseases, especially in variola, typhus, and typhoid 
fever. 

The bone-marrow presents quite a characteristic ap- 
pearance in those diseases that produce changes in the 
serum and the cells of the blood, such as pernicious 
anemia and leukemia. In pernicious anemia the yellow 
marrow of the long hone- changes to red marrow, which 
contain- all the element- normally found in this -ort of 
marrow, such a- marrow-cells, giant cell-, eosinophilous 
cells, and nucleated red corpuscles, 'flic last, as well as 
nonnucleated, red corpuscles, may assume a remarkably 
larg nacroerythrocytes, Ehrlich) ; some may contain 

two or more -mall, dense nuclei. In addition, there are 
usually found numerous cells containing blood-corpuscles : 
these cells are presumably marrow-cells, idled with red 
blood-corpuscles, which have undergone disintegration and 
have been taken up by the phagocytic cells. The fat-tissue 
i- usually reduced to a minimum. 

In leukemia yellow marrow i- also commonly changed 

grayish-red or red ; in the mosl advanced stages it 
becomes ud puriform, a- in the myelogenic form of 

leukemia, in which tin- change in the marrow i- regarded 
5 



66 PATHOLOGIC HISTOLOGY. 

as a primary condition. The reticulum contains marrow- 
cells in large numbers — that is, large, round cells with a 
narrow, protoplasmic ring and large, lightly stained, 
round or oval nuclei, from which the smaller and dark 
nuclei of the lymphocytes are sharply differentiated. In 
this form the blood is also loaded with myelocytes. The 
fat-tissue may be crowded out completely. 

The infectious processes in the bone-marrow, as sup- 
purative and tuberculous osteomyelitis, are considered in 
connection with diseases of the bones. 






II. RESPIRATORY ORGANS. 

THE NOSE. 

The mucous membrane of the nose is lined with a 
single layer of ciliated epithelium, exec])! in that part of 
its cavity known as the auricle, which is covered by 
stratified, flat epithelium. Under the epithelial covering 
is a stratum proprium, richly infiltrated with leukocytes. 
The epithelium of the olfactory region carries the special 
olfactory cells. — peculiarly transformed ganglion cells, — 
which communicate with the olfactory lobes by means of 
nerve-fibers that originate at the base of the cells. The 
stratum proprium also contains alveolar glands. The 
loose submucous tissue supports a well-developed plexus 
of vein-. 

One of the most frequent pathologic processes in the 
nasal mucous membrane is the so-called nasal catarrh, or 
coryza. Histologically, this is characterized by great hy- 
peremia, edema, and increased secretion of the glands, so 
that many of their cells are converted into goblet cells. 
let cells also appear among the ciliated surface cells. 
The Leukocytes of the stratum proprium are increased ; 
they penetrate the epithelium and become mixed with the 
tion, which, in proportion to the Dumber of cells, 
assumes a more or less well-marked purulent character. 
I >• squamated epithelial cells also become mixed with the 
etion, which, furthermore, contains bacteria among 

which diplococci and Friedender'- pneumobacülus pre- 
dominate ; staphylococci are also met with. 

67 



68 PATHOLOGIC HISTOLOGY. 

Should the catarrh become chronic under the influence 
of long-continued, injurious agencies, then the mucous 
membrane becomes thicker than normal on account of the 
extensive development of the veins and of the increase of 
tissue in the stratum proprium. The stroma of the mu- 
cous membrane is infiltrated with young connective tissue 
and round cells, and the glands are enlarged and greatly 
convoluted. In the latter stages it is common to find an 
atrophy of the whole mucous membrane. The glands 
shrink and disappear ; the vessels show a marked thick- 
ening of their walls with narrowing of the lumen, which 
may become wholly closed. The mucous membrane 
becomes dry, the epithelium falls oif or is much atrophied, 
the cells in the stratum proprium and the submucosa 
disappear, and a thin layer of stiff connective tissue 
develops. Such atrophic changes are generally found in 
connection with processes that are designated as ozena ; 
ulcers in the altered mucous membrane are also occasion- 
ally found. 

Chronic catarrh of the nasal mucous membrane is 
not infrequently associated with the development of cir- 
cumscribed and, later, pedunculated swellings or polypi, 
the structure of which resembles that of the mucosa ; the 
stroma is fibrous connective tissue, which is more or less 
swollen by virtue of an accumulation of edematous fluid in 
its meshes ; at times this may give it a typical myxomatous 
appearance, especially when the fluid contains mucinous 
substances ; the nuclei become spindle-shaped, and when 
the cell-body can be demonstrated, it is found to present 
numerous radiating processes. In addition, the spaces of the 
tissue contain numerous round cells, of the type of lymph- 
ocytes, which are found especially numerous in the vicin- 
ity of the vessels, and also some polymorphonuclear leuko- 
cytes. The glands of the normal mucous membrane are 
found also in the polypoid outgrowth ; not infrequently, the 
glands show an extraordinary development, and when their 






ÜESPIXATOSY OBGANS. 69 

ducts are closed or narrowed, cystic dilatations result, which 
may become so large and so numerous that they constitute 
the principal mass of the polyp (cystic polyp). The sur- 
face of these new formations are covered with cylindric 
epithelium — at least, in their earlier stages; later, the 
epithelium may become much reduced or even wholly de- 
stroyed. On the whole, these polyps are best regarded 
as fibromata, which, when edematous, approach the type 
of myxomata. The word polyp does not convey any idea 
of the histologic structure of the growth; it refers only 
to the ur<>— form — /. e., a pedunculated growth, no matter 
whether it is a fibroma, -arc» una, or epithelioma. 

Infectious processes, such as tuberculosis, syphilis, and 
glanders, are met with in the nasal mucous membrane. 
The tuberculous and syphilitic lesions differ in no way 
from the same processes as they occur in other mucous 
membranes; and the nodules of glanders, which may de- 
velop upon the nasal lining of man and animals, are also 
composed of epithelioid cells — derived from the fixed cells 
— and lymphocyte- and leukocytes. Central necrosis 
occur- early, and may lead to perforation of the free sur- 
face and the formation of sinuous ulcer-. 

Diphtheria of the nose, which is not so infrequent, pre- 
sents n<» histologic peculiarities, and further reference is 
made t<> what i- -aid concerning diphtheria of the larynx, 
trachea, and the pharynx. 



LARYNX, TRACHEA, AND BRONCHI. 

The larynx, trachea, and bronchi are covered by a mu- 
cous membrane lined with ciliated cells. Each epithelial 
cell passes through the entire thickness of the epithelial 
ering, hut on account of mutual pressure the form may 
h«' varying, Buch a- conic and spindle-shaped. The 
nuclei are situated at the broadest part of the cell, and, 



70 PATHOLOGIC HISTOLOGY. 

PLATE 26. 

Fig. I.— Diphtheria of the Trachea. (Bird's-eye view.) X 18. 
1, Cartilage of the trachea ; 2, mucous glands ; 3, infiltrated sub- 
mucosa ; 4, false membrane on the mucous surface, composed of fibrin 
and necrotic elements. 

Fig. II.— Diphtheria of the Trachea. X 130. Weigert's fibrin 
stain. 1, Infiltrated tissue of the tunica propria ; 2, fibrin layer, cov- 
ering the largely necrotic mucous membrane ; 3, remains of epithe- 
lium ; 4, peripheral layer of the diphtheric pseudomembrane, consist- 
ing of nuclear fragments and leukocytes ; 5, nonnucleated necrotic 
masses. 

consequently, they occur at varying levels, so that at first 
glance the impression is given of several layers of cells. 
The thread-like, basal processes of the cells end in a 
dense, homogeneous basement membrane. Normally, 
there are found in the epithelium a large number of gob- 
let cells whose protoplasm is the seat of mucoid change. 
In the larynx, however, the most exposed parts, the parts 
subjected to the most movement, are supplied with a more 
substantial and more protective covering — namely, strati- 
fied, squamous epithelium ; situated upon the basal layer 
of cylindric cells is the stratum Malpighii with its char- 
acteristic prickle cells. The parts thus covered are the 
free margins of the epiglottis, a part of its upper and 
lower surfaces, the region between the arytenoid cartilages, 
and the vocal cords. Under the basement membrane 
lies a stratum proprium composed of fibrillated connec- 
tive tissue, elastic elements, and blood-vessels ; scattered 
throughout are numerous lymphocytes. In some points 
of the larynx and trachea the accumulation of lympho- 
cytes becomes more dense, a true lymphadenoid tissue 
being formed ; and at times complete lymph-follicles 
result (posterior surface of epiglottis). The stratum 
proprium of the true vocal cords is, for the most part, 
composed of stiff, parallel, elastic fibers. The glands 



Tab.26. 







Fiff.I. 












■ 





Fig. u. 



I, i lh. Anal E Reuhhold, Manchen . 



RESPIRATORY ORGANS. 71 

in the submucosa and in the deeper layers of the stratum 
proprium belong to the compound, alveolar, mucous glancte. 
The cells, which produce mucus, are cubic or goblet- or 
balloon-shaped. The gland ducts are lined with cylin- 

dric epithelium, which may be provided with cilia for a 
distance into the duct. There are do aland- at all in the 
true cords. The submucosa of the larynx is separated 
from the cartilage by muscular tissue ; in the trachea and 
larger bronchi a -mall amount of tat and of' connective 
tissue separates the submucosa from the internal perichon- 
drium. The cartilage is hyaline except in the epiglottis, 
the cartilages of Santorini and of Wrisberg, which are 
composed <>f elastic <>r reticular cartilage. The external 
surface of all the cartilages is covered by fibrous, ex- 
ternal perichondrium. 

As in the nose, simple catarrh is the most frequent form 
of inflammation in the larynx. In the acute form there 
are diffuse swelling and redness of the mucous membrane. 
The vessels are distended, and frequently small hemor- 
rhages are observed. The stratum proprium of the 
mucosa, a- well a- the submucosa, are more or les< 
crowded with leukocytes, which infiltrate the epithelium 
also and appear in the secretion. Small losses of substance 
frequently appear in the epithelial lining, due mucous 
-land- are -wollen and in a condition of hypersecretion; 
numerous goblet cells appear among the cylindric cells of 
the lining. 

In the course of the infection- diseases, especially 
typhoid fever, numerous bacteria, principally staphylococci 

and streptococci, lodge upon the loosened epithelium, 

which they probably also penetrate. The collection of 
leukocytes in the mucous membrane increases greatly ; 
the superficial parts of the infiltrated area may become 
necrotic, and on being cast off ulcers form whose wall- and 
floors are formed by the pus-cells. In the vicinity the 
epithelüi appear without nuclei and are often occupied by 



72 PATHOLOGIC HISTOLOGY. 

PLATE 27. 

Fig. I. — Ulcer of the Larynx in Typhoid Fever. X35. 1, 
The epithelium still present around the border of the ulcer (stratified 
squamous epithelium, vocal cord) ; 2, epithelium falling off toward 
floor of the ulcer, over which it is completely necrotic ; 3, bacterial 
masses ; 4, tunica propria of the mucosa infiltrated with leukocytes ; 
5, sections of blood-vessels; 6, mucous glands; 7, transverse section 
of striated muscle-fibers. 

Fig. IL— Pachydermia Laryngis. X 60. 1, Cylindric epithe- 
lium ; 2, area of transition into (3) stratified squamous epithelium ; 
4, papillary body ; 5, dilated blood-vessels of tunica propria ; 6, 
mucous glands. 

heaps of cocci. Similar ulcerations occur in the larynx in 
variola. 

In chronic catarrh the entire mucous membrane is 
thicker than normal, due to infiltration of round cells, 
which occur chiefly in small masses, and to the increase of 
the fixed connective-tissue elements of the stratum pro- 
prium. The mucous glands are enlarged, frequently their 
ducts are plugged by secretions, when the overlying epi- 
thelium is liable to be pushed forward a little so that the 
surface of the mucous membrane appears granular (granu- 
lar laryngitis). 

In chronic catarrh of the larynx the epithelial covering 
is the seat of the most important changes. Where strati- 
fied squamous epithelium is present (margins of epiglottis, 
interarytenoid region, margins of vocal cords), the layers 
become increased in number, and in the superficial ones 
hornification is likely to occur. Squamous epithelium may 
also appear in places normally covered by cylindric cells 
but which have fallen off; such islands of flat cells may 
coalesce to form larger areas, which may be recognized 
macroscopically as whitish, usually definitely circum- 
scribed thickenings of the mucous membrane, known as 
pachydermia laryngis (Virchow). Underneath the epi- 



/ 



Fuf.l. 



Tab. 27. 




6 Füf.2- 

Litli.Anst /■: Reichhold, München. 



BESPIBATOXY ORGANS. 



73 



thelium a papillary body may form, the vascular papilhe 
at times growing in length so that warty excrescences! 
irregular thickenings, and branching polypoid outgrowths 
arc produced. A large part of the so-called laryngeal 
polypi owe their development to such chronic catarrhal 
conditions. 

In children croupous and diphtheric inflammations of 
the upper air-passages arc frequent. The characteristic 
feature of such processes is the formation of fibrinous 
membranes associated with necrosis oi' the mucosa. AVhen 
the membrane is easily removable and only the superficial 
layers of the mucosa undergo necrosis, the term croup is 
usually applied ; but when the fibrinous membrane extends 
into the tissue of the mucosa because the necrosis involves 
the deeper layer- of the mucous membrane, then the con- 
dition is anatomically a true diphtheric inflammation, no 
matter whether caused by Löffler's bacillus or by strepto- 
cocci, or by chemic agents. 

In both cases the fibrinous membrane presents a retic- 
ular structure. Between the fibrinous threads lie leu- 
kocytes and desquamated, more or less necrotic, cells. 
In croup this layer of fibrin simply covers the mucous 
membrane, which retains its normal structure though 
usually thickly infiltrated with leukocyte- ; the superfi- 
cial epithelium i- the only part that undergoes necrosis, 
but after the separation of the false membrane perfect 
regeneration of the epithelium usually takes place. In 
diphtheria, on the other hand, the precipitation of fibrin 
rids into the deeper layers of the stratum proprium, 
which thereby lose their distinctness and become ne- 
crotic. Between the layers of fibrin are seen the ami- 
clear scales of the dead epithelium. The gland ducts are 
usually covered by membrane, so thai the secretion ac- 
cumulates in the glands, which may also fall victims to 
necrosis. At the border of \\\<' necrotic tissue is found a 
wall of leukocytes of considerable thickness, which cir- 



74 PATHOLOGIC HISTOLOGY. 

PLATE 28. 

Fig. I.— Tuberculosis of the Larynx. X 16. The epithelium 
is completely destroyed and is absent at many places. The free sur- 
face is formed by the floor of the tuberculous ulcer, which resulted 
from the growth of tubercles in the submucosa, and the tunica propria 
of the mucosa, and upward extension, the tubercles coalescing and 
breaking through the epithelial lining. At times the caseous centers 
of the tubercles, and at times their richly cellular peripheries, are seen 
on the free border of the ulcer. 1, Deep-seated tubercle in submu- 
cosa ; 2, remains of mucous glands j 3, cartilage. 

Fig. II. — Tuberculosis of a Large=sized Bronchus. X54. 
Epithelium entirely disappeared. 1, Cartilage ; 2, mucous glands, the 
interstitial tissue of which is greatly iniiltrated ; 3, tubercle, with 
beginning caseation of the center and numerous giant cells ; 4, greatly 
distended blood-vessels, reaching to the surface of the ulcer. 



cumscribes the area doomed to mortification. The sepa- 
ration of the dead tissue, iniiltrated with fibrin, leaves a 
deep defect, — the diphtheric ulcer, — which in healing 
often gives rise to extensive cicatricial deformation of the 
mucous membrane ; usually, the mucous glands are per- 
manently lost in such areas. 

Tuberculosis of the larynx is frequently associated with 
pulmonary tuberculosis, to which it is usually secondary ; 
a primary laryngeal tuberculosis is much more rare. The 
macroscopic appearances and the histologic characteristics 
vary greatly. In the early stages are found small, sub- 
epithelial, more rarely submucous, nodules, which are 
composed of round and epithelioid cells, and frequently lift 
up the epithelium. With increasing growth the central 
necrosis, which is quite constant, also increases, several 
neighboring areas may coalesce, or solitary nodules increase 
and break through the superficial epithelium and dis- 
charge the caseous and necrotic material in the center ; 
thus arise sinuous ulcerations with overhanging margins. 
Simultaneously, the caseating infiltrations may extend 



Tab. 28. 




vz>. 



tfÜi M 



i 



♦ ',- 



a 



41 



i^./. 






■ ■ •••• 
_> 















/•///// 






LUfuAnst /-.' Reichhold, Manchen, 



KESPIEATOßY ORGANS. 75 

downward and involve the perichondrium, which is de- 
stroyed, bo that the cartilage is laid bare (tuberculous 
perichondritis), and eventually larger and smaller ne- 
crotic pieces may be exfoliated. 

In addition to this common form of ulcerative tuber- 
culosis of the larynx other varieties also occur that 
oftenest arc recognized as tuberculosis only by the micro- 
scopic examination ; in these varieties distinct nodules 
and ulcer- may not be formed, but large, often extensive, 
polypoid excrescences, composed of a diffuse, tuberculous, 
granulation tissue with epithelioid and giant cells. Dis- 
integration and ulceration frequently appear late in this 
so-called polypoid, laryngeal tuberculosis. 

Like tuberculosis, syphilis of the larynx may cause 
granulomatous areas, which disintegrate and form ulcers 
— gummatous laryngitis; extensive necrosis of the laryn- 
geal wall may result, and especially of the epiglottis, 
loading to sequestration of large portions. Healing and 
cicatrization of syphilitic defects frequently lead to exten- 
sive connective-tissue formations, followed by contractions 
and narrowing of the larynx and trachea. 

Leprosy and glanders produce laryngeal nodules and 
ulcers, whose true nature is recognized by microscopic 
examination and the demonstration of the specific mi- 
crobes. 



TRACHEA, BRONCHI. 

The diseases of the trachea and larger bronchi are 
histologically similar to those of the larynx. The dis- 
- of the smaller and smallest bronchi are to bo studied 
in connection with the surrounding lung tissue. 

Acute trachea] and bronchial catarrh manifest them- 
selves by desquamation of the epithelial cell-, enlargement 

the mucous glands, marked vascular injection, and more 
or less leukocytic infiltration of the epithelium and strar 



76 PATHOLOGIC HISTOLOGY. 

PLATE 29. 

Fig. I.— Ectasia of a Small Bronchus. X10. 1, Irregularly 
dilated lumen ; the epithelium, the whole of the mucosa, and a large 
part of the submucosa have disappeared ; at 2 a small portion of car- 
tilage is still present ; the wall is greatly infiltrated with round cells, 
and penetrated throughout with numerous blood-vessels filled with 
blood (3). Externally, a dense, fibrillar, connective tissue is seen in- 
filtrated with dust. 

Fig. IL— Bronchiectatic Wall. X 127. (Part of the foregoing 
section.) 1, Lumen ; 2, cartilage; lacunae in cartilage, dilated and 
filled with leukocytes ; 4, dilated blood-vessels, filled with blood. 

tum proprium. When the catarrh becomes chronic, then 
the swelling of the mucous membrane may persist ; but in 
the later stages the opposite may occur — namely, atrophy. 
The desquamated epithelium is not replaced, the stratum 
proprium and the submucosa become thin, deficient in cells, 
stiff, and fibrous ; the glands shrink and in part disap- 
pear. Macroscopically, the mucous membrane is pale, 
thin, adherent to the cartilages, and traversed by occa- 
sional prominent bands. Frequently, the chronic inflam- 
mation is not confined to the bronchial mucosa but spreads 
to the subjacent structures. The submucous and muscu- 
lar vessels, and the vessels in the connective tissue outside 
the cartilages are dilated and filled and surrounded by 
leukocytes and lymphocytes. The elastic and muscular 
elements are pressed apart ; the leukocytes may penetrate 
through the perichondrium into the cartilage, the ground 
substance of which becomes eroded and absorbed. Finally, 
the cartilaginous spaces are opened and filled with pus- 
cells and the cartilage cells are destroyed (peribronchitis). 
(Plate 29, Figs. I and II.) By these processes and 
through the edema that accompanies the inflammatory 
hyperemia, the whole wall becomes softened and may 
give way. If there occurs a hindrance to the outflow of 
the secretion, or if there is present a strong, positive 



Ift I 






Fig.1. 



Tab. 2!). 






..-4 






Fig. S. 



l.ilh.An.sl /< Houlilwlil München . 



RESPIRATORY (Uta Ays. 77 

pressure in the # bronchial lumen, as in the case of severe 
coughing, larger or smaller areas of permanent dilatation 
may result | bronchiectasis). 

Oftentimes the mucous membrane of such dilatations is 
win »11 v destroyed, and the lumen is bounded by a greatly 
infiltrated, richly vascular, connective tissue, the vessels of 
which are thin walled and dilated ; the continuity of the 
muscle layer is lost, and of the cartilage also, so that 
there i- found only cartilaginous rudiment- or islands. 
In the later stages the connective tissue becomes acellular 
and avascular, and, finally, the irregularly dilated lumen 
is surrounded by cicatricial connective tissue. 



LUNGS. 

A- they become smaller and smaller, the branching, 
arborescent bronchioles lose altogether the cartilage and 
the mucous glands in their walls ; the cylindric, ciliated 
epithelium diminishes in length, becomes polyhedral and 
granular, while below the epithelium lies a thin stratum 
proprium and a circular layer of smooth muscle-fibers, 
and internally a layer of Loose vascular connective tissue 
with numerous elastic fibers. 

In this manner arc formed the respiratory or terminal 
bronchioles. Each continues a- a short, tubular struc- 
ture, the alveolar passage or duet, which in returfi ter- 
mini tes as a funnel-shaped expansion — the terminal vesi- 
• r infundibulum. 
Tic- wall of the terminal vesicle becomes pouched out 
gularly into saccular dilatations, generally half- 
>ular in shape, and designated a- the alveoli or lung 
These alveoli communicate freely with the in- 
fundibulum. and also with one another through minute 
ii their walls — the so-called stigmata of Cohn. 
walls of the alveoli and the terminal vesicles, in addi- 



78 PATHOLOGIC HISTOLOGY. 

PLATE 30. 

Fig. I.— Colloid Goiter. The glandular acini are dilated (1) and 
filled with an increased amount of homogeneous, colloid material 
(stained light red in color). The epithelium (2) is somewhat flattened 
in places. The connective-tissue septa are thickened. 

Fig. IL— Parenchymatous Goiter with Hyaline Degenera- 
tion of the Interstitial Substance. X 70. 1, Dilated acini partly 
filled with colloid material ; 2, epithelium of the same ; 3, hyaline 
connective tissue, the nuclei of which have disappeared. 

tion to the small polyhedral cells, are also lined with 
larger, flat cells, which are extremely thin, clear, and 
polygonal, and partly nonnucleated. They directly cover 
the capillaries, which surround the alveoli in the form of 
a network. When the lung is fully expanded, there are 
present small openings or stomas between the cells, through 
which communications between the alveoli and the finer 
lymph-channels are established. It is believed that it is 
through these stomas that corpuscular elements are carried 
by inspiration into the lymph-stream. The layer of 
smooth muscle is present in the wall of the infundibula 
in the form of remnants from the end bronchioles, but 
muscle-cells are not found in the alveolar walls. The 
framework of the alveolar walls consists of a thin net of 
elastic fibers that continue directly from the end bronchi- 
oles, and of a delicate, fibrillar, connective tissue with 
star-shaped cells. 

A respiratory bronchiole with its infundibula and 
alveoli is surrounded by a layer of connective tissue that 
is continuous at the proximal end with the adventitia of 
the larger bronchial stem, while at the distal end it be- 
comes lost in the connective tissue of the pulmonary 
pleura. In this way sharply outlined areas result, pyram- 
idal in shape, the bases lying under the pleura, while the 
apices point toward the hilus of the lung. These areas 
are known as lobules, and are especially well marked in 






Tab. 30- 






.; 






. 



Tig.l. 









/•>// S. 



RESPIRATORY ORGANS. 79 

the lungs of children and in highly pigmented lunge. 
The capillaries of the pulmonary artery, surrounding the 
alveoli, anastomose more or less freely with the capillaries 
of the bronchia] artery. 

Normally, the alveoli contain air since the very firsl 
inspiration after birth ; under pathologic conditions, how- 
ever, the air may be pressed out either through sinking 
together of the alveolar walls, which come in contact with 
each other, or by other substances thai completely fill the 
lumen of the alveoli. The firsl condition is designated 
as atelectasis. Its prototype is present physiologically 
during fetal life. In the fetus no air enters the alveoli ; 
they are not expanded, but lie close together; at this 
time the alveolar epithelium has nuclei, and the flat, 
thin, nonnucleated platelet- area- yet absent. (Plate 31, 
Fig. I.) Microscopically, the organ shows a compact 
appearance. The few spaces present correspond to the 
lumen- of the bronchi and bronchioles, while the infun- 
dibula are hardly to be made out. 

Under various pathologic conditions part of the whole 
organ may present the same appearance a- during fetal 
life. This is frequently the case when a part or the whole 
of a lobe is pressed upon, a- by tumors, exudates, transu- 
dates, by the enlargement of neighboring organs, etc. 
The lower sharp borders of the lower lobe- frequently 
become compressed and airless a- the result of a high 
position of the diaphragm. Such conditions are desig- 
nated a- compression atelectasis, in contradistinction to 
rption oi- collapse atelectasis, which i- also frequent 
and due to the occlusion of a larger bronchial stem by 
foreign bodies, mucus, etc., when the air present in the 
affected district is gradually absorbed. In consequence, 
the alveoli collapse because no longer exposed to the 
pressure of the air, and the alveolar lumen- become 
pbliterated. 

When sections of this kind are stained to bring out 



80 PATHOLOGIC HISTOLOGY. 

PLATE 31. 

Fig. I.— Fetal Atelectasis of Lung. X 70. The alveolar walls 
are very close together, the alveoli not expanded. The tissue, there- 
fore, appears more cellular than normal, aerated, lung tissue. 1, Bron- 
chioles ; 2, infundibula ; 3, pleura. 

Fig. II.— Compression Atelectasis of the Lung in Sero= 
fibrinous Pleuritis. X 70. The elastic fibers stained. The alveo- 
lar walls with their elastic fibers are approximated and compressed, 
especially at the peripheral portions. 1, Thickened pleura as a result 
of inflammation. 

the elastic elements, the elastic fibers of the alveolar walls 
and the walls themselves will be found wrinkled or 
crumpled and in close contact with each other. (Plate 31, 
Fig. II.) In compression atelectasis the capillaries, in 
contrast to fetal atelectasis, are mostly empty and hardly 
visible ; while in resorption atelectasis they usually con- 
tain the same amount of blood, if not more, than the 
surrounding vessels. If the cause in either compres- 
sion or resorption atelectasis is removed in a certain 
length of time, it is possible for the affected lung area to 
return to its normal state. The air-cells become inflated, 
and their walls are smoothed out. If, however, the con- 
dition of atelectasis is present for a longer time, then 
adhesions take place between the folded alveolar septa. 
First, the alveolar epithelium degenerates, and then the 
fixed, connective-tissue cells proliferate, and finally lead 
to the formation of a cicatricial area which remains per- 
manently airless. When the atelectatic area is located at 
the periphery of the lung, the pleural or subpleural con- 
nective tissue takes an active part in the proliferation and 
formation of the new tissue. The capillaries are fre- 
quently in a state of hyperemia and stasis ; they may rup- 
ture and lead to extravasations into the thickened tissue, 
with subsequent deposit of pigments. 

Resorption atelectasis, when resulting from bronchitis 



Tab. 31. 




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• ,- W% ;eyim a .-■■-■■. - 

i>V/./. 






t 













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J ith . AftSt /:' ReiChhold, München 



RESPIRATORY ORGANS. 81 

(especially in children), is usually a forerunner of inflam- 
matory processes that extend from the bronchial wall 
down into the airless lung tissue. (See Peribronchitis and 
Lobular Pneumonia.) 

The reverse condition of atelectasis is emphysema of 
the lune. By this term we understand an increase of 
the air contained within the lungs. Sometimes it occurs 
acutely after severe coughing orforcible inspiration, which 

ds to rupture of the air-passages or space-, and extra- 
vasation of the air into the interlobular septa as well as 
under the pleura. This condition is designated as inter- 
stitial or intervesicular or subpleural emphysema, and 
shows no changes <>f any particular interest from a histo- 
logic point of view. 

Important histologic changes are found, however, in 
the substantial er vesicular form of emphysema. This 
consists in the distention of the air-cells or spaces, and a 
simultaneous disappearance of their walls or septa so that 
an apparent increase in the volume of the whole organ is 
produced. Vesicular emphysema must be distinguished 
from atrophy of the lung, which always occurs more or less 
in old age and is distinguished histologically from emphy- 
sema only with difficulty. The alveoli, first of all, are 
flattened <>nt. the edge-like partitions which project into the 
infundibular spaces become shorter, while the infundibula 
;i- a result become larger. Constant and increased intra- 
vesicular pressure causes the alveolar septa to become 
• xtended, stretched, and thinned out. Naturally, thi- 
n-ion first shows it-elf at those areas where the walls 
contain minute openings. The stigmas of Cohn are ren- 
dered dehiscent, and in the thicker sections they can he 
recognized on the surface of the alveolar wall- as round 
oi' oval holes. It' the extension continues, the alveoli 
become confluent with the infundibular spaces in larger 

as : the increased rarefaction of the lung and the dis- 
appearance of tin- elastic fibers and blood-vessels produce 
8 



82 



PATHOLOGIC HISTOLOGY. 



PLATE 32. 

Fig. I.— Anthracosis of the Lung. X 100. The lung tissue 
is very much indurated as the result of newly formed connective tissue 
in which are embedded star-shaped masses of fine, granular, blackish 
pigment of inhaled coal particles. 

Fig. IL— Siderosis of Lung (Red Iron Lung). X330. The 
lung tissue is loaded with numerous masses of iron-dust, which 
are found mostly within the cells in the thickened alveolar walls, 
the nuclei being covered by the pigment. Between the pigment 
cells the connective tissue is fibrillar and contains but few nuclei. 
Alveoli partly compressed. Atypical, proliferated epithelium in the 
alveoli. 



large, bladder-like, thin-walled spaces, varying in size, 
according to circumstances, from that of a pea to that of 
a large walnut, and even larger (bullous emphysema). 
(Plate 33, Figs. I, II, and III.) 

The normal elastic fibers, always slightly tortuous or 
bent, become stretched, give way gradually, and are 
finally torn in half. The same changes take place in 
the capillaries in the intervesicular and infundibular 
walls. Their lumen becomes narrower and narrower 



PLATE 33. 



Fig. I.— Emphysema of the 

alveolar spaces, extraordinarily thin 
and torn at many places so that the 
one another. 1, Interlobular septum 
3, dilated and confluent alveoli. 

Fig. IL— Emphysema of the 

seen, whose interalveolar septa are 
and about to be torn through in the 



Lung. X40. Greatly dilated 
alveolar septa, deficient in cells 
several alveoli communicate with 

; 2, contiguous but normal alveoli ; 

Lung. X 340. Two alveoli are 
extremely thin, deficient in cells, 
center. 



Fig. III. — Emphysema of the Lung. X 54. From an injected 
preparation. 



Tab. 32. 







Ms 



' ^Mf: 






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• •■' * • 




JHG&y* ■>■■ 

Fn,.L 



im 










V38 






LUfuAnst /•■' Reichhold, München. 



Tab. .33- 












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Mg.l. 






*« 



V 
»9 










/•v; 7 ,y. 



///fl. /Jz/.v/ A' Reichhold, München. 



RESPIRATORY ORGANS. 83 

from the constant stretching, until finally the walls 
for some distance lie in such close contact that a solid 
fiber results : eventually this i< torn, and the stump may 
-till he found projecting into the dilated space. Rudi- 
ments of degenerated or obliterated vessels are especially 
well shown in injected preparations. In severe forms 
of emphysema there i- also noticed a similar oblitera- 
tion of the -mailer arteries and veins with eventual dis- 
appearance <>f the walls. Naturally, the alveolar epithe- 
lium also becomes destroyed through fatty degeneration. 
Usually the emphysematous portion- are less pigmented 
than the normal lung tissue. This is due, first, to the 
fact that the pigment masses lie further apart on account 
of the widening of the tissues, which macroscopically 
gives it a lighter appearance, and, secondly, to the resorp- 
tion of the original pigment inclosed within the alveolar 
and vascular epithelium, which, on breaking down, sets 
free the pigment. 



Circulatory Disturbances. 

In long-continued obstruction to the outflow of blood 
from the hmg- to the left auricle, especially from insuffi- 
ciency and stenosis of the mitral valves, there result- a 
passive hyperemia of the lungs. Later, the organ in- 
creases in consistency, due to hyperplasia of the connec- 
tive tissue. With the deposition of blood pigments the 
tissue acquires a brownish discoloration, and the condition 
i- th<-n designated a- brown or cyanotic induration. 

A- a resull of the damming back of blood in the vein-, 

tin- capillaries in the alveolar walls are greatly distended ; 
they become twisted and tortuous, and projeci irregularly 
into the alveolar lumen. In this manner the alveolar 
spaces become contracted and the respiratory surface 
diminished. (Plate34, Figs. I and II.) With the increase 
of intracapillary pressure more or less diapedesis of red 



84 PATHOLOGIC HISTOLOGY. 

PLATE 34. 

Fig. I.— Brown Induration of the Lung. X 130. Thickened 
alveolar septa, due to newly formed connective tissue arranged around 
the blood-vessels. Large, round cells containing amorphous granular 
blood pigment partly in the septa and partly within the alveoli (so- 
called "Herzfehlerzellen"). 

Fig. IL— Passive Hyperemia of the Lung. X 250. 1, Ectatic 
and distended blood-vessels, filled with blood ; 2, engorged and tor- 
tuous capillaries ; 3, lumen of alveolus ; 4, increased interlobular con- 
nective tissue ; 5, cells, containing blood pigment, within the alveolar 
lumen ; 6, free, amorphous blood pigment. 



(also white) blood-corpuscles takes place and, occasionally;, 
rupture of the capillaries. The extravasated blood is 
found in the alveoli as well as in the tissues of the alveolar 
septa, and the same changes occur as in extravasated 
blood in general. Later, the red blood-corpuscles are 
taken up by the desquamated alveolar epithelium, as well 
as by wandering cells (lymphocytes and leukocytes), and 
also by young connective-tissue cells that proliferate from 
the alveolar walls as a result of the irritation of the 
hemorrhage. The alveolar lumen and the alveolar septa 
are then found to contain cells loaded with masses of 
yellowish or brownish pigment. The pigment-containing 
cells are expectorated and appear in the sputum as the 
cells of heart-disease (" Herzfehlerzellen "). 

The deposit of pigment and subsequent proliferative 
changes in the alveolar walls lead to thickening of the 
walls and increased consistency. The elasticity of the 
tissue is lessened while the respiratory surface becomes 
encroached upon on account of the continued compression 
of the alveoli. Sometimes areas of alveoli are completely 
filled with pigment-containing cells, so that there results 
a condition of catarrhal inflammation. In addition to 
blood pigment the cells may also contain coal pigment, 



Tub. 34. 



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XU 



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.-■■ 








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Fu,l 



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, > . • • ' * ' * « 



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l.ith. Ansl /•' ReüMiold, München*. 



RESPIRATORY ORGANS, 85 

which is easily distinguished, however, on account of its 
black color. When the cells break down, the pigment is set 

free and is then deposited in the thiekened alveolar septa, 
the peribronchial and perivascular connective tissue, and 
lymph-spaces as amorphous, hematoidin granules arranged 
in n»\\-. Hematoidin crystals are rare in the lung. 

In severe chronic passive hyperemia there often occurs 
complete stasis in many of the capillaries. The blood- 
corpuscles are then changed into pigment within the ves- 
sels, and in such instances we find the lumen of the 
capillaries and the smaller arteries dilated and completely 
filled with pigment, some of which is inclosed within cells. 
In obstructed vessels of this kind the circulation entirely 
ceas 

This form of passive hyperemia must not be mistaken 
for another that develops in the posterior portions» of the 
lower lohe- in cases of heart failure and asthenia — namely, 
hypostatic congestion. Here we also have dilatation 
of the vessels with passing out of the red blood-corpuscles 
into the alveolar tissue. If, in addition, inflammatory 
change- occur, the process is designated marantic spleni- 
zation. Likewise, edema of the lung is the result of a 
passive hyperemia that, however, often occurs first during 
the death agony. (Plate 36, Fig. I.) It may either 
develop acutely or in a more chronic way; oftentimes 
it accompanies inflammation of the surrounding lung 
area, or it i- a forerunner of inflammation, being then 
known a- inflammatory edema. In edema the alveoli are 
filled with a richly albuminous fluid and cell- (alveolar 
epithelium and round cells). For microscopic examination 
it i- besl to preserve the fluid by throwing -mall piece- of 
edematous lung tissue into boiling water for one or two 
minutes. This causes the fluid to become coagulated, and 
it is found in the alveoli as an opaque, grayish, crumbling, 
oi' thread-like mass. 

'I hi- procedure i- advisable when it is necessary to 



86 PATHOLOGIC HISTOLOGY. 

PLATE 35. 

Fig. I.— Marginal Zone of Hemorrhagic Infarct of Lung. 

X 40. 1, Lung tissue in which the alveoli are normal ; 2, compressed 
and airless lung tissue ; 3, infarcted lung tissue infiltrated throughout 
with red blood-corpuscles ; the nuclei are poorly stained, and necrosis 
has occurred in places. 

Fig. II. — Fat Embolism of the Lung, Resulting from Frac= 
ture of a Long Bone. X 100. Fresh preparation. There is seen 
an infundibulum with several alveoli, in the wall of which are present 
globular, sausage-shaped, and branched, shining, yel low bodies, partly 
inclosed within the capillaries and partly free as a result of the teasing. 



differentiate between edematous fluid in the lung and 
aspirated water as a result of death by drowning. 

Oftentimes the alveolar walls and interlobular septa also 
become saturated with the edematous fluid. The inter- 
stitial tissue is then found swollen and expanded, and the 
same coagulated mass is seen in the spaces. In inflamma- 
tory edema the fluid is often mixed with numerous cells, 
especially leukocytes. 

Infarction. 

It has been pointed out that the lung tissue is richly 
supplied with blood-vessels ; therefore, in case of occlusion 
of an arterial branch the conditions are favorable for the 
establishment of collateral circulation. For, as a matter 
of fact, we frequently find on the postmortem table larger 
or smaller arterial branches of the lung occluded with 
thrombi without leading to any consecutive tissue changes. 
This being the case, then the cause of infarction of the 
lung must be sought for in other injuries of the vessel 
wall, and this is found in chronic passive congestion. For 
that reason infarction occurs most frequently in lungs that 
are the seat of passive hyperemia. (Plate 35, Fig. I.) 
If in such a lung one of the arterial branches is occluded 



»J 






Fig.1. 



Tab.35. 






■ 
- 






; ; 



& 









l.ith. A/i.st F Reichhold, München. 



, 



RESPIRATORY ORGANS. 87 

by an embolus, the area of tissue beyond the vessel be- 
comes anemia Blood now flows from the surrounding 
capillaries into the empty vessels, but the walls have lost 
their integrity ; the blood-corpuscles pass out, as through 
a sieve, into the lumen of the alveoli, infundibula, and 
oftentimes into the smaller bronchi, infiltrating in a diffuse 
manner these structures. All forms of infarction of the 
lung are, without exception, hemorrhagic. Anemic infarc- 
tion does not occur, on account of the peculiar arrange- 
ment of the blood-vessels. 

At this stage the infarcted lung tissue is found more or 
less necrotic, manifested by the absence of the nuclei j 
while the tissue itself is infiltrated with closely packed red 
blood-corpuscles. Frequently, the capillaries are occluded 
with fibrinous or hyaline thrombi, which can be removed 
as fine bands or strings. Occasionally, fine fibrin threads 
arc demonstrable between the extravasated red blood- 
corpuscles. The infarcted area is usually sharply out- 
lined from the surrounding tissue. 

After the infarct lias existed for some time it may be- 
come absorbed. The necrotic lung tissue breaks down 
through fatty degeneration, while the blood is transformed 
into pigment, which is taken up by wandering cells. The 
infarct may also become organized — that is to say, it i< 
replaced by granulation tissue that is derived from the 
surrounding connective tissue, especially the peribronchial 
— and finally transformed into a fibrous scar. (See 
( organization, in ( reneral Part. ) 

A lbnn of embolism peculiar to the lung is fat em- 
bolism. It occurs after extensive crushing and bruising 
of the Bubcutaneous fat-tissue and the fatty marrow of 
bones, as a result of traumatism or fractures. (Plate 35, 
Fig. II. The f;it droplets are absorbed by the open veins 
and transported to the right side of the heart and then to 
the lungs. It may also occur, though rarely, in cases of 
spontaneous lipemia, ;i- a result of diabetes. The inter- 



88 PATHOLOGIC HISTOLOGY. 

alveolar capillaries and, occasionally, the smaller arteries 
are found plugged with yellowish, transparent fat droplets 
or fat-globules. These are partly seen singly or in the form 
of branched or sausage-shaped masses. The fat can be 
fixed in loco with osmic acid or it can be stained with 
sudan III in frozen sections after hardening in formalin. 
The sections must not be too thin. 

Occasionally, we have pulmonary emboli that are cel- 
lular in their nature. Thus, in cases of malignant tumors 
the metastases in the lung can oftentimes be traced to 
small emboli of tumor cells. (See Metastasis, General 
Part.) 

True parenchyma cell emboli also occur in the lung. 
Thus, for instance, after traumatic injury of the liver as 
well as in the course of the acute infectious diseases and 
intoxications, liver cells may be carried to the lungs as 
emboli. Placental cells, especially in eclampsia, and giant 
cells from the bone-marrow after injury to, or operations 
on, bones, may also be carried to the lungs as emboli. 

Pneumoconiosis. 

Dust is constantly carried into the respiratory organs 
with the inhaled air ; some of the dust is caught in the 
upper respiratory tract by the ciliated cylindric epithelium 
and again discharged, while the rest reaches the alveoli of 
the lungs. Even in the trachea and bronchi the inhaled 
dust particles are found partly inclosed by cells ; in the 
lung tissue the dust is also found either free or intracellular. 
These cells, which are known as dust cells, are partly 
small and round, with a darkly granular, richly chromatic, 
and sometimes lobulated nucleus, while others are larger, 
flat, and have clear vesicular nuclei. The former are 
lymphoid elements that have wandered out from the blood- 
stream, while the latter are desquamated, alveolar, epithe- 
lial cells. In the bronchi the cylindric epithelial cells 



RESPIRATORY ORGANS. 89 

and tile so-called goblet cells are transformed into dust 
cells. Occasionally, the still adherent epithelium is Pound 
filled with dust particles. Sometimes a number of such 
epithelial cells are detached from the underlying basement 
membrane while joined, and appear as small, membranous 
flakes. In cases of excessive inhalation of dust larger 
area- are found, in which the alveoli are completely filled 
with dust cells. 

The larger part of the free and intracellular dust is 
again discharged through the bronchi : the rest, however, is 
retained within the lung and deposited at certain fixed 
depot-. Hen- it may accumulate in stich quantities as 
to give the tissue a distinct, oftentimes intense, discolo- 
ration. The free particles and the dust cells find their 
way between the epithelial cell- of the alveolar walls, 
through line stomas in the lymph-spaces of the connective 
tissue, and from thence into the narrow lymphatic vessels 
in which the dust, especially coal dust, is closely packed in 
row- and fill- up the lumen. The free granules are swept 
along by the lymph-stream, while the dust cells, besides a 
passive, also play an active, part and penetrate into the 
lymph-stream by their own ameboid movements. Both 
lymphoid and epithelial cell- have this power. 

Usually, the dust i- found accumulated largely in the 
inter- and peri-infundibular a- well as peribronchial and 
perivascular connective tissue : in the latter it accumulates 
in the adventitial lymph-spaces of the -mall, pulmonary, 
lymphatic nodules. Here the dust may he arrested for 
-«»in.- tiiii.- ; later, it may break through tin- filter, whence 
it i- transported to the pleura, the pleural, peribronchial, 
and mediastinal lymph-glands. Not rarely the dust 

crowds into the wall- of the blood-vessels a- far a- to the 

internal elastic coat. 

Inhaled dost, when present in large quantities, has 
th.- power, by virtue of it- chemic or physical nature, to 
stimulate or irritate the lung tissue to an inflammatory 



90 PATHOLOGIC HISTOLOGY. 

reaction. The protoplasm and the nuclei of the dust cells 
break down with the formation of fatty granules, while 
the surrounding alveolar wall is infiltrated with numerous 
round cells and eventually replaced by fibrous tissue. 
The alveolar wall finally becomes very much thickened, 
and there results a small connective-tissue nodule, which 
contains more or less free pigment granules. Later, the 
nodule may undergo hyaline degeneration ; so much so 
that it becomes hard to trace its genesis. It is difficult 
to draw a sharp line between these processes and certain 
forms of true inflammation of the lungs, which are classed 
as circumscribed indurative bronchopneumonia (endoperi- 
vasculitis nodosa of Arnold). 

In long-continued inhalations of dust in large amount 
such nodular masses may fuse and give rise to extensive 
indurations. 

The pigment masses deposited in the peri-infundibular, 
peribronchial, and perivascular tissue may excite the latter 
to similar connective-tissue proliferation, which leads 
to further enlargement of the indurated areas (peri- and 
endolymphangitis fibrosa or peribronchitis and perivascu- 
litis nodosa). In the same way similar nodules may 
arise in the pleura, as in the case of the so-called miliary 
fibromas of the pleura observed in stone-cutters. 

The extent and intensity of the histologic processes 
described depend upon the kind of dust, as well as on 
the amount of dust, inhaled. Fine amorphous soot — 
that is, amorphous coal dust — is found in the lungs of 
nearly every individual of adult age. This condition is 
designated as simple anthracosis. Since soot-particles 
have no sharp edges, indurations are but seldom ob- 
served. In exceptional cases, when the deposit is exten- 
sive, nodular or larger indurations occur in the lungs. 
(Plate 32, Fig. I.) The dust of bituminous coal acts 
more intensely, since the fine, sharp-edged, chip-like 
particles give rise to considerable irritation and inflam- 



RESPIBATOBY OEGAXs. 91 

nation in the lung tissue. (Plato 32, Fig. II.) This is 
even more 90 in case of inhalation of stone dust (chaßöO- 
sis pulmonis) and metal dust (siderosis pulmonis). In 
these cases it may load to circumscribed necrosis of lung 
tissue, and finally to cavity formation. 

Du-t thai on account of its chemic or physical nature 
acts injuriously upon the lung tissue produces thereby an 
increased susceptibility to infection. The predisposition 
to tuberculosis excited by metal and stone dust is gener- 
ally known and feared. 



Pneumonia. 

By the term pneumonia we understand the filling up of 
the air-cells with inflammatory exudate, as a result of 
which area- of lung tissue become airless. When the in- 
flammatory irritant acts directly upon the inner surface of 
the lung, larger portions of lung tissue (one or more lobes) 
may become simultaneously involved. In that ease the 
inflammatory exudate, which is derived from the alveoli 
themselves, develops suddenly, and the condition is known 
as genuine or lobar pneumonia. 

More frequently, inflammation of the lung results from 
extension of a primary affection in the larger or smaller 
bronchi. It may either spread by continuity — that is to 
say, along the inner surface of the bronchi, bronchioles, 
infundibula, and then to the alveoli — or by contiguity — 
that is, perpendicular to the long axis of the bronchus, 
spreading transversely outward to the surrounding hing 
tissue. The inflammation spreads from the epithelial sur- 
face to the stratum proprium, and then outward into the 
peribronchial connective tissue. In this manner develops 
an area of peribronchitis. 

In both instances the pneumonic process that results is 
d< signated as bronchopneumonia. 1 1> manner of spread- 
ing is lobular in character — thai is to say, the inflamma- 



02 PATHOLOGIC HISTOLOGY. 

tion does not usually extend beyond the limit of a lobule 
and its accompanying bronchiole. 

Furthermore, areas of pneumonic infiltrations may be 
the result of emboli lodged in the blood-vessels of the 
lung and containing substances acting as inflammatory 
irritants. Around the embolic thrombus there usually de- 
velops a purulent inflammation (embolic or metastatic 
pneumonia). Its mode of spreading is not dependent 
upon the course of the bronchi, but is wholly an irregular 
one — the so-called insular form. 

Finally, inflammation of the lung may be secondary to 
primary inflammatory affections of the pleura ; the in- 
flammatory processes extending usually along the course 
of the interlobular connective tissue toward the centrally 
located alveolar areas — the so-called pleurogenic pneu- 
monia. 

All the different special forms of inflammation known 
(see General Pathologic Anatomy) may run their course 
in the lung ; and exudation, cellulation, and emigration 
share in different degrees in building up the pneumonic 
infiltrate. Under certain conditions we find the alveoli 
filled only with a richly albuminous fluid in which are 
present but a few cells (inflammatory edema or serous 
pneumonia). The exudate may be fixed in situ by boiling 
portions of the lung tissue. Frequently, this condition is 
only an early stage of other inflammatory changes. This 
is due to the fact that the bacteria that we believe cause 
the cellular or fibrinous form of pneumonia are often found 
in the inflammatory, edematous fluid in very large num- 
bers. The serous exudate may become cloudy and partly 
crowded out by the admixture of cells or through the pre- 
cipitation of fibrin. Occasionally, there are present a con- 
siderable number of red blood-corpuscles, so that the exu- 
date is distinctly hemorrhagic in character (hemorrhagic 
pneumonia). If the process occurs suddenly and exten- 
sively, it usually leads to fatal results, and it may then be 



RESPIRATORY ORGANS 93 

gnized upon the postmortem table only. I sually, in- 
flammatory edema occurs in parts of the lung surrounding 
inflammatory areas (collateral edema), and may appear in 
the same or neighboring lol 

Most frequently, the exudate filling the alveoli is cellu- 
lar in nature from the very beginning ; two types of cells 
are recognized — first, large, flat, epithelial cells from the 
alveolar lining, and, second, leukocytes. It' the alveolar 
epithelium prevails and if desquamation is combined with 
active proliferation, the process is designated as catarrhal 
pneumonia. On the other hand, if the leukocytes are 
more numerous or present exclusively, the term purulent 
pneumonia is employed. 

The leukocytes (pus-cells) not only till the lumen of 
the alveoli, but oftentimes infiltrate throughout the alveo- 
lar septa, infundibular walls, and occasionally the inter- 
lobular connective tissue. If the leukocyte- accumulate 
in large numbers, it may lead to larger areas of necrosis. 
Tlii- is frequently the case in the hematogenous, embolic 
pneumonia. 

In nearly all cases there is present in the inflammatory 
exudate a varying amount of thread-like fibrin, the dis- 
tribution of which will be referred to later. 

In special forms of pneumonia, especially the genuine 
pneumonia, which is distinguished by the fact that large 

is, usually a whole lobe, become simultaneously 
inflammatory exudate which rapidly fills the 
alveoli soon coagulates, so that there appears in cadi 
alveolus a plug of fibrin mixed with but few cells. This 
form is, therefore, known as croupous or fibrinous pneu- 
monia in the strict sense. 

A.8 the termination- of pneumonia differ clinically from 
one another, so, in like manner, the histologic picture is a 
variable one. The most frequent termination — namely, 
resolution of the inflammatory consolidation and resorp- 
tion of the exudate — is manifested by a progressive fatty 



94 PATHOLOGIC HISTOLOGY. 



PLATE 36. 



Fig. I.— Edema of the Lung. X127. Section through a por- 
tion of boiled lung. In the somewhat dilated alveoli is seen a grayish, 
opaque, homogeneous mass (the coagulated edematous fluid) in which 
are intermingled single, desquamated, alveolar, epithelial cells and 
leukocytes. 

Fig. IL— Marantic Splenization of the Lung. X 360. 1, 
Elastic fibers, sharply outlining an alveolus ; in the latter (2) coagu- 
lated edematous fluid ; 3, desquamated alveolar epithelium ; 4, leuko- 
cytes ; 5, red blood- corpuscles. 

Fig. III.— Beginning Red Hepatization of Lung in Croupous 
Pneumonia. X 340. Weigert's fibrin stain. Alveolar walls appar- 
ently broadened, owing to the great distention with blood of the capil- 
laries, which are tortuous and project into the lumen of the alveoli. 
In the alveoli are seen red blood-corpuscles, a few desquamated alveo- 
lar epithelial cells, and fine, thread-like bunches of fibrin. 

degeneration and breaking down of the cells and the 
fibrin, and gradual emulsification of the fibrinous plugs. 

Occasionally, the pneumonic area may become purulent, 
due to the presence of a large number of emigrated leu- 
kocytes and the melting down of the lung tissue ; this 
leads to the formation of an abscess cavity filled with pus. 
The cause of this result is to be found in the kind and 
number of micro-organisms present in the exudate. Fre- 
quently, partial or total purulent softening may occur in 
fibrinous pneumonia as a result of the penetration within 
the exudate of pus-producing microbes. 

If putrefactive bacteria gain entrance into an inflam- 
matory area in the lung, — for instance, by aspiration of 
fluid substances from the mouth, — the exudate may then 
undergo putrid decomposition ; the surrounding lung 
tissue as well as the part primarily affected may undergo 
necrosis and putrefaction, large gangrenous shreds being 
thrown off (termination in gangrene of the lung). 

Finally, the various forms of pneumonic exudates^ in- 



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RESPIRATORY ORGANS. « >: > 

stead of becoming resolved, undergo organization, the end 
of which is the filling up and the compression of the lung 
tissue by fibrillar connective tissue ; as a result, larger 
portions of the lung become converted into a resisting, 
tough mass. This condition is designated as carnification, 
because the lung tissue, as a result of this process, has a 
flesh-like consistence. 



Croupous Pneumonia. 

Croupous pneumonia is, in a certain manner, the para- 
digm of a typical inflammation of the lung, and therefore 
i- here considered first The inflammation starts in the 
lung tissue proper — that is t<> say, the alveoli — and affects 
usually large ana-, mostly a whole lobe, occasionally 
ral at the same time, and in rare instances even both 
lungs. It is characterized by the coagulation of the exu- 
date within the alveoli. 

From the microscopic appearances croupous pneumonia 
is usually divided into four stages, which, however, are not 
sharply separable from one another, hut microscopically 
they clearly show recognizable differences. 

L Tin Stage qf Congestion. — The affected lung area is 
highly injected, the capillaries of the alveolar walls are 
filled to their full extent with blood and partly bulge in a 
tortuous manner into the alveolar lumen.-. The latterare 
filled with a fluid substance composed largely of albumin, 
which, after boiling small pieces or hardening in the ordi- 
nary fixing solutions, appears a- a homogeneous, coagulated 
mass that stains readily with the acid aniline dyes. Even 
;it this stage line thread- of fibrin are found, usually as star- 
diaped bunches, radiating from particular point- upon the 
alveolar surface " coagulative centers/' Häuser). Among 
the fibrin are intermingled a few large, vesicular, alveolar, 
epithelial cells, m- well a- a variable number of leukocytes 
and red blood-corpuscles. 'Plat.;;!;, Fig, III.) 



96 PATHOLOGIC HISTOLOGY. 

PLATE 37. 

Fig. I.— Croupous Pneumonia at the Height of Hepatiza= 
tion. X 88. Weigert's fibrin stain. The infundibula and alveoli 
are filled with a thick network of fibrin (stained blue) ; owing to the 
hardening agent, it has retracted from the walls. In several of the 
alveoli the exudate has altogether or partly dropped out. 

Fig. II.— Croupous Pneumonia, Stage of Gray Hepatization. 

X 360. Weigert's fibrin stain. The fibrin network is beginning to 
break up (1) ; at 2 exudate passing through Cohn's interalveolar 
spaces ; 3, leukocytes ; 4, alveolar epithelium mixed with exudate. 



#. The Stage of Red Hepatization. — The hyperemia still 
continues, but the separation of fibrin has increased in pro- 
portion, so that the affected lung area has more of a liver- 
like consistence. 

The fibrin threads fill the alveoli in the form of plugs or 
skeins that are more compact at their periphery, while the 
central parts are looser in structure, inclosing Avithin the 
meshes some leukocytes and swollen or broken down alve- 
olar epithelium. The cells and fibrin are not necessarily 
uniformly distributed ; there is usually a sort of a lobular 
arrangement, the cells being found most numerous within 
the bronchioles and the central alveoli, while the peripheral 
alveoli contain principally a fibrinous exudate (Bezzola). 
At many points fibrinous bands are found to pass over from 
one alveolus to another through their walls, and form inter- 
alveolar bridges. Occasionally, the bridges consist of single 
fibrinous threads, oftentimes of whole bundles, with their 
broad bases toward the skeins in which they become lost. 1 

At times we see fibrinous deposits within the capillaries 
of the alveolar walls, in the larger arterial and venous 
branches, as well as within the lymph-vessels of the inter- 
lobular connective tissue. (Plate 37, Figs. I and II.) 

1 Formerly, it was believed that the spaces were the result of the pneu- 
monia, but the investigations of Hansemann have shown that they are 
normally present in the lung (Cohn's stigmas). 



Tab. 37. 



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RESPIRATORY ORGANS. 



97 



3. Gradually, the condition passes over into the third 
stage — Üu stagi of gray hepatization. The cut surface is 
granular, due to the projecting fibrinous plugs ; it is grayish 

in color, explained by two factors — namely (1) the deple- 
tion of the alveolar capillaries, caused by the increased pres- 
sure of tli«' ever-increasing fibrinous exudate, and (2) to the 
retrograde metamorphosis of the exudate itself. At this 
-tau*' Hi»' <nt surface, when -craped, will yield an opaque, 
puriform, viscid, juicy substance. The latter, when freshly 
mined, is found t<> he composed of fatty plugs, partly of 
shining, fibrinous masses, and of cells which have under- 
gone marked fatty changes. Stained sections will show 
the exudate t<> he partly broken down into fine, molecular 
granules, or changed into thick clumps that give the fibrin 
reaction hut do not .-how the single threads of which they 
are formed. 

4. The exudate, which gradually softens and becomes 
similar to an emulsion of milk, is expectorated and ab- 
sorbed, and finally the stage of gray hepatization passes 
into the fourth stage — the stage of resolution or lysis. 
This stage is recognized histologically by the complete 
disintegration of the fibrinous network and of the cells, 
and by the gradual emptying of the alveolar spaces. 
The lung tissue, a- a rule, is wholly restored. 

The specific micro-organisms which are looked upon as 
the causative i : i < • t « > i - of croupous pneumonia are, in the 
firs! place, the diplococcus pneumoniae of Fränkel and 
Weichselbaum (micrococcus lanceolatus), less frequently, 
pneumobacillus of Friedländer (bacillus mucosus cap- 
sulata»), and sometimes the pyogenic staphylococci and 
streptococci. A- a rule, the bacteria are demonstrable 
microscopically in large numbers in the early stages of 
the inflammation. They are seen sometime- in thick 
clumps, especially in the central lobules, which contain 

many cells and hut little fibrin. [It is exceedingly prob- 
able thai the micrococcus lanceolatus or the diplococcus 



98 PATHOLOGIC HISTOLOGY. 

PLATE 38. 

Fig. I.—** Carnification" of the Lung, Following Croupous 
Pneumonia. X 170. Stained with orcein. There is passing into 
the alveoli, which are sharply outlined by the staining of the elastic 
fibers (1), a dense, fibrillar, and somewhat richly cellular, connective 
tissue in the form of loops or garland-like bundles (2) ; at areas is 
still recognized the swollen, partly desquamated epithelium (3). 

Fig. IL— Organization of the Exudate in Bronchopneu= 
monia. A proliferating connective-tissue shoot within a small bron- 
chus. X 200. 1, Epithelium of bronchus ; 2, plug of connective 
tissue. 

pneumonia is the essential cause of croupous pneumonia, 
the other bacteria met with being due to a secondary, 
mixed infection.] 

The regular typical course of croupous pneumonia 
depends evidently on the vitality of the micro-organisms 
in question ; with the death of the latter disintegration of 
the exudate soon follows. 

Occasionally, resolution does not take place ; the fibrin 
may disappear, but in its place the leukocytes increase. 
The latter fill the lumens of the alveoli, break through 
their walls, and infiltrate the lobular septa of connective 
tissue. In this way, as a result of either a continued in- 
crease or growth of the pneumococci (Zenker) or through 
subsequent infection with pus organisms, pneumonia is 
succeeded by either focal or more extensive suppuration 
and destruction of lung tissue. Not infrequently, espe- 
cially in cachectic individuals, in children, and in the 
aged, putrefactive bacteria may gain entrance through the 
bronchial tract into pneumonic areas, or areas previously 
the seat of purulent infiltration, and set up a putrefactive 
destruction of the lung — gangrene and sequestration. 

In croupous pneumonia the stage of resolution is some- 
times retarded ; the fibrin remains present for an unus- 
ually long time, and finally becomes replaced by the in- 



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RESPIBATOBY OBGANS. 99 

growth into the alveoli of fibrous tissue. The latter 
eventually converts portions of lung tissue into a resisting, 
flesh-like mass — carnification, or chronic fibrous pneu- 
monia. 

In sections of this kind (chiefly when stained especially 
for elastic fibers) there will be seen shoot- of spindle- 
shaped, connective-tissue cells (fibroblasts) breaking 
through the alveolar walls and passing in a wreath-like 
manner from alveolus to alveolus, filling up and distending 
the Lumens. The connective tissue is moderately cellular, 
cially in the central portions of the shoots, in which 
arc seen richly protoplasmic, epithelioid cells, as well as 
dark, small, round cells. An increase in the thickness of 
the alveolar walls does not usually take place. The 
rather -canty vascular connective tissue does not, there- 
fore, originate from the alveolar walls, but rather from the 
-canty connective tissue surrounding the end bronchioles. 
Sometimes the shoots also penetrate into the finer bron- 
chiole-. The unresolved fibrin seems to play the role of 
bridges, which the connective tissue follows in passing 
through Cohn's >paces, which become dilated. Polypoid 
connective-tissue plugs are -ecu penetrating into smaller 
bronchioles, and finally occluding them. Detached alveo- 
lar epithelium may -till be found within the alveoli 
.-nid near the connective-tissue shoots. Occasionally, 
these -li<".t- become lined with extensive row- of cuboid 
epithelium. 

Quite frequently, there i- Been a proliferation of the 
remaining epithelium of the alveoli not altogether idled 
with the connective-tissue plugs. These new cells do not 
remain flat and low. bin become higher, cuboid, oftentimes 
cylindric in shape, bo thai adenoma-like structures resull 
iedlander's atypical proliferation of the alveolar epi- 
thelimn). This atypical proliferation occurs in all those 
processes in which the lung tissue becomes indurated, in- 
cluding tuberculosis and syphilis, and depend- undoubt- 



10Ö PATHOLOGIC HISTOLOGY. 

edly on the removal of the pressure of the air on the walls 
of the partially occluded alveoli. 

Naturally, such fibrous, "carnified" portions of the 
lung are rendered useless for respiratory purposes. In 
such areas are sometimes found glistening, concentrically 
lamellated, globular bodies, the so-called corpora amy- 
loidea. (See General Part.) 

Bronchopneumonia. 

All the remaining forms of pneumonia (with the excep- 
tion of the tuberculous) are macroscopically distinguished, 
in the early stages, by the appearance of circumscribed 
areas of inflammation, usually affecting single lobules. 
Through confluence of many lobules it may lead to larger 
areas of infiltration : sometimes a whole lobe may in this 
manner become solidified. When this occurs, it is known 
as " pseudolobular " extension. All these forms of 
pneumonia are most commonly the result of extension 
from a primary infection of the smaller bronchioles. A 
simple catarrhal inflammation of a bronchiole may spread 
to the surrounding lung tissue, which the bronchiole 
supplies. Usually, the bronchial stem becomes occluded 
by the accumulation of cells and increased mucous secre- 
tion, as a result of which the alveolar area that it supplies 
collapses and becomes atelectatic. Later, these collapsed 
alveoli become distended, not with air, but with cellular 
elements, especially with alveolar epithelium. The latter 
find their way into the lumen partly through desquamation 
and, on the other hand, as a result of active proliferation. 
Some of the cells are still flat and polygonal in shape, 
while others have become swollen, vesicular, or globular, 
and may easily be distinguished from other cellular 
elements by their vesicular nuclei. Around tuberculous 
areas in the lung similar forms of pneumonia may develop 
(desquamative pneumonia of Buhl, see Tuberculosis). 



RESPIRATORY ORGANS. 101 

In the later stages those cells become mixed with a 
variable number of leukocytes as well as red blood- 
corpuscles which have passed out from the alveolar cap- 
illaries. Fibrin is not found in the purely catarrhal 
forms of bronchopneumonia ; if present, it is only met 
with in limited amount. Macroscopically, the cut surface 
of such inflammatory areas is always smooth. Resolution 
takes place through fatty degeneration of the cells that 
till tin- alveoli. 

A form o{ consolidation that resembles catarrhal pneu- 
monia very much in structure is the so-called marantic 
splenization of the lung. It is usually found in con- 
nection with long-standing, hypostatic congestion, especially 
when edema is also present. (Plate 36, Fig. II.) 

Complicated in structure as well as in genesis is the 
-«»-called lobular pneumonia that occurs secondarily to 
various other diseases, and especially in children after the 
acute infections, such as diphtheria, measles, scarlatina, 
smallpox, whooping-cough, influenza, etc. These forms of 
pneumonia are also of bronchiogenic development, but the 
inflammation, instead of extending along the long axis of 
the bronchial tube into the corresponding lobule, spreads 
into the bronchial walls and the surrounding peribron- 
chial tissue, whence it passes over into the neighboring 
groups of alveoli. Since the latter do not belong to the 
lobule supplied by the affected bronchus, the typical 
lobular arrangement of the consolidation is. disturbed, and 
there are produced variously <ize<], rounded, elongated or 
circular, infiltrated areas, which surround a bronchus and 
are noi confined to the lobular limit or border. Trans- 
verse sections through a bronchus and it- surrounding 
lung tissue will show, even macroscopically, the central 
yellow-stained portion — namely, the bronchus — filled 
with the purulent exudate, and its infiltrated wall, while 
the periphery of the nodule i- deeper in color. 

Microscopically, the bronchus is tilled with pus-cells 



102 



PATHOLOGIC HISTOLOGY. 



PLATE 39. 

Fig. I.— Beginning Catarrhal Pneumonia. X 250. In the 
alveoli is seen a purely cellular exudate ; the latter consists of large, 
swollen, polygonal or round, alveolar, epithelial cells (1) and a few 
leukocytes. 

Fig. II. — A Peribronchial Inflammatory Area with Begin= 
ning Extension into the Surrounding Lung Tissue. X 80. 

1, Lumen of small bronchus filled with pus-cells and cocci (diplo- 
coccus pneumoniae and streptococcus) ; 2, epithelium of bronchus infil- 
trated with leukocytes ; 3, muscularis, also infiltrated with leuko- 
cytes ; 4, peribronchial tissue greatly infiltrated with leukocytes ; the 
blood-vessels are greatly dilated ; 5, the infiltration extends to the 
walls as well as to the lumen of the adjacent alveoli. 



as well as detached cylindric epithelium, sometimes in 
rows, and also numerous micro-organisms. The connective 
tissue and muscular layers are densely infiltrated with 
leukocytes ; sometimes the muscle-fibers are so pressed 
apart by the pus-cells that they are hardly recog- 
nizable. The blood-vessels of the bronchial wall are 
greatly distended with red blood- corpuscles, oftentimes 
occluded with fibrin and leukocytic thrombi. The sur- 
rounding alveoli are not sharply outlined, as their walls 
are also infiltrated with polymorphonuclear leukocytes 
filling the lumen. The composition of the exudate is a 
variable one, especially as regards the amount of fibrin 
present, and its manner of distribution is often irregular. 
(Plate 39, Fig. II.) 

There are cases of bronchopneumonia in which the 
exudate is purely cellular, in other instances fibrin pre- 
dominates at the peripheral alveoli of the lobule, while in 
the central ones the cellular elements of the exudate pre- 
dominate. Sometimes areas are found in which single 
fields can not be distinguished from a typical croupous 
pneumonia. The fibrinous plugs are quite numerous, 
while interalveolar fibrin threads and bundles are also 



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JRESPIKATOBY OKGAXS. 103 

present, and oftentimes the fibrinous exudate Extends into 
the bronchi themselves, from which it may also start. 
The variability of the exudate does not depend so much 
upon the kind of micro-organism present as upon their 
number. The micro-organisms that arc found are the 
diplococcus pneumoniae (Fränkel-Weichselbaum), the 
streptococcus pyogenes, the pyogenic staphylococci, the 
pneumobacillus <>t' Friedlander, the diphtheria bacillus, 
the influenza bacillus, and the tubercle bacillus which 
i- found in the bronchopneumonia around tuberculous 
areas. 

Generally speaking, it may be -aid that the amount of 
fibrin found i- in inverse proportion to the number of 
bacteria present ; in other words, the greater the number 
<>t' bacteria, the -mailer i> the amount of fibrin. The 
whole process really depends upon the chemotactic action 
of bacteria on the leukocytes. (See General Part, In- 
flammation.) 

Under peculiar circumstances there are formed in the 
exudate of the alveoli a larger or smaller number of giant 
eel!-, especially in cases of postdiphtheric pneumonia and 
in cases following measles. They are seen in the alveoli 
a- massive, polynuclear, occasionally extraordinarily large- 
sized, polygonal, or irregularly pointed cells that inclose 
within their cytoplasm a number of white blood-corpus- 
cles, nuclear and cellular fragments, and clumps of fibrin. 
(Plate 10, Fig. II.) These cells are formed by the con- 
glutination of a number of detached, alveolar, epithelial 
cells, a- well ;i- by the multiplication of the nucleus 
in the cell without subsequent division of the cell-body. 
asionally, they are found in fibrous indurated lungs, 
resulting from the "atypically proliferated" epithelium. 

The embolic and pleurogenous forms of pneumonia have 
been mentioned. The embolic forms are often accom- 
panied with the formation of infarction ; tin- occurs 
when bacteria alone do not reach the lung, but are car- 



104 PATHOLOGIC HISTOLOGY. 

PLATE 40. 

Fig. I.— Purulent (Lobular) Pneumonia Following Diph= 
theria. X 250. I, Bronchus filled with pus-corpuscles and loosened 
epithelium, the latter in form of rows. The wall of the bronchus is 
infiltrated with leukocytes (pus-cells). Alveolar septa contain greatly 
injected blood-vessels. The alveoli are filled with a purely cellular 
exudate, composed largely of leukocytes and partly of desquamated 
epithelium. 

Fig. IL— Postdiphtheric Lobular Pneumonia. X 280. 
Weigert's fibrin stain. The exudate in the alveoli is partly cellular 
and partly fibrinous (2) ; capillaries of the alveolar walls are greatly in- 
jected ; the cellular material in the alveoli consists largely of leuko- 
cytes, less so of alveolar, epithelial, and giant cells (1). The giant 
cells are the result of the melting together of a number of the alveolar 
epithelial cells ; their protoplasmic bodies are filled with various kinds 
of detritus, nuclear fragments, and particles of fibrin, etc. 



ried there by an embolus in which they are inclosed. The 
most frequent points of origin are infectious thrombi in 
veins in various parts of the body : for instance, the uter- 
ine veins in puerperal septicopyemia ; more rarely, endo- 
carditic vegetations in the right side of the heart. First, 
there is formed a hemorrhagic infarct in the affected area 
that soon becomes infiltrated with leukocytes as a result of 
the peculiar action of the micro-organisms, and more or less 
purulent softening of the surrounding tissue (embolic ab- 
scess) soon takes place. The picture of an insular pneu- 
monia in this instance is of brief duration, as the process 
of softening of larger areas is soon accomplished. Some- 
times the clump-like masses of cocci are visible with the 
low power. 

Tuberculosis. 

The histologic appearance of pulmonary tuberculosis is 
extremely varying and polymorphous. Formerly, before 
the discovery of the tubercle germ led to the establishment 



Tab. 40. 




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%./. 







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RESPIRATORY organs. 105 

of their etiologic unity, these processes were looked upon 
as a -eric- of distinct diseases (phthisis, caseous pneumonia, 
cirrhosis, etc. }. 

The localization, distribution, and course of the tuber- 
culous disease - of the lungs are so manifold that it becomes 
well nigh impossible to consider these processes from a 
common histologic standpoint. All the forms of inflam- 
mation and their several terminations, which were referred 
to previously, may run their course side by side with the 
specific tuberculous processes ; no organ in the body un- 
dergoes so many alterations from tuberculosis as the Lung. 

The tuberculous virus may reach and spread throughout 
the lung along three distinct routes : the circulating blood, 
by inhalation through the bronchi, and by way of the 
lymph-vessels. In the first case we speak of a hemato- 
genous or embolic tuberculosis, or of an acute miliary 
tuberculosis, because in this case the tuberculous eruptions 
at the time of death generally reach the size of millet 
seeds. This form of tuberculosis most frequently develops 
as the result of a tuberculous focus in some part of the 
body — e. g. } a tuberculous lymphatic gland rupturing into 
a vein, the infectious material being carried by the blood 
to the right heart and thence into the lungs. A somewhat 
similar event occur- after the rupture of a tuberculous 
focus into a larger lymphatic vessel, followed by a trans- 
port of tuberculous material into the circulating blood. 
Circumscribed miliary tuberculosis of parts of the lung 
tissue may result from the breaking into an arterial 
branch of a preexisting tuberculous focus in the lung 
itself. 

In all these cases there circulate in the blood tubercle 
bacilli that, if arn-ted in the capillaries, produce multi- 
ple, miliary, embolic, tuberculous foci, the beginning of 
which takes place in the capillary wall- and their imme- 
diate surround in 

A- elsewhere, tubercle bacilli in the lung- cause first 



106 PATHOLOGIC HISTOLOGY. 

a proliferation of the fixed tissue cells. The capillary 
endothelium, the connective-tissue cells of the alveolar 
septa, the alveolar epithelium in the neighborhood of 
the bacilli begin to proliferate, and there are produced the 
so-called epithelioid cells that form the basis for the pul- 
monary tubercle. At this stage a purely cellular nodule 
is found, usually surrounded by the elastic fibers of the 
alveolar walls, and projecting into the adjacent alveolar or 
infundibular lumen. Under the influence of this nodule 
the alveolar epithelium begins to desquamate at the same 
time that inflammatory exudation also occurs, so that a 
varying amount of fibrin is deposited in the affected 
alveoli and around the cellular nodules. Histologically, 
the pulmonary tubercles of hematogenous origin differ 
in no way from miliary tuberculopneumonic foci that 
develop in lymphogenic or bronchiogenic tuberculosis of 
the lung. Several adjacent tubercles may coalesce with 
one another, thus giving origin to large conglomerations 
of tubercles, which for some time remain microscopically 
distinct. 

In acute general miliary tuberculosis the nodules do 
not, as a rule, reach beyond the stages just described. 
Occasionally, such nodules are found in the lumen of an 
infundibulum or an alveolus ; their localization is readily 
seen in preparations in which the elastic fibers are stained 
by special methods. It is then seen that, according to 
age, the cellular or more or less caseous centers are en- 
circled by the elastic fibers of the walls of these spaces. 

The epithelioid cells may form giant cells in varying 
numbers. Frequently, giant cells are seen with numer- 
ous protoplasmic pseudopods extending out and becoming 
lost in the reticulum of the tubercle. (See General Part, 
Tuberculosis.) With increasing growth there develops in 
the center of the cellular complexus a caseous necrosis 
which steadily advances. 

The forms of tuberculosis that begin in and spread 



HESPIEATORY OEGAXS. 107 

along the bronchial tree or the lymphatic vessels, while 
presenting the same histologic changes in their inception, 
differ markedly in their further course. 

By far the most frequent mode of tuberculous infection 
of the lung and of the body as a whole is by way of the 
inspiration. Through the respiratory passages the bacilli 
nach the -mall bronchial branches where they become 
arrested and produce in the walls the earliest changes, or 
they reach the inthndibnla or alveoli, where the specific 
changes then develop. In the first case processes de- 
velop similar to those seen in the evolution of broncho- 
pneumonia. Bronchitis, peribronchitis, and bronchopneu- 
monia develop successively, the inflammation extending 
through the bronchial wall into the surrounding tissue ; 
histologically, these changes are modified only in so far as 
the specific effects on the tissues of the tubercle bacillus 
come into play. There is formation of nodules and then 
the caseous necrosis, which, as a rule, befalls tuberculous 
tissue at a certain stage. 

It may be assumed that the bacilli are arrested in a plug 
of mucus in a small bronchus, and next come in contact 
with the epithelial cells of the Avails ; the toxic action of 
the bacilli at once induces a proliferation of the cells and 
leukocytic emigration, and a bronchial tubercle is formed. 
The nodules enlarge ; the smaller the bronchus, the sooner 
the nodules coalesce; caseation occurs, and the caseous 
era aoon run together and form a partial or complete 
ous ring around the bronchial lumen. At this point 
the neighborhood of the bronchus is extensively involved ; 
the nodules spread to the external layer- of the bronchial 
wall, which are destroyed and included in the caseous 
riii-. Gaseous material either partially or wholly fills the 
lumen, and, in consequence, the corresponding alveolar 
area -ink- together in atelectasis. Furthermore, the peri- 
bronchial connective tissue and the alveoli adjacent there- 
to present consecutive changes: the alveolar wall- are 



108 PATHOLOGIC HISTOLOGY. 

PLATE 41. 

Fig. I.— Embolic Abscess of Lung in Pyemia. X 75. (In- 
sular, embolic, purulent pneumonia.) Around the blue stained coccal 
masses lie a great number of leukocytes in the alveolar lumens and 
septa. The lung tissue is in part undergoing purulent softening. 

Fig. IL— Caseous Bronchitis. X 40. Transverse section 
through a small bronchus and surrounding lung tissue. The wall of 
the bronchus is completely broken down, caseated (1), its lumen 
partly rilled with the cheesy material (2). The tuberculous process 
extends in a circular manner outward to the surrounding lung tissue ; 
the alveoli of the latter are infiltrated and filled with numerous con- 
fluent tubercles (3). 



infiltrated with numerous round cells and appear thick- 
ened ; in the alveolar lumen a lively desquamation of the 
epithelium occurs, and the cells are mixed with red and 
white blood-corpuscles ; at certain points large accumula- 
tions of leukocytes appear, which obscure the outlines of 
the alveolar walls. Fibrin, in greater or less quantity, 
may also be precipitated in the surrounding alveoli ; in 
brief, at a short distance from the caseated bronchus there 
exists a typical bronchopneumonic focus, which at first 
presents nothing to betray its tuberculous origin ; gradu- 
ally, the picture changes, however ; tubercle bacilli enter 
this zone also, either directly by virtue of their own pro- 
liferation, or, more frequently by far, they are imported by 
wandering cells. And now there appear in the walls of 
the alveoli new nodules, which grow eccentrically wdrile 
central necrosis takes place ; or, when bacilli are present 
in large numbers, the cellular exudate already present in 
the alveoli undergoes caseation to a larger extent, so that 
now a focus of caseous pneumonia results. 

Further inflammatory changes of a consecutive nature 
also develop in the lobule of the occluded bronchus. The 
atelectasis is succeeded by a lively proliferation and des- 



Tab At. 












•I • 



Fig. I 






• 




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Luh.An.st r Reichhold, Muuuhui* 






6 



RESPIRATORY ORGANS. 109 

quamation of the alveolar epithelium, which tills the 
alveolar spaces ; often some fibrin is also precipitated, and 
this gives the tissue a certain compactness and a peculiar 
gelatinous consistence. In the absence in the closed 
alveoli of all interalveolar pressure on part of the air- 
currenl the proliferating epithelium frequently assumes 
the cubic and atypical forms referred to, which bear such 

mblance to glandular epithelium. The connective 
tissue of the interlobular septa, or the peribronchial tissue, 
if not alnady tuberculous, may inaugurate the same pro- 
>f organization that are seen in the common pneu- 
monia, and that lead t<> fibrous induration and obliteration 
<»f the pulmonary area involved. Frequently, however, 
the collapsed and gelatinous Inno; tissue becomes infected 
with tubercle bacilli, either from the surrounding tuber- 
culous bronchopneumonia or from the tuberculous plug in 
the bronchial lumen, and in this case it undergoes a rapid 
caseous necrosis (caseous pneumonia). When fibrin is 
present in larger quantities in the alveoli, then it may — 
as also the elastic tissue in the alveolar walls — resist the 
necrotic action of the bacilli longer than the cells in the 
alveoli. The bodies of the cells run together, and the in- 
dividual colls are no longer distinguishable, but disintegrate 
into a finely granular, opaque mass ; peculiar distortions 
occur in the nuclei which undergo fragmentation, the result- 
in- (»article- often retaining for a long time their affinity 
for stains. Gradually, this process extend- to the cells of 
the alveolar walla and destroys the epithelium, the cap- 
illaries, and the connective-tissue liber- and cells. At 
tlii- tin- necrotic lung tissue may <till contain 

dense, easily stainable plugs of fibrin ; even the inter- 
alveolar connecting bands may he retained. Eventually, 
the fibrin also disintegrates, leaving only the elastic 
fibers, which, :i- a rule, break up into segments arranged 
in rows before disappearing. Finally, there result larger 

3 composed of an unstainable and almost structureless 



110 PATHOLOGIC HISTOLOGY. 

PLATE 42. 

Fig. I.— Miliary Tuberculosis of the Lung. X 35. The 

tubercles are caseated in the center (2), and are surrounded by air- 
containing,- alveolar tissue (1) ; at parts the tubercles are so close to 
each other that larger nodules are formed ; giant cell (3). 

Fig. IL— Caseous Pneumonia. Weigert's fibrin stain and elas- 
tic-fiber stain. X 70. The tissue has undergone complete necrosis ; 
nuclei can not be recognized either in the alveolar walls or in their 
lumens ; in the latter are seen an opaque, granular (cheesy) detritus 
with some chromatin fragments ; 3, well-preserved fibrin is seen in the 
peripheral parts, and a few alveoli are filled with closely packed fibrin, 
as is seen in croupous pneumonia ; the elastic fibers in the alveolar 
walls (1) and blood-vessels (2) are still well preserved. 

material, — the caseous material, — which is rather dry and 
wholly bloodless, hence the well-known yellowish-white 
color. The blood-vessels in areas of caseous pneumonia 
are usually stopped up by fibrinous and leukocytic thrombi 
— a dense network of fibrin adhering to the intim a. 

Tuberculous bronchopneumonia, and caseous, circum- 
scribed pneumonic foci are commonly succeeded by a 
further spread of the tuberculous process through the 
lymphatic system. The lymph-vessels run parallel with 
the bronchi and with the vessels, being situated in the 
peribronchial and perivascular connective tissue ; their 
roots and radicles are, therefore, inclosed in the tubercu- 
lous granulation tissue in the forms of pulmonary tuber- 
culosis now described, and bacilli naturally find their 
way into the lymph-current, by which they are then 
carried further. In this way multiple tubercles form in 
the lymph-vessels themselves, which, on account of the 
resulting swellings, may appear as strings of beads, as 
they run around the bronchi. This may be properly 
designated as peribronchial tuberculous lymphangitis. 

In this case the tubercles originate from the lymphatic 
epithelium. The concentric enlargements extend, on the 



/ 



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Ff//. 2. 



Tab. 42. 



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. 






































/,////. Anst F. Reichhold . München. • 



RESPIRATORY ORGANS. Ill 

one hand, toward the bronchi ; on the other hand, toward 
the Burronnding alveolar tissue. When several lymph- 
vessels in the circumference of a bronchus become tuber- 
culous, thm caseous rings may form around the bronchi, 
due to the circular confluence of spreading tubercles which 
may attack the bronchial wall secondarily, and eventually 
ml to the lumen. It sometimes happen- that in 
favorable sections of a pulmonary lobe the yellowish, 
nodular cords can be followed with the naked eye clear 
to the hilus, where they end in the peribronchial lymph- 
id-. In the latter stages of the disease, when the 
confluent aodules have destroyed the bronchus and invaded 
the surrounding tissue, the exact genesis of the disease can 
no longer be followed. 

When the tubercle bacilli enter the alveolar tissue 
directly through the bronchi, which is often the case in the 
apices of the lungs, then there develops a minute pneu- 
monic infiltration in case the bacilli remain ; or they may 
he taken up bywandering cells and carried into the lymph- 
vessels of the interstitial tissue, become arrested here, and 
induce the formation of nodules. In the first case there 
i- produced a miliary, tuberculous pneumonia ; in the 
iid, a pulmonary tubercle. But the histologic differ- 
ences a- to position and mode of further spreading are 
early obliterated, because the interstitial tubercle very 
caus< - pneumonie changes, while the primary foci 
in the alveoli, in their turn, soon induce interstitial 
changes. In the beginning the alveolar foci consist prin- 
cipally of proliferated, alveolar epithelium and wandering 
cells, while the interstitial foci are built up by connective- 
tissue cells and vascular epithelium. Prom the resulting 
epithelioid cells giant cells are formed with pseudopodial 
pro* (tending into the reticulum of the tubercle j 

the protoplasm of the giant cells frequently <*« »nt ;ii n- 
tubercle bacilli a- well as disintegration product- of such. 
In genera] the giant cells are the more numerous the 



112 PATHOLOGIC HISTOLOGY. 

PLATE 43. 

Fig. I.— Miliary Tuberculous Pneumonia. X 170. Wei- 

gert's fibrin stain and elastic-fiber stain. Several alveoli adjoining 
each other are filled with a cellular and fibrinous exudate. The cells 
consist largely of desquamated epithelium ; some of their nuclei have 
not taken the stain (beginning caseation). The attached alveolar epi- 
thelium is undergoing proliferation. 

Fig. II. —Caseation of the Exudate in an Alveolus in a Case 
of Caseous Pneumonia. X 360. Elastin staining. The alveolus 
is filled up with a grayish, fine, granular mass, containiüg a larger num- 
ber of nuclei which are undergoing degeneration. The cell-bodies are 
no longer visible. 

slower the process of nodule formation ; in the rapidly 
spreading, diffusely pneumonic, and extensively caseated 
forms giant cells are often absent. As elsewhere, the 
center of the nodules, after a time, becomes caseous, and 
larger caseous areas result from the confluence of groups 
of nodules. 

The further fate of such isolated tuberculous foci may 
vary much. The form of healing through connective- 
tissue encapsulation is relatively common. In this case 
the exudation does not progress further into the adjacent 
alveolar groups, but from the margins of the nodules 

PLATE 44. 

Fig. I.— Desquamative Pneumonia (Buhl) Around a Tuber= 
culous Area of the Lung. X 340. 1, " Atypically proliferated," 
cuboid, and cylindric, alveolar epithelium ; 2, desquamated, vesicu- 
lated, swollen, alveolar, epithelial cells ; 3, epithelial cells loaded with 
anthracotic pigment. 

Fig. II. — Proliferation and Desquamation of the Alveolar 
Epithelium in Tuberculous Pneumonia. X 520. 1, Fibrin plug 
in an alveolus ; 2, interalveolar fibrin bridge (Cohn's stigma) ; 3, pro- 
liferated alveolar epithelium partly detached from the underlying 
membrane ; 4, elastic fibers of the alveolar wall. 



7 ab. 43. 










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LUfuAnst ERekhhoUt, München. 



Tab A4. 



- • 



*J 



■ - 



r* ■ 






r # a 



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V 






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RESPIBÄTOJRY OEGAXS. 113 

springs a cellular connective tissue which gradually 
becomes more and more fibrous and less cellular at the 
same time as it surrounds and encroaches upon the case- 
on- zone ; the epithelioid cells, which often are arranged 
in a radiating manner around the caseous center, and also 
the more peripheral round cells, disappear, and in their 
place connective-tissue hands appear derived from the in- 
terstitial tissue, especially the peribronchial. The advanc- 
ing connective tissue frequently takes up the giant cells, 
which may remain inclosed with the new tissue. The 
caseous material dries up more and more, and shrinks, and 
calcareous salts are frequently deposited here; the caseous 
focus, at first soft and gritty, later becomes converted into 
a dry and brittle calcareous mass. The connective-tissue 
formation i- not always limited to encapsulation of a pre- 
existing focus, but may assume a more progressive charac- 
ter and give rise to a cirrhotic induration of the surround- 
ing tissue ; fibroplastic sprouts, similar to those observed 
in the organization after lobar pneumonia, grow into the 
alveoli, fill up the lumens, and eventually change the tis- 
sue into a hard, cicatricial mass. Such scars are favorite 
places for the deposition of coal pigment, which is scattered 
about in stellate and spindle-shaped groups between the 
librilhe a- well as in the persisting cells (slaty induration). 
The alveoli immediately adjacent are often the seat of a 
vicarious emphysema. (Plate 45, Fig. II.) The epithe- 
lium of the alveoli that are not obliterated often assumes 
a cubic form, giving rise to gland-like spaces and tubules. 
(Plate H. Fig, I.) [f living tubercle bacilli are not pres- 
ent in the caseous or calcareous focus, then the tuberculosis 
i^ to I».- regarded a- healed. 

Bui the course is not always so favorable as this; fre- 
quently, indeed, does the opposite happen — namely, soft- 
eningand -<»lnti<»n of the foci. Two conditions are to be 
considered in connection with this process — namely, the 
mechanical and the infectious. 

8 






114 PATHOLOGIC HISTOLOGY. 



PLATE 45. 



Fig. I. — Wall of a Tuberculous Cavity in the Lung with 
Cirrhosis of the Apex. X 16. 1, Cavity ; 2, shreddy, caseous 
masses ; 3, closely fibrillar fibrous tissue with authracotic pigment ; 4, 
compressed alveoli with proliferating epithelium. 

Fig. II.— Slaty Induration of the Lung in Obsolete Fibrous 
Tuberculosis (Cirrhosis). X 55. 1, Emphysematous lung tissue ; 
2, an indurated area of lung, composed of a close, fibrillar, and slightly 
cellular, connective tissue (scar), infiltrated with masses of black pig- 
ment. 

If the tuberculous focus either starts from a bronchus or 
a bronchiole or reaches them in the course of its extension, 
then the bronchial wall becomes involved in the necrotic 
process ; no longer able to withstand the inspiratory pres- 
sure, the wall dilates, and in the necrotic district there 
results a cavity which is in connection with the bronchus — 
the so-called bronchiectatic cavity. Such cavities may 
arise in the smaller bronchi and, by amalgamation, form 
larger, irregular caverns. 

The majority of the cavities, how r ever, are the result of 
mixed infections with pneumococci, streptococci, etc., which 
reach the tuberculous pneumonic areas with the air. This 
mixed infection leads to a softening of the caseous material 
and a progressive suppuration at the periphery of the focus ; 
sooner or later the focus empties itself through a bron- 
chus. The innermost layer of the walls of a cavity like 
this consists of necrotic tissue containing innumerable 
tubercle bacilli ; the adjacent layers are infiltrated very 
densely with leukocytes ; following the evacuation there 
ensues an active and productive inflammation, the result 
of which is the production of a connective-tissue sac 
around the cavity ; this sac has a structure similar to the 
slaty induration around caseous foci ; coal pigment may 
be deposited in fibrous lamellae, and the epithelium of the 
adjacent alveoli may assume a cuboid form. 






Sgl. 



Tab. 4-5. 



4 
4 



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wv. 




Eig.2. 



LUhmAnst /•' HpichhoUL, München. 



RESPIRATORY ORGANS. 1 1 : > 

As the cavities enlarge, a few persisting bands or ridges 
of tissue are usually found to pass across the spaces. 
On examination, these are found to consist largely of 
blood-vessels with greatly thickened walls, the lumens 
being wholly or partly closed by endarteritic or endophle- 
lutie changes, (See Circulatory Organ-, p. 3 ( J.) 

Syphilis. 

Tlicr«- is no doubt but that syphilis of the lungs 
occurs in the adult, but its histologic changes are little 
kn<»wn. It is probably frequently confounded with the 
chronic indurative forms of tuberculosis, both macroscopi- 
cally and microscopically. The tubercle bacilli are 
absent, of course. In the new-born, however, and the 
prematurely still-born the pulmonary lesions of congeni- 
tal hies present characteristic appearances. Two chief 
forms are distinguished — the pneumonic form, which in- 
volve- whole lobes and often the entire lung, and the 
circumscribed, nodular form. 

The diffuse form is characterized by a general increase 
of the interstitial connective tissue, interlobular as well as 
peribronchial ; the alveolar septa are also thickened; this 
Lb due to the presence of numerous, spindle-shaped and 
polygonal, fibroblastic cells. The alveolar spaces become 
contracted ; they usually contain a rather richly cellular 
exudate composed of Borne leukocytes and numerous, dv<- 
quamated, epithelial cells, which have a pronounced ten- 
dency to fatty changes. The blood-vessels present thick- 

d walls; in the adventitia arc connective tissue 
proliferation and follicular heaps of rounds cells, and in 
the intima is hyperplasia of the subepithelial connective 
tissue, so thai the lumen becomes greatly narrowed and 
even wholly closed. Tin- render- the organ anemic. 
This combined with the fatty changes in the alveolar epi- 
thelium gives the involved district a yellowish-white 



116 PATHOLOGIC HISTOLOGY. 



PLATE 46. 



Fig. I. — Syphilitic " White" Pneumonia of the New=born. 

X 250. The alveolar walls are considerably thickened with a richly 
cellular, connective tissue (1). In the alveolar lumen numerous large, 
desquamated, epithelial cells (2) and several leukocytes are seen. 

Fig. IL— Indurative Interstitial Pneumonia in Hereditary 
Syphilis. X 250. The connective-tissue septa of the alveoli are 
considerably broadened (1). The alveolar lumens are small and 
tubular in appearance (2), with atypically proliferated, cuboid epi- 
thelium. 



appearance and a firm consistence, and hence the term 
" white pneumonia." 

In many cases the lungs of syphilitic fetuses contain 
larger or smaller, light-colored, dry nodules, which are 
usually not sharply circumscribed. Examined micro- 
scopically, it is seen that the changes evidently date from 
an early embryonal period. The principal part of these 
nodules consists of a dry connective tissue with long fi- 
brillse and spindle-shaped nuclei. This tissue is arranged 
in dense bands, and incloses gland-like and branching 
centers lined with a cubic, cylindric, or quite regular epi- 
thelium. These spaces correspond to the alveoli whose 
development was arrested by the growth of connective 
tissue in an early period when the alveolar lining in 
general is cubic in character. The centers of these nod- 
ules are often caseous — that is, the nuclei are not stained 
while the coarser structure is quite distinct, as is often the 
case in the caseation of syphilitic lesions. In the lung 
tissue about the nodules the alveolar septa are usually 
thickened for a considerable extent, and frequently a 
" white pneumonia" is also present. 



TabA6. 



/a fiT J, 




/ ///. J. 










i-'.'/n 

Ltlh. Ans/ /:' Hciclihnlil . Mnnrhcn 



IBATOBT ORGANS. 117 



PLEURA. 

The pulmonary and costal (including the diaphragmatic) 
pleura consists of a layer of parallel connective-tissue 
rs with l>ui few nuclei and interspersed with numerous 
■ rs, 1 ":.' free surface is covered with flat, polyg- 
onal epithelium« The pleura is involved in all pul- 
monary inflammations that reach the pleural surface of 
the lung. The character of the exudate varies from a 
fine, macroscopically barely visible layer of fibrin to 
voluminous, fibrinous precipitates or purulent collections. 
In fibrinous pleuritis the epithelium is losl early through 
1 fatty changes ; where it is still retained it 
shows loosening and Granular disintegration; rarely docs 
it appear to proliferate. The fibrin, which is derivedfrom 
the exudation and coagulation of plasmatic fluid, may 
appear first upon or under the epithelial cells. The con- 
nective tissue shows much vascular congestion, the blood- 
sels often containing leukocytes or thrombi of filamen- 
s fibrin ; the lymph-vessels are widened and often con- 
tain fibrin in addition to desquamated cells. Between 
the connective-tissue fibers lie leukocyte-, which usually 
i infiltrate the fibrinous deposit ; the cells of the oon- 
- le proliferate freely and a granulation tissue 
<I of fibroblasts, leukocytes, and new 
*, which push toward and eventually replace 
the fibrin, [stands of fibrin may be found inclosed in the 
tissue; such fibrinous masses often undergo 
hyaline -. and form glistening, homogeneous flakes 

which do I-' i the fibrin stain. < rradually, the gran- 

ulation tissue changes into a densely fibrillated, fibrous 
diminish, it- vessels becoming obliterated. 
- igations by Ziegler, hyaline 
ccur in mature connective tissue, prob- 
ably due to an infiltration of the connective tissue with 
Ibuminoufl body that has coagulated in hyaline form. 



118 PATHOLOGIC HISTOLOGY. 

PLATE 47. 

Fig. I.— Acute Fibrinous Pleuritis in Croupous Pneumonia. 

X 66. Weigert's fibrin stain. 1, Deposit of fibrin inclosing leuko. 
cytes ; 2, lung tissue infiltrated with pneumonic exudate ; 3, thick- 
ened pleura infiltrated with young connective-tissue cells and shoots 
of thin walled blood-vessels, in the lumen of which are seen leuko- 
cytes and fibrin (2). 

Fig. II.— Beginning Organization in Fibrinous Pleuritis. 

A part of the preceding figure X 340. 1, Layer of fibrin (the pleura 
is to be thought as near 2) ; 3, young blood-vessels growing toward 
the fibrinous layer ; 4, as a result of fibrinous accumulation, one of 
the vessels has become thrombosed ; 5, large epithelioid cells with 
vesicular nuclei ; 6, spindle-shaped, young, connective-tissue cells ; 7, 
lymphocytes ; 8, leukocytes. 



In this way arise the connective-tissue band s, wide-spread 
fibrous adhesions, and extensive scars in which lime-salts are 
later deposited. 

The tuberculous pleuritis is distinguished from the sim- 
ple by the presence of tubercles and caseating nodules in 
the granulation tissue. Otherwise, the same processes of 
exudation, proliferation, and organization occur. 



THYROID GLAND. 

The thyroid gland is a compound tubular gland whose 
duct, — the thyroglossal, — which at one time opens at the 
foramen cecum on the back of the tongue, becomes oblit- 
erated in early embryonal life. The tubules are blind at 
both ends, and dense strands of fibrous tissue separate them 
into lobules. Clothed with a cubic and cylindric epithelium, 
which is arranged upon a basement membrane, the tubules 
at all stages contain a homogeneous, so-called colloid mass 
which also fills the lymph-vessels. The stroma is richly 
vascular. 






Tab A). 



/•;•-.;%' 






- 



',. Wi . 





' 






Tig- 1. 3 2 






1 * fa 






--» 















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i 















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i 



J.if/i . . Inst /'•' Heult hold Mmirhcn 



BESPlRATORY ORGANS. 119 

The commonest change of the thyroid is an increase in 
volume, called goiter or struma, which may depend on 
various histologic processes. From embryonal remnants 
of epithelial cells, which arc not arranged as tubules, 
there may develop solid columns and loops the ends (A' 
which are expanded, bul in which the amount of colloid 
usually is slight. This is generally called adenoma of 
the thyroid, or parenchymatous goiter. At other times 
the preexisting tubules increase both in length and breadth 
at the same time as the amount of colloid greatly increases. 
This is known as colloid goiter. 

The colloid material is secreted by the cells, which may 
also change directly into colloid material ; in that case 
there appear in the cells small, glistening drops of colloid 
substance which gradually coalesce to form larger masses, 
crowding the nucleus and obscuring the cell outline. 
When such changes occur over a considerable part of an 
acinus, the colloid material lies in direct contact with the 
connective tissue. Desquamated epithelial cells, or frag- 
ments of such, are often found in the colloid material. 
It' the epithelial cells do not degenerate, the constantly 
increasing ma— of colloid flattens the cell- more and 
more. The colloid contents of the lymph- vessels are also 
often much increased. The great dilatation of adjacent 
follicles may lead to their confluence with lymph-vessels, 
whereby larger cystic spaces filled with colloid material 
are produc d (cystic goiter). Hemorrhages may render the 
contents rusty red or brownish in color, and mixed with 
blood pigment (hemorrhagic goiter). The surrounding 
stroma often proliferates, sometimes in the form of papil- 
lary ingrowths into the follicular spaces, the epithelium 
of which i- lifted up and carried inward. 

Among the frequent degenerative changes in the fibrous 
tissue of :i goiter may be mentioned hyaline changes, 
which are among the more common. Broad, glistening, 
hom< a is bands without nuclei are then formed between 



120 PATHOLOGIC HISTOLOGY. 

the gland spaces ; the hyaline changes frequently occur in 
an extensive degree in the walls of the blood-vessels, 
whose lumen often appears greatly narrowed. 

Calcareous salts are frequently deposited in goiters, so 
that very hard and extensive calcification results (calcareous 
goiter). Goiter is also accompanied with telangiectatic 
dilatations of the blood-vessels, leading to formal cavern- 
ous spaces (vascular goiter). 

Carcinoma is the most frequent tumor in the thyroid 
gland ; sarcoma is more rare, and osteosarcoma sometimes 
occurs. 



III. THE DIGESTIVE ORGANS. 

The oral cavity is lined by a mucous membrane com- 
posed of a squamous, stratified epithelium and tunica pro- 
pria. The latter rises up into papillae of varying heights, 
-nine being very high. The basal layer of the epithelium 
is eylindrie, then comes the stratum Malpighii with its 
prickle cells, which become flatter and flatter toward the 
surface. The tunica propria, which is composed of con- 
nective tissue, elastic fibers, and fine vessels, contains 
lymphocytes, scattered either diffusely or accumulated in 
follicular masses. Below, the tunica propria merges gradu- 
ally into the submucous coat, which contains the glands. 
The glands are compound, tubulo-acinous, mucous glands ; 
the duet-, lined principally with flat cells, empty upon the 
surface of the mucous membrane: not infrequently, small 
accessory glands empty into the main ducts. In several 
places occur striped muscles under the oral mucosa. 

The bulk of the tongue consists of striated muscles, the 
bundles of which interlace in various directions. A median 
septum divides the muscular mass into a right and a left 
halt*. The musculature is surrounded by a submucous coat, 
which contains numerous mucous and serous glands, some of 
which extend into the muscles. The papillae, formed by the 
tunica propria, are more or less complicated. In man four 
general types are distinguished : (1) The filiform papillae, 
which arc eylindrie elevations with numerous dichotomous 
branches a< the free end; (2) the fungiform papillae, situ- 
ated "ii ;i broad base and covered by numerous secondary 
papillae; (3) the circumvallate papillae, especially large 



122 PATHOLOGIC HISTOLOGY. 

and separated from the surrounding mucosa by a circular 
furrow ; (4) the papillae foliate, which are parallel folds at 
the lateral margins of the tongue. All papillae are cov- 
ered with stratified squamous epithelium. The summits of 
the filiform papillae are not infrequently hornified. In the 
epithelium covering the sides of the circumvallate papillae 
lie the end-organs of the nerves of taste ; the taste-buds ; 
elongated epithelial cells, forming oval bodies in which the 
nerves end. At the base of the tongue the tunica propria 
and even the epithelium are infiltrated with numerous 
lymphocytes, which at various points are gathered into 
denser nodules, the lymph- follicles of the tongue. 

All the salivary glands in the oral mucous membrane 
and the vicinity of the mouth are built upon the tubulo- 
acinous plan — that is, clustered about the ends of branch- 
ing ducts as small round saccules, the whole somewhat 
resembling a bunch of grapes. According to the secre- 
tion produced, there are distinguished : (1) Pure mucous 
glands, without demilunes, occurring at the root of the 
tongue, on the hard palate, and at the anterior margin of 
the soft palate. (2) Mixed mucous glands, with demi- 
lunes, occurring in the lips, the cheeks, in the tip of the 
tongue (Nuhn's glands) ; here belong also the lingual 
glands. (3) Mixed serous glands — the submaxillary 
glands. (4) Pure serous glands, occurring in the tongue 
in the vicinity of the circumvallate papillae and the pa- 
pillae foliate ; also the parotid glands. 

The demilunes, or marginal cells, are flat cells in close 
contact with the basement membrane of the glands ; these 
cells produce a secretion that differs from that of the mu- 
cous cells proper. 

The faucial tonsils consist of from ten to twenty 
lymph-nodes. The adenoid tissue contains numerous 
follicles with germinal centers. The surface of the tonsils 
is marked by depressions, lined with epithelium — the 
so-called crypts ; numerous lymphocytes are always found 



THE DIGESTIVE ORGANS. 123 

migrating through the epithelium, and constitute a fertile 
source of the salivary corpuscles. The tunica propria of 
the pharynx is also infiltrated with leukocytes which 
migrate through the epithelium. 

In the esophagus three coats arc present : The mucosa, 
covered by stratified squamous epithelium, and containing 
in the tunica propria a longitudinal muscularis mucosae; 
the submucosa ; and the internal circular and the external, 
longitudinal, muscular layers. In the upper fourth the 
muscular tissue is exclusively striated ; in the lower fourth 
it is exclusively unstriated ; and in the middle two-fourths 
the two are mixed. Outside of the muscular coat are 
connective-tissue bundles, interspersed with elastic fibers, 
among which run vessels and nerves. The submucosa 
contains mucous glands ; in the upper and lower ends of 
the esophagus are glands which correspond in structure to 
the fundus glands of the stomach. Leukocytes commonly 
inn* It rate the neighborhood of the glands. 

Throughout the entire intestinal tract, from the stomach 
to the rectum, the walls comprise three layers : The serous 
coat, the muscular, and the mucous. Between the mucous 
and the muscular lies the submucous. 

The serous coat, or the visceral layer of the peritoneum, 
consists of interlacing bundles of connective-tissue and 
numerous elastic networks, which externally in places arc 
condensed to \\>v\n a distinct limiting membrane. The 
five surface is covered by a single layer of Hat, polygonal, 
epithelial cells. In various places the subserous connec- 
tive tissue contains a varying amount of fat-cells. The 
parietal peritoneum ;ii some points contains smooth muscle- 
fibers. 

The muscular ooa< of the stomach has three layers — 
namely, external longitudinal fibers, a central circular 
layer, and an oblique inner layer which in the fundus pre- 
sents ;i complicated arrangement. Throughout the large 
and small intestines the muscularis presents bul an inner 



124 PATHOLOGIC HISTOLOGY. 

circular and an external longitudinal coat. Normally, the 
spindle-shaped muscle-cells in the adult contain some pig- 
ment granules about the nucleus. Between the two mus- 
cular layers occurs Auerbachs nerve-plexus. 

The submucous coat consists of fibrillated connective 
tissue with numerous elastic elements ; it contains spindle- 
shaped, stellate, and other cells, and also small masses of 
fat-cells. Internally, this layer passes on into the stratum 
proprium of the mucous coat, in which there are no elastic 
elements, but it contains a varying number of lymphoid 
cells and thus acquires the characteristics of the so-called 
cytogenic connective tissue (adenoid tissue). 

The muscularis muscosse, which occurs throughout the 
Avhole gastro-intestinal tract, may be regarded as the 
boundary between the submucous coat and the tunica pro- 
pria of the mucous layer. The muscularis mucosae con- 
sists, as a general rule, of a single layer of longitudinal, 
smooth muscle-bundles, which at certain places (the villi) 
send prolongations into the mucous membrane proper. 

The epithelium from the cardiac end of the stomach to 
the anus is a single layer of cylindric cells. In the sub- 
mucous coat lies a second nerve-plexus with ganglion cells, 
the so-called Meissners plexus. The transition between 
the flat epithelium of the esophagus and the cylindric epi- 
thelium of the stomach is sudden and sharp. 

The epithelium of the stomach covers its interior com- 
pletely ; it continues into the mouths of the glands and 
produces mucus, in consequence of w T hich there are found 
a varying number of goblet cells. There is no cuticular 
formation. 

Three forms are recognized among the tubular glands : 
(1) The cardiac glands, occupying a small zone at the 
transition of the esophagus into the stomach. They are 
compound, tubular glands, which empty into pit-like de- 
pressions lined by typical gastric epithelium. (2) The 
gastric glands proper, which are found in the fundus and 






THE DIGESTIVE ORGANS. 125 

the body of the stomach. They rest upon the museularis 
mucosae, and are simple tubular glands, often branched. 
They contain two distinct kinds of cells — the chief or 
central cells which, small and prismatic, line the principal 

part of the tubule and secrete pepsin ; and the parietal or 
aeid cells, which occur at irregular intervals along the 
membrana propria and outside of the chief cells. The 
parietal cells appear to secrete the acids of the gastric 
juice, (3) The pyloric glands, occurring in the pyloric 
part of the stomach, and distinguished from the preceding 
by numerous turns and divisions of the tubules and by 
entire absence of the parietal cells. In addition, the 
mucous membrane of the stomach contains closed follicles 
similar in structure t<> that of the solitary follicles of the 
intestine. 

The mucous membrane of the intestine presents nu- 
merous elevations., — the intestinal villi, — which consist 
of a prolongation of the tunica propria, smooth muscle- 
fiber-, a capillary network with small meshes, and also, as 
a rule, one, or rarely several, central chyle vessels. In 
the duodenum the villi are broad and leaf-like. Two 
kind- of epithelium cover the villi — the epithelial cells 
proper, of cylindric form and provided with a distinct 
CUticular border on their free surface, the nucleus lying in 
the inferior half of the cells; between these occur the 
>iid kind of cells, the goblet cells. 

The glands of the small intestine are formed by the sim- 
ple tubular depressions, or Lieberkühn's crypts, between 
the villi, and they are lined with cylindric cells and goblet 
cells. Between the epithelial cells of the villi and of the 
crypts migratory leukocytes are found in varying numbers. 

In the duodenum there occur also branched tubular 
glands of Brunner, which pierce the museularis mucosae, 
:md are lined with darkly granular, cylindric cell-. 

The large intestine is devoid of villi ; the crypts of 
Lieberkühn are larger and contain numerous goblet cell.-. 



126 PATHOLOGIC HISTOLOGY. 

The surface epithelium presents a cuticular or basal 
border. 

In the mucous membrane of both large and small intes- 
tines are numerous lymph-nodules, occurring either singly 
(solitary follicles) or in flattened groups (agminated 
follicles or Peyer's patches). They lie partly in the 
mucous membrane itself, partly in the submucous tissue ; 
they reach, on the one hand, to the surface epithelium ; 
on the other, to the muscular coat. They possess 
a delicate connective-tissue capsule and a delicate reticulum, 
in the spaces of which lie the lymphocytes. The interior 
presents a distinct germinal center. 

In the large intestine are found only solitary follicles 
that here are embedded a little deeper in the mucosa, the 
epithelium forming small crypt-like depressions upon their 
surface. 



ORAL CAVITY, PHARYNX, ESOPHAGUS. 

In the mouth and pharynx occur simple catarrhal pro- 
cesses that histologically resemble those of the upper 
air-passages, except in so far as the stratified squamous 
epithelium naturally is more resistant than the cylindric. 

The vessels of the stratum proprium and of the submu- 
cosa are strongly injected. The wandering cells, present 
normally, are now increased, lymphocytes and numerous' 
leukocytes are present, and in the act of passing out be- 
tween the epithelial cells, in whose interior they also fre- 
quently are found. 

The mucous glands are enlarged ; here and there a duct 
is dilated and cystic, filled with mucus. The epithelium 
shows a granular cloudiness of its protoplasm, especially 
in the upper layers, and there is an increased desquama- 
tion ; on the tongue the loosened cells dry up and form 
brownish masses, which contain numerous bacteria and 
thread fungi • the adenoid tissue is often considerably 



THE DIGESTIVE ORGANS, 127 

increased, especially in the pharynx in chronic catarrhal 
conditions, leading to follicular nodules, which give the 
mucous membrane a granular appearance (granular phar- 
yngitis). 

The papillae of the tongue, especially the secondary 
papillae of the filiform variety, are often covered by the 
thread- ()f a fungus (Leptothrix bnccalis, Robin), which 
must not he con founded with the hair-like prolongations 
of the apices of the filiform papillae, produced by increased 
growth of the epithelium ; in marked eases the tongue 
appear- a- if covered witli hairs, from nine to thirteen 
millimeters long and pointing backward (lingua hirsuta 
or villosa ; frequently, the hornified epithelium assumes 
a black color (black, hairy tongue). 

Infant- that are poorly nourished, marantic individuals 
in general, and especially diabetics, frequently present 
whitish-yellow, circumscribed deposits upon the lining of 
the mouth, pharynx, esophagus, and in children even of 
the stomach ; these deposits are easily removable and at 
first glance they are not unlike diphtheric membranes. 
Microscopically, they are found to consist almost wholly 
of a branching network of the mycelium of the thrush 
fungus, or oidium or saecharomyces albicans. The 
thread- are septate, and the hyphae carry oval conidia or 
spores. Between the threads lie masse- of desquamated, 
partly necrotic, epithelium. In sections it i> -ecu that the 
mycelium passes deeply into the softened epithelium, 
which is infiltrated with leukocytes. On the surface of 
the mass lie masses of spores and bacteria of various kinds. 
Tin- loosened epithelial cells frequently show poorly 
stained nuclei, <>r no nuclei. Occasionally, the mycelium 
penetrates the entire thickness of the epithelium and 
reaches down into the stratum proprium. 

Tuberculosis of the mucous membrane of the mouth 
and <>t' the pharynx, ;i- well a- of the esophagus^ is rela- 
tively tare; histologically, it is devoid of peculiarities \ 



128 PATHOLOGIC HISTOLOGY. 

PLATE 48. 

Fig. I.— Variola Vera of the Tongue. X 75. 1, The whole 
thickness of the epithelial lining is broken down and necrotic ; sub- 
mucosa penetrated with greatly injected blood-vessels ; 2, the sub- 
mucous glands are necrotic, with cyst-like dilatation of the acini ; 
3, musculature. 

Fig. IL— Tuberculosis of the Pharynx. X 75. 1, Epithe- 
lium in places very thin and at the point of rupture ; in stratum 
proprium numerous confluent tubercles with beginning necrosis and 
many giant cells (2) ; 3, mucous glands. 



the nodules develop in the stratum proprium of the 
mucosa, and consist of epithelioid and giant cells and 
peripherally arranged round cells. The center early be- 
comes caseous, and as the process invades the epithelium 
this becomes thinner and thinner and infiltrated with 
round cells, until, finally, rupture takes place ; caseous 
material is then discharged, and a tuberculous ulcer with 
sinuous outlines is formed ; the development of new 
tubercles followed by caseation leads to increase in ex- 
tent and depth of the ulcer, whose surroundings are 
usually widely infiltrated with round cells. 



PLATE 49. 

Fig. I. — Diphtheria of the Pharynx. X 80. The exudation 
of fibrin (1) between the necrotic epithelial cells is far advanced ; the 
necrosis has not yet reached the superficial surface. In the submucosa 
(2) the blood-vessels are dilated, some filled with fibrinous thrombi 

(3). 

Fig. II— Diphtheria of the Tonsil. X 280. 1, Fibrinous de 
posit, inclosing in its meshes nuclei which are disintegrating ; 2, zone 
of- the former epithelial layer ; epithelial cells largely disintegrated ; 
3, nuclei of disintegrated epithelial cells ; 4, lymphocytes of tonsillar 
follicle. 



Tab.43. 













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TabAv. 






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LitfuAnst /-.' Reichhold. Mum hen . 



THE DIGESTIVE ORGANS 1*29 

Noma i- the name given to an inflammation beginning 
in the mucous membrane of the lips or the mouth, especi- 
ally in children after severe infectious diseases. At first 
the mucous and submucous coats become edematous and 
infiltrated with blood, followed by leukocytic accumulation 
and an extensive and rapid gangrene, which spreads in ex- 
tent and depth, involving all the adjacent soft tissues, such 

glands, muscles, fat, and external skin. Previous to 
their total disappearance the nuclei break up into frag- 
ment- and deeply staining, minute particles. The blood- 
vessels generally are thrombotic. 

In smallpox the mouth, pharynx, and also the esopha- 
gus are often the seal ^\' eruptions quite similar histo- 
logically to the cutaneous pustules of variola. The epi- 
thelium becomes the seat of vesicular spaces filled with 
serous fluid, and formed by the pressing asunder of 
the cells that may remain connected by protoplasmic 
hand- and bridges, so that the cavity of the vesicle is sub- 
divided into many compartments. The accumulation of 
emigrating leukocytes ultimately renders the contents 
wholly purulent. Through rupture of the summit of the 
pustule a flattened ulcer is formed ; usually, this occurs 
earlier in the eruption- upon mucous surfaces than on the 
externa] -kin, whose horny layer i> more resistant. The 
floor of the ulcer is formed by necrotic epithelium and 
bacterial masses, especially staphylococci and streptococci. 
The stratum proprium and the submucosa are much con- 
■ d and infiltrated with leukocyte-. 'Flic mucous elands 
of the submucosa may present similar pustular efflores- 
cences with necrosis of the glandular epithelium and also 
cystic dilatations of some acini, which become filled with 
masses of mucus owing to occlusion of some of the secretory 
ducts. The infiltration usually extends to the underlying 
tissues. 



130 PATHOLOGIC HISTOLOGY. 



Croupous and Diphtheric Inflammation. 

Croupous and diphtheric processes occur frequently, 
especially in children, upon the soft palate, the tonsils, in 
the pharynx, and more rarely in the mouth itself. Ana- 
tomically, the terms croupous and diphtheric signify an 
inflammation in which are combined necrosis of the 
mucous membrane and fibrinous exudation, so that a 
membrane ("pseudomembrane") is formed. If the 
necrosis involves only the superficial layers of the mucosa, 
— merely the epithelial layer or perhaps only the outer 
layers of this, — the affection is called croup ; while diph- 
theria, in the anatomic sense, is characterized by a deeper 
necrosis, which extends into the stratum proprium. Prac- 
tically, the two forms are hard to differentiate from each 
other ; transitional stages occur from superficial fibrinous 
deposits with but a slight necrosis, to a severe mortification 
with the formation of fibrinous material in the deepest lay- 
ers of the mucous membrane. The necrosis and precipitation 
of fibrin go hand in hand, and stand in direct causal rela- 
tion with each other because the death of the tissue cells sets 
free fibrin ferment which induces coagulation in the plas- 
matic fluid exuded from the dilated vessels. This process 
can be observed histologically in various stages of the 
disease. In the beginning the vessels of the stratum 
proprium are greatly dilated and filled to distention with 
blood ; mixed among the red blood-corpuscles are 
numerous leukocytes which are also found free in the con- 
nective tissue and the epithelial layer. In some vessels 
occlusion by fibrinous filaments can be recognized. The 
epithelium is swollen, the protoplasm of the cells in the rete 
Malpighii is granular, and the intercellular cement lines 
appear broad. And now the first threads of fibrin can be 
observed as broad, glistening bands between the cells ; the 
bands or layers unite to form a network the meshes of 
which become narrower and narrower while the inclosed 






THE DIGESTIVE ORGANS. 131 

epithelial cells undergo a progressive solution. Gradually, 
the nuclear chromatin becomes condensed (pyknosis), fol- 
lowed by disintegration into minute fragments ; eventually, 
the fragments disappear wholly, and the destruction of 
the epithelium is now complete. In the mean time other 
nuclei appear in the fibrin, due to the migration of 
numerous leukocytes and nuclear fragmentation ; occasion- 
ally, lymphocytes are also visible. Usually, the exudation 
rises above the epithelium. The plasmatic fluid emerges 
upon its surface and runs over it for a distance before 
filiation takes place ; on this account the margins of 
the pseudomembrane are usually easily separated from the 
underlying tissue. Sometimes the emigration of leuko- 
cyte- into the membrane is very marked, so that it be- 
come- softened and assumes a purulent appearance. A 
dense, leukocytic wall forms at the margins of the zone of 
coagulation necrosis; finally, the new membrane separates 
either in the form of large shreds or as smaller, softer 
pieces, due to fatty changes, so that a more or less deep 
Loss of substance results — the diphtheric ulcer. Healing 
results from proliferation of the epithelium in the vicinity, 
and new cells gradually cover the defect. 

The disease just described is caused in the pharyngeal 
cavity and in the respiratory mucous membranes princi- 
pally by Löffler^ bacillus of diphtheria; in the latter 
stages other micro-organisms, especially streptococci, are 
also found present^ often in dense layers. At times these 
only are active — a-, for instance, in scarlatinal diphtheria. 
Bui chemic agents, especially corroding substances such as 
ammonia, can also produce the anatomic picture of a 
croupous-diphtheric inflammation. This form of inflam- 
mation i- consequently not of itself absolutely distinctive 
of a definite infection, 



132 PATHOLOGIC HISTOLOGY. 

PLATE 50. 
Fig. I.— Acute Suppurative Embolic Parotitis. X 70. (In 

appendicitis.) The interstitial tissue of the lobules is purulently in- 
filtrated, the acini themselves are largely destroyed and also greatly 
infiltrated with leukocytes (2) ; a few are still present (1). At several 
areas accumulations of pyogenic cocci (3) are seen. 

Fig. II.— Thrush Vegetations in Esophagus. X 270. Stained 
by Gram's method. The upper epithelial layers are loosened in their 
connections, separated and infiltrated with the mycelium of the thrush 
fungus (oidium or saccharomyces albicans) ; the threads are septate. 
In the lower layers of the epithelium (right) numerous leukocytes are 
present. 

SALIVARY GLANDS. 

The salivary glands, especially the parotid, are not 
rarely the seat of inflammation. In addition to the epi- 
demic form of acute parotitis or mumps, the parotid 
gland is frequently involved in suppurative processes, 
principally in the acute infectious diseases — typhoid fever, 
dysentery, cholera, scarlet fever, diphtheria, sepsis, pyemia. 
The pyogenic microbes in most cases probably enter the 
ducts of the gland (Stenson's duct) from the oral cavity. 
There results an acute sialodochitis with occlusion of the 
salivary passages by pus-cells, desquamated epithelial cells, 
and bacterial masses. The overflow of secretion is hin- 
dered and the entrance of bacteria into the substance of 
the gland favored. The interstitial tissue, and later the 
acini, become densely infiltrated with leukocytes : the epi- 
thelial cells may be covered over by leukocytes ; numer- 
ous cloud-like masses of cocci are seen. Finally, multiple 
abscesses are formed, which coalesce, and thus establish 
suppuration throughout the whole gland. Frequently, 
the purulent process extends to the periglandular tissue. 

The diseases of the esophagus do not demand any sepa- 
rate consideration from the histologic standpoint, resem- 
bling those of the mouth and the pharynx. 



Tab. JO. 










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/•'// *• 



///// . . I//.S/. /■: Reichhold, München , 



THE DIGESTIVE ORGANS. 133 

Corrosion of the esophagus by caustic alkalies and by 
acid- presents the appearance of a more or less deep-seated 
necrosis, with a fibrinous exudation between the necrotic 
epithelial cells and even in the deeper layers of the 
mucosa. Ammonia and carbolic acid especially produce 
typical lesions. 

In cardiac insufficiency and in cirrhosis of the liver the 
submucous veins o{ the esophagus frequently become 
varicose, and this may result in rupture and hemorrhage 
a- well a- in the formation of genuine varicose ulcers. 



STOMACH. 

Circulatory disturbances of the stomach are observed in 
cardiac insufficiency and in obstruction of the portal circu- 
lation, a- in cirrhosis of the liver. The veins of the mu- 
cosa become dilated and small hemorrhages frequently 
occur ) yellow or brownish blood-pigment is often found 
in the stratum proprium, and the tissue of the submncosa 
may be edematous. 

Acute catarrhal gastritis does not present any histologic 
peculiarities. In chronic gastric catarrh, as seen so com- 
monly in drunkards, noteworthy changes occur in the 
mucous membrane, affecting the glands as well as the 
stratum proprium. Usually, the surface epithelium ap- 
pears increased a- compared with the glandular epithelium 
proper; frequently, it contains remarkably tall cylindrie 
cells and also numerous goblet cells. In the glands the 
parietal cells especially appear atrophic ; often they disap- 
pear wholly. The chief cells occasionally present numer- 
ous karyokinetic figures and other evidences of prolifera- 
tion. They also form numerous goblet cells, which are 
found from tic mouth to the fundus of the glands, giving 
tin- mucosa a certain resemblance to that of the rectum. 
r I he specific glandular elements disappear more and more, 
and in the stratum proprium proliferative processes on 



PATHOLOGIC HISTOLOGY. 



PLATE 51. 



Fig. I. —Chronic Granular Gastritis. X 30. 1, Mucosa; 2, 
proliferated and greatly convoluted gastric glands ; 3, stratum pro- 
prium, thickened, infiltrated with round cells, and provided with pa- 
pillary elevations ; below, the muscularis mucosae and the submucosa ; 
4, tunica muscularis ; 5, serosa with subserous fat-layer. 

Fig. II.— Chronic Catarrh of the Stomach. X 160. The 
cells of the stratum proprium much increased in number. Interstices 
between the glands broadened. In the glandular cells are numerous 
mitotic figures ; many are changing into goblet cells (1). 



part of the connective tissue are very prominent. The 
cells are increased in number, and there is also leukocytic 
infiltration, so that the glands and their ducts are crowded 
apart and forced above the level of the surrounding mu- 
cosa as small papilla, which form especially in the course 
of the large submucous vessels (granular gastritis). The 
resulting irregularity and granular condition of the mucous 
membrane and the increased consistence are readily recog- 
nized macroscopically, and, when marked, frequently 
referred to as the so-called etat mamelonne. Occasionally, 
the increasing proliferation of the connective-tissue ele- 



PLATE 52. 

Fig. I.— Hemorrhagic, Necrotic Gastritis in Sulphuric Acid 
Poisoning (from Dog). X80. The upper layers of the mucosa 
form a necrotic scab, infiltrated with numerous red blood-corpuscles ; 
the glands are not visible (1); 2, areas still containing glands; in 
stratum proprium many round cells ; 3, muscularis mucosae ; 4, sub- 
mucosa. 

Fig. II.— Hemorrhagic Erosion of the Stomach. X 57. The 

superficial layers of the mucosa are destroyed. 1, Remains, of glands ; 
2, deposit composed of conglutinated red blood-corpuscles and portions 
of necrotic mucosa ; 3, the stratum proprium is exposed ; 4, muscu- 
laris mucosae ; 5, submucosa ; 6, circular muscular layer. 



Tab. sr. 



. 



OCgfö 




„-0 



Fig.1. 




Fig.2. 



/.////.Ans/ F. Reichhold, München,. 



Tab. 52. 







j^.j. 










. <J 






LOA. Aast. F ReuchJtwUl, Mu/i/Jwn 



THE DIGESTIVE ORGANS. 135 

ments and the elongation and cystic dilatation of the glands 
become bo marked at certain places that pedunculated 
polypoid excrescences arise (polypoid gastritis). Such 
polypoid outgrowths may acquire very considerable dimen- 
sions j in rare cases masses are formed as large as goose 
2jgs 3 consisting of the proliferated elements of the normal 
mucous membrane. The submucous connective tissue also 
take- part in these polypoid formations, so that the mus- 
cularis mucosae at their base may he broken through. The 
lymph-follicles frequently undergo considerable hyperplasia 
in these chronic inflammatory condition-. 

Diphtheric eschars appear on the gastric mucous mem- 
brane after the action of' acids or alkalies ; sulphuric acid 
produces a linn, brownish or greenish, pseudomembranous 
layer, consisting of the necrotic mucous membrane into 
which fibrin has been precipitated, usually freely mixed 
with red blood-corpuscles. 

Phlegmonous gastritis is the term applied to purulent 
inflammation of the wall of the stomach. It concerns a 
focal <>r diffuse, purulent infiltration, especially of the sub- 
mucosa. The muscularis mucosae and the stratum pro- 
prium arc densely infiltrated with leukocytes, which also 
gather between the glandular epithelium, which may be 
wholly covered over. In this way multiple abscesses are 
formed in the mucous membrane, which, on rupturing, 
Liivr rise t<> ulcer- ; at other times large shreds of the 
mucosa are exfoliated in continuity on account of the sub- 
mucous suppuration. 

Gastric Ulcer. 

Defects «•!' varying -i/o and depth appear upon the 
mucous membrane of the stomach. Such defects are 
produced, in the first place, by the digestive action of 
the gastric juice after injuries of various kind- to the 
inner layer of the wall. Small, circumscribed hemor- 



136 PATHOLOGIC HISTOLOGY. 

PLATE 53. 

Fig. I.— Round Ulcer of the Stomach with Erosion of a 
Blood=vessel. X16- 1> Ulcerated margin, with surrounding 
mucosa, muscularis mucosae, and submncosa ; the ulcer extends to the 
inner muscle layer ; its rloor (2) is covered with necrotic material ; 3, 
eroded arterial blood-vessel with thrombotic lumen. 

Fig. II.— Margin of a Round Ulcer of the Stomach. X 64. 

1, Mucosa ; 2, muscularis mucosae ; 3, submucosa ; 4, muscularis ; 
6, infiltrated floor of the ulcer in the outer layers of the muscular coat. 



rhages, as occur in gastric catarrh and passive congestion, 
are, perhaps, the most frequent first cause for the su- 
perficial defects, usually called hemorrhagic erosions. 
These are frequently multiple, and at times the mucous 
membrane is thereby given a sieve-like appearance ; they 
generally involve the mucous coat only, reaching rarely 
through the muscularis mucosae ; the surface epithelium is 
destroyed, while the lower part of the glands may be 
present, especially in the slanting margins ; the tissue im- 
mediately adjacent is usually necrotic and infiltrated with 
disintegrated red blood-corpuscles and brownish blood- 
pigment ; below this zone there is proliferation of cells 
and leukocytic accumulations. 

Superficial defects like these commonly heal ; the tunica 
propria is repaired by scar tissue, and new epithelium 
covers the surface. 

Should the peptic action last for a longer time, the 
defect becomes deeper and wider and there is formed the 
round ulcer of the stomach. This ulcer extends through 
the entire thickness of the mucosa, the muscularis mucosae, 
and the submucosa ; frequently, part or all of the mus- 
culature is also eaten away, and even the serous coat may 
be perforated. 

Generally, the margins of the ulcer appear terraced or 
step-like, because the loss of substance in the mucosa is 







Fig.l. 



Tab. S3- 



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Bfi ä - W2£, 



^^Säft? 



.. 



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Z^/l. ,4^ /T Jteichhofd '. München . 



THE DIGESTIVE OEGAXS. 137 

larger than in the inner layers of the muscular coat, and 
tin- again larger than in the outer layers. AVith low powers, 
section- of the nicer show that the margins rapidly slope 
to the hot torn, that the mucosa is frequently contracted in 
a somewhat funnel-shaped manner,, that the immediate 
vicinity of the delect is necrotic while the more distant 
parts are infiltrated with round cells. The bottom of the 
nicer also presents a thin, necrotic, anuclear layer. Blood- 
vessels arc often eroded and fatal hemorrhage may occur. 
Microscopically, the vessel walls are then found cut 
through just as sharply as the single layers in the margins 
of the ulcer. Usually, the lumen of the vessels is partly 
or wholly closed by thrombi. It is highly probable that 
a part of the round ulcers of the stomach originate upon 
the basis «>f a hemorrhagic infarction of the gastric wall 
with consecutive digestion of the mortified area. 

Simple atrophy of the mucous membrane of the stomach 
with disappearance of the glands occurs in chronic gastric 
catarrh, in carcinoma of the stomach, also in the marantic, 
and especially in atrophic infants. 

Amyloid degeneration occasionally occurs simultaneously 
with amyloidosis of the intestinal mucous membrane. 

Fatty changes of the epithelial and connective-tissue 
elements are observed, especially in acute phosphorous, 
and also in arsenous, poisoning. 

Tuberculosis and syphilis of the wall of the stomach 
are of rare occurrence; the specific granulomatous pro- 

a is form in the stratum proprium and in the submu- 
oosa. 

Tumors. — The adenomas of the mucous membrane 
frequently originate from the polypi previously mentioned. 
Of the connective-tissue tumors, fibroma, myoma, lipoma, 
and sarcoma are observed. All forms of carcinoma occur 
in the stomach, from the hard, fibrous scirrhous to soft, 
almost confluent colloid. 

Opportunity is occasionally given for the study of 



138 PATHOLOGIC HISTOLOGY. 

the beginning of the development of carcinoma in the 
mucous membrane of the stomach. It is then seen that 
many layered or solid epithelial masses, starting from the 
lower parts of the glands, perforate the stratum proprium 
and the muscularis mucosae, and infiltrate the submucosa 
in nest-like groupings. The carcinoma in this case grows 
into the w T all of the stomach without first destroying the 
overlying mucous membrane. At times larger portions 
of the wall of the stomach are diffusely infiltrated with 
carcinomatous masses, and thus rendered greatly thickened 
and stiff, while the mucosa does not show any loss of sub- 
stance. 

The hard or scirrhous forms of carcinoma are quite 
prone to cause much narrowing of the lumen, especially 
of the pylorus. Microscopically, the walls are composed 
of broad fibrous masses in w T hich are narrow slit-shaped 
alveoli, filled with a sparse, low epithelium, also present 
in the muscular coat, which is then usually hypertrophied. 



INTESTINE. 

Passive congestion of the intestines with marked injec- 
tion of the vessels and edema of the walls occurs in car- 
diac insufficiency and in obstruction to the portal circula- 
tion ; when of longer duration, it is usually associated 
with the manifestations of a chronic gastric catarrh. 

Hemorrhagic infarction and necrosis of larger segments 
of the intestine occur only after complete occlusion of the 
superior mesenteric artery. The occlusion of small arte- 
ries is generally without effect, because of the numerous 
anastomoses. 

Atrophy of the intestinal wall is found in prolonged 
inanition, especially in atrophic infants. The lumen is 
then usually widened by the presence of gas, the walls 
are thin as paper, transparent, and exceedingly pale. 



THE DIGESTIVE ORGANS. 139 

Microscopically, all layers appear uniformly thinned. The 
surface epithelium is lost, as a rule, the glands are short, 
the lymph-follicles have generally disappeared, and both 
muscle-layers are greatly attenuated. On account of the 
diminution of the muscle-cells, the lymph-vessels appear 
more distinct. (Plate 55, Fig. I.) 

A peculiar form of atrophy, associated with pigmenta- 
tion of the musculature, is observed in old age, in marantic 
and cachectic persons, in alcoholics, and also in cases of a 
simultaneous pigmentation of other organs, such as the 
lymph-glands, spleen, kidneys, and liver — the so-called 
hemochromatosis of Recklinghausen, a disease which appar- 
ently depends on an increased destruction of the red 
1 >1( »od-c< »rpuseles. 1 Examined fresh, the muscle-cells are 
found somewhat enlarged and partly, or in severe cases 
wholly, filled with numerous, minute pigment-granules, 
which do not always give the iron reaction. Often the nuclei 
are covered by the pigment particles. The longitudinal mus- 
cular layer is commonly more pigmented than the circular. 
Occasionally, pigment is found in the muscularis mucosae 
and the submucosa. The process has a marked similarity 
to the brown atrophy of striped muscle as seen in the 
heart. (Plate 55, Fig. II.) 

Amyloid degeneration of the intestinal mucosa is occa- 
sionally observed in amyloidosis of other organs (kidney, 
spleen, liver). A- elsewhere, the degeneration of the in- 
testinal mucosa also begins in the .-mailer arteries and 
preferably in the branches within the villi ; glistening 
masses, giving the well-known specific reactions, are de- 
posited in their walls. The further increase causes a nar- 
rowing of the vessels, the mucous membrane becomes 
anemic and acquires a peculiar stiffness ; the epithelium is 
lost, and many villi appear as if broken across; in some 

For a full discussion of hemochromatosis ><■<• Opie, "The Journal 
tperimenta] Medicine," 1--!». iv. 279, and " Transactions <>t' the 
Association of Ajnerican Physicians/' !-!>!). \iv, 253. 



140 PATHOLOGIC HISTOLOGY. 

PLATE 54. 

Fig. I.— Beginning Carcinoma of the Stomach. X 54. At 

left, free surface of mucosa. 1, Proliferated glands with several layers 
of epithelial cells ; 2, muscularis mucosae, at one point ruptured by 
glandular proliferation ; 3, submucosa ; 4, in the submucosa are seen 
the alveoli of the carcinoma. 

Fig. II.— Marked Stenosis of the Pylorus as a Result of a 
Scirrhous Carcinoma. X 13. The lumen is extraordinarily nar- 
rowed ; the mucosa is wholly destroyed. 1, Connective-tissue bauds 
with small, slit like, cancer alveoli ; greatly hypertrophied muscularis. 

cases the villi are represented by short, broad, anuclear 
projections. The vessels in the muscular coat are also 
liable to amyloid change, but the process does not extend 
to the muscle itself, which may, however, undergo a 
secondary atrophy. 

Inflammations. 

In acute catarrhal enteritis the intestinal mucous mem- 
brane is swollen, hyperemic, and edematous. The epithe- 
lium contains an increased number of goblet cells, and 
often extensive mucous degeneration is observed, not 
only in the surface epithelium, but also in the glandular ; 
the mucus accumulates as large, viscid, flocculent, grayish 



PLATE 55. 

Fig. I. — Atrophy of the Large Intestine ; Chronic Tuber= 
culosis in a Child. X 85. Mucous membrane very thin, with short 
glands (1) and somewhat increased stratum proprium (2); 2, muscu- 
laris mucosae ; 3, submucosa ; 4, muscularis ; 5, serosa. 

Fig. II. — Brown Atrophy of the Muscularis of the Small 
Intestine in Cachexia Due to Cancer. X 330. Almost all muscle- 
cells filled with fine, granular, brownish pigment ; the nuclei are covered 
by the latter. 



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THE DIGESTIVE ORGANS. 141 

masses. The lymphatic apparatus is also involved ; the 
follicles are swollen and often project above the level of 
the mucosa as small nodules as large as a grain of wheat 
(follicular enteritis). The germinal centers are enlarged 
on account of an increased formation of lymphocytes ; 
frequently , the centers become necrotic, and, on rupture 
into the lumen, small, follicular ulcers are produced, 
which usually heal promptly by proliferation of the ret- 
iculum, leaving, however, a small depression easily recog- 
nized by the presence of blackish pigment. 

In chronic catarrh, which frequently develops as a con- 
sequence of long-continued passive hyperemia, the changes 
described are supplemented by an increase in the stratum 
proprium and the submucosa, owing to round-cell infiltra- 
tion and proliferation of the fixed cells. The continua- 
tion of this process may lead to partial destruction of the 
intestinal glands, the mucous membrane becomes irregu- 
larly uneven, and polypoid protuberances may be formed 
by the connective-tissue proliferation (polypoid enteritis). 
The frequent, minute hemorrhages may lead to an exten- 
sive punctiform, blackish pigmentation. 

Genuine croupous enteritis — L <?., formation of a fibrin- 
ous layer upon the surface of the necrotic intestinal 
epithelium — is a very rare disease ; on the other hand, 
various etiologic agents may produce the anatomic picture 
of diphtheria ; deep necrosis of the mucosa with precipi- 
tation of a varying amount of fibrin. Toxic agents are 
the most common ; in mercurial poisoning the action of 
the corrosive chlorid eliminated by the mucous membrane 
of the colon produces a diphtheric colitis ; and uremic 
colitis is a diphtheria caused by an elimination of deriva- 
tives from urea ; diphtheric inflammation is also the 
result of pressure-necrosis of the mucous membrane, 
caused by inspissated fecal masses or hard foreign bodies ; 
in severe septic and pyemic processes diphtheric inflam- 
mation of the large intestine arises by metastasis ; finally, 



142 PATHOLOGIC HISTOLOGY. 



PLATE 56. 



Fig. I.— Diphtheric Colitis in Corrosive Sublimate Poison- 
ing. X 20. 1, Necrotic mucous membrane, covered by eschar ; 2, 
leukocytic wall at margin of slough ; 3, greatly injected submucosa ; 
4, muscularis. 

Fig. II.— Dysentery of Large Intestine. X 50. The super- 
ficial layers of the mucosa are necrotic. In the deeper layers between 
the glands many leukocytes have accumulated (1) ; 2, fibrinous 
thrombus in a small artery ; 3, muscularis mucosae ruptured in many 
places by leukocytic accumulations ; 4, submucosa with greatly 
dilated blood-vessels. 



some forms of the so-called dysentery are anatomically 
diphtheria of the colon. In sublimate poisoning the 
diphtheric changes may be very extensive ; the entire 
mucous membrane may be converted into a solid, hard 
eschar, composed of an opaque, grayish layer, which 
microscopically is found to be without nuclei and infil- 
trated with hemorrhages and small chromatin fragments ; 
Lieberkühn' s glands may be recognized in the form of 
shadowy and indistinct outlines. Externally, the zone of 
necrosis is bounded by a thick layer of polynuclear leuko- 
cytes, the subjacent submucosa is highly congested, hem- 
orrhagic, and infiltrated with round cells ; similar, but 
not so well-marked, changes may be present in the mus- 
cular coat. By means of the fibrin stain the necrotic 
eschar and also the submucous tissue are shown to contain 
a fine, fibrinous network ; many of the vessels are also 
often the seat of fibrin formation. (Plate 56, Figs. I 
and II.) 

Dysentery, in the strict sense, is characterized by a 
purulent infiltration of the mucous and submucous coats. 
The glands are compressed and separated from each other 
by the accumulation of cells, and pus may form in the 
glandular lumen, Simultaneously, fibrin is deposited in 



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THE DIGESTIVE OEGAXS. 143 

the superficial layers of the epithelium, which undergoes 
necrosis. The process may spread toward the submucosa 
and lead to an extensive and deep coagulation necrosis of 
the mucous membrane. In the beginning the necrotic 
areas may be separated from each other, but later they 
coalesce to form thick, stiff, brownish or greenish crusts 
and membranes. The increasing accumulation of the 
leukocytes gradually separates the crusts and ulcers, at 
the base of which appears the hypercmic and infiltrated 
submucosa, which may continue to suppurate for a long 
time. The lymphatic follicles are also much swollen, 
and a central necrosis may produce crater-shaped losses of 
substance. [In amebic dysentery the ulcers have over- 
hanging margins.] 

In these processes, as well as in the typhoid intestinal 
lesions, the lymph-vessels are involved in a characteristic 
manner. They appear as remarkably distinct, richly 
cellular cords at the boundary of the submucosa and 
between the muscular layers. Their lumen is filled with 
large, polygonal, and flat cells, — desquamated epithelial 
cells, — which often appear necrotic or filled with fat- 
vacuoles ; in addition, are seen leukocytes and deeply 
stained bacterial masses. (Plate 58, Fig. II.) 

On account of its rapid course cholera does not produce 
extensive or noteworthy histologic changes in the intes- 
tines. In the ea-es that die in the stage of asphyxia 
there are found small hemorrhages, extensive desquama- 
tion of the surface epithelium, necrosis of the summits of 
the villi ; occasionally, the necrosis may extend to the 
base of the villi; the submucosa usually contains numer- 
ous mast-cells. 

The changes in the intestines in typhoid lever are more 
characteristic and more severe. 'Die specific microbes 
localize in the lymphatic apparatus of the mucous mem- 
brane, and it i- here that the most marked changes occur. 
[These changes correspond in a general way with those 



144 PATHOLOGIC HISTOLOGY. 

PLATE 57. 

Fig. I.— Typhoid Fever. Medullary Swelling of Follicle of 
Large Intestine. X 50. The follicle is greatly enlarged, and 
shades into the surrounding infiltration ; at its upper part the mucous 
membrane is almost displaced. 1, Remains of the glands of Lieber- 
kühn ; 2, infiltrated submucosa ; 3, remains of follicle. 

Fig. IL— Typhoid Fever. Medullary Swelling with Begin= 
ning Necrosis of a Follicle. X 50. In the center of the follicle 
necrosis has taken place ; a small amount of fibrin is here found (3) ; in 
the submucosa (4) greatly inj ected blood-vessels and numerous, large, 
round cells (deeply stained with eosin) ; 1, mucosa infiltrated with 
leukocytes ; 2, muscularis mucosae ; 5, muscularis. 



that occur in the mesenteric lymph-glands and in the 
spleen, and which have been referred to. In the first 
stage, corresponding to the first two weeks of the disease, 
the solitary follicles and Peyer's patches, especially those 
near the ileocecal valve, become considerably enlarged, 
of soft consistence, rising above the surrounding mucosa 
(so-called medullary infiltration). 

Microscopically, the swelling of the follicles is found to 
depend upon a marked multiplication and enlargement of 
the cells in the germinal centers and their vicinity. In 
place of the lymphocytes appear numerous, large, roundish 
cells, with a large amount of acidophilous protoplasm, 
the nuclei being mostly vesicular, although some may be 
richer in chromatin and often a number are present in one 
cell. The appearance resembles very much those pre- 
sented by mesenteric glands that are the seat of typhoid 
swelling. (Plate 14, Fig. II.) This similarity is in- 
creased by the appearance of fat-vacuoles in the plasmatic 
cells, [phagocytic cells that often contain red corpuscles, 
etc.] in the intestinal follicles. 

In the beginning masses of typhoid bacilli are found 
just as in the lymph-glands (Plate 14 ; Fig. II) ; later, the 



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THE DIGESTIVE ORGANS. 145 

bacilli disappear, while other micro-organisms may invade 
the tissue secondarily. Mast-cells appear in the vicinity 
oi the swollen follicles almost without exception ; these 
cells are large, round cells filled with small, roundish 
granules, which stain deeply with alkaline, aniline dyes. 
The limits of the follicles become obscured on account of 
the leukocytic infiltration of the adjacent mucosa and sub- 
mucosa. 

[Mast-cells are cells whose protoplasm is filled with 
basophile granules that stain red (metachromatically) with 
polychrome methylene-blue. 1 Ma-ma cells are cells of 
oval, cubic, or rhombic form, whose protoplasm retains a 
blue color when stained with methylene-blue, while the 
nucleus, generally eccentric in its situation, stains more 
lightly and presents a few blue, chromatic masses. It is 
regarded as derived from preexisting or emigrated lympho- 
cytes, and occurs in various cell accumulations of inflam- 
matory nature.] 

The mucous membrane covering the follicles is raised 
so that the crypts at the side of the swelling acquire 
an oblique position ; very soon retrogressive changes 
make their appearance in these parts of the mucosa. The 
superficial epithelium, and also, in part, that lining the 
crypts, becomes in erotic ; the villi also undergo necrosis ; 
fibrin is deposited in the necrotic layer, so that at a 
certain definite stage there is a diphtheric inflammation 
over the follicles. The surrounding blood-vessels are 
greatly congested. Occasionally, the medullary infiltra- 
tion of the follicle- subsides, and a simple resolution 
ensues without extensive and general necrosis 5 theswollen 
and enlarged cell- undergo fatty changes, and the fat-drops 
are absorbed. | Plate 07. Figs. I and IT.) Usually, how- 
ever, the end of the second or the beginning of the third 
week witnesses the appearance of an at firsl limited and 
superficial necrosis that gradually involves the whole fol- 
licle. A delicate, fibrinous network appears between the 

10 



146 PATHOLOGIC HISTOLOGY. 

PLATE 58. 
Fig. I.— Typhoid Fever. Ulcer after Detachment of Slough. 

X 50. The margins of the defect end abruptly ; in the floor of the 
ulcer, which reaches into the submucosa, are seen a few necrotic por- 
tions of tissue with extensive infiltration of leukocytes. 1, Mucosa ; 2, 
muscularis mucosae ; 3, submucosa with overfilled blood-vessels ; 4, 
muscularis. 

Fig. IL— Intestinal Lymphangitis. Cellular " Thrombus" 
in a Lymph=vessel of the Submucosa of the Large Intestine 
in Dysentery. X 360. 1, In the lymph-vessel are seen large 
polygonal, partly necrotic cells, some with two nuclei ; among these 
are several leukocytes. 

disintegrating cells ; eventually, the necrotic follicle and 
the necrotic mucous membrane are changed into a struc- 
tureless mass, often stained greenish by the bile, and sur- 
rounded by a dense leukocytic wall. This is the typhoid 
slough. 

Toward the end of the third or the beginning of the 
fourth week this slough becomes loosened from the sur- 
roundings and thrown off — the typhoid ulcer has formed. 
(Plate 58, Fig. I.) The margins of the ulcer are usually 
abrupt ; the depth varies, depending on the extent of the 
necrosis and the size of the follicles involved ; it always ex- 
tends at least to the submucosa, and not rarely the necrosis 
may involve the muscular coat, so that at times there is ex- 
posed the serous membrane, which may become perforated. 
The floor of the ulcer is at first brownish or blackish from 
the extravasated blood, but soon it becomes clean, so that 
the tissue exposed is readily recognizable. Later, the 
tissue forming the floor of the ulcer produces granulation 
tissue from newly formed connective-tissue cells and em- 
bryonic vessels, until the defect is filled up. The surface 
epithelium may be regenerated from that at the margin ; 
even the villi are partly reproduced, but the glands do not 
seem to be reproduced. 



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THE DIGESTIVE ORGANS. 147 

These regenerative processes do not generally appear 
before the fifth to the sixth week of the disease. 

As in diphtheric enteritis and in dysentery, so also in 
typhoid, the lymph-vessels of the intestinal wall become 
involved through extensive desquamation and new forma- 
tion of their epithelium. 

Tuberculosis. 

Primarily, tuberculosis of the intestines also tends to 
become localized in the lymphatic apparatus of the mu- 
cous membrane. As the leukocytes accumulate, large 
polygonal cells, with vesicular, clear nuclei, — the so-called 
epithelioid cells, — appear among them and often form 
giant cells. The epithelioid cells are undoubtedly deriv- 
atives of connective-tissue cells, and the cells lining lymph- 
vessels. 

While different cells accumulate about the small nodules 
and densely infiltrate the mucous membrane, the center of 
the mass undergoes coagulation necrosis ; the nuclei disin- 
tegrate into fine fragments and finally disappear wholly. 
The caseous area spreads and involves the surrounding 
tissue, so that the mucous membrane is broken through 
and the caseous center empties itself into the lumen of the 
intestine ; the follicular, tuberculous ulcer which is thus 
formed corresponds to the caseous area, and has over- 
hanging, irregularly thickened, -wollen margins. The 
defect increases rapidly because new tubercles form in the 
Moor and undergo caseation ; the process frequently 
spreads in a circular direction — that is, perpendicularly 
to the long axis of the intestine. In advanced instances 
all the layer- of the intestinal wall — the submucous, mus- 
cular, and serou become infiltrated with nodules that 

may undergo necrosis, until eventually perforation takes 
place. ( Plate 59, Figs. I and 1 1. 1 

Syphilitic granulomas occur in the intestinal walls in 
congenital syphilis of the new-horn a.- well as in adults 



148 PATHOLOGIC HISTOLOGY. 

PLATE 59. 
Fig. I.— Beginning Tuberculosis in the Vermiform Ap= 
pendix. X 80. Mucosa about normal, but with infiltrated stratum 
proprium. 1, Moderately sharply circumscribed, cellular nodule in 
the submucosa with beginning central necrosis. 

Fig. IL— From the Margin of a Tuberculous Ulcer of the 
Intestine. X 80. The greater part of the mucosa is destroyed by 
exfoliation of the caseous tissue. 3, The overhanging margin of the 
tuberculous ulcer; 2, floor of ulcer ; at (1) is a newly formed nodule. 
All the blood-vessels are greatly distended with blood. 

in the later stages of acquired lues. The nodules differ 
from tuberculosis on account of their tendency to fibrous 
encapsulation and the constant presence of syphilitic en- 
darteritis in their vicinity. The confluence of adjacent 
nodules may occasionally produce larger sclerotic patches 
in the mucosa and submucosa. 

PERITONEUM. 

The inflammations (including tuberculosis) of the peri- 
toneum resemble, histologically, the same processes in the 
pleura. In order to avoid repetitions, it is sufficient to 
refer the reader to page 117. 

PLATE 60. 
Fig. I.— Beginning Suppurative Peritonitis, Twenty=four 
Hours after Ligating the Intestine (from Guinea=pig). X 625. 

1, Peritoneal connective tissue in longitudinal and transverse section ; 

2, epithelium ; 3, exudate, consisting of a moderate amount of fibrin 
(several of the threads are also deposited between the epithelial cells 
and the connective tissue of the serosa), numerous leukocytes, and red 
blood-corpuscles. Scattered about are nuclei of detached epithelium 
and various bacteria. 

Fig. IL— Tuberculous Peritonitis. X 72. 1, Epithelium; 2, 
infiltrated connective tissue of the serosa ; 3, subserous fat-layer ; 4, 
tubercle with giant-cells ; 5, villus-like elevations. 



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INDEX, 



A. 

Abscess, embolic, 23 ; PL 3 
of lang, PI. 41 
of spleen, 57 
purulent, of lymphatic glands, 

49 
splenic, 59 
Acute inflammation of lymph- 
gland, 51 
Adenoma of stomach, 137 
Adipositas cardis, 20 : PI. 2 
Albuminous degeneration of 

heart-muscle, 18 
Amebic dysentery, 143 
Amyloid degeneration of intes- 
tine, 139 
of spleen, 61 ; PL 21, 22 
of stomach, 137 
Amyloidosis of spleen, 61 ; PL 

2 1 22 
Anemia, pernicious, bone-mar- 
row in, 65 ; PL 25 
Aneurysm. 12 

of aorta. PL 10 a 
Anthraeosis of lung, 90 ; PL 32 

of spleen, 55 
Aorta, aneurysm of, PL 10a 
Arteries, fatty degeneration of, 
37; PI. 10 
structure of, 33 
Arteriosclerosis. 35 : PL 9, 10 
Arteriosclerotic myocarditis, 25 
Arteritis, 39 

gummatous. 11 : PL 10 b 

in tuberculous leptomeningitis, 

29, 10 : PL 10 1) 
obliterans, PL 11 
tuberculous, PL 12 



149 



Artery, atheroma of, 34, 35 ; PL 
10 

calcification of, 37 

inflammation of, 39 
Atelectasis, 79 

collapse, 79 

compression, 79, 80 ; PL 31 

fetal, 79 ; PL 31 

resorption, 80 
Atheroma of artery, 34, 35 ; PL 

10 
Atheromatosis, 35 
Atheromatous patch, Cholesterin 

plates from, 37 ; PL 10 
Atrophy of heart-muscle, brown, 
20, 21 ; PL 2 

of intestine, 138 ; PL 55 
brown, 139 ; PL 55 

of mucous membrane of stom- 
ach, 137 

of spleen, senile, PL 18 



Bacon spleen, 61 ; PL 21 
Black tongue, hairy, 127 
Blood-vessels, structure of, 33 
Bone-marrow, gelatinous, 65 

in acute leukemia, 65 ; PL 25 

in pernicious anemia, 05 ; PL 
25 

necrosis of, 65 

structure of, 64 
Bronchi, diseases of, 75 

structure of, 69, 71 
Bronchia] catarrh, 75 
Bronchiectasis, 76 ; PL 29 



150 



INDEX. 



Bronchiectatic cavity, 114 ; PI. 

45 
Bronchitis, caseous, 207 ; PL 41 
Bronchopneumonia, 91, 100 

circumscribed indurative, 90 

organization of exudate in, PI. 
38 
Bronchus, ectasia of, PI. 76 

tuberculosis of, PI. 28 
Brown atrophy of heart-muscle, 
20, 21 ; PI. 2 

induration of lung, 83 ; PI. 34 
Bullous emphysema of lung, 82 



C. 

Calcareous goiter, 120 
Calcification of artery, 37 

of veins, 45 
Capillaries, structure of, 34 
Carcinoma of stomach, 137 ; PI. 
54 
of thyroid gland, 120 
Cardiac glands, 124 
Carnification of lung, 95, 99 ; PL 

38 
Caseation of lymph-glands, 52 
Caseous bronchitis, 107 ; PL 41 
necrosis in gummatous arteritis, 
41 ; PL 10 b 
of pericardium, 32 
pneumonia, 108, 109 ; PL 42 
Catarrh, bronchial, 75 
nasal, 67 

chronic, 68 
of larynx, 71 
chronic, 72 
of oral cavity, 126 
of pharynx, 126 
Catarrhal enteritis, acute, 140 
chronic, 141 
gastritis, acute, 133 

chronic, 133 ; PL 51 
pneumonia, 93 ; PL 39 
Chalkosis pulmonis, 91 
Cholera, effect on intestine, 143 
Cholesterin plates from athero- 
matous patch, 37 ; PL 10 



Circulatory disturbances in the 
lungs, 83 
of myocardium, 21 
of stomach, 133 
Circum vallate papillae, 121 
Cirrhotic induration of lung, 113 ; 

PL 45 
Cloudy swelling in heart-muscle, 

18 
Coagulative centers in croupous 

pneumonia, 95 
Cohnheim's experiment, 39 
Cohn's stigmas, 77, 96 
Colitis, diphtheric, 141 ; PL 56 

uremic, 141 
Collapse atelectasis, 79 
Collateral edema of lung, 93 
Colloid goiter, 119 
Colon, diphtheria of, 142 
Compression atelectasis, 79 
Congestion, passive, of intestine, 
138 
of spleen, 54 

stage of, in croupous pneumo- 
nia, 95 
Coronary arteries, embolism of, 

21 
Corpora amyloidea, 100 
Corrosion of esophagus, 133 
Cor villosum, 31 ; PL 7 
Coryza, 67 
Croup, 73, 130 
Croupous enteritis, 141 

laryngitis, 73 

pneumonia, 93, 95 
Cyanotic induration of lung, 83 ; 

PL 34 
Cystic goiter, 119 

polyp of nose, 69 



D. 

Degeneration, albuminous, of 

heart-muscle, 18 
amyloid, of intestine, 139 

of spleen, 61 ; PL 21,22 

of stomach, 137 
fatty, of arteries, 37 ; PL 10 

of heart, 19 ; PL 1 






IXDEX. 



151 



Degeneration, hyaline, of lymph- 
glands, 51 ; PL 16 

of spleen, 61 
Demilune cells, 1*22 
Desquamative pneumonia, 100 ; 

PI. 44 
Diphtheria, 130 

Loffler's bacillus in, 131 

of colon, 142 

of nose, 69 

of pharynx, 130 ; PI. 49 

of tonsil, 130: PI. 49 

of trachea, PI. 26 

spleen-follicle in, PI. 24 
Diphtheric colitis, 141 ; PI. 56 

endocarditis. 26, 29 

eschars, 135 

laryngitis. 73 

ulcer, 74, 131 
Diplococcus pneumoniae, 97 
Dust in lungs. 88, 89, 90 
Dust-cells in lungs, 88 
Dysentery. 142 : PI. 56 

amebic. 143 

E. 

Ectasia of bronchus, PI. 76 
Edema of lung, 85 ; PI. 36 
collateral, 93 
inflammatory. 92 
Embolic abscess,' 23 ; PL 3 
of lung, PL 41 
of spleen, 57 
parotitis, acute suppurative, 

132 ; PL 50 
pneumonia, 92, 93, 103 
scars of spleen, 57 
tuberculosis. 105 
Embolism of coronary arteries, 21 
of lung, fiat, 87 ; PL 35 
of spleen, staphylococcal, PL 
23 
Emphysema of lung, 81 ; PL 33 
bullous. 82; PL 33 
interstitial subpleural, 81 
intervesicular, 81 
Endarteritis. 35 
obliterans. 41 
tuberculous, 39, 40 



Endocarditis, 26 

diphtheric, 26, 29 

mycotic, 27 : PL c 

rheumatic, 26, 27 

ulcerative, 26, 29 

verrucose, 26, 27 
mycotic, 28 ; PL 6 
organized, 28 ; PL 6 
Endocardium, inflammation of, 
26 

structure of, 18 
Endolymphangitis fibrosa, 90 
Endoperivasculitis nodosa, 90 
Endophlebitis, 43 
Enteritis, 140 

acute catarrhal. 140 

chronic catarrhal, 141 

croupous, 141 

follicular, 141 

polypoid, 141 
Epicardium, milk spots of, PL 8 

sclerotic spots of, PL 8 

structure of, 17 
Erosion, hemorrhagic, of stomach, 

PL 52 
Eschars, diphtheric, 135 
Esophagus, corrosion of, 133 

diseases of, 126, 132 

in smallpox, 129 

structure of, 123 

tuberculosis of, 127 

tuberculous ulcer of, 128 

varicose veins of, 133 



F. 

Fat-embolism of lung, 87 ; PL 35 
Fatty degeneration of arteries, 37 ; 
PL 10 
of heart, 19 ; PL 1 
Faucial tonsils, 122 
Fetal gelatinous nodule, 18 ; PL 5 
Fibrinous pericarditis, acute, 31 ; 
PL 7 
pleuritis, 117 ; PL 47 
pneumonia, 93 
Fibroma of stomach, 137 
Fibrous myocarditis, chronic, 25; 
PL 4 



152 



INDEX. 



Filiform papillae, 121 

Follicles of lymphatic glands, 46 

splenic, 53 
Follicular enteritis, 141 
Fragmentation of myocardium, 

21, 24 
Fungiform papillae, 121 



Gastric glands, 124 

ulcer, 135 
Gastritis, acute catarrhal, 133 

chronic catarrhal, 133 ; PI. 51 

granular, 134 ; PL 51 

hemorrhagic, PI. 52 

necrotic, PL 52 

phlegmonous, 135 

polypoid, 135 
Gelatinous bone-marrow, 65 
Glanders of larynx, 75 

of nose, 69 
Glands, lymphatic, structure of, 

45 
Goiter, 119 

calcareous, 120 

colloid, 119 

cystic, 119 

hemorrhagic, 119 

parenchymatous, 119 

vascular, 120 
Granular gastritis, 134 ; PL 51 

laryngitis, 72 

pharyngitis, 127 
Gray hepatization, 96, 97 
Gummatous arteritis, 41 ; PL 10 b 

laryngitis, 75 



H. 

Heart, fatty degeneration, 19 
Heart-muscle, albuminous degen- 
eration of, 18 
brown atrophy of, 20, 21 ; PL 

2 
cloudy swelling in, 18 
diseases of, 18 

infarction of, organized, 23 ; 
PL 5 



Hematogenous pneumonia, 93 
tuberculosis, 105 

Hematoidin crystals in lung, 85 

Hemochromatosis, 139 

Hemorrhagic gastritis, PL 52 
goiter, 119 

infarction of intestine, 138 
pneumonia, 92 

Hepatization, gray, 97 ; PL 37 
in croupous pneumonia, 96 
red, 95, 96 ; PL 36 

Herzfehlerzellen, 84 

Hyaline degeneration of lymph- 
glands, 51; PI. 16 

Hyperemia of lung, passive, 83, 
85 ; PL 34 
of spleen, passive, 54 ; PL 18 

Hyperplasia, cellular, of lymph- 
gland, PL 15 

Hypostatic congestion of lung, 85 



I. 

Indurative lymphadenitis, PL 16 
Infarction of heart-muscle, or- 
ganized, 23 ; PL 3 

of intestine, hemorrhagic, 138 

of lung, 86 ; PL 35 

of spleen, anemic, 56 ; PL 19 
Infarcts in spleen, 55 

hemorrhagic, 56 ; PL 19 
Infiltration, medullary, in lymph- 
atic glands, 50 
Inflammation, interstitial, of 
lymph-glands, 51 

of artery, 39 

of endocardium, 26 

of intestine, 140 

of larynx, 71 

of lung, 91 

of lymph-glands, 47 
acute, 51 
suppurative, 49 

of pericardium, 30 

of perineum, 148 

of stomach, 133 

of veins, 43 
Inflammatory edema of lung, 85 



IXDEX. 



153 



Interstitial inflammation of 

lymph-glands, 51 
myocarditis, 24 ; PL 4 
Intestinal lymphangitis, 143 ; 

PI. d8 
villi, 125 
Intestine, amyloid degeneration 

of, 139 
atrophy of, 138 ; PL 55 

brown. 139 ; PL öd 
diphtheric inflammation of, 141 
diseases of. 138 
effect of cholera on, 143 
effect of typhoid fever on, 143 
follicular nicer of. 141 
hemorrhagic infarction of, 138 
inflammation of, 140 
large, structure of, 125, 126 
passive congestion of, 138 
small, structure of, 125. 126 
syphilitic granuloma of, 147 
tuberculosis of. 147 
tuberculous ulcer of, 147 



L. 

Large intestine, structure of, 125, 
126 

Laryngeal ulcer, 71 ; PI. 27 
Laryngitis, 71 

croupous, 73 

diphtheric. 73 

granular. 72 

gummatous. 75 
Larynx, catarrh of, 71 
chronic, 72 

glanders of. 75 

inflammation of, 71 

leprosy of, 75 

structure of, 69, 70, 71 

syphilis of, 75 

tuberculosis of, 74 ; PL 28 

ulcerations of, 74, 75 
Leprosy of larynx, 75 
Leptomeningitis, tuberculous, in 

arteritis, 39, 40 ; PL 10 b 
Leptothrix buccal is. 127 
Leukemia, acute, bone-marrow 

in, 65 ; PL 25 



Leukemia, myelogenic, 63 

spleen in, 62 ; PL 23 
Lingua hirsuta, 127 
Lipoma of stomach, 137 
Lipomatosis cordis, 20 ; PL 2 
Lobar pneumonia, 91 
Lobular pneumonia, 101 ; PL 40 

postdiphtheric, 103 ; PL 40 
Löffler's bacillus, 131 
Lung, anthracosis of, 90 ; PL 32 
atelectasis of, 79 

of fetal, 79; PL 31 
brown induration of, 83 ; PL 

34 
bullous emphysema of, 82 ; PL 

33 
carnification of, 95, 99 ; PL 38 
chalicosis of, 91 
cirrhotic induration of, 113 ; 

PL 45 
collateral edema of, 93 
cyanotic induration of, 83 ; PL 

34 
edema of, 85 ; PL 36 
embolic abscess of, PL 41 
emphysema of, 81 ; PL 33 
interstitial, 81 
intervesicular, 81 
fat embolism of, 87 ; PL 35 
hypostatic congestion of, 85 
infarction of, 86 ; PL 35 
inflammation of, 91 
inflammatory edema of, 85, 92 
marantic splenization of, 101 ; 

PL 36 
nodular syphilis of, 115, 116 
passive hyperemia of, 83, 85 ; 

PL 34 
red iron, PL 32 
siderosisof, 91 ; PL 32 
slaty induration of, 113 ; PL 45 
syphilis of, 115 
tuberculosis of, 104 
Lungs, circulatory disturbances 
in, 83 
dust in, 88, 89, 90 
embolism of, cellular, 88 
hematoidin crystals in, 85 
structure of, 77 



154 



- INDEX. 



Lymphadenitis, 47 ; PI. 15 

indurative, PI. 16, 17 
Lymphangitis, intestinal, 143 ; 
PI. 58 

peribronchial tuberculous, 110 
Lymph-glands, acute inflamma- 
tion of, 51 

caseation of, 52 

cellular hyperplasia of, PI. 15 

deposition of pigment in, due to 
tattooing, 48 ; PI. 14 

follicles of, 46 

hyaline degeneration of, 51 ; 
PI. 16 

inflammation of, 47 

interstitial inflammation of, 51 

in typhoidal diseases, 50 ; PI. 
14, Fig. 2 

medullary infiltration in, 50 

necrosis of, 51 

purulent abscess of, 49 

secondary nodules of, 46 

structure of, 45 

suppurative inflammation of, 
49 

tuberculosis of, 51 ; PI. 17 
Lymph-sinuses, 46 
Lymph -vessels, 46 
Lysis, stage, of, in croupous pneu- 
monia, 97 

M. 

Macroerythrocytes, 65 
Malpighian bodies, 53 
Marantic splenization, 85 ; PI. 36 

of lung, 101 ; PI. 36 
Marginal lymph-sinuses, 46 
Mast-cells, 145 

Medullary infiltration in lymph- 
atic glands, 50 
Mesarteritis, 35 
Mesophlebitis, 43 
Metastatic pneumonia, 92 
Micrococcus lanceolatus, 97 
Miliary tuberculosis, acute, 105, 

106 ; PI. 42 
tuberculous pneumonia, 111 ; 

PI. 43 
Milk spots of epicardium, PI. 8 



Mouth, croupous inflammation of, 
130 

diphtheric inflammation of, 130 

in smallpox, 129 
Mucous glands, mixed, 122 

pure, 122 
Mumps, 132 
Muscularis mucosae, 124 
Mycotic endocarditis, 27 ; PL 5 

verrucose, 28 ; PI. 6 
Myelogenic leukemia, 63 
Myeloplaxes, 65 
Myocardial scars, 23, 25 ; PI. 4 
Myocardite segmentaire, 24 
Myocarditis, arteriosclerotic, 25 

fibrous, chronic, 25 ; PI. 4 

interstitial, 24 ; PI. 4 
Myocardium (see also Heart-mus- 
cle), circulatory disturbances 
of, 21 

fragmentation of, 21, 24 

segmentation of, 21, 24 

structure of, 17 
Myoma of stomach, 137 
Myomalacia cordis, 22 



N. 

Nasal catarrh, 67 
chronic, 68 

polypi, 68 
Necrosis, caseous, in gummatous 
arteritis, 41 ; PI. 10 b 
of pericardium, 32 

of bone-marrow, 65 

of lymphatic glands, 51 
Necrotic gastritis, PL 52 
Nodular syphilis of lung, 115, 116 
Nodule, fetal gelatinous, 18 ; PL 5 
Nodules, secondary, of lymphatic 

glands, 46 
Noma, 129 
Nose, diphtheria of, 69 

glanders of, 69 

structure of, 67 

syphilis of, 69 

tuberculosis of, 69 
Nuhn's glands, 122 






INDEX. 



155 



o. 

Obesitas cordis, 20 ; PI. 2 
Oidium albicans, 127 
Oral cavity, 121 

catarrh of, 126 

diseases of, 126 

tuberculosis of, 127 

tuberculous ulcer of, 128 
Organs of circulation, 17 
Osteosarcoma of thyroid gland, 

120 
Ozena, 63 

P. 

Pachydermia laryngis, 72 ; PL 

27 
Papillae foliatae, 122 
Parenchyma, splenic, 53 
Parenchymatous goiter, 49 
Parotid glands, 122 
Parotitis, 132 

embolic, acute suppurative, 
132 ; PL 50 
Periarteritis, 35 

Peribronchial tuberculous lymph- 
angitis, 110 
Peribronchitis, 76 

nodosa, 90 
Pericarditis, 30 

fibrinous, acute, 31 ; PL 7 

tuberculous, 31 

subacute, 31 ; PL 8 
Pericardium, caseous necrosis of, 
32 

diseases of. 30 

inflammation of. 30 
Perichondritis, tuberculous, 75 
Perilymphangitis fibrosa, 90 
Periphlebitis, 43 

Peritoneum, inflammation of, 148 
Peritonitis, 148 

suppurative, PL 60 

tuberculous, 148 ; PL 60 
Perivasculitis nodosa, 90 
Pharyngitis, granular. 127 
Pharynx, catarrh of, 126 

croupous inflammation of, 130 

diphtheria of. 130 ; PL 49 

diseases of, 126 

in smallpox, 129 



Pharynx, tuberculosis of, 127, 

123 ; PL 48 
Phlebectasia, 45 
Phlebitis, 43, 44 

suppurative, PL 13 

thrombo-, 43 
Phlegmonous gastritis, 135 
Pigmentation in spleen, 55 
Plasma cells, 145 
Pleura, structure of, 117 
Pleuritis, fibrinous, 117 ; PL 47 

tuberculous, 118 
Pleurogenic pneumonia, 92 
Pleurogenous pneumonia, 103 
Pneumobacillus of Friedländer, 

97 
Pneumoconiosis, 88 
Pneumonia, 91 

caseous, 108, 109 ; PL 42 

catarrhal, 93 ; PL 39 

croupous, 93, 95 

desquamative, 100 ; PL 44 

embolic, 92, 93, 103 

hematogenous, 93 

hemorrhagic, 92 

lobar, 91 

lobular, 101; PL 40 

postdiphtheric, 103 ; PL 40 

metastatic, 92 

miliary tuberculous, 111 ; PL 
43 

pleurogenic, 92 

pleurogenous, 103 

pseudolobular, 100 

purulent, 93 ; PL 40 

serous, 92 

syphilitic, 115; PL 46 

white, 115; PL 46 
Polyp, cystic, of nose, 69 
Polypi, nasal, 68 
Polypoid enteritis, 141 

gastritis, 135 
Pseudolobular pneumonia, 100 
Pseudomembrane, 130 
Pulmonary tubercle, 111 
Pulp of spleen, 53 
Purulent abscess of lymphatic 
glands, 49 

pneumonia, 93 ; PL 40 



156 



INDEX. 



Pyknosis, 131 
Pyloric glands, 125 



Red hepatization, 96 
Red iron lung, PL 32 
Resolution, stage of, in croupous 

pneumonia, 97 
Resorption atelectasis, 79 
Respiratory organs, 67 
Rheumatic endocarditis, 26, 27 
Round ulcer of stomach, 136 



Saccharomyces albicans, 127 
Sago spleen, 61; PI. 22 
Salivary glands, 122 
diseases of, 132 
Sarcoma of stomach, 137 

of thyroid gland, 120 
Sclerotic spots of epicardium, PL 

8 
Scrofula, 52 
Secondary nodules of lymphatic 

glands, 46 
Segmentation of myocardium, 21, 

24 
Serous glands, mixed, 122 
pure, 122 

pneumonia, 92 
Sialodochitis, acute, 132 
Siclerosis of lung, 91 ; PL 32 
Sinuous ulcers of arteries, 37 
Slaty induration of lungs, 112 ; 

PL 45 
Small intestine, structure of, 125, 

126 
Smallpox, esophagus in, 129 

mouth in, 129 

pharynx in, 129 
Soldier-spots, 31 

Spleen, amyloid degeneration of, 
61 ; Plate 21, 22 

amyloidosis of, 61 ; PL 21, 22 

anemic infarction of, 56 ; PL 
19 

anthracosis of, 55 



Spleen, bacon, 61 ; PL 21 

embolic scars of, 57 

hemorrhagic infarct of, 26 ; PL 
19 

infarcts in, 55 

in leukemia, 62 ; PL 23 

in pseudoleukemia, 62 

passive congestion of, 54 
hyperemia of, 54 ; PL 18 

pigmentation in, 55 

sago, 61; PL 22 

senile atrophy of, PL 18 

staphylococcal embolism of, PL 
23 

structure of, 53 

tubercle of, 63 

tuberculosis of, PL 24 
Spleen-follicle in diphtheria, PL 

24 
Splenic abscess, 59 

follicles, 53 

parenchyma, 53 

pulp, 53 

tumor, acute, 57 

hyperplastic, 58 ; PL 20 
chronic, 59 ; PL 20 
infectious, PL 20 
Splenization, marantic, 85 ; PL 
36 
of lung, 101 ; PL 36 
Spots, tendinous, 31 
Stigmata of Cohn, 77, 96 
Stomach, adenoma of, 137 

amyloid degeneration of, 137 

atrophy of mucous membrane 
of, 137 

carcinoma of, 137 ; PL 54 

circulatory disturbances of, 133 

diseases of, 133 

fibroma of, 137 

hemorrhagic erosion of, PL 52 

inflammation of, 133 

lipoma of, 137 

myoma of, 137 

round ulcer of, 136 ; PL 53 

sarcoma of, 137 

structure of, 123 

syphilis of, 137 

tuberculosis of, 137 



IXDEX. 



157 



Stomach, tumors of, 137 
Struma. 119 

Submaxillary glands, 1*2*2 
Suppurative inflammation of 
lymphatic glands, 49 

phlebitis. PL 13 
Swelling, cloudy, iu heart-muscle, 

18 
Syphilis of larynx, 75 

of lung, 115 

of nose, 69 

of stomach, 137 
Syphilitic granuloma of intestine, 
147 

pneumonia, 115 ; PL 46 



T. 

Tattooing, deposition of pigment 

in lymphatic glands as result 

of, 47 ; PL 14 
Tendinous spots, 31 
Terminal lymph-sinuses, 46 
Throinbo-phlebitis, 43 
Thrush. 127 ; PL 50 
Thyroid gland, carcinoma of, 120 
osteosarcoma of. 120 
sarcoma of. 120 
structure of, 118 
struma of, 119 
Tongue, black, hairy, 127 

structure of. 121 

variola vera of, PL 48 
Tonsil, croupous inflammation of, 
130 

diphtheria of, 130 : PL 49 

diphtheric inflammation of, 
130: PL 49 
Tonsils, faucial. 122 
Trachea, diphtheria of. PI. 26 

diseases of. 76 

structure of, 09. 70, 71 
Trachea] catarrh, 75 
Tubercle in vein-wall. PI. 12 

of spleen, (ü) 

pulmonary, 111 
Tuberculosis, embolic. 105 

hematogenous, 105 

in vermiform appendix, PL 59 



Tuberculosis, miliary, acute, 105, 
106 ; PL 42 
of bronchus. PI. 28 
of esophagus, 127 
of intestine, 147 
of larynx, 74 ;" PL 28 
of lung, 104 
ol' lymph-gland, PL 17 
of lymph-glands, 51 
of nose, 69 
of oral cavity, 127 
of pharynx, 127; PL 48 
of spleen, PL 24 
of stomach, 137 
Tuberculous arteritis, PL 12 
endoarteritis, 39, 40 
leptomeningitis, arteritis in, 39, 

40; PL 10 b 
pericarditis, 31: PL 8 
perichondritis. 75 
peritonitis, 148 ; PL 60 
pleuritis, 118 
Tumor, splenic, acute, 57 

hyperplastic, 58 ; PL 20 
chronic, 59 : PL 20 
infectious, PL 20 
Tumors of stomach, 137 
Typhoid fever. PL 57 

effect on intestine, 143 
Typhoidal disease, lymphatic 
glands in, 50 ; PL 14, Fig. 2 



U. 

L^lcer, diphtheric, 74. 131 
follicular, of intestine, 141 
gastric, 135 
laryngeal, 71; PL 27 
round, of stomach, 136 ; PL 

sinuous, of arteries, 37 
tuberculous, of esophagus, 128 
of intestine, 147 
of oral cavity, 128 
of pharynx, 12ft 
Ulcerations of larynx, 74. 75 
Ulcerative endocarditis, 26, 29 
Uremic colitis, 141 



158 



INDEX. 



V. 

Varicose veins of esophagus, 133 
Variola vera of tongue, Pi. 48 
Varix, 45 ; PI. 13 
Vascular goiter, 120 
Veins, calcification of, 45 

inflammation of, 43 

structure of, 34 
Vein-wall, tubercle in, PI. 12 



Verrucose endocarditis, 26, 27 
mycotic, 28 ; PI. 6 
organized, 28 ; PL 6 

Villi, intestinal, 125 



W. 

White pneumonia, 115 ; PI. 46 



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Throat and Nose Department, Hospital of the University of Pennsylvania. 
With 107 colored figures on 44 plates, 25 text-illustrations, and 103 pages 
of text. Cloth, $2.50 net. 

"Aided as it is by magnificently executed illustrations in color, it cannot fail of being of 
the greatest advantage to students, general practitioners, and expert laryngologists." — St. 
Louis Medical and Surgical Journal. 

Atlas and Epitome of Operative Surgery. By Dr. O. Zuckerkandl, 

of Vienna. Edited by J. Chalmers DaCosta, M. D., Clinical Professor 
of Surgery, Jefferson Medical College, Philadelphia. With 24 colored plates, 
217 text-illustrations, and 395 pages of text. Cloth, $3.00 net. 

" We know of no other work diat combines such a wealth of beautiful illustrations with 
clearness and conciseness of language, that is so entirely abreast of the latest achievements, 
and so useful both for the beginner and for one who wishes to increase his knowledge of oper- 
ative surgery." — Münchener medicinische Wochenschrift. 

Atlas and Epitome of Syphilis and the Venereal Diseases. By 

Prof. Dr. Franz Mracek, of Vienna. Edited by L. Bolton Bangs, 
M. D., Professor of Genito-Urinary Surgery, University and Bellevue Hos- 
pital Medical College, New York. With 71 colored plates, 16 black-and- 
white illustrations, and 122 pages of text. Cloth, $3.50 net. 

"A glance through the book is almost like actual attendance upon a famous clinic." — 
Journal of the American Medical Association. 

Atlas and Epitome of External Diseases of the Eye. By Dr. O 

Ha ab, of Zurich. Edited by G. E. de Schweinitz, M. D., Professor of 
Ophthalmology, Jefferson Medical College, Philadelphia. With 76 colored 
illustrations on 40 plates, and 228 pages of text. Cloth, $3.00 net. 

" It is always difficult to represent pathological appearances in colored plates, but this 
work seems to have overcome these difficulties, and the plates, with one or two exceptions, 
are absolutely satisfactory." — Boston Medical and Surgical Journal. 

Atlas and Epitome of Skin Diseases. By Prof. Dr. Franz Mracek, 
of Vienna. Edited by Henry W. Stelwagon, M. D., Clinical Professor 
of Dermatology, Jefferson Medical College, Philadelphia. With 63 colored 
plates, 39 half-tone illustrations, and 200 pages of text. Cloth, $3.50 net. 
" The importance of personal inspection of cases in the study of cutaneous diseases is 
readily appreciated, and next to the living subjects are pictures which will show the appear- 
ance of the disease under consideration. Altogether the work will be found of very great 
value to the general practitioner." — Journal of the American Medical Association. 

4 



SAUNDERS' MEDICAL HAND-ATLASES- 



VOLUMES IN PRESS FOR EARLY PUBLICATION. 

Atlas and Epitome of Diseases Caused by Accidents. By Dr. Ed. 
GOLEBIEWSKI, of Berlin. Translated and edited with additions by Pearce 
Bailey, M.D., Attending Physician to the Department of Corrections 
and to the Almshouse and Incurable Hospitals, New York. With 40 
colored plates, 143 text-illustrations, and 600 pages of text. 

Atlas and Epitome of Special Pathological Histology. By Dr. H. 
DÖRCK, of Munich. Edited by Ludvig Hektoen, M.D., Professor of 
Pathology, Rush Medical College, Chicago. Two volumes, with about 
120 colored plates, numerous text-illustrations, and copious text. 

Atlas and Epitome of General Pathological Histology. With an 
Appendix on Patho-histological Technic. By Dr. H. Dürck, of Munich. 
Edited by Ludvig Hektoen, M.D., Professor of Pathology, Rush Medi- 
cal College, Chicago. With 80 colored plates, numerous text-illustrations, 
and copious text. 

Atlas and Epitome of Gynecology. By Dr. O. Schäffer, of the 
University of Heidelberg. With 90 colored plates, 65 text-illustrations, 
and 308 pages of text. Edited by Richard C. Norris, A. M„ M. D., 
Gynecologist to the Philadelphia and the Methodist Episcopal Hospitals. 

IN PREPARATION. 

Atlas and Epitome of Orthopedic Surgery. By Dr. Schultess and 

Dr. LöNINGj of Zurich. About 100 colored illustrations. 
Atlas and Epitome of Operative Gynecology. By Dr. O. Schäffer, 

of Heidelberg. With 40 colored plates and numerous illustrations in 

black and white from original paintings. 
Atlas and Epitome of Diseases of the Ear. Edited by Prof. Dr. 

POLITZER, of Vienna, and Dr. G. Brühl, of Berlin. With 120 colored 

illustrations and about 200 pages of text. 
Atlas and Epitome of General Surgery. Edited by Dr. Marwedel, 

with the cooperation of Prof. Dr. Czerny. With about 200 colored 

illustrations. 

Atlas and Epitome of Psychiatry. By Dr. Wilh. Weygandt, of Würz- 
burg. With about 120 colored illustrations. 

Atlas and Epitome of Normal Histology. By Dr. Johannes Sobotta, 
of Würzburg. With 80 colored plates and numerous illustrations. 

Atlas and Epitome of Topographical Anatomy. By Prof. Dr. 
Schultze, of Würzburg. About 100 colored illustrations and a very 
copious text. 

5 



W. B. SAUNDERS' 



*THE INTERNATIONAL TEXT-BOOK OF SURGERY. In 

two volumes. By American and British authors. Edited by J. Col- 
lins Warren, M.D., LL.D., Professor of Surgery, Harvard Medical School, 
Boston ; Surgeon to the Massachusetts General Hospital ; and A. Pearce 
Gould, M. S., F. R. C. S., Eng., Lecturer on Practical Surgery and Teacher 
of Operative Surgery, Middlesex Hospital Medical School; Surgeon to the 
Middlesex Hospital, London, England. Vol. I. — General and Operative 
Surgery. — Handsome octavo volume of 947 pages, with 458 beautiful 
illustrations, and 9 lithographic plates. Vol. II. — Special or Regional 
Surgery. — Handsome octavo volume of 1050 pages, with over 500 wood- 
cuts and half-tones, and 8 lithographic plates. Prices per volume : Cloth, 
$5.00 net; Half-Morocco, $6.00 net. 



Just Issued. 

In presenting a new work on surgery to the medical profession the publisher 
feels that he need offer no apology for making an addition to the list of excellent 
works already in existence. Modern surgery is still in the transition stage of its 
development. The art and science of surgery are advancing rapidly, and the 
number of workers is now so great and so widely spread through the whole of 
the civilized world that there is certainly room for another work of reference 
which shall be untrammelled by many of the traditions of the past, and shall at 
the same time present with due discrimination the results of modern progress. 
There is a real need among practitioners and advanced students for a work on 
surgery encyclopedic in scope, yet so condensed in style and arrangement that 
the matter usually diffused through four or five volumes shall be given in one- 
half the space and at a correspondingly moderate cost. 

The ever-widening-field of surgery has been developed largely by special 
work, and this method of progress has made it practically impossible for one 
man to write authoritatively on the vast range of subjects embraced in a modern 
text-book of surgery. In order, therefore, to accomplish their object, the editors 
have sought the aid of men of wide experience and established reputation in the 
various departments of surgery. 

CONTRIBUTORS : 






Dr. Robert W. Abbe. 
C.H.Golding Bird. 
E. H. Bradford. 
W. T. Bull. 
T. G. A. Burns. 
Herbert L. Burrell. 
R. C. Cabot. 
I. H. Cameron. 
James Cantlie. 
W . Watson Cheyne. 
William B. Clarke. 
William B. Coley. 
Edw. Treacher Collins. 
H. Holbrook Curtis. 
J. Chalmers Da Costa. 
N. P. Dandridge. 
John B. Deaver. 
J. W. Elliot. 
Harold Ernst. 



Dr. Christian Fenger. 
W. H. Forwood. 
George R. Fowler. 
George W. Gay. 
A. Pearce Gould. 
J. Orne Green. 
John B. Hamilton. 
M. L. Harris. 
Fernand Henrotin. 
G. H. Makins. 
Rudolph Matas. 
Charles McBurney. 
A. J. McCosh. 
L. S. McMurtry. 
J. Ewing Mears. 
George H. Monks. 
John Murray. 
Robert W. Parker. 



Dr. 



Rushton Parker. 
George A. Peters. 
Franz Pfaff. 
Lewis S. Pilcher. 
James J. Putnam. 
M. H. Richardson. 
A. W. Mayo Robson. 
W. L. Rodman. 
C. A. Siegfried. 
G. B. Smith. 
W. G. Spencer. 
J. Bland Sutton. 
L. McLane Tiffany. 
H. Tuholske. 
Weiler Van Hook. 
James P. Warbasse. 
J. Collins Warren. 
De Forest Willard. 



CATALOGUE OF MEDICAL WORKS. 



*AN AMERICAN TEXT-BOOK OF PHYSIOLOGY. Edited by 
WILLIAM H. Howell, Ph. D., M. D., Professor of Physiology in the 
Johns Hopkins University, Baltimore, Nfd. One handsome octavo volume 
of 1052 pages, fully illustrated. Prices : Cloth, $6.00 net; Sheep or Half- 
Morocco, S7.00 net. 

This work is the most notable attempt yet made in America to combine in 
nne volume the entire subject of Human Physiology by well-known teachers 
who have given especial study to that part of the subject upon which they write. 
The completed work represents the present status of the science of Physiology, 
particularly from the standpoint of the student of medicine and of the medical 
practitioner. 

The collaboration of several teachers in the preparation of an elementary text- 
book of physiology is, unusual, the almost invariable rule heretofore having been 
for a single author to write the entire book. One of the advantages to be derived 
from this collaboration method is that the more limited literature necessary for 
consultation by each author has enabled him to base his elementary account 
upon a comprehensive knowledge of the subject assigned to him ; another, and 
perhaps the most important, advantage is that the student gains the point of view 
of a number of teachers. In a measure he reaps the same benefit as would be 
obtained by following courses of instruction under different teachers. The 
different standpoints assumed, and the differences in emphasis laid upon the 
various lines of procedure, chemical, physical, and anatomical, should give the 
student a better insight into the methods of the science as it exists to-day. The 
work will also be found useful to many medical practitioners who may wish to 
keep in touch with the development of modern physiology. 

CONTRIBUTORS : 

HENRY P. BOWDITCH, M. D., WARREN P. LOMBARD, M.D., 

Professor of Physiology, Harvard Medi- Professor of Physiology, University of 

cal School. Michigan. 

JOHN G. CURTIS, M. D., PP ATTAM TTTqiT Ph n 

Professor of Physiology, Columbia Uni- ^AtiAiYl 1»U&Ä, rn. U., ..... 

Professor of Physiology, \ ale Medica- 



and Surgeons). 

HENRY H. DONALDSON, Ph.D., 

Head-Professor of Neurology, Univer- 
sity of Chicago. 

W. H. HOWELL, Ph. D.M. D., EDWARD T. REICHERT, M.D., 



W. T. PORTER, M.D., 

Assistant Professor of Physiology, Har* 
vard Medical School. 



Pr fessor of Physiology, Johns Hopkins 
University. 

FREDERIC S. LEE, Ph.D., 

Adjunct Professor of Physiology, Colum- 
bia University, X. V. (College of 
Physicians and Surgeons). 



Professor of Physiology, University of 
Pennsylvania, 

HENRY SEWALL, Ph. D., M. D.. 

Professorof Physiology, Medical Depart- 
ment, University of Denver. 



" We can commend it most heartily, not only to all students of physiology, but to every 
physician and pathologist, as a valuable and comprehensive work of reference, written by 
men who are of eminent authority in their own special subjects." — London Lancet. 

" To the practitioner of medicine and to the advanced student this volume constitutes, 
we believe, the best exposition of the present status of the science of physiology in the Eng- 
lish language."— American Journal of the Medical Sciences. 



8 



W. B. SAUNDERS' 



*AN AMERICAN TEXT-BOOK OF APPLIED THERAPEU- 
TICS. For the Use of Practitioners and Students. Edited by 
James C. Wilson, M. D., Professor of the Practice of Medicine and of 
Clinical Medicine in the Jefferson Medical College. One handsome octavo 
volume of 1326 pages. Illustrated. Prices: Cloth, $7.00 net; Sheep or 
Half- Morocco, $8.00 net. 

The arrangement of this volume has been based, so far as possible, upon 
modern pathologic doctrines, beginning with the intoxications, and following 
with infections, diseases due to internal parasites, diseases of undetermined 
origin, and finally the disorders of the several bodily systems — digestive, re- 
spiratory, circulatory, renal, nervous, and cutaneous. It was thought proper to 
include also a consideration of the disorders of pregnancy. 

The articles, with two exceptions, are the contributions of American writers. 
Written from the standpoint of the practitioner, the aim of the work is to facili- 
tate the application of knowledge to the prevention, the cure, and the allevia- 
tion of disease. The endeavor throughout has been to conform to the title of 
the book — Applied Therapeutics — to indicate the course of treatment to be 
pursued at the bedside, rather than to name a list of drugs that have been used 
at one time or another. 

The list of contributors comprises the names of many who have acquired dis- 
tinction as practitioners and teachers of practice, of clinical medicine, and of 
the specialties. 

CONTRIBUTORS : 



Dr. I. E. Atkinson, Baltimore, Md. 
Sanger Brown, Chicago, lil. 
John B. Chapin, Philadelphia, Pa. 
William C. Dabney, Charlottesville, Va. 
John Chalmers DaCosta, Philada., Pa. 
I. N. Danforth, Chicago, 111. 
John L. Dawson, Jr., Charleston, S. C. 
F. X. Dercum, Philadelphia, Pa. 
George Dock, Ann Arbor, Mich. 
Robert T. Edes, Jamaica Plain, Mass. 
Augustus A. Eshner, Philadelphia, Pa. 
J. T. Eskridge, Denver, Col. 
F. Forchheimer, Cincinnati, O. 
Carl Frese, Philadelphia, Pa. 
Edwin E. Graham, Philadelphia, Pa. 
John Guiteras, Philadelphia, Pa. 
Frederick P. Henry, Philadelphia, Pa. 
Guy Hinsdale, Philadelphia, Pa. 
Orville Horwitz, Philadelphia, Pa. 
W. W. Johnston, Washington, D. C. 
Ernest Laplace, Philadelphia, Pa. 
A. Laveran, Pans, France. 

" As a work either for study or reference it will be of great value to the practitioner, as 
it is virtually an exposition of such clinical therapeutics as experience has taught to be of 
the most value. Taking it all in all, no recent publication on therapeutics can be compared 
with this one in practical value to the working physician." — Chicago Clinical Review. 

"The whole field of medicine has been well covered. The work is thoroughly practical, 
and while it is intended for practitioners and students, it is a better book for the general 
practitioner than for the student. The young practitioner especially will find it extremely 
suggestive and helpful." — The Indian Lancet. 



Dr. James Hendrie Lloyd, Philadelphia, Pa. 
John Noland Mackenzie, Baltimore, Md. 
J. W. McLaughlin, Austin, Texas. 
A. Lawrence Mason, Boston, Mass. 
Charles K. Mills, Philadelphia, Pa. 
John K. Mitchell, Philadelphia, Pa. 
W. P. Northrup, New York City. 
William Osier, Baltimore, Md. 
Frederick A. Packard, Philadelphia, Pa. 
Theophilus Parvin, Philadelphia, Pa. 
Beaven Rake, London, England. 
E. O. Shakespeare, Philadelphia, Pa. 
Wharton Sinkler, Philadelphia. Pa. 
Louis Starr, Philadelphia, Pa. 
Henry W. Stelwagon, Philadelphia, Pa. 
James Stewart, Montreal, Canada. 
Charles G. Stockton, Buffalo, N. Y. 
James Tyson, Philadelphia, Pa. 
Victor C. Vaughan, Ann Arbor, Mich. 
James T. Whittaker, Cincinnati, O. 
J. C. Wilson, Philadelphia, Pa. 






CATALOGUE OF MEDICAL WORKS. 



*AN AMERICAN TEXT-BOOK OF OBSTETRICS. Edited by 
Richard C. Norris, M. D. ; Art Editor, Robert L. Dickinson, M. D. 
One handsome octavo volume of over iooo pages, with nearly 900 colored 
and half-tone illustrations. Prices: Cloth, $7.00 net; Sheep or Half 
Morocco, SS.00 net. 

The advent of each successive volume of the series of the American Text- 
Book^ has been signalized by the most Mattering comment from both the Press 
and the Profession. The high consideration received by these text-books, and 
their attainment to an authoritative position in current medical literature, have 
been matters of deep international interest, which finds its fullest expression in 
the demand for these publications from all parts of the civilized world. 

In the preparation of the " American Text-Book of Obstetrics" the 
editor has called to his aid proficient collaborators whose professional prominence 
entitles them to recognition, and whose disquisitions exemplify Practical 
Obstetrics. While these writers were each assigned special themes for dis- 
cussion, the correlation of the subject-matter is, nevertheless, such as ensures 
logical connection in treatment, the deductions of which thoroughly represent 
the latest advances in the science, and which elucidate the best modern methods 
of frocedu 

The more conspicuous feature of the treatise is its wealth of illustrative 
matter. The production of the illustrations had been in progress for several 
years, under the personal supervision of Robert L. Dickinson, M. D., to whose 
artistic judgment and professional experience is due the most sumptuously 
illustrated work of the period. By means of the photographic art, combined 
with the skill of the artist and draughtsman, conventional illustration is super- 
seded by rational methods of delineation. 

Furthermore, the volume is a revelation as to the possibilities that may be 
reached in mechanical execution, through the unsparing hand of its publisher. 



CONTRIBUTORS: 



Dr. James C. Cameron, 
vard P. Davis. 
:rt L. Dickinson. 
Charles Warrington Earle. 
James H. Etheridge. 
Henry J. Garripies. 
Barton Cooke I1 
Charles Jewett. 



Dr. Howard A. Kelly. 
Richard C. Norris. 
Chauncey D. Palmer. 
Theophilus Parvin. 
George A. Piersol. 
Edward Reynolds. 
Henry Schwarz. 



" At first glance we are overwhelmed by the magnitude of thh work in several respects, 
viz. : First, by the size of the volume, then by the array of eminent teachers in this depart- 
ment who have taken part in its production, then by the profuseness and character of the 
illustrations, and last, but not least, the conciseness and clearness with which the text is ren- 
dered. This is an entirely new composition, embodying the highest knowledge of the art as 
it stands to-day by authors who occupy the front rank in their specialty, and there are many 
of them. We cannot turn ov thout being struck by the superb illustrations 

which adorn ^0 many of them. We .ire confident that this most practical work will find 
instant appreciation by practitioners as well as students." — Neiv York Medical Tunes. 

Permit me to say that your American Text-Book of Obstetrics is the most magnificent 
medical work that 1 have ever seen. I congratulate you and thank you for this superb work, 
which alone is sufficient to place you first in the ranks of medical publishers. 

With profound respect I am sincerely yours, Alex. J. C. Skene. 



IO IV. B. SAUNDERS* 



*AN AMERICAN TEXT-BOOK OF THE THEORY AND 
PRACTICE OF MEDICINE. By American Teachers. Edited 
by William Pepper, M. D., LL.D., Provost and Professor of the Theory 
and Practice of Medicine and of Clinical Medicine in the University of 
Pennsylvania. Complete in two handsome royal- octavo volumes of about 
iooo pages each, with illustrations to elucidate the text wherever necessary. 
Price per Volume: Cloth, $5.00 net; Sheep or Half-Morocco, $6.00 net. 

VOJLUME I. CONTAINS: 



Hygiene. — Fevers (Ephemeral, Simple Con- 
tinued, Typhus, Typhoid, Epidemic Cerebro- 
spinal Meningitis, and Relapsing). — Scarla- 
tina, Measles, Röthein, Variola, Varioloid, 
Vaccinia, Varicella, Mumps, Whooping-cough, 
Anthrax, Hydrophobia, Trichinosis, Actino- 



mycosis, Glanders, and Tetanus.— Tubercu- 
losis, Scrofula, Syphilis, Diphtheria, Erysipe- 
las, Malaria, Cholera, and Yellow Fever. — 
Nervous, Muscular, and Mental Diseases etc. 



VOLUME II. CONTAINS: 



Urine (Chemistry and Microscopy). — Kid- 
ney and Lungs. — Air-passages (Larynx and 
Bronchi) and Pleura. — Pharynx, (Esophagus, 
Stomach and Intestines (including Intestinal 
Parasites)., Heart, Aorta, Arteries and Veins. 



— Peritoneum, Liver, and Pancreas. — Diathet- 
ic Diseases (Rheumatism, Rheumatoid Ar- 
thritis, Gout, Lithaemia, and Diabetes.)— 
Blood and Spleen. — Inflammation, Embolism, 
Thrombosis, Fever, and Bacteriology. 



The articles are not written as though addressed to students in lectures, but 
are exhaustive descriptions of diseases, with the newest facts as regards Causa- 
tion, Symptomatology, Diagnosis, Prognosis, and Treatment, including a large 
number of approved formulae. The recent advances made in the study 
of the bacterial origin of various diseases are fully described, as well as the 
bearing of the knowledge so gained upon prevention and cure. The subjects 
of Bacteriology as a whole and of Immunity nre fully considered in a separate 
section. 

Methods of diagnosis are given the most minute and careful attention, thus 
enabling the reader to learn the very latest methods of investigation without 
consulting works specially devoted to the subject. 

CONTRIBUTORS : 



Dr. J. S. Billings, Philadelphia. 

Francis Delafield, New York. 
Reginald H. Fitz, Boston. 
James W. Holland, Philadelphia. 
Henry M. Lyman, Chicago. 
William Osier, Baltimore. 



Dr. William Pepper, Philadelphia. 

W. Oilman Thompson, New York. 
W. H. Welch, Baltimore. 
James T. Whittaker, Cincinnati. 
James C. Wilson, Philadelphia. 
Horatio C. Wood, Philadelphia. 






" We reviewed the first volume of this work, and said : ' It is undoubtedly one of the best 
text-books on the practice of medicine which we possess.' A consideration of the second 
and last volume leads us to modify that verdict and to say that the completed work i-s, in our 
opinion, the best of its kind it has ever been our fortune to see. It is complete, thorough, 
accurate, and clear. It is well written, well arranged, well printed, well illustrated, and well 
bound. It is a model of what the modern text-book should be." — New York Medical Journal. 

" A library upon modern medical art. The work must promote the wider diffusion of 
sound knowledge." — American Lancet. 

" A trusty counsellor for the practitioner or senior student, on which he may implicitly 
rely." — Edinburgh Medical Journal. 



CATALOGUE OF MEDICAL WORKS. II 

UN AMERICAN TEXT-BOOK OF SURGERY. Edited by Wil- 
liam AY. Keen, M. I> , LL.D., and J. William White, M. D., Ph.D. 
Forming one handsome royal octavo volume of 1250 pages (10 x 7 inches , 
with 496 wood-cuts in text, and 37 colored and half-tone plates, many of 
them I from original photographs and drawings furnished by the 

autnors. Price : Cloth, $7.00 net: Sheep or Half Morocco, $S.oo net. 

THIRD EDITION. THOROUGHLY REVISED. 

resent edition, among the new topics introduced are a lull considera- 
tion of serum-therapy ; leucocytosis ; post-operative insanity; the use of dry heat 
at high temperatures; Krönlein's method of locating the cerebral fissures; 
.is and Lorenz's operations of congenital dislocations of the hip; Allis's re- 
searches on dislocations of the hip-joint ; lumbar puncture; the forcible reposi- 
tion of the spine in Pott's disease; the treatment of exophthalmic goiter; the 
surgery of typhoid fever; gastrectomy and other operations on the stomach; 
new methods of operating upon the intestines; the use of Kelly's rectal specula; 
the surgery of the ureter; Schleicht infiltration-method and the use of eucain 
for local anesthesia : Krause's method of skin-grafting ; the newer methods of 
disinfecting the hands; the use of gloves, etc. The sections on Appendicitis, 
on Fractures, and od Gynecological Operations have been revised and enlarged. 
Dsiderable number of new illustrations have been added, and enhance the 
vaiue of the work. 

The text of the entire book has been submitted to all the authors for their 
mutual criticism and revision — an idea in book-making that is entirely new and 
original. The book as a whole, therefore, expresses on all the important sur- 
gical topics of the day the consensus of opinion of the eminent surgeons who 
have joined in its preparation. 

One of the most attractive features of the book is its illustrations. Very 
many of them are original and faithful reproductions of photographs taken 
directly from patients or from SD-ecimens. 

«OXTRIBtTORS: 



Dr. Phineas S. Conner. Cincinnati. 
Frederic S. De >' >rk. 

1. Philadelphia. 
Charles B Nancrede, Ann Arbor. Mich. 

11 Park. B . Vork. 

Lewis 5. Pilcher. New York. 



Dr. Nicholas Senn, Chicago. 

Francis J. Shepherd, Montreal, Canada. 
Lewis A. Siimson, New York. 

lins Warren, 15 >>ton. 
J. William White, Philadelphia. 



<f If this text-book is a fair reflex of the present position of American surgerv. we must 
admit it is of a very high order of merit, and that English surgeons will have to' look very 
'V to their laurei> it they are to preserve a position in the van of surgical practice."— 
London Lancet. 

Mild n t mind it being called TH1 k (instead of A I 
r no single volume which contains so readal pete an account of the 

science and art of - EDMUND ber of the i 

of Examitiers of :h- . s <r 0/ Surgeons, £ 



12 W. B. SAUNDERS' 



*AN AMERICAN TEXT-BOOK OF GYNECOLOGY, MEDICAL 
AND SURGICAL, for the use of Students and Practitioners. 

Edited by J. M. Baldy, M. D. Forming a handsome royal-octavo volume 
of 718 pages, with 341 illustrations in the text and 38 colored and half- 
tone plates. Prices : Cloth, $6.00 net; Sheep or Half-Morocco, $7.00 net. 

SECOND EDITION, THOROUGHLY REVISED. 

In this volume all anatomical descriptions, excepting those essential to a clear 
understanding of the text, have been omitted, the illustrations being largely de- 
pended upon to elucidate the anatomy of the parts. This work, which is 
thoroughly practical in its teachings, is intended, as its title implies, to be a 
working text-book for physicians and students. A clear line of treatment has 
been laid down in every case, and although no attempt has been made to dis- 
cuss mooted points, still the most important of these have been noted and ex- 
plained. The operations recommended are fully illustrated, so that the reader, 
having a picture of the procedure described in the text under his eye, cannot fail 
to grasp the idea. All extraneous matter and discussions have been carefully 
excluded, the attempt being made to allow no unnecessary details to cumber 
the text. The subject-matter is brought up to date at every point, and the 
work is as nearly as possible the combined opinions of the ten specialists who 
figure as the authors. 

In the revised edition much new material has been added, and some of the 
old eliminated or modified. More than forty of the old illustrations have been 
replaced by new ones, which add very materially to the elucidation of the 
text, as they picture methods, not specimens. The chapters on technique and 
after-treatment have been considerably enlarged, and the portions devoted to 
plastic work have been so greatly improved as to be practically new. Hyste- 
rectomy has been rewritten, and all the descriptions of operative procedures 
have been carefully revised and fully illustrated. 



CONTRIBUTORS : 



Dr. Henry T. Byford. 
John M. Baldy. 
Edwin Cragin. 
!. H. Etheridge. 
William Goodell. 



Howard A. Kelly. 
Florian Krug. 
E. E. Montgomery. 
William R. Pryor. 
George M. Tuttle. 



"The most notable contribution to gynecological literature since 1887, .... and the most 
complete exponent of gynecology which we have. No subject seems to have been neglected, 
.... and the gynecologist and surgeon, and the general practitioner who has any desire 
to practise diseases of women, will find it of practical value. In the matter of illustrations 
and plates the book surpasses anything we have seen." — Boston Medical and Surgical 
Journal. 

" A thoroughly modern text-book, and gives reliable and well-tempered advice and in- 
struction." — Edinburgh Medical Journal. 

" The harmony of its conclusions and the homogeneity of its style give it an individuality 
which suggests a single rather than a multiple authorship." — Annals of Surgery. 

" It must command attention and respect as a worthy representation of our advanced 
clinical teaching." — American Journal of Medical Sciences. 



CATALOGUE OF MEDICAL WORKS. 



13 



*AN AMERICAN TEXT-BOOK OF THE DISEASES OF CHIL- 
DREN. By American Teachers. Edited by Louis Starr, M. D., 
assisted by THOMPSON S. WESTCOTT, M. D. In one handsome royal-8v<i 
volume o[ 1244 pages, profusely illustrated with wood-cuts, half-tone and 
colored plates. Net Prices: Cloth. 57. 00; Sheep or Half- Morocco, $8.00. 

SECOND EDITION, REVISED AND ENLARGED. 

The plan of this work embraces a series of original articles written by some 
sixty well-known podiatrists, representing collectively the teachings of the most 
prominent medical schools and colleges of America. The work is intended to 
be a practical book, suitable for constant and handy reference by the practi- 
tioner and the advanced student. 

Especial attention has been given to the latest accepted teachings upon the 
etiology, symptoms, pathology, diagnosis, and treatment of the disorders of chil- 
dren, with the introduction o\ many special formulae and therapeutic procedures. 

In this new edition the whole subject matter has been carefully revised, new 
articles added, some original papers emended, and a number entirely rewritten. 
The new articles include "Modified Milk and Percentage Milk-Mixtures," 
" Lit hernia," and a section on "Orthopedics." Those rewritten are "Typhoid 
v." "Rubella,"' "Chicken-pox,'' "Tuberculous Meningitis," "Hydroceph- 
alus.*" and "Scurvy;" while extensive revision has been made in "Infant 
Feeding," " Measles," " Diphtheria," and " Cretinism." The volume has thus 
been much increased in size by the introduction of fresh material. 

CONTRIBUTORS t 



Dr. S. S. Adams, Washington. 

John Ashhurst, Jr., Philadelphia. 
A. D. Blackader, Montreal, Canada 

I Bovaird, New York. 
Dillon Brown. New York. 
Edward M. Buckingham, Boston. 
Charles W. Burr, Philadelphia. 
W. E. Casselberry, Chicago. 
Henry Dwight Chapin, New York. 
VI . S. Christopher, Chicago. 
Archibald Church, Chicago. 

d M. Crandall, New York. 
Andrew F. Currier, New York. 
ind G. Curtin, Philadelphia 
J. M. DaCos'a, Philadelphia. 
I. N. Danforth, Chicago. 
Edward P. Davis, Philadelphia. 
John B. Deaver, Philadelphia. 
G. E. de Schweinitz, Philadelphia. 
John Dorr. Y >rk. 

Charles Warringl Chicago. 

\Vm. A. Edwards. San Diego, Cal. 
F. Forchheimer, Cincinnati. 
I. Henry Fruitnight, New York. 
J. P. Cr zer Griffith, Philadelphia. 
W. A. Hardawav. St. Louis. 
M. P Hatfield, Chi 
Barton Cooke Hir>t, Philadelphia. 
H. Illoway, Cincinnati. 

-v Jackson 
Charles > I »etroit. 

Henry Koplik. New York. 



Dr. Thomas S. Latimer, Baltimore. 

Albert R. Leeds, Hoboken, N. J. 

J. Hendrie Lloyd, Philadelphia. 

George Roe Lockwood, New York. 

Henry M. Lyman, Chicago. 

Francis T. Miles, Baltimore. 

Charles K Mills, Philadelphia. 

James F Moore. Minneapolis. 

F. Gordon Morrill, Boston. 

John H. Musser, Philadelphia. 

Thomas R. Neilson, Philadelphia. 

\V. P. Northrup, New York. 

William Osier, Baltimore. 

Frederick A. Packard, Philadelphia. 

William Pepper, Philadelphia. 

Frederick Peterson, New York. 

W. T. Plant, Syracuse, New York 
William M. Powell. Atlantic City. 
B. K. Rachford, Cincinnati. 
B. Alexander Randall, Philadelphia. 
Edward O. Shakespeare, Philadtlphi; 
F. C. Shattuck, Boston. 

T. Lewis Smith, New York. 

Louis Starr, Philadelphia. 

M. Allen Starr, New York. 

Charles W. Townsend, Boston. 

Tames Tyson, Philadelphia. 

W. S. Thayer, Baltimore. 

Victor C. Vaughan, Ann Arbor, Mich 

Thompson S. Westcott, Philadelphia. 

Henry R. Wharton, Philadelphia. 

J William Whit«.-, Philadelphia. 

J. C. Wilson, Philadelphia. 



H 



W. B. SAUNDERS' 



*AN AMERICAN TEXT-BOOK OF GENITO-URINARY AND 
SKIN DISEASES. By 47 Eminent Specialists and Teachers. Edited 
by L. Bolton Bangs, M. D., Professor of Genito-Urinary Surgery, Uni- 
versity and Bellevue Hospital Medical College, New York; and W. A. 
Hardaway, M. D., Professor of Diseases of the Skin, Missouri Medicai 
College. Imperial octavo volume of 1229 pages, with 300 engravings and 
20 full-page colored plates. Cloth, $7.00 net ; Sheep or Half Morocco, 
$8.00 net. 

This addition to the series of " American Text-Books," it is confidently be- 
lieved, will meet the requirements of both students and practitioners, giving, as 
it does, a comprehensive and detailed presentation of the Diseases of the 
Genito-Urinary Organs, of the Venereal Diseases, and of the Affections of the 
Skin. 

Having secured the collaboration of well-known authorities in the branches 
represented in the undertaking, the editors have not restricted the contributors 
ik regard to the particular views set forth, but have offered every facility for the 
free expression of their individual opinions. The work will therefore be found 
to be original, yet homogeneous and fully representative of the several depart- 
ments of medical science with which it is concerned. 



CONTRIBUTORS s 



■. Chas. W. Allen, New York. 
I. E. Atkinson, Baltimore. 
L Bolton Bangs, New York. 
P. R. Bolton, New York. 
Lewis C. Bosher, Richmond, Va. 
John T. Bowen, Boston. 
J. Abbott Cantrell. Philadelphia. 
William T. Corlett, Cleveland, Ohio. 
B. Farquhar Curtis, New York. 
Condict W. Cutler, New York. 
Isadore Dyer, New Orleans. 
Christian Fenger, Chicago. 
John A. Fordyce, New York, 
Eugene Fuller, New York. 
R. H. Greene, New York. 
Joseph Grindon, St. Louis. 
Graeme M. Hammond, New York. 
W. A. Hardaway, St. Louis. 
M. B. Hartzell, Philadelphia. 
Louis Heitzmann, New York. 
James S. Howe, Boston. 
George T. Jackson, New York. 
Abraham Jacobi, New York. 
James C. Johnston. New Yoik. 



Dr. Hermann G. Klotz, New Yorj?.. 
J. H. Linsley, Burlington, V t. 
G. F. Lydston, Chicago. 
Hartwell N. Lyon, St. Louis. 
Edward Martin, Philadelphia. 
D. G. Montgomery, San Francisco. 
James Pedersen, New York. 
S. Pollitzer, New York. 
Thomas R. Pooley, New York. 
A. R. Robinson, New York. 
A. E. Regensburger, San Francisco. 
Francis J. Shepherd, Montreal, Can. 
S. C. Stanton, Chicago, 111. 
Emmanuel J. Stout. Philadelphia. 
Alonzo E. Taylor Philadelphia. 
Robert W. Taylor, New York. 
Paul Thorndike, Boston. 
H. Tuholske, St. Louis. 
Arthur Van Harlingen, Philadelphia. 
Francis S. Watson, Boston. 
J. William White, Philadelphia. 
J. McF. Winfield. Brooklyn. 
Alfred C. Wood, Philadelphia. 






"This voluminous work is thoroughly up to date, and the chapters on gemto-unnary dis- 
eases are especially valuable. The illustrations are fine and are mostly original. The section 
on dermatology is concise and in every way admirable,"— Journal of the American Medical 
Association. 

"This volume is one of the best yet issued of the publisher's series of 'American Text- 
Books.' The list of contributors represents an extraordinary array of talent and extended 
experience. The book will easily take the place in comprehensiveness and value of the 
half dozen or more costly works on these subjects which have hitherto been necessary to a 
well-equipped librarv." — New York Polyclinic, 



\LOGUE OF MEDICAL WORKS. 



15 



* AN AMERICAN TEXT-BOOK OF DISEASES OF THE EYE, 
EAR, NOSE, AND THROAT. Edited by George E. de Schweinitz, 

A. M.. M. D., Professor of Ophthalmology, Jefferson Medical College; and 

B. Ai EXANDER RAND AI 1 . A. M., M. D., Clinical Professor of Diseases of 
the Kar, University oi Pennsylvania. One handsome imperial octavo 
volume oi 1251 pages; 700 illustrations, 59 of them colored. Prices: 
Cloth, 57.00 net; Sheep or Half-Morocco, 38.00 net. 

Just Issued. 

The present work is the only book ever published embracing diseases of the 
intimately related organs of the eye, ear, nose, and throat. Its special claim 
to favor is based on encyclopedic, authoritative, and practical treatment of the 
subjects. 

Each section of the book has been entrusted to an author who is specially 
identified with the subject on which he writes, and who therefore presents his 
case in the manner of an expert. Uniformity is secured and overlapping pre- 
vented by careful editing and by a system of cross-references which forms a 
special feature of the volume, enabling the reader to come into touch with all 
that is said on any subject in different portions of the book. 

Particular emphasis is laid on the most approved methods of treatment, so 
that the book shall be one to which the student and practitioner can refer for 
information in practical work. Anatomical and physiological problems, also, 
are fully discussed for the benefit of those who desire to investigate the more 
abstruse problems of the subject. 



CONTRIBUTORS : 



. Henry A. Alderton, Brooklyn. 
n Allen, Philadelphia. 
Frank. All pore, Chicago. 

York. 
\vre-. Cincinnati. 
R. O Be trd, Minn apolis. 
Clarence I -ton. 

Arthur . liladelphia. 

Albert 1'. Brub ker, Philadelphia. 
J. H. Brv ). C. 

Albert H. Buck, New York. 
II' Ian. 

Swan M. Burnett, Washington, D C. 
Flemming Carrow, Am Mich. 

W. E. C selberry, Ch 
Colra in \V. Or rk. 

rk. 

. Dennett, New York. 

hweinitz, Philadelphia. 
A 
John \V. 1 

i, Philadelp 
H . Giffor 

lis. 

Christian R < incinnati. 

F. C. Hotz, Chicago. 
Lucien Howe, Buffalo, N. V. 



Dr. Alvin A. Hubbell, Buffalo, N. Y. 
Edward Jackson, Philadelphia. 
J. Ellis Jennings. St. Louis. 
Herman Knapp, New York. 
Chas. W. Kollock, Charleston, S. C. 
( t. A Leland, Boston. 
J. A. Lippincott, Pittsburg, Pa. 
G. Hudson Makuen, Philadelphia. 
John H. McColl* i 
II. G. Miller, Providence, R I. 

B f.. Milliken, Cleveland, Ohio. 
R »bert C. Myles, New York. 
Jam. 5 I \ ■ ml), New York. 
R. J. Phillips, Philadelphia. 

Piersol. Philadelphia. 
W. P P rcher, Charleston, S. C. 

B AU x Randall. Philadelphia. 

Randolph, Baltimore. 
John O. K \ Y. 

Philadelphia. 
1 I. Shepp ird, Brooklyn, N. Y. 
II. Shui y, I »• troit, Mich. 
Willi • t, Philadelphia. 

Samu< . Baltimore, Aid. 

. Philadelphia. 

hiladelphia. 

. 111. 
han Wright, Brooklyn. 
II. V, Würdemann. Milwaukee, Wis. 



i6 



W. B. SAUNDERS 1 



*AN AMERICAN YEAR-BOOK OF MEDICINE AND SUR- 
GERY. A Yearly Digest of Scientific Progress and Authoritative 
Opinion in all branches of Medicine and Surgery, drawn from journals» 
monographs, and text-books of the leading American and Foreign authors 
and investigators. Collected and arranged, with critical editorial com- 
ments, by eminent American specialists and teachers, under the general 
editorial charge of George M. Gould, M. D. Volumes for 1896, '97, 
'98, and '99 each a handsome imperial octavo volume of about 1200 pages. 
Prices : Cloth, $6.50 net ; Half-Morocco, $7.50 net. Year-Book for 1900 in 
two octavo volumes of about 600 pages each. Prices per volume : Cloth, 
$3.00 net; Half-Morocco, $3.75 net. 

In Two Volumes* No Increase in Price. 

In response to a widespread demand from the medical profession, the pub- 
lisher of the "American Year-Book of Medicine and Surgery" has decided to 
issue that well-known work in two volumes, Vol. I. treating of General Medi- 
cine, Vol. II. of General Surgery. Each volume is complete in itself, and 
the work is sold either separately or in sets. 

This division is made in such a way as to appeal to physicians from a class 
standpoint, one volume being distinctly medical, and the other distinctly surgi- 
cal. This arrangement has a two-fold advantage. To the physician who uses 
the entire book, it offers an increased amount of matter in the most convenient 
form for easy consultation, and without any increase in price ; while the man 
who wants either the medical or the surgical section alone secures the complete 
consideration of his branch without the necessity of purchasing matter for which 
he has no use. 

CONTRIBUTORS : 



Vol. I. 
Dr. Samuel W. Abbott, Boston. 
Archibald Church, Chicago. 
Louis A. Duhring, Philadelphia. 
D. L. Edsall, Philadelphia. 
Alfred Hand, Jr., Philadelphia. 
M. B. Hartzell, Philadelphia. 
Reid Hunt, Baltimore. 
Wyatt Johnston, Montreal. 
Walter" Jones, Baltimore. 
David Riesman, Philadelphia. 
Louis Starr, Philadelphia. _ 
Alfred Stengel, Philadelphia. 
A. A. Stevens, Philadelphia. 
G. N. Stewart. Cleveland. 
Reynold W. Wilcox, New York City. 



Vol. II. 
Dr. J. Montgomery Baldy, Philadelphia. 
Charles H. Burnett, Philadelphia. 
J. Chalmers DaCosta, Philadelphia. 
W. A. N. Dorland, Philadelphia. 
Virgil P. Gibney, New York City. 
C. H. Hamann, Cleveland. 
Howard F. Hansell, Philadelphia. 
Barton Cooke Hirst, Philadelphia. 
E. Fletcher lr.eals, Chicago. 
W. W. Keen, Philadelphia. 
Henry G. Ohls, Chicago. 
Wendell Reber, Philadelphia. 
J. Hilton Waterman, New York City. 



" It is difficult to know which to admire most— the research and industry of the distin- 
guished band of experts whom Dr. Gould has enlisted in the service of the Year-Book, or the 
wealth and abundance of the contributions to every department of science that have been 
deemed worthy of analysis. ... It is much more than a mere compilation of abstracts, for, 
as each section is entrusted to experienced and able contributors, the reader has the advan- 
tage of certain critical commentaries and expositions . . . proceeding from writers fully 
qualified to perform these tasks. ... It is emphatically a book which should find a place in 
every medical library, and is in several respects more useful than the famous ' Jahrbucher 
of Germany." — London Lancet. 



CATALOGUE OF MEDICAL WORKS. \J 

* ANOMALIES AND CURIOSITIES OF MEDICINE. By George 
M. Gould, M.D., and Walter L. Pyle, M.D. An encyclopedic collec- 
tion of are and extraordinary cases and of the most striking instances of 
abnormality in all branches of Medicine and Surgery, derived from an ex- 
haustive research of medical literature from its origin to the present day, 
abstracted, classified, annotated, and indexed. Handsome imperial octavo 
volume o( 908 pages, with 295 engravings in the text, and 12 full-page 
plates. Cloth, $3.00 net; Half-Morocco, $4.00 net. 

POPULAR EDITION REDUCED FROM $6.00 to $3.00. 

In view of the gre.it success of this magnificent work, the publisher has decided 
to issue a " Popular Edition '' at a price so low that it may be procured by every 
student and practitioner of medicine. Notwithstanding the great reduction in 
price, there will be no depreciation in the excellence of typography, paper, and 
binding that characterized the earlier editions. 

Several years of exhaustive research have been spent by the authors in the 
great medical libraries of the United States and Europe in collecting the mate- 
rial for this work. Medical literature of all ages and all languages has 
been carefully searched, as a glance at the Bibliographic Index will show. The 
facts, which will be of extreme value to the author and lecturer, have been 
arranged and annotated, and full reference footnotes given. 

"One of the most valuable contributions ever made to medical literature. It is, so far as 
we know, absolutely unique, and every page is as fascinating as a novel. Not alone for the 
medical profession has this volume value : it will serve as a book of reference for all who are 
interested in general scientific, sociologic, or medico-legal topics." — Brooklyn Medical your- 
nal. 

NERVOUS AND MENTAL DISEASES. By Archibald Church, 
M. D., Professor of Clinical Neurology, Mental Diseases, and Medical 
Jurisprudence, Northwestern University Medical School; and Frederick 
Peterson, M. D., Clinical Professor of Mental Diseases, Woman's Medi- 
cal College, New York. Handsome octavo volume of 843 pages, with 
over 300 illustrations. Prices: Cloth, 55.00 net; Half-Morocco, $6.00 
net. 

Second Edition, 

This book is intended to furnish students and practitioners with a practical, 
working knowledge of nervous and mental diseases. Written by men of wide 
experience and authority, it presents the many recent additions to the subject. 
The book is not filled with an extended dissertation on anatomy and pathology, 
but, treating these points in connection with special conditions, it lays particular 
stress on methods of examination, 1 . and treatment. In this respect the 

work is unusually complete and valuable, laying down the definite courses of 
procedure which the authors have found to be most generally satisfactory. 

" The work is an epitome of what is to-day known of nervous diseases prepared for the 
student and practitioner ill the light of the author's experience . . . We believe that no work 
presents the difficult subject of insanity in such a reasonable and readable way." — Chicago 
Medical Recorder. 



1 8 W. B. SAUNDERS' 



DISEASES OF THE NOSE AND THROAT. By D. Braden Kyle, 
M. D., Clinical Professor of Laryngology and Rhinology, Jefferson Medi- 
cal College, Philadelphia; Consulting Laryngologist, Rhinologist, and 
Otologist, St. Agnes' Hospital. Octavo volume of 646 pages, with over 
150 illustrations and 6 lithographic plates. Cloth, $4.00 net; Half-Mo- 
rocco, $ 5. 00 net. 

Just Issued. 

This book presents the subject of Diseases of the Nose and Throat in as con- 
cise a manner as is consistent with clearness, keeping in mind the needs of the 
student and general practitioner as well as those of the specialist. The arrange- 
ment and classification are based on modern pathology, and the pathological 
views advanced are supported by drawings of microscopical sections made in the 
author's own laboratory. These and the other illustrations are particularly fine, 
being chiefly original. With the practical purpose of the book in mind, ex- 
tended consideration has been given to details of treatment, each disease being 
considered in full, and definite courses being laid down to meet special condi- 
tions and symptoms. 

" It is a thorough, full, and systematic treatise, so classified and arranged as greatly to facili- 
tate the teaching of laryngology and rhinology to classes, and must prove most convenient 
and satisfactory as a reference book, both for students and practitioners." — International 
Medical Magazine. 

THE HYGIENE OF TRANSMISSIBLE DISEASES ; their Causa- 
tion, Modes of Dissemination, and Methods of Prevention. By 
A. C. Abbott, M. D., Professor of Hygiene in the University of Pennsyl- 
vania; Director of the Laboratory of Hygiene. Octavo volume of 311 
pages, with charts and maps, and numerous illustrations. Cloth, $2.00 net. 



Just Issued. 

It is not the purpose of this work to present the subject of Hygiene in the 
comprehensive sense ordinarily implied by the word, but rather to deal directly 
with but a section, certainly not the least important, of the subject — viz., that 
embracing a knowledge of the preventable specific diseases. The book aims to 
furnish information concerning the detailed management of transmissible dis- 
eases. Incidentally there are discussed those numerous and varied factors that 
have not only a direct bearing upon the incidence and suppression of such dis- 
eases, but are of general sanitary importance as well. 

" The work is admirable in conception and no less so in execution. It is a practical work, 
simply and lucidly written, and it should prove a most helpful aid in that department of 
medicine which is becoming daily of increasing importance and application — namely, prophy- 
laxis." — Philadelphia Medical Journal. 

'* It is scientific, but not too technical ; it is as complete as our present-day knowledge of 
hygiene and sanitation allows, and it is in harmony with the efforts of the profession, which 
are tending more and more to methods of prophylaxis. For the student and for the practi- 
tioner it is well nigh indispensable." — Medical News, New York. 



CATALOGUE OF MEDICAL WORKS. ig 

A TEXT-BOOK OF EMBRYOLOGY. By John C. Heisler, M. D, 
Professor of Anatomy in the Medico- Chirurgical College, Philadelphia. 
Octavo volume of 405 pages, with 190 illustrations, 26 in colors. Cloth 
52.50 net. 

Just Issued. 

The facts of embryology having acquired in recent years such great interesl 
in connection with the teaching and with the proper comprehension of human 
anatomy, it is of first importance to the student of medicine that a concise and 
yet sufficiently full text-book upon the subject be available. It was with the 
aim of presenting such a book that this volume was written, the author, in his 
experience as a teacher of anatomy, having been impressed with the fact that 
students were seriously handicapped in their study of the subject of embryology 
by the lack of a text-book full enough to be intelligible, and yet without that 
minuteness of detail which characterizes the larger treatises, and which so often 
serves only to confuse and discourage the beginner. 

" In short, the book is written to fill a want which has distinctly existed and which it 
definitely meets ; commendation greater than this it is not possible to give to anything." — 
Medi New Yurk. 

A MANUAL OF DISEASES OF THE EYE. By Edward Jack- 
son, A. M., M. D., sometime Professor of Diseases of the Eye in the Phila- 
delphia Polyclinic and College for Graduates in Medicine. I2mo, 604 
pages, with 178 illustrations from drawings by the author. Cloth, $2.50 net. 

Just Issued. 

This book is intended to meet the needs of the general practitioner of medi- 
cine and the beginner in ophthalmology. More attention is given to the condi- 
tions that must be met and dealt with early in ophthalmic practice than to the 
, rarer diseases and more difficult operations that may come later. 

It is designed to furnish efficient aid in the actual work of dealing with dis- 
ease, and therefore gives the place of first importance to the recognition and 
management of the conditions that present themselves in actual clinical work. 

, LECTURES ON THE PRINCIPLES OF SURGERY. By Charles 
B. NANCREDE, M. D., LL.D., Professor of Surgery and of Clinical Surgery, 
University of Michigan, Ann Arbor. Handsome octavo, 398 pages, illus- 

\ trated. Cloth, $2.50 net. 

Just Issued. 

The present book is based on the lectures delivered by Dr. Nancrede to his 
undergraduate classes, and is intended as a text-book for students and a practi- 
cal help for teachers. By the careful elimination of unnecessary details of 
pathology, bacteriology, etc., which are amply provided for in other courses of 
study, space is gained for a more extended consideration of the Principles of 
Surgery in themselves, and of the application of these principles to -methods 
of practice. 



20 W. B. SAUNDERS' 



A TEXT-BOOK OF PATHOLOGY. By Alfred Stengel, M. D., 

Professor of Clinical Medicine in the University of Pennsylvania; Physi- 
cian to the Philadelphia Hospital; Physician to the Children's Hospital, 
Philadelphia. Handsome octavo volume of 848 pages, with 362 illustra- 
tions, many of which are in colors. Prices: Cloth, $4.00 net; Half- 
Morocco, $5.00 net. 

Second Edition. 

In this work the practical application of pathological facts to clinical medicine 
is considered more fully than is customary in works on pathology. While the 
subject of pathology is treated in the broadest way consistent with the size of 
the book, an effort has been made to present the subject from the point of view 
of the clinician. The general relations of bacteriology to pathology are dis- 
cussed at considerable length, as the importance of these branches deserves. It 
will be found that the recent knowledge is fully considered, as well as older and 
more widely-known facts. 

" I consider the work abreast of modern pathology, and useful to both students and prac- 
titioners. It presents in a concise and well-considered form the essential facts of general and 
special pathological anatomy, with more than usual emphasis upon pathological physiology." 
— William H. Welch, Professor of Pathology , Johns Hopkins University , Baltimore, Md. 

" I regard it as the most serviceable text-book for students on this subject yet written by 
an American author." — L. Hektoen, Professor of Pathology, Rush Medical College, 
Chicago, III. 

A TEXT-BOOK OF OBSTETRICS. By Barton Cooke Hirst, M.D., 
Professor of Obstetrics in the University of Pennsylvania. Handsome oc- 
tavo volume of 846 pages, with 618 illustrations and seven colored plates. 
Prices: Cloth, $5.00 net; Half-Morocco, $6.00 net. 

Second Edition. 

This work, which has been in course of preparation for several years, is in- 
tended as an ideal text-book for the student no less than an advanced treatise 
for the obstetrician and for general practitioners. It represents the very latest 
teaching in the practice of obstetrics by a man of extended experience and 
recognized authority. The book emphasizes especially, as a work on obstetrics 
should, the practical side of the subject, and to this end presents an unusually 
large collection of illustrations. A great number of these are new and original, 
and the whole collection will form a complete atlas of obstetrical practice. 
An extremely valuable feature of the book is the large number of refer- 
ences to cases, authorities, sources, etc., forming, as it does, a valuable bib- 
liography of the most recent and authoritative literature on the subject 
of obstetrics. As already stated, this work records the wide practical ex- 
perience of the author, which fact, combined with the brilliant presentation 
of the subject, will doubtless render this one of the most notable books on 
obstetrics that has yet appeared. 

" The illustrations are numerous and are works of art, many of them appearing for the 
first time. The arrangement of the subject-matter, the foot-notes, and index are beyond 
criticism. The author's style, though condensed, is singularly clear, so that it is never 
necessary to re-read a sentence in order to grasp its meaning. As a true model of what a 
modern text-book in obstetrics should be, we feel justified in affirming that Dr. Hirst's 
book is without a rival." — New York Medical Record. 



CATALOGUE OF MEDICAL WORKS. 21 

A TEXT-BOOK OF THE PRACTICE OF MEDICINE. By 

James M. Anders. M.D., Ph.D., LL.D., Professor of the Practice of 
Medicine and of Clinical Medicine, Medico-Chirurgical College, Philadel- 
phia. In one handsome octavo volume of 1292 pages, fully illustrated. 
Cloth, $5.50 net; Sheep or Half-Morocco, $6.50 net. 

THIRD EDITION, THOROUGHLY REVISED. 

The present edition is the result of a careful and thorough revision. A few 
new subjects have been introduced : Glandular Fever, Ether-pneumonia, Splenic 
Anemia, Meralgia Paresthetica, and Periodic Paralysis. The affections that 
have been substantially rewritten are: Plague, Malta Fever, Diseases of the 
Thymus Gland, Liver Cirrhoses, and Progressive Spinal Muscular Atrophy. 
The following articles have been extensively revised : Typhoid Fever, Yellow 
Fever, Lobar Pneumonia, Dengue, Tuberculosis, Diabetes Mellitus, Gout, Ar- 
thritis Deformans, Autumnal Catarrh, Diseases of the Circulatory System, more 
particularly Hypertrophy and Dilatation of the Heart, Arteriosclerosis and 
Thoracic Aneurysm. Pancreatic Hemorrhage, Jaundice, Acute Peritonitis, Acute 
Yellow Atrophy, Hematoma of Dura Mater, and Scleroses of the Brain. The 
preliminary chapter on Nervous Diseases is new, and deals with the subject of 
localization and the various methods of investigating nervous affections. 

" It is an excellent book — concise, comprehensive, thorough, and up to date. It is a 
credit to you ; but, more than that, it is a credit to the profession of Philadelphia— to us." 
—James C. Wilson, Professor of the Practice of Medicine and Clinical Medicine, Jeffer- 
son Medical College, Philadelphia. 

" The book can be unreservedly recommended to students and practitioners as a safe, full 
compendium of the knowledge of internal medicine of the present day ... It is a work 
thoroughly modern in every sense." — Medical News, New York. 

DISEASES OF THE STOMACH. By William W. Van Valzah, 
M. L)., Professor of General Medicine and Diseases of the Digestive System 
and the Blood, New York Polyclinic; and J. DOUGLAS NlSBET, M. D., 

Adjunct Professor of General Medicine and Diseases of the Digestive Sys- 
tem and the Blood, New York Polyclinic. Octavo volume of 674 pages, 
illustrated. Cloth, S3. 50 net. 

An eminently practical book, intended as a guide to the student, an aid to the 
:ian, and a contribution to scientific medicine. It aims to give a complete 
description of the modern methods of diagnosis and treatment of diseases of the 
ich, and to reconstruct the pathology of the stomach in keeping with the 
revelations of scientific research. The book is clear, practical, and complete, 
and contains the results of the authors' investigations and of their extensive ex- 
perience as specialists. Particular attention is given to the important subject of 
dietetic treatment. The diet-lists are very complete, and are so arranged that 
selections can readily be made to suit individual cases. 

"This is the most satisfactory work on the subject in the English language." — Chicago 

"The article on diet and general medication is one of the most valuable in the book, and 
should be read by every practising physician." — New York Medical Journal. 



22 W. B. SAUNDERS' 



SURGICAL DIAGNOSIS AND TREATMENT. By J. W. Mao 

Donald, M. D., Edin., F. R. C. S., Edin., Professor of the Practice of Sur- 
gery and of Clinical Surgery in Hamline University ; Visiting Surgeon to St. 
Barnabas' Hospital, Minneapolis, etc. Handsome octavo volume of 800 
pages, profusely illustrated. Cloth, $5.00 net; Half- Morocco, $6.00 net. 
This work aims in a comprehensive manner to furnish a guide in matters of 
surgical diagnosis. It sets forth in a systematic way the necessities of examina- 
tions and the proper methods of making them. The various portions of the 
body are then taken up in order and the diseases and injuries thereof succinctly 
considered and the treatment briefly indicated. Practically all the modern and 
approved operations are described with thoroughness and clearness. The work 
concludes with a chapter on the use of the Röntgen rays in surgery. 

" The work is brimful of just the kind of practical information that is useful alike to 
students and practitioners. It is a pleasure to commend the book because of its intrinsic 
value to the medical practitioner." — Cincinnati Lane et- Clinic. 

PATHOLOGICAL TECHNIQUE. A Practical Manual for Laboratory 
Work in Pathology, Bacteriology, and Morbid Anatomy, with chapters on 
Post-Mortem Technique and the Performance of Autopsies. By Frank 
B. MALLORY, A. M., M. D., Assistant Professor of Pathology, Harvard 
University Medical School, Boston; and James H. Wright, A. M., M.D., 
Instructor in Pathology, Harvard University Medical School, Boston. Oc- 
tavo volume of 396 pages, handsomely illustrated. Cloth, $2.50 net. 
This book is designed especially for practical use in pathological laboratories, 
both as a guide to beginners and as a source of reference for the advanced. The 
book will also meet the wants of practitioners who have opportunity to do general 
pathological work. Besides the methods of post-mortem examinations and of 
bacteriological and histological investigations connected with autopsies, the 
special methods employed in clinical bacteriology and pathology have been 
fully discussed. 

" One of the most complete works on the subject, and one which should be in the library 
of every physician who hopes to keep pace with the great advances made in pathology." — 
yournal of American Medical Association. 

THE SURGICAL COMPLICATIONS AND SEQUELS OF TY- 
PHOID FEVER. By Wm. W. Keen, M. D., LL.D., Professor of the 
Principles of Surgery and of Clinical Surgery, Jefferson Medical College, 
Philadelphia. Octavo volume of 386 pages, illustrated. Cloth, $3.00 net. 
This monograph is the only one in any language covering the entire subject 
of the Surgical Complications and Sequels of Typhoid Fever. The work will 
prove to be of importance and interest not only to the general surgeon and phy- 
sician, but also to many specialists — laryngologists, ophthalmologists, gynecolo- 
gists, pathologists, and bacteriologists — as the subject has an important bearing 
upon each one of their spheres. The author's conclusions are based on reports 
of over 1700 cases, including practically all those recorded in the last fifty years. 
Reports of cases have been brought down to date, many having been added 
while the work was in press. 

" This is probably the first and only work in the English language that gives the reader a 
clear view of what typhoid fever really is, and what it does and can do to the human organ- 
ism. This book should be in the possession of every medical man in America." — American 
Medico-Surgical Bulletin. 



CATALOGUE OF MEDICAL WORKS. 23 



MODERN SURGERY, GENERAL AND OPERATIVE. By John 
Chalmers DaCosta, M.D., Clinical Professor of Surgery, Jefferson Medi- 
cal College, Philadelphia; Surgeon to the Philadelphia Hospital, etc. 
Handsome octavo volume of 911 pages, profusely illustrated. Cloth, $4.00 
net ; Half-Morocco, $5.00 net. 

Second Edition, Beitritten and Greatly Enlarged. 

The remarkable success attending DaCosta's Manual of Surgery, and the 
general favor with which it has been received, have led the author in this 
revision to produce a complete treatise on modern surgery along the same lines 
that made the former edition so successful. The* book has been entirely re- 
written and very much enlarged. The old edition has long been a favorite not 
only with students and teachers, but also with practising physicians and sur- 
geons, and it is believed that the present work will find an even wider field of 
usefulness. 

" We know of no small work on surgery in the English language which so well fulfils the 
requirements of the modern student." — Medico-Chirurgical Journal , Bristol, England. 

" The author has presented concisely and accurately the principles of modern surgery. 
The book is a valuable one which can be recommended to students and is of great value to 
the general practitioner." — American Journal of the Medical Sciences. 

A MANUAL OF ORTHOPEDIC SURGERY. By James E. Moore, 
M.D., Professor of Orthopedics and Adjunct Professor of Clinical Surgery, 
University of Minnesota, College of Medicine and Surgery. Octavo volume 
of 356 pages, with 177 beautiful illustrations from photographs made spec- 
ially for this work. Cloth, $2.50 net. 

A oractical book based upon the author's experience, in which special stress 
is laid upon early diagnosis and treatment such as can be carried out by the 
general practitioner. The teachings of the author are in accordance with his 
belief that true conservatism is to be found in the middle course between the 
surgeon who operates too frequently and the orthopedist who seldom operates. 

" A very demonstrative work, every illustration of which conveys a lesson. The work is 
: excellent and commendable one, which we can certainly endorse with pleasure."" — 
St. Louis Medical and Surgical journal. 

ELEMENTARY BANDAGING AND SURGICAL DRESSING. 

With Directions concerning the Immediate Treatment of Cases of Emer- 
gency. For the use of Dressers and Nurses. By Walter Pye, F.R.C.S., 
late Surgeon to St. Mary's Hospital, London. Small i2mo, with over 80 
illustrations. Cloth, flexible covers, 75 cents net. 

This little book is chiefly a condensation of those portions of Pye's " Surgical 
Handicraft'' which deal with bandaging, splinting, etc!, and of those which 
treat of the management in the first instance of cases of emergency. The 
directions given are thoroughly practical, and the book will prove extremely use- 
ful to students, surgical nurses, and dressers. 

" The author writes well, the diagrams are clear, and the book itself is small and portable, 
although the paper and type are good." — British Medical Journal. 



24 W. B. SAUNDERS' 



A TEXT-BOOK OF MATERIA MEDICA, THERAPEUTICS 
AND PHARMACOLOGY. By George F. Butler, Ph.G., M.D., 
Professor of Materia Medica and of Clinical Medicine in the College of 
Physicians and Surgeons, Chicago ; Professor of Materia Medica and 
Therapeutics, Northwestern University, Woman's Medical School, etc 
Octavo, 874 pages, illustrated. Cloth, $4.00 net; Sheep, $5.00 net. 
Third Edition, Thoroughly Revised. 
A clear, concise, and practical text-book, adapted for permanent reference no 
less than for the requirements of the class-room. 

The recent important additions made to our knowledge of the physiological 
action of drugs are fully discussed in the present edition. The book has been 
thoroughly revised and many additions have been made. 

" Taken as a whole, the book may fairly be considered as one of the most satisfactory of any 
single-volume works on materia medica in the market."— Journal of the A7nerican Medical 
Association. 

TUBERCULOSIS OF THE GENITO-URINARY ORGANS, 
MALE AND FEMALE. By Nicholas Senn, M.D., Ph.D., LL.D., 
Professor of the Practice of Surgery and of Clinical Surgery, Rush Medical 
College, Chicago. Handsome octavo volume of 320 pages, illustrated^ 
Cloth, $3.00 net. 

Tuberculosis of the male and female genito-urinary organs is such a frequent, 
distressing, and fatal affection that a special treatise on the subject appears to 
fill a gap in medical literature. In the present work the bacteriology of the sub- 
ject has received due attention, the modern resources employed in the differen- 
tial diagnosis between tubercular and other inflammatory affections are fully 
described, and the medical and surgical therapeutics are discussed in detail. 

"An important book upon an important subject, and written by a man of mature judg- 
ment and wide experience. The author has given us an instructive book upon one of the 
most important subjects of the day." — Clinical Reporter. 

"A work which adds another to the many obligations the profession owes the talented 
author." — Chicago Medical Recorder. 

A TEXT-BOOK OF DISEASES OF WOMEN. By Charles B. 
Penrose, M.D., Ph.D., Professor of Gynecology in the University of 
Pennsylvania; Surgeon to the Gynecean Hospital, Philadelphia. Octavo 
volume of 531 pages, with 217 illustrations, nearly all from drawings made 
for this work. Cloth, $3.75 net. 

Third Edition, Revised. 
In this work, which has been written for both the student of gynecology and 
the general practitioner, the author presents the best teaching of modern gyne- 
cology untrammelled by antiquated theories or methods of treatment. In most 
instances but one plan of treatment is recommended, to avoid confusing the 
student or the physician who consults the book for practical guidance. 

" I shall value very highly the copy of Penrose's ' Diseases of Women ' received. I have 
already recommended it to my class as THE BEST book." — Howard A. Kelly, Professor 
of Gynecology and Obstetrics , Johns Hopkijis University, Baltimore, Md. 

" The book is to be commended without reserve, not only to the student but to the general 
practitioner who wishes to have the latest and best modes of treatment explained with absolute 
clearness." — Therapeutic Gazette. 



CATALOGUE OF MEDICAL WORKS. 



SURGICAL PATHOLOGY AND THERAPEUTICS. By John 
Collins WARREN, M.D., LL.D., Professor of Surgery, Medical Depart- 
ment Harvard University. Handsome octavo, S32 pages, with 136 relief 
and lithographic illustrations, 33 of which are printed in colors. 

Second Edition, 

with an Appendix devoted to the Scientific Aids to Surgical Diagnosis, and 
a series of articles on Regional Bacteriology. Cloth, $5.00 net; Half- 
Morocco. 56.00 net. 

Without Exception, the Illustrations are the Best ever Seen in a 
Work of this Kind. 

"A most striking and very excellent feature of this book is its illustrations. Without ex- 

•. the point ot accuracy and artistic merit, they are the best ever seen in a work 

of this kind. * * * Many of those representing microscopic pictures are so perfect in their 

coloring and detail as almost to give the beholder the impression that he is looking down the 

barrel of a microscope at a well-mounted section." — Annals of Surgery, Philadelphia. 

" It is the handsomest specimen of book-making * * * that has ever been issued from the 
American medical press." — American Journal of the Medical Sciences, Philadelphia. 

PATHOLOGY AND SURGICAL TREATMENT OF TUMORS. 
By N. SENN, M. D., Ph. D., LL. D., Professor of Practice of Surgery and 
of Clinical Surgery, Rush Medical College; Professor of Surgery, Chicago 
Polyclinic ; Attending Surgeon to Presbyterian Hospital ; Surgeon-in-Chief, 
St. Joseph's Hospital, Chicago. One volume of 710 pages, with 515 
engravings, including full-page colored plates. New and enlarged Edition 
in Preparation. 

Books specially devoted to this subject are few, and in our text-books and 
ms of surgery this part of surgical pathology is usually condensed to a de- 
gree incompatible with its scientific and clinical importance. The author spent 
many years in collecting the material for this work, and has taken great pains 
to present it in a manner that should prove useful as a text-book for the student, 
a work of reference for the practitioner, and a reliable guide for the surgeon. 

"The m.st exhaustive of any recent book in English on this subject. It is well illus- 
trated, and will doubtless remain as the principal monograph on the subject in our language 
for some years. The book is handsomely illustrated and printed, .... and the author has 
given a notable and lasting contribution to surgery." — Journal of the America?! M 
Association, Chicago. 

LECTURES ON RENAL AND URINARY DISEASES. By 

in., Fellow of the Royal College of Physicians, 
London, and of the Royal Medico-Chirurgical Society; Physician to the 
Genera] Hospital. volume of 434 pages, with numerous illustra- 

tions and 4 colored plates. Cloth, $2.50 1 

"The volume makes a favorable impression at once. The style is clear and succinct. 

nnot find any part oftl in which th- ■ carefully tl. 

out and fortified by evidence drawn from the m The book may be cordially 

recommended." — British Medical Journal. 



26 W. B. SAUNDERS' 



A HANDBOOK FOR NURSES. By J. K. Watson, M. D., Edin., 

Assistant House-Surgeon, Sheffield Royal Hospital. American Edition, 
under the supervision of A. A. Stevens, A. M., M. D., Professor of 
Pathology, Woman's Medical College, Philadelphia. i2mo, 413 pages, 
73 illustrations. Cloth, $1.50 net. 

This work aims to supply in one volume that information which so many 
nurses at the present time are trying to extract from various medical works, and 
to present that information in a suitable form. Nurses must necessarily acquire 
a certain amount of medical knowledge, and the author of this book has aimed 
judiciously to cater to this need with the object of directing the nurses' pursuit 
of medical information in proper and legitimate channels. The book represents 
an entirely new departure in nursing literature, insomuch as it contains useful 
information on medical and surgical matters hitherto only to be obtained from 
expensive works written expressly for medical men. 

A NEW PRONOUNCING DICTIONARY OF MEDICINE, with 
Phonetic Pronunciation, Accentuation, Etymology, etc. By John 
M. Keating, M.D., LL.D., Fellow of the College of Physicians of Phila- 
delphia; Editor "Cyclopaedia of the Diseases of Children," etc.; and 
Henry Hamilton, with the Collaboration of J. Chalmers DaCosta, 
M. D., and Frederick A. Packard, M. D. One very attractive volume 
of over 800 pages. Second Revised Edition. Prices: Cloth, $5.00 net ; 
Sheep or Half-Morocco, $6.00 net; with Denison's Patent Ready- Refer- 
ence Index ; without patent index, Cloth, $4.00 net ; Sheep or Half- 
Morocco, $5.00 net. 

PROFESSIONAL. OPINIONS. 

" I am much pleased with Keating's Dictionary, and shall take pleasure in recommending 
it to my classes." 

Henry M. Lyman, M. D., 
Professor of Principles and Practice of Medicine , Rush Medical College, Chicago, III. 

" I am convinced that it will be a very valuable adjunct to my study-table, convenient in 
size and sufficiently full for ordinary use." 

C. A. LlNDSLEY, M. D., 

Professor of Theory and Practice of Medicine, Medical Dept. Yale University; 

Secretary Connecticut State Board of Health, New Haven, Conn, 

AUTOBIOGRAPHY OF SAMUEL D. GROSS, M. D., Emeritus Pro- 
fessor of Surgery in the Jefferson Medical College of Philadelphia, with 
Reminiscences of His Times and Contemporaries. Edited by his sons, 
Samuel W. Gross, M. D., LL.D., and A. Haller Gross, A.M., of the 
Philadelphia Bar. Preceded by a Memoir of Dr. Gross, by the late 
Austin Flint, M. D., LL.D. In two handsome volumes, each containing 
over 400 pages, demy 8vo, extra cloth, gilt tops, with fine Frontispiece 
engraved on steel. Price per Volume, $2.50 net. 






TALOGUE OF MEDICAL WORKS. 2*] 

PRACTICAL POINTS IN NURSING. For Nurses in Private 
Practice. By Emily A. M, Stoney, Graduate of the Traming-School 
tor Nurses, Lawrence, Mass.; Superintendent of the Training-School for 

Nurses, Carney Hospital, South Boston, Mass. 456 pages, handsomely 
illustrated with 73 engravings in tne text, and 9 colored and half-tone 
mates. Cloth. Price, M.Js net. 

SECOND EDITION, THOROUGHLY REVISED. 

In this volume the author explains, in popular language and in the shortest 
possible form, the entire range of private nursing as distinguished from hospital 
nursing, and the nurse is instructed how best to meet the various emergencies of 
medical and surgical cases when distant from medical or surgical aid or when 
thrown on her own resources. 

An especially valuable feature of the work will be found in the directions to 
the nurse how to improvise everything ordinarily needed in the sick-room, where 
the embarrassment of the nurse, owing to the want of proper appliances, is fre- 
quently extreme. 

The werk has been logically divided into the following sections: 

I. The Nurse : her responsibilities, qualifications, equipment, etc. 
II. The Sick-Room : its selection, preparation, and management. 
TIL The Patient : duties of the nurse in medical, surgical, obstetric, and gyne- 
cologic cases. 
IV. Nursing in Accidents and Emergencies. 
V. Nursing in Special Medical Cases. 
VI. Nursing of the New-born and Sick Children. 
VII. Physiology and Descriptive Anatomy. 

The Appendix contains much information in compact form that will be found 
of great value to the nurse, including Rules for Feeding the Sick; Recipes for 
Invalid Foods and Beverages; Tables of Weights and Measures; Table for 
Computing the Date of Labor; List of Abbreviations : Dose-List; and a full 
and complete Glossary of Medical Terms and Nursing Treatment. 

"This is a well-written, eminently practical volume, which covers the entire range of 

private nursing as distinguished from hospital nursing, and instructs the nurse how best to 

meet the various - which may arise and how to prepare everything ordinarily 

needed in the illness of her patient." — American Journal of Obstetrics and Diseases of 

n and Children, Aug., 1896. 

A TEXT-BOOK OF BACTERIOLOGY, including the Etiology and 
Prevention of Infective i and an account of Yeasts and Moulds, 

kiaematozoa, a By Edgar M. Crookshank, M. B., Pro- 

! thology and Bacteriology, King's College, London. 
A handsome octavo volume of 700 pages, with 273 engravings in the text, 
ana and colored plates. Price, $6.50 net. 

"'his hook, though nominally a Fourth Edition of Professor Crookshank's 

,( Manual 01 \V\< rERIOLOGY," is practically a new work, the old one having 
been reconstructed, greatly enlarged, revised throughout, and largely rewritten, 
forming a text-book for the Bacteriological Laboratory, for Medical Officers of 
Health, and for Veterinary InsoecU 



28 IV. B. SAUNDERS' 



MEDICAL DIAGNOSIS. By Dr. Oswald Vierordt, Professor of 
Medicine at the University of Heidelberg. Translated, with additions, 
from the Fifth Enlarged German Edition, with the author's permission, by 
Francis H. Stuart, A. M., M. D. In one handsome royal-octavo volume 
of 600 pages« 194 fine wood-cuts in the text, many of them in colors. 
Prices: Cloth, $4.00 net; Sheep or Half-Morocco, $5.00 net. 

FOURTH AMERICAN EDITION, FROM THE FIFTH REVISED AND 
ENLARGED GERMAN EDITION. 

In this work, as in no other hitherto published, are given full and accurate 
explanations of the phenomena observed at the bedside. It is distinctly a clin- 
ical work by a master teacher, characterized by thoroughness, fulness, and accu- 
racy. It is a mine of information upon the points that are so often passed over 
without explanation. Especial attention has been given to the germ-theory as a 
factor in the origin of disease. 

The present edition of this highly successful work has been translated from 
the fifth German edition. Many alterations have been made throughout the 
book, but especially in the sections on Gastric Digestion and the Nervous System. 

It will be found that all the qualities which served to make the earlier editions 
so acceptable have been developed with the evolution of the work to its present 
form. 

THE PICTORIAL ATLAS OF SKIN DISEASES AND SYPHI- 
LITIC AFFECTIONS. (American Edition.) Translation from 
the French. Edited by J. J. Pringle, M. B., F. R. C. P., Assistant Phy- 
sician to, and Physician to the department for Diseases of the Skin at, the 
Middlesex Hospital, London. Photo-lithochromes from the famous models 
of dermatological and syphilitic cases in the Museum of the Saint-Louis 
Hospital, Paris, with explanatory wood-cuts and letter-press. In 12 Parts, 
at $3.00 per Part. 

" Of all the atlases of skin diseases which have been published in recent years, the present 
one promises to be of greatest interest and value, especially from the standpoint of the 
general practitioner."— American Medico-Surgical Bulletin, Feb. 22, 1896. 

"The introduction of explanatory wood-cuts in the text is a novel and most important 
feature which greatly furthers the easier understanding of the excellent plates, than which 
nothing, we venture to say, has been seen better in point of correctness, beauty, and general 
merit." — Neiv York Medical Journal ', Feb. 15, 1896. 

" An interesting feature of the Atlas is the descriptive text, which is written for each picture 
by the physician who treated the case or at whose instigation the models have been made. 
We predict for this truly beautiful work a large circulation in all parts of the medical world 
where the names St. Louis and Baretta have preceded it." — Medical Record, N. Y., Feb. 1, 
1896. 

A TEXT-BOOK OF MECHANO-THERAPY (MASSAGE AND 
MEDICAL GYMNASTICS). By Axel V. Grafstrom, B. Sc, 
M. D., late Lieutenant in the Royal Swedish Army; late House Physi- 
cian, City Hospital, BlackwelPs Island, New York. i2mo, 139 pages, 
illustrated. Cloth, $1.00 net. 



CATALOGUE OF MEDICAL WORKS. 2g 

DISEASES OF THE EYE. A Hand-Book of Ophthalmic Prac- 
tice. By G. E. DE SCHWRINITZ, M. D., Professor of Ophthalmology in 

the Jefferson Medical College, Philadelphia, etc. A handsome royal- 
octavo volume of 696 pages, with 255 fine illustrations, many of which are 
original, and 2 chromo-lithographic plates. Prices : Cloth, $4.00 net ; 
Sheep or Half-Morocco, $5.00 net. 

THIRD EDITION, THOROUGHLY REVISED. 

In the third edition of this text-book, destined, it is hoped, to meet the favor- 
able reception which has been accorded to its predecessors, the work has been 
revised thoroughly, and much new matter has been introduced. Particular 
attention has been given to the important relations which micro-organisms bear 
to many ocular diseases. A number of special paragraphs on new subjects have 
been introduced, and certain articles, including a portion of the chapter on 
Operations, have been largely rewritten, or at least materially changed. A 
number of new illustrations have been added. The Appendix contains a full 
description of the method of determining the corneal astigmatism with the 
ophthalmometer of Javal and Schiötz, and the rotation of the eyes with the 
tropometer of Stevens. 

" A work that will meet the requirements not only of the specialist, but of the general 
practitioner in a rare degree. I am satisfied that unusual success awaits it." 

William Pepper, M. D. 
Froz'ost and Professor of Theory and Practice of Medicine and Clinical Medicine 
in the University of Pennsylvania. 

"A clearly written, comprehensive manual. . . . One which we can commend to students 
as a reliable text-book, written with an evident knowledge of the wants of those entering upon 
the study of this special branch of medical science." — British Medical Journal. 

" It is hardly too much to say that for the student and practitioner beginning the study of 
Ophthalmology, it is the best single volume at present published." — Medical News. 

" It is a very useful, satisfactory, and safe guide for the student and the practitioner, and 
one of the best works of this scope in the English language." — Annals of Ophthalmology. 

DISEASES OF WOMEN. By J. Bland Sutton, F.R.C.S., Assistant 

.' sc x I [ospital, and Surgeon to Chelsea Hospital, London ; 

and Arthur E. Giles, M. D., B.Sc, Lond., F.R.C.S., Edin., Assistant 

on to Chelsea Hospital, London. 436 pages, handsomely illustrated. 

Cloth, 52.50 net. 

The author- have placed in the hands of the physician and student a concise 
yet comprehensive guide to the study of gynecology in its most modern develop- 
ment. It has been their aim to relate facts and describe methods belonging to 
the science and art of gynecology in a way that will prove useful to students for 
mination purposes, and which will also enable the general physician to prac- 
tice thi- important department of surgery with advantage to his patients and with 
satisfacti' 

" The bnok is very well prepared, and i be well received by the medical public." 

— British M 'Hal. 

"The text has been carefully prepnr N tl ing essential has been omitted, and its 

teaching are those recommended by the leading authorities of the day." — 'Journal of the 
American Medical Association. 



30 m M. SAUNDE&S* 



TEXT-BOOK UPON THE PATHOGENIC BACTERIA. Spe- 
cially written for Students of Medicine. By Joseph McFarland, 
M. D., Professor of Pathology and Bacteriology in the Medico-Chirurgical 
College of Philadelphia, etc. 497 pages, finely illustrated. Price, Cloth, 
$2.50 net, 

SECOND EDITION, REVISED AND GREATLY ENLARGED, 
The work is intended to be a text-book for the medical student and for the 
practitioner who has had no recent laboratory training in this department of medi- 
cal science. The instructions given as to needed apparatus, cultures, stainings, 
microscopic examinations, etc. are ample for the student's needs, and will afford 
to the physician much information that will interest and profit him relative to a 
subject which modern science shows to go far in explaining the etiology of many 
diseased conditions. 

In this second edition the work has been brought up to date in all depart- 
ments of the subject, and numerous additions have been made to the technique 
in the endeavor to make the book fulfil the double purpose of a systematic work 
upon bacteria and a laboratory guide. 

" It is excellently adapted for the medical students and practitioners for whom it is avowedly- 
written. . . . The descriptions given are accurate and readable, and the book should prove 
useful to those for whom it is written. — London Lancet, Aug. 29, 189Ö. 

" The author has succeded admirably in presenting the essential details of bacteriological 
technics, together with a judiciously chosen summary of our present knowledge of pathogenic 
bacteria. . . . The work, we think, should have a wide circulation among English-speaking 
students of medicine." — N. Y. Medical Journal, April 4, 1896. 

" The book wiU be found of considerable use by medical men who have not had a special 
bacteriological training, and who desire to understand this important branch of medical 
science." — Edinburgh Medical Journal, July, 1896. 

LABORATORY GUIDE FOR THE BACTERIOLOGIST. By 

Langdon Frothingham, M. D. V., Assistant in Bacteriology and Veteri- 
nary Science, Sheffield Scientific School. Yale University. Illustrated. 
Price, Cloth, 75 cents. 

The technical methods involved in bacteria-culture, methods of staining, ana 
microscopical study are fully described and arranged as simply and concisely as 
possible. The book is especially intended for use in laboratory work, 

" It is a convenient and useful little work, and will more than repay the outlay necessary 
for its purchase in the saving of time which would otherwise be consumed in looking up the 
various points of technique so clearly and concisely laid down in its pages." — American Med.- 
Surg. Bulletin, 

FEEDING IN EARLY INFANCY. By Arthur V. Meigs. M. D. 
Bound in limp cloth : flush edges. Price, 25 cents net. 

Synopsis : Analyses of Milk — Importance of the Subject of Feeding in Early 
Infancy — Proportion of Casein and Sugar in Human Milk — Time to Begin Arti- 
ficial Feeding of Infants — Amount of Food to be Administered at Each Feed- 
ing — Intervals between Feedings — Increase in Amount of Food at Different 
Periods of Infant Development — Unsuitableness of Condensed Milk as a Sub- 
stitute for Mother's Milk — Objections to Sterilization or " Pasteurization y ' ot 
Milk — Advances made in the Method of Artificial Feeding of Infants. 



CATALOGUE OF MEDICAL WORKS. 3 1 

MATERIA MEDICA FOR NURSES. By Emily A. M. STQNEY, 
Graduate of the Training-school for Nurses, Lawrence, Mass. ; late 
Superintendent of the Training-school for Nurses, Carney Hospital, South 
Boston. Mass. Handsome octavo, 300 pages. Cloth, $1.50 net. 

The present book differs from other similar works in several features, all of 
which are introduced to render it more practical and generally useful. The 
general plan o\ contents follows the lines laid down in training-schools for 
nurses, but the book contains much useful matter not usually included in works 
o\ this character, such as emergencies, Ready Dose-list, Weights and 

sures, etc., as well as a Glossary, defining all the terms in Materia Medica, 
and describing all the latest drugs and remedies, which have been generally 
neglected by other books of the kind. 

ESSENTIALS OF ANATOMY AND MANUAL OF PRACTI- 
CAL DISSECTION, containing « Hints on Dissection." By Charles 
B. Nancrede, M. D., Professor of Surgery and Clinical Surgery in the 
University of Michigan, Ann Arbor; Corresponding Member of the Royal 
Academy of Medicine, Rome, Italy ; late Surgeon Jefferson Medical Col- 
lege, etc. Fourth and revised edition, lost 8vo, over 500 pages, with 
handsome full-page lithographic plates in co.ors, and over 200 illustrations. 
Price : Extra Cloth or Oilcloth for the dissection-room, 32.00 net. 

Neither pains nor expense has been spared to make this work the most ex- 
haustive yet concise Student's Manual of Anatomy and Dissection ever pub- 
lished, either in America or in Europe. 

The colored plates are designed to aid the student in dissecting the muscles, 
arteries, veins, and nerves. The wood-cuts have all been specially drawn and 
engraved, and an Appendix added, containing 60 illustrations representing the 
structure of the entire human skeleton, the whole being based on the eleventh 
edition of Gray's Anatomy. 

A MANUAL OF PRACTICE OF MEDICINE. By A. A. Stevens, 
A. M .. M. D., Instructor in Physical Diagnosis in the University of Penn- 
sylvania, and Professor of Pathology in the Woman's Medical College of 
Pennsylvania. Specially intended for students preparing for graduation 
and hospital examinations. Post Svo, 519 pages. Numerous illustrations 
and selected formulae. Price, bound in flexible leather, $2.00 net. 

FIFTH EDITION, REVISED AND ENLARGED. 

Contributions to the science of medicine have poured in so rapidly during the 
last quarter of a century that it is well-nigh impossible for the student, with the 
limited time at his disposal, to master elaborate treatises or to cull from them 
ihat knowledge which is absolutely essential. From an extended experience in 
teaching, the author has been enabled, by classification, to group allied symp- 
toms, and by the judicious elimination of theories and redundant explanations 
to bring within a comparatively small compass a complete outline of the prac- 
tice of medicine. 



32 W. ß. SAUNDERS 



MANUAL OF MATERIA MEDICA AND THERAPEUTICS. 

By A. A. Stevens, A. M., M. D., Instructor of Physical Diagnosis in the 
University of Pennsylvania, and Professor of Pathology in the Woman's 
Medical College of Pennsylvania. 445 pages. Price, bound in flexible 
leather, $2.25. 

SECOND EDITION, REVISED. 

This wholly new volume, which is based on the last edition of the Pharma- 
copoeia, comprehends the following sections : Physiological Action of Drugs ; 
Drugs; Remedial Measures other than Drugs; Applied Therapeutics; Incom- 
patibility in Prescriptions; Table of Doses; Index of Drugs; and Index of 
Diseases; the treatment being elucidated by more than two hundred formulae. 

" The author is to be congratulated upon having presented the medical student with as 
accurate a manual of therapeutics as it is possible to prepare." — Therapeutic Gazette. 

" Far superior to most of its class ; in fact, it is very good. Moreover, the book is reliable 
and accurate." — New York Medical Journal. 

" The author has faithfully presented modern therapeutics in a comprehensive work, . . . 
and it will be found a reliable guide."— University Medical Magazine. 

NOTES ON THE NEWER REMEDIES: their Therapeutic Ap- 
plications and Modes of Administration. By David Cerna, M. D., 
Ph. D., Demonstrator of and Lecturer on Experimental Therapeutics in 
the University of Pennsylvania. Post-octavo, 253 pages. Price, #1.25. 

SECOND EDITION, RE-WRITTEN AND GREATLY ENLARGED. 

The work takes up in alphabetical order all the newer remedies, giving their 
physical properties, solubility, therapeutic applications, administration, and 
chemical formula. 

It thus forms a very valuable addition to the various works on therapeutics 
now in existence. 

Chemists are so multiplying compounds, that, if each compound is to be thor- 
oughly studied, investigations must be carried far enough to determine the prac- 
tical importance of the new agents. 

"Especially valuable because of its completeness, its accuracy, its systematic consider- 
ation of the properties and therapy of many remedies of which doctors generally know but 
little, expressed in a brief yet terse manner." — Chicago Clinical Review. 



TEMPERATURE CHART. Prepared by D. T. Laine, M. D. Size 
8x 13^ inches. Price, per pad of 25 charts, 50 cents. 

A conveniently arranged chart for recording Temperature, with columns for 
daily amounts of Urinary and Fecal Excretions, Food, Remarks, etc. On the 
back of each chart is given in full the method of Brand in the treatment of 
Typhoid Fever. 



CATALOGUE OF MEDICAL WORKS. 33 



A TEXT-BOOK OF HISTOLOGY, DESCRIPTIVE AND PRAC- 
TICAL. For the Use of Students. By Arthur Clarkson, M. B., 
C. M., Edin., formerly Demonstrator of Physiology in the Owen's College, 
Manchester; late Demonstrator of Physiology in the Yorkshire College, 
Leeds. Large Svo, 554 pages, with 22 engravings in the text, and 174 
beautifully colored original illustrations. Price, strongly bound in Cloth, 
54.00 net. 

The purpose of the writer in this work has been to furnish the student of His- 
tology, in one volume, with both the descriptive and the practical part of the 
science. The first two chapters are devoted to the consideration of the general 
methods of Histology ; subsequently, in each chapter, the structure of the tissue 
or organ is first systematically described, the student is then taken tutorially over 
the specimens illustrating it, and, finally, an appendix affords a short note of the 
methods of preparation. 

" The work must be considered a valuable addition to the list of available text-books, and 
is to be highly recommended." — New York Medical Journal. 

" One of the best works for students we have ever noticed. We predict that the book will 
attain a well-deserved popularity among our students." — Chicago Medical Recorder. 

THE PATHOLOGY AND TREATMENT OF SEXUAL IM- 
POTENCE. By Victor G. Vecki, M. D. From the second Ger- 
man edition, revised and rewritten. Demi-octavo, about 300 pages. 
Cloth, $2.00 net. 

The subject of impotence has but seldom been treated in this country in the 
trulv scientific spirit that it deserves, and this volume will come to many as a 
revelation of the possibilities of therapeusis in this important field. Dr. Vecki's 
work has long been favorably known, and the German book has received the 
highest consideration. This edition is more than a mere translation, for, although 
based on the German edition, it has been entirely rewritten by the author in 
English. 

" The work can be recommended as a scholarly treatise on its subject, and it can be read 
with advantage by many practitioners." — Journal of the American Medical Association. 

THE TREATMENT OF PELVIC INFLAMMATIONS 
THROUGH THE VAGINA. By \V. R. Pryor, M. D., Pro- 
fessor of Gynecology in the New York Polyclinic. i2mo, 248 pages, 
handsomely illustrated. Cloth, $2.00 net. 

In this book the author directs the attention of the general practitioner to a 
surgical treatment of the pelvic diseases of women. There exists the utmost 
confusion in the profession regarding the most successful methods of treating 
pelvic inflammation- ; and inasmuch as inflammatory lesions constitute the ma- 
jority of all pelvic diseases, the subject is an important one. It has been the 
endeavor of the author to put down every little detail, no matter how insig- 
nificant, which might be of service. 



34 W. B. SAUNDERS' 



DISEASES OF WOMEN. By Henry J. Garrigues, A.M., M.D., 
Professor of Gynecology in the New York School of Clinical Medicine; 
Gynecologist to St. Mark's Hospital and to the German Dispensary, New 
York City. In one handsome octavo volume of 728 pages, illustrated by 
335 engravings and colored plates. Prices: Cloth, $4.00 net; Sheep or 
Half-Morocco, $5.00 net. 

A PRACTICAL work on gynecology for the use of students and practitioners, 
written in a terse and concise manner. The importance of a thorough know- 
ledge of the anatomy of the female pelvic organs has been fully recognized by 
the author, and considerable space has been devoted to the subject. The chap- 
ters on Operations and on Treatment are thoroughly modern, and are based 
upon the large hospital and private practice of the author. The text is eluci- 
dated by a large number of illustrations and colored plates, many of them being 
original, and forming a complete atlas for studying embryology and the anatomy 
of the female genitalia, besides exemplifying, whenever needed, morbid condi- 
tions, instruments, apparatus, and operations. 

Second Edition, Thoroughly Revised. 

The first edition of this work met with a most appreciative reception by the 
medical press and profession both in this country and abroad, and was adopted 
as a text-book or recommended as a book of reference by nearly one hundred 
colleges in the United States and Canada. The author has availed himself of 
the opportunity afforded by this revision to embody the latest approved advances 
in the treatment employed in this important branch of Medicine. He has also 
more extensively expressed his own opinion on the comparative value of the 
different methods of treatment employed. 

"One of the best text-books for students and practitioners which has been published in 
the English language ; it is condensed, clear, and comprehensive. The profound learning 
and great clinical experience of the distinguished author find expression in this book in a 
most attractive and instructive form. Young practitioners, to whom experienced consultants 
may not be available, will find in this book invaluable counsel and help." 

Thad. A. Reamy, M. D., LL.D., 
Professor of Clinical Gynecology ', Medical College of Ohio ; Gynecologist to the Good 

Samaritan and Cincinnati Hospitals. 



A SYLLABUS OF GYNECOLOGY, arranged in conformity witn 
"An American Text-Book of Gynecology. " By J. W. Long, M. D., 
Professor of Diseases of Women and Children, Medical College of Vir- 
ginia, etc. Price, Cloth (interleaved), $1.00 net. 

Based upon the teaching and methods laid down in the larger work, this will 
not only be useful as a supplementary volume, but to those who do not already 
possess the text-book it will also have an independent value as an aid to the 
practitioner in gynecological work, and to the student as a guide in the lecture- 
room, as the subject is presented in a manner at once systematic, clear, succinct, 
pad practica.!. 



CATALOGUE OF MEDICAL WORKS. 35 

THE AMERICAN POCKET MEDICAL DICTIONARY. Edited 
by W. A. NEWMAN Dor land, M. D., Assistant Obstetrician to the Hospital 
of the University of Pennsylvania; Fellow of the American Academy of 
Medicine. Containing the pronunciation and definition of all the principal 
words used in medicine and the kindred sciences, with 64 extensive tables. 
Handsomely bound in flexible leather, limp, with gold edges and patent 
thumb index. Price, Si. 00 net ; with thumb index, $1.25 net. 

SECOND EDITION, REVISED. 

This is the ideal pocket lexicon. It is an absolutely new book, and not a re- 
vision of any old work. It is complete, defining all the terms of modern medi- 
cine and forming an unusually complete vocabulary. It gives the pronunciation 
of all the terms. It makes a special feature of the newer words neglected by 
other dictionaries. It contains a wealth of anatomical tables of special value to * 
students. It forms a handy volume, indispensable to every medical man. 

SAUNDERS* POCKET MEDICAL FORMULARY. By William 

M. Powell. M. D., Attending Physician to the Mercer House for Invalid 
Women at Atlantic City. Containing 1800 Formulae, selected from several 
hundred of the best-known authorities. Forming a handsome and con- 
venient pocket companion of nearly 300 printed pages, with blank leaves 
for Additions; with an Appendix containing Posological Table, Formulae 
and Doses for Hypodermatic Medication, Poisons and their Antidotes, 
Diameters of the Pemale Pelvis and Fcetal Head, Obstetrical Table, Diet 
List for Various Diseases, Materials and Drugs used in Antiseptic Surgery, 
Treatment of Asphyxia from Drowning, Surgical Remembrancer, Tables 
of Incompatibles, Eruptive Fevers, Weights and Measures, etc. Hand- 
somely bound in morocco, with side index, wallet, and flap. Price, $1.75 
net. 

FIFTH EDITION, THOROUGHLY REVISED. 

"This little book, that can be conveniently carried in the pocket, contains an immense 
amount of material. It is very useful, and as the name of the author of each prescription is 
given, is unusually reliable." — New York Medical Record. 

A COMPENDIUM OF INSANITY. ByJOHN B. Chapin, M.D., LL.D., 

■ician-in-Chief, Pennsylvania Hospital for the Insane; late Physician- 
Superintendent oPthe Willaid State Hospital, New York; Honorary Mem- 
ber of the Medico-Psychological Society of Great Britain, of the Society of 
Mental Medicine of Belgium, I2mo, 234 pages, Must, (loth, $1.25 net. 

The author has given, in a condensed and concise form, a compendium of 
fthe Mind, for the convenient use and aid of physicians and students. 
It contains a clear, concise Statement of the clinical aspects of the various ab- 
normal mental conditions, with directions as to the most approved methods of 
managing and treating the insane. 

he practical parts of Dr. Chapin' s book are what constitute its distinctive merit. We 
especially, however, to call attention to the fa< t that in the subje« t of the therapeutics 
of insanity the work is exceedingly valuable. The author has made a distinct addition to the 
literature of his specialty." — Philadelphia Mcdi<al Journal . 



3 6 W. B. SAUNDERS' 



AN OPERATION BLANK, with Lists of Instruments, etc. re- 
quired in Various Operations. Prepared by W. W. Keen, M. D., 
LL.D., Professor of Principles of Surgery in the Jefferson Medical Col- 
lege, Philadelphia. Price per Pad, containing Blanks for fifty operations, 
50 cents net. 

SECOND EDITION, REVISED FORM. 

A convenient blank, suitable for all operations, giving complete instructions 
regarding necessary preparation of patient, etc., with a full list of dressings and 
medicines to be employed. 

On the back of each blank is a list of instruments used — viz. general instru 
ments, etc., required for all operations ; and special instruments for surgery of 
the brain and spine, mouth and throat, abdomen, rectum, male and femah 
genito-urinary organs, the bones, etc. 

The whole forming a neat pad, arranged for hanging on the wall of a sur- 
geon's office or in the hospital operating-room. 

"Will serve a useful purpose for the surgeon in reminding him of the details of prepa- 
ration for the patient and the room as well as for the instruments, dressings, and antiseptics 
needed ." — New York Medical Record 

*' Covers about all that can be needed in any operation." — American Lancet. 

" The plan is a capital one." — Boston Medical and Surgical Journal. 

LABORATORY EXERCISES IN BOTANY. By Edson S. Bastin, 
M. A., Professor of Materia Medica and Botany in the Philadelphia Col- 
lege of Pharmacy. Octavo volume of 536 pages, 87 full-page plates. Price, 
Cloth, #2.50. 

This work is intended for the beginner and the advanced student, and it fully 
covers the structure of flowering plants, roots, ordinary stems, rhizomes, tubers, 
bulbs, leaves, flowers, fruits, and seeds. Particular attention is given to the gross 
and microscopical structure of plants, and to those used in medicine. Illustra- 
tions have freely been used to elucidate the text, and a complete index to facil- 
itate reference has been added. 

" There is no work like it in the pharmaceutical or botanical literature of this country, and 
we predict for it a wide circulation." — American Journal of Pharmacy. 

DIET IN SICKNESS AND IN HEALTH. By Mrs. Ernest Hart, 
formerly Student of the Faculty of Medicine of Paris and of the London 
School of Medicine for Women; with an Introduction by Sir Henry 
Thompson, F. R. C. S., M. D., London. 220 pages ; illustrated. Price, 
Cloth, J 1. 50. 

Useful to those who have to nurse, feed, and prescribe for the sick. In 
each case the accepted causation of the disease and the reasons for the special 
diet prescribed are briefly described. Medical men will find the dietaries and 
recipes practically useful, and likely to save them trouble in directing the dietetic 
treatment of patients. 



CATALOGUE OF MEDICAL WORKS. 



A MANUAL OF PHYSIOLOGY, with Practical Exercises. For 
Students and Practitioners. By G. N. Stewart, M. A., M. D., D. Sc, 

lately Examiner in Physiology, University of Aberdeen, and of the New 
Museums, Cambridge University ; Professor of Physiology in the Western 
Reserve University, Cleveland, Ohio. Handsome octavo volume of 848 
pages, with 300 illustrations in the text, and 5 colored plates. Price, Cloth, 
53.75 net. 

THIRD EDITION, REVISED. 

" It will make its way by sheer force of merit, and amply deserves to do so. It is one oj 
the very best English text-books on the subject." — London Lancet. 

M Of the many text-books of physiology published, we do not know of one that so nearly 
comes up to the ideal as does Professor Stewart's volume." — British Medical Journal. 

ESSENTIALS OF PHYSICAL DIAGNOSIS OF THE THORAX. 

By Arthur M. Corwin, A. M., M. D., Demonstrator of Physical Diagno- 
sis in the Rush Medical College, Chicago; Attending Physician to the 
Central Free Dispensary, Department of Rhinology, Laryngology, and 
Diseases of the Chest. 219 pages. Illustrated. Cloth, flexible covers. 
Price, $1.25 net. 

THIRD EDITION, THOROUGHLY REVISED AND ENLARGED. 
SYLLABUS OF OBSTETRICAL LECTURES in the Medical 
Department, University of Pennsylvania. By Richard C. Norris, 
A. M., M. D., Lecturer on Clinical and Operative Obstetrics, University 
of Pennsylvania. Third edition, thoroughly revised and enlarged. Crown 
8vo. Price, Cloth, interleaved for notes, $2.00 net. 

" This work is so far superior to others on the same subject that we take pleasure in call- 
ing attention briefly to its excellent features. It covers the subject thoroughly, and will 
prove invaluable buth to the student and the practitioner. The author has introduced a 
number of valuable hints which would only occur to one who was himself an experienced 
teacher of obstetrics. The subject-matter is clear, forcible, and modern. We are especially 
pleased with the portion devoted to the practical duties of the accoucheur, care of the child, 
etc. The paragraphs on antiseptics are admirable, there is no doubtful tone in the direc- 
tions given. No details are regarded as unimportant; no minor matters omitted. We ven- 
ture to say that even the old practitioner will find useful hints in this direction which he can- 
not afford to despise." — New York Medical Record. 

A SYLLABUS OF LECTURES ON THE PRACTICE OF SUR- 
GERY, arranged in conformity with " An American Text-Book 
of Surgery." By X. Si. NN, M. D., Ph. D., Professor of Surgery in Rush 
Medical College, Chicago, and in the Chicago Polyclinic. Price, $2.00. 

This work by so eminent an author, himself one of the contributors to 
"An American Text-Book of Surgery," will prove of exceptional value to 
the advanced student who hns adopted that work as his text-book. It is not 
only the syllabus of an unrivalled course of surgical practice, but it is also an 
epitome of or supplement to the larger work. 

" The author has evidently spared no pains in making his Syllabus thoroughly comprehen- 
sive, and har. added new matter and alluded to the most recent authors and operations. Full 
references are aUo given to all requisite details of surgical anatomy and pathology." — British 
Medical Journal, London. 



38 W. B. SAUNDERS' 



THE CARE OF THE BABY. By J. P. Crozer Griffith, M. D., 
Clinical Professor of Diseases of Children, University of Pennsylvania; 
Physician to the Children's Hospital', Philadelphia, etc. 404 pages, with 
67 illustrations in the text, and 5 plates. i2mo. Price, #1.50. 

SECOND EDITION, REVISED. 

A reliable guide not only for mothers, but also for medical students and 
practitioners whose opportunities for observing children have been limited. 

" The whole book is characterized by rare good sense, and is evidently written by a mas. 
ter hand. _ It can be read with benefit not only by mothers, but by medical students and by 
any practitioners who have not had large opportunities for observing children/'— American 
Journal of Obstetrics. 

THE NURSE'S DICTIONARY of Medical Terms and Nursing 
Treatment, containing Definitions of the Principal Medical and Nursing 
Terms, Abbreviations, and Physiological Names, and Descriptions of the 
Instruments, Drugs, Diseases, Accidents, Treatments, Operations, Foods, 
Appliances, etc. encountered in the ward or the sick-room. By Honnor 
Morten, author of " How to Become a Nurse," " Sketches of Hospital 
Life," etc. i6mo, 140 pages. Price, Cloth, $1.00. 

This little volume is intended for use merely as a small reference-book which 
can be consulted at the bedside or in the ward. It gives sufficient explanation 
to the nurse to enable her to comprehend a case until she has leisure to look up 
larger and fuller works on the subject. 

DIET LISTS AND SICK-ROOM DIETARY. By Jerome B. Thomas, 
M. D., Visiting Physician to the Home for Friendless Women and Children 
and to the Newsboys' Home ; Assistant Visiting Physician to the Kings 
County Hospital ; Assistant Bacteriologist, Brooklyn Health Department. 
Price, Cloth, $1.50 (Send for specimen List.) 

One hundred and sixty detachable (perforated) diet lists for Albuminuria, 
Anaemia and Debility, Constipation, Diabetes, Diarrhoea, Dyspepsia, Fevers, 
Gout or Uric- Acid Diathesis, Obesity, and Tuberculosis. Also forty detachable 
sheets of Sick-Room Dietary, containing full instructions for preparation of 
easily-digested foods necessary for invalids. Each list is numbered only, the 
disease for which it is to be used in no case being mentioned, an index key 
being reserved for the physician's private use. 

DIETS FOR INFANTS AND CHILDREN IN HEALTH AND 
IN DISEASE. By Louis Starr, M. D., Editor of " An American 
Text-Book of the Diseases of Children. ,, 230 blanks (pocket-book size), 
perforated and neatly bound in flexible morocco. Price, $1.25 net. 

The first series of blanks are prepared for the first seven months of infant 
life; each blank indicates the ingredients, but not the quantities, of the food, 
the latter directions being left for the physician. After the seventh month, 
modifications being less necessary, the diet lists are printed in full. Formula 
to" trie preparation of diluents and foods are appended. 



CATALOGUE OF MEDICAL WORKS. 39 

HOW TO EXAMINE FOR LIFE INSURANCE. By Jofn M. 
Keating, M. D., Fellow of the College of Physicians and Surgeons of 
Philadelphia; Vice-President of the American Pediatric Society; Ex- 
President of the Association of Life Insurance Medical Directors. Royal 
8vo, 211 pages, with two large half-tone illustrations, and a plate prepared 
by Dr. McClellan from special dissections ; also, numerous cuts to elucidate 
the text. Third edition. Price, Cloth, $2.00 net. 

" This is by far the most useful book which has yet appeared on insurance examination, a 
subject of growing interest and importance. Not the least valuable portion of the volume is 
Part II., which consists of instructions issued to their examining physicians by twenty-four 
representative companies of this country. As the proofs of these instructions were corrected 
by the directors of the companies, they form the latest instructions obtainable. If for these 
alone, the book should be at the right hand of every physician interested in this special branch 
of medical science." — The Medical News, Philadelphia. 

NURSING: ITS PRINCIPLES AND PRACTICE. By Isabel 

Adams Hampton, Graduate of the New York Training School for 
Nurses attached to Bellevue Hospital; Superintendent of Nurses and 
Principal of the Training School for Nurses, Johns Hopkins Hospital, 
Baltimore, Md. ; late Superintendent of Nurses, Illinois Training School 
for Nurses, Chicago, 111. In one very handsome i2mo volume of 512 
pages, illustrated. Price, Cloth, $2. 00 net. 

SECOND EDITION, REVISED AND ENLARGED. 

This original work on the important subject of nursing is at once comprehensive 
and systematic. It is written in a clear, accurate, and readable style, suitable 
alike to the student and the lay reader. Such a work has long been a desidera- 
tum with those entrusted with the management of hospitals and the instruction of 
nurses in training-schools. It is also of especial value to the graduated nurse 
who desires to acquire a practical working knowledge of the care of the sick 
and the hygiene of the sick-room. 

OBSTETRIC ACCIDENTS, EMERGENCIES, AND OPERA- 
TIONS. By L. CH. Boisliniere, lit. D., late Emeritus Professor of 
Obstetrics in the St. Louis Medical College. 381 pages, handsomely illus- 
trated. Price, $2.00 net. 

" For the use of the practitioner who, when away from home, has not the 
opportunity of consulting a library or of calling a friend in consultation. He 
then, being thrown upon his own resources, will find this book of benefit in 
guiding and assisting him in emergencies." 

INFANT'S WEIGHT CHART. Designed by J. P. Crozer Griffith, 
M. D., Clinical Professor of Diseases of Children in the University of Penn- 
sylvania. 25 charts in each pad. Price per pad, 50 cents net. 

A convenient blank for keeping a record of the child's weight during the first 
two years of life. Printed on each chart is a curve representing the average weight 
of a healthy infant, so that any deviation from the normal can readily be detected 




Saunders' 
New Series 
of Manuals 



for Students 
and 
Practitioners* 



THAT there exists a need for thoroughly reliable hand-books on the leading 
branches of Medicine and Surgery is a fact amply demonstrated by the 
favor with which the SAUNDERS NEW SERIES OF MANUALS have been 
received by medical students and practitioners and by the Medical Press. 
These manuals are not merely condensations from present literature, but 
are ably written by well-known authors and practitioners, most of them being 
teachers in representative American colleges. Each volume is concisely and 
authoritatively written and exhaustive in detail, without being encumbered 
with the introduction of " cases," which so largely expand the ordinary text- 
book. These manuals will therefore form an admirable collection of advanced 
lectures, useful alike to the medical student and the practitioner : to the latter, 
too busy to search through page after page of elaborate treatises for what he 
wants to know, they will prove of inestimable value ; to the former they will 
afford safe guides to the essential points of study. 

The SAUNDERS NEW SERIES OF MANUALS are conceded to be 
superior to any similar books now on the market. No other manuals afford so 
much information in such a concise and available form. A liberal expenditure 
has enabled the publisher to render the mechanical portion of the work worthy 
of the high literary standard attained by these books. 

Any of these Manuals will be mailed on receipt of price (see next page 
for List). 



SAUNDERS' NEW SERIES OE MANUALS, 



VOLUMES PUBLISHED. 



PHYSIOLOGY. By Joseph Howard Raymond, A. M., M. D., Professor 
of Physiology and Hygiene and Lecturer on Gynecology in the Long 
Island College Hospital, etc. Price, $1.25 net. 

SURGERY, General and Operative. By John Chalmers DaCosta, 
M. D., Professor of Clinical Surgery, Jefferson Medical College, Philadel- 
phia. Second edition, revised and greatly enlarged. Octavo, 911 pages, 
3S6 illustrations. Cloth, $4.00 net ; Half-Morocco, $5.00 net. 

DOSE-BOOK AND MANUAL OF PRESCRIPTION- WRITING. 

By E. Q. Thornton, M. D., Demonstrator of Therapeutics, Jefferson 
Medical College, Philadelphia. Price, $1.25 net. 

MEDICAL JURISPRUDENCE. By Henry C. Chapman, M. D., Pro- 
fessor of Institutes of Medicine and Medical Jurisprudence in the Jeffer- 
son Medical College of Philadelphia, etc Price, $1.50 net. 

SURGICAL ASEPSIS. By Carl Beck, M.D., Surgeon to St. Mark's 
Hospital and to the German Poliklinik ; Instructor in Surgery, New York 
Post-Graduate Medical School, etc. Price, $1.25 net. 

MANUAL OF ANATOMY. By Irving S. Haynes, M.D., Adjunct 
Professor of Anatomy and Demonstrator of Anatomy, Medical Department 
of the New York University, etc. Price, $2.50 net. 

SYPHILIS AND THE VENEREAL DISEASES. By James 
Nevins Hyde, M. D., Professor of Skin and Venereal Diseases, and 
Frank H. Montgomery, M. D., Lecturer on Dermatology and Genito- 
urinary Diseases in Rush Medical College, Chicago. Price, $2.50 net. 

PRACTICE OF MEDICINE. By George Roe Lockwood, M. D., 
Professor of Practice in the Woman's Medical College of the New York 
Infirmary, etc. Price, $2.50 net. 

OBSTETRICS. By W. A. Newman Dorland, M. D., Assistant Demon- 
strator of Obstetrics, University of Pennsylvania ; Chief of Gynecological 
Dispensary, Pennsylvania Hospital. Price, $2.50 net. 

DISEASES OF WOMEN. By J. Bland Sutton, F. R. C. S., Assistant 
Surgeon to the Middlesex Hospital, and Surgeon to the Chelsea Hospital 
for Women, London; and Arthur E. Giles, M. D., B. Sc. Lond., F. R. C. S. 
Edin., Assistant Surgeon to the Chelsea Hospital for Women, London. 436 
pages, handsomely illustrated. Price, $2.50 net. 

IN PREPARATION. 

NERVOUS DISEASES. By Chari.es W. Burr, M. D„ Clinical Profes- 
sor of Nervous Diseases, Medico-Chirurgical College, Philadelphia, etc. 

%* There will be published in the same series, at short intervals, carefully prepared works 
on various subjects, by prominent specialists. 



SAUNDERS' QUESTION COMPENDS. 

Arranged in Question and Answer Form, 

THE LATEST, MOST COMPLETE, and BEST ILLUSTRATED 
SERIES OF COMPENDS EVER ISSUED. 



Now the Standard Authorities in Medical Literature 



Students and Practitioners in every City of the United 
States and Canada. 



THE REASON WHY. 

They are the advance guard of " Student's Helps " — that DO HELP; they are 
the leaders in their special line, well and authoritatively written by able men, 
who, as teachers in the large colleges, ktiow exactly what is wanted by a student 
preparing for his examinations. The judgment exercised in the selection of 
authors is fully demonstrated by their professional elevation. Chosen from the 
ranks of Demonstrators, Quiz-masters, and Assistants, most of them have be- 
come Professors and Lecturers in their respective colleges. 

Each book is of convenient size (5x7 inches), containing on an average 250 
pages, profusely illustrated, and elegantly printed in clear, readable type, on 
fine paper. 

The entire series, numbering twenty- four subjects, has been kept thoroughly 
revised and enlarged when necessary, many of them being in their fourth and 
fifth editions. 

TO SUM UP. 

Although there are numerous other Quizzes, Manuals, Aids, etc. in the mar- 
ket, none of them approach the " Blue Series of Question Compends;" and 
the claim is made for the following points of excellence : 

1. Professional distinction and reputation of authors. 

2. Conciseness, clearness, and soundness of treatment. 

3. Size of type and quality of paper and binding. 

%* Any of these Compends will be mailed on receipt of price (see next 

page for List). 

42 









SAUNDERS' QUESTION-COMPEND SERIES. 



Price, Cloth, $J*00 per copy, except when otherwise noted* 

1. ESSENTIALS OF PHYSIOLOGY. 4th edition. Illustrated. Revised and enlarged. 

By H. A. Hare, M. D. (Price, $1.00 net.) 

2. ESSENTIALS OF SURGERY. 7th edition, with a chapter on Appendicitis. 90 illus- 

trations. By Edward Martin, M. D. (Price, £t.oo net.) 

3. ESSENTIALS OF ANATOMY. 6th edition, thoroughly revised. 151 illustrations. 

By Charles B. Nancrede, M. D. (Price, $1.00 net.) 

4. ESSENTIALS OF MEDICAL CHEMISTRY, ORGANIC AND INORGANIC. 

5th edition, revised, with an Appendix. By Lawrence Wolff, M. D. ($1. 00 net.) 

5. ESSENTIALS OF OBSTETRICS. 4th edition, revised and enlarged. 75 illustra- 

tions. By W. Easterly Ashton, M. D. 

6. ESSENTIALS OF PATHOLOGY AND MORBID ANATOMY. 7 th thousand. 

46 illustrations. By C. E. Armand Semple, M. D. 

7. ESSENTIALS OF MATERIA MEDICA, THERAPEUTICS, AND PRE- 

SCRIPTION-WRITING. 5th edition. By Henry Morris, M. D. 

8. g. ESSENTIALS OF PRACTICE OF MEDICINE. By Henry Morris, M.D. 

An Appendix on Urine Kxamin ation. Illustrated. By Lawrence Wolff, M. D. 
3d edition, enlarged by some 300 Essential Formulae, selected from eminent authori- 
ties, by W.m. M. Powell, M. D. (Double number, price $2.00.) 

10. ESSENTIALS OF GYNECOLOGY. 4th edition, revised. With 62 illustrations. 

By Edwin B. Cragin, M. D. 

11. ESSENTIALS OF DISEASES OF THE SKIN. 4th edition, revised and enlarged. 

71 letter-press cuts and 15 half-tone illustrations. By Henry W. Stelwagon, M.D. 
(Price, $1.00 net.) 

12. ESSENTIALS OF MINOR SURGERY, BANDAGING, AND VENEREAL 

DISEASES. 2d edition, revised and enlarged. 78 illustrations. By Edward 
Martin, M. D. 

13. ESSENTIALS OF LEGAL MEDICINE, TOXICOLOGY, AND HYGIENE. 

130 illustrations. By C. E. Armand Semple, M. D. 

14. ESSENTIALS OF DISEASES OF THE EYE, NOSE, AND THROAT. 124 

illustrations. 2-i edition, revised. By Edward Jackson, M. D., and E. Baldwin 
Glkason, M. D. 

15. ESSENTIALS OF DISEASES OF CHILDREN. 2d edition. By William M. 

Powell, M. D. 

16. ESSENTIALS OF EXAMINATION OF URINE. Colored " Vogel Scale," 

and numerous illustrations. By Lawrence Wolff, M. D.. (Price, 75 cents.) 

17. ESSENTIALS OF DIAGNOSIS. 2d edition, thoroughly revised. 60 illustrations. 

By S. - OH EN, M. I)., and A. A. Eshner, M. D. (Price, $1. 00 net.) 

18. ESSENTIALS OF PRACTICE OF PHARMACY. 2d edition, revised. By L. 

■.VRE. 

20. ESSENTIALS OF BACTERIOLOGY. 3d edition. 82 illustrations. By M. V. 

Ball, M D. 

21. ESSENTIALS OF NERVOUS DISEASES AND INSANITY. 48 illustrations. 

3d edition, revised. By John C. Shaw, M. D. 

22. ESSENTIALS OF MEDICAL PHYSICS. 155 illustrations. 2d edition, revised. 

By Fred J. Bro< kway, M. D. (Price, $1.00 net.) 

23. ESSENTIALS OF MEDICAL ELECTRICITY. 65 illustrations. By David D. 

ART, M. 1).. and Kdwahd S. Lawrance, M. D. 

24. ESSENTIALS OF DISEASES OF THE EAR. 114 illustrations. 2d edition, re- 

vised and enlarged. By E. Baldwin Gleason, M. D. 

43 



Some of the Books in Preparation for 
Publication during 1900. 



AMERICAN Text=Book of Pa= 
thology. 

Edited by Ludvig Hektoen, M.D., Pro- 
fessor of Pathology, Rush Medical College, 
Chicago; and David Riesman, M.D., De- 
monstrator of Pathological Histology, Uni- 
versity of Pennsylvania. 

AMERICAN Text=Book of Legal 
Medicine and Toxicology. 

Edited by Frederick Peterson, M.D., 
Chief of Clinic, Nervous Department, College 
of Physicians and Surgeons, New York City ; 
and Walter S. Haines, M.D., Professor of 
Chemistry, Pharmacy, and Toxicology, Rush 
Medical College, Chicago. 

BECK— Fractures. 

By Carl Beck, M.D., Professor of Surgery 
in the N. Y. School of Clinical Medicine. 

BÖHM, DAVIDOFF, and HU= 
BER— A Text=Book of Human 
Histology. 

Including Microscopic Technic. By 
Dr. A. A. Böhm and Dr. M. von Davidoff, 
of the Anatomical Institute of Munich, and 
G. C. Huber,M.D., Junior Professor of Anat- 
omy and Histology, University of Michigan, 
Ann Arbor. 

EICH HORST- A Text=Book of 
the Practice of Medicine. 

By Dr. Herman Eichhorst, Professor of 
Special Pathology and Therapeutics and Di- 
rector of the Medical Clinic, University of 
Zurich. Translated and edited by Augustus 
A. Eshner, M.D , Professor of Clinical 
Medicine in the Philadelphia Polyclinic. 

FRIEDRICH — Rhinology, La= 
ryngology, and Otology in 
their Relations to General 
Medicine. 

By Dr. E. P. Friedrich, of the Univer- 
sity of Leipsig. 

LEVY AND KLEMPERER — 
The Elements of Clinical Bac= 
teriology. 

By Dr. Ernst Levy, Professor in the 
University of Strassburg, and Dr. Felix 
Klemperer, Privat-Docent in the Univer- 
sity of Strassburg. Translated and edited 
by Augustus A. Eshner, M.D., Professor 
of Clinical Medicine in the Philadelphia Poly- 
clinic. Just Ready. Cloth, $2 5c net. 



McFARLAND— A Text=Book of 
Pathology. 

By Joseph McFarland, M.D., Professor 
of Pathology and Bacteriology, Medico-Chi- 
rurgical College, Philadelphia. 

OGDEN — Clinical Examination 
of the Urine. 

By J. Bergen Ogden, M.D., Assistant in 
Chemistry, Harvard Medical School. 

PYLE— A Manual of Personal 
Hygiene. 

Edited by Walter L. Pyle, M.D., Assis- 
tant Surgeon to Wills' Eye Hospital, Philada. 

SCUDDER— The Treatment of 
Fractures. 

By Charles L. Scudder, M.D., Assistant 
in Clinical and Operative Surgery, Harvard 
University. 

SENN— Practical Surgery. 

By Nicholas Senn, M.D., Ph.D., LL.D., 

Professor of the Practice of Surgery and of 
Clinical Surgery, Rush Medical College, Chi- 
cago. Octavo volume of about 800 pages, 
profusely illustrated. 

The Pathology and Treatment 
of Tumors. 

By Nicholas Senn, M.D., Ph.D., LL.D., 

Professor of the Practice of Surgery and of 
Clinical Surgery, Rush Medical College, Chi- 
cago. A New and Thoroughly Revised Edi- 
tion in preparation. 

STENGEL AND WHITE — The 
Blood in its Clinical and Patho= 
logical Relations. 

By Alfred Stengel, M.D., Professor of 
Clinical Medicine, University of Pennsyl- 
vania; and C. Y. White, M.D., Instruc- 
tor in Clinical Medicine, University of Penn- 
sylvania. 

STEVENS— The Physical Diag= 
nosis of Diseases of the Chest. 

By A. A. Stevens, A.M., M.D., Lecturer 
on Terminology, and Instructor in Physical 
Diagnosis, University of Pennsylvania. 

STONEY — Surgical Technique 
for Nurses. 

By Emily A. M. Stoney, late Superin- 
tendent of the Training Schools for Nurses, 
Carney Hospital, South Boston, Mass. 



MAY 31 1900 






VOLUMES NOW READY. 

Atlas of Internal Medicine and Clinical Diagnosis. By 

Dr. Chr. Jakob, of Erlangen. Edited by Augustus A. 
Eshner, M.D., Professor of Clinical Medicine in the Phila- 
delphia Polyclinic ; Attending Physician to the Philadelphia 
Hospital. 68 colored plates. Cloth, $3.00 net. 

Atlas of Legal Medicine. By Dr. E. von Hofmann, of 
Vienna. Edited by Frederick Peterson, M.D. , Clinical 
Professor of Mental Diseases, Woman's Medical College, New 
York; Chief of Clinic, Nervous Dept., College of Physicians 
and Surgeons, New York. With 120 colored figures on 56 
plates, and 193 half-tone illustrations. Cloth, $3.50 net. 

Atlas of Diseases of the Larynx. By Dr. L Grünwald, 
of Munich. Edited by Charles P. Grayson, M.D., Lec- 
turer on Laryngology and Rhinology in the University of 
Pennsylvania; Physician-in -Charge, Throat and Nose Depart- 
ment, Hospital of the University of Penna. With 107 colored 
figures on 44 plates, and 25 text-illustrations. Cloth, $2.50 net. 

Atlas of Operative Surgery. By Dr. O. Zuckerkandl, of 
Vienna. Edited by J. Chalmers DaCosta, M.D., Clinical 
Professor of Surgery, Jefferson Medical College, Philadelphia ; 
Surgeon to the Philadelphia Hospital. With 24 colored plates, 
and 217 illustrations in the text. Cloth, $3.00 net. 

Atlas of Syphilis and the Venereal Diseases. By Prof. 
Dr. Franz Mracek, of Vienna. Edited by L. Bolton 
Bangs, M.D., late Professor of Genito-Urinary and Venereal 
Diseases, New York Post-Graduate Medical School and Hos- 
pital. With 71 colored plates from original water-colors by 
A. Schmitson. Cloth, $3.50 net. 

Atlas of External Diseases of the Eye.— By Dr. O. Haab, 
of Zurich. Edited by G. E. de Schweinitz, M. D., Profes- 
sor of Ophthalmology, Jefferson MedicaJ College, Philadel- 
phia. With 76 colored illustrations on 40 plates. Cloth, 
$3.00 net. 

Atlas of Skin Diseases. — By Prof. Dr. Franz Mracek, of 
Vienna. Edited by Henry W. Stelwagon, M. D., Clinical 
Professor of Dermatology, Jefferson Medical College, Phila- 
delphia. With 63 colored plates and 39 beautiful half-tone 
illustrations. Cloth, $3.50 net. 

IN PREPARATION. 

Atlas of Pathological Histology. Atlas of Operative Gynecology. 

Atlas of Orthopedic Surgery. Atlas of Psychiatry. 

Atlas of General Surgery. Atlas of Diseases of the Ear.