Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 89

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189

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VOLUME XIII. 605 pages, with 6 plates, 201 figures, ax 1 colored chart.

Studies in Genito-Urinary Surgery.

The Seven-Glass Test. By HUGH H. YOUNG, M. D.

The Possibility of Avoiding Confusion by Bacillus smegmatis (Soya bacillus) In the Diagnosis of Urinary and Genital Tuberculosis u Experimental Study. By HUGH H. YOUNG, M. D., and Joms CHURCHMAN, M. D.

Urethral Diverticula In the Male. By STEPHEN H. WATTS, M. D. An Unusual Case of Urethrorrhagia. By H. A. FOWLER, M. D. Paraurethritis. By JOHN W. CHURCHMAN, M. D.

Use of Ointments in the Urethra In the Treatment of Chronle Urethra HUGH H. YOUNG, M. D.

Treatment of Stricture of the Urethra. By HUGH H. YOUNG, M. D. uf JOHN T. GERAGHTY, M. D.

The Treatment of Impermeable Stricture of the Urethra. By HUGE E YOUNG, M. D.

(

The Treatment of Bacteriuria by Internal Medication. By JOBS i CHURCHMAN, M. D.

Use of the Cystoscope in the Diagnosis of Diseases of the Prostate. E HUGH H. YOUNG, M. D.

Chronic Prostatitis. An Analysis of 358 Cases. By HOGH H. Yors M. D., JOHN T. GERAGHTY, M. D., and A. R. STEVENS, M. D. Modern Method for the Performance of Perineal Lithotomy. By Hoc E YOUNG, M. D.

Operative Treatment of Vesical Diverticula. By HUGH H. YOUNG, M. D Case of Double Renal Pelvis and Bifid Ureter. By HUGH H. YOUNG, Y! Pyonephrosis Due to Bacillus Typhosus. By HUGH H. YOUNG, M. D. IN LOUIS C. LEHR, M. D.

The Use of the X-ray In the Diagnosis of Renal and Ureteral Calcull : F. H. BAETJER, M. D. Nephritis and Hæmaturia. By H. A. FOWLER, M. D.

The Microscopic Structure of Urinary Calculi of Oxalate of Lime I B, M. Cystinuria with Formation of Calcull. By H. A. FOWLER, M. D. Post-Traumatic Atrophy of the Testicle. By JOHN W. CHURCHMAN, M. A Description of the Dispensary for Treatment of Genito-Urinary Surla Cases at the Johns Hopkins Hospital. By HUGH H. YOUNG, M.D.

VOLUME XIV. 632 pages, with 97 figures.

Studies in Genito-Urinary Surgery.

The Treatment of Prostatic Hypertrophy by Conservative Perineal Pret tatectomy. An analysis of cases and results based on a detailed report of 145 cases. By HUGH H. YOUNG, M. D.

Recto-Urethral Fistula. Description of New Procedures for their Pr vention and Cure. By HUGH H. YOUNG, M. D. The Early Diagnosis and Radical Cure of Carcinoma of the Prostate, belay a study of 40 cases and presentation of a radical operation whis was carried out in four cases. By HUGH H. YOUNG, M. D.

VOLUME XV. 542 pages, with 87 illustrations.

Twelve papers on pneumonia. By DRS. CHATARD, FABYAN, EMERSE, MARSHALL, MCCRAE, STEINER, HOWARD and HAINES. A Study of Diarrhea in Children. By J. H. MASON KNOX. JR., M. D. E. EDWIN H. SCHORER, M. D.

Skin Transplantation. By JOHN STAIGE DAVIS, M. D. Epidemic Cerebrospinal Meningitis and Serum Therapy at the Johns Hopkins Hospital. By FRANK J. SLADEN, M. D.

VOLUME XVI. 670 pages with 151 figures. (Now in press. Studies in the Experimental Production of Tuberculosis in the Gerlo Urinary Organs. By GEORGE WALKER, M. D. The Effect on Breeding of the Removal of the Prostate Gland or of 12 Vesiculæ Seminales, or of Both; together with Observations on the Condition of the Testes after such Operations on White Rats By GEORGE WALKER, M. D. Scalping Accidents. By JOHN STAIGE DAVIS, M. D. Obstruction of the Inferior Vena Cava with a Report of Eighteen Cass. By J. HALL PLEASANTS, M. D. Physiological and Pharmacological Studies on Cardiac Tonicity in Mar- mals. By PERCIVAL DOUGLAS CAMERON, M. D.

The set of sixteen volumes will be sold, bound in cloth, for ninety dollars, net. Volume II will not be sold separately. Volumes I, IL IV, V, VI, VII, VIII, X, XI, XII, XIII, XIV, XV, XVI will be sold for $5.00, net, bound in paper, and $5.50, net, bound in cloth. Volume II will be sold for ten dollars, net.

Orders should be addressed to The Johns Hopkins Press, Baltimore, Xa

a year (foreign postage, 50 cents), may be addressed to the publishers, THE JOHNS HOPKINS PRESS. BALTIMORE : single copies will be an"

The Johns Hopkins Hospital Bulletins are issued monthly. They are printed by the LORD BALTIMORE PRESS, Baltimore.

Subscriptions, $2.00 mail for twenty-five cents each. Single copies may also be procured from the BALTIMORE NEWS CO., Baltimore.

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BULLETIN

THE LIBRARY 11

RECEIVED

THE JOHNS HOPKINS HOSPITAL

Entered as Second-Class Matter at the Baltimore, Maryland, Postodice.

'ol. XXII .- No. 240.]

BALTIMORE, MARCH, 1911.

[Price, 25 Cents

CONTENTS.

PAGE

Acute Tuberculous Endaortitis. (Illustrated.) By PAUL G. WOOLLEY, M. D.

yphoid Spine; with the Report of Two Additional Cases with Bony Changes in the Vertebra.

By THOMAS. MCCRAE, M. D., F. R. C. P. .

By WILLIAM S. THAYER, M. D., and ROGER S. MORRIS, M. D. 85

Notes on New Books .

By H. P. PARKER, M. D., and H. H. HAZEN, M. D. . · · 79

Books Received

CIRRHOSIS OF THE LIVER. FIVE DIFFERENT TYPES OF LESIONS FROM WHICH IT MAY ARISE.'

By F. B. MALLORY, M. D.

(From the Pathological Laboratory of the Boston City Hospital.)

Introduction .- In some organs the late stages of certain sions have received more attention than the beginnings of nese lesions. The emphasis has been placed on the wrong end f the process. This statement is particularly true of the flammatory changes in the liver and in the central nervous 'stem.

Now, in order to understand a pathological process, it is cessary to find and study its beginning and to trace its logical development. It is with this view in mind that I 1] present to you to-night a study of five different types of ly lesions of the liver so that you may see for yourselves the late stages of these lesions resulting in sclerosis would be classed under the term cirrhosis. It will enable you ter to appreciate what very different kinds of pathological tesses the term covers.

shall not present these different types of lesions in the of their relative frequency and importance, but in such ence as will throw most light on certain features common nem all, especially the changes in the connective tissue na.

the clinician the term cirrhosis usually means a chronic, ressive, destructive lesion of the liver combined with re- ad before the Johns Hopkins Hospital Medical Society, Nov. 0.

parative activity and contraction on the part of the connective tissue. This contraction of the connective tissue may lead to obstruction of bile ducts, causing more or less jaundice, and to interference with the flow of blood through the blood vessels resulting in portal congestion and ascites.

The pathologist uses the term cirrhosis in a broader sense. He applies it to all sclerosed conditions of the liver, whether progressive or not, in which destruction of liver cells is asso- ciated with real or apparent increase of connective tissue. It is from the pathologists' point of view that I approach the subject.

I shall have to refer first to three pathological conditions which may complicate some of the changes terminating in sclerosis.

The first of these, fatty infiltration, is common but of little significance except that under certain conditions the fat pres- ent in the cells seems to serve as nutrition and thus aids to protect to some extent the liver cells containing it from under- going necrosis as readily as surrounding cells containing none.

The second is chronic passive congestion. When this con- dition is uncomplicated it seems not to cause disappearance of the liver cells around the hepatic vein in the lobule as is gen- erally taught. The cells disappear as the result of a toxic necrosis complicated with hemorrhage. If, as is usually the

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irythema Multiforme Iris during the Course of Typhoid Fever.

· 96

· 99

irrhosis of the Liver. Five Different Types of Lesions from which it May Arise. (Illustrated.) By F. B. MALLORY, M. D. 69 :

Report of a Case of Extensive Tiersch Skin Graft. (Illustrated.) By W. D. GATCH, M. D. 184 Two Cases of Congenital Haemolytic Jaundice with Splenomegaly. Observations on Hemolytic Jaundice.

JOHNS HOPKINS HOSPITAL BULLETIN.

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case, the necrosis is recent, due to a terminal infection, it is easy to demonstrate the necrotic liver cells in the midst of the red blood corpuscles filling the trabecular spaces. If the necrosis is of longer standing the necrotic cells will have par- tially or entirely disappeared under the solvent action of polynuclear and endothelial' leucocytes. The trabecular spaces, dilated and filled with blood, are readily mistaken for distended sinusoids. As a matter of fact the sinusoids are usually more or less compressed as the result of the hemor- rhage. In time the hemorrhage disappears and the sinusoids again dilate. Owing to the condition of congestion the liver cells do not regenerate. Consequently, in time, the trabecular spaces shrink and the connective tissue contracts and thickens, although it does not increase in amount, and the liver by its consistence may suggest a mild uniform type of sclerosis.

The third and most important pathological condition to which I must refer is general bile stasis due usually to obstruc- tion of the common bile duct by a calculus or by a tumor. This condition leads to marked dilatation of the bile capil- laries around the hepatic vein, to rupture of them, and to the escape of masses of inspissated bile into the lymph space be- tween the liver cells and the wall of the sinusoid. Here the bile is incorporated by endothelial leucocytes and gradually dissolved. After solution it seems to pass, perhaps by osmosis, directly into the blood stream, not along the lymph channels to the thoracic duct. Apparently uncomplicated bile stasis does not result in any sclerotic process around the hepatic veins where the chief lesion is located and it certainly does not around the portal vessels.

I. TOXIC CIRRHOSIS.

A fairly common affection of the liver is necrosis of the cells around the hepatic vein, the so-called central necrosis, due to toxins in the circulation. It is a frequent terminal lesion. Occasionally the necrosis is limited more or less definitely to the midzonal region. This type of lesion may be slight, or very extensive involving nearly all the cells in a lobule. It is usually quite uniformly distributed throughout the whole liver. In the milder degrees of necrosis the liver cells are quickly invaded by polymorphonuclear or endothelial leucocytes (Fig. 1) or by both, dissolved, and removed. If the patient survives, the liver cells usually regenerate and the liver lobules are restored to their normal appearance. Some- times, however, the liver cells do not regenerate. Then the

"The endothelial leucocyte arises by proliferation and desqua- mation of endothelial cells lining blood and lymph vessels. It emigrates from vessels like the other leucocytes, multiplies by mitosis in the vessels and tissues like the lymphocyte, and possesses one especially distinguishing property, that of being under certain circumstances very phagocytic for the other leuco- cytes as well as being able to incorporate red blood corpuscles, various microorganisms, and foreign bodies of all sorts. This leucocyte is known by various names, the large mononuclear of the blood, the nongranular leucocyte, the macrophage, etc. Its origin is best studied in the early lesions of typhoid fever, in very young miliary tubercles, and experimentally by the subcutaneous injection of agar.

walls of the sinusoids collapse, the lobules shrink, and zie connective tissue around the hepatic veins appears thickene. just as may happen in connection with chronic passive aus- gestion. Experimentally it has been shown that this form ?. lesion may be produced by chloroform narcosis and that ze generation will quickly take place.

Occasionally this type of necrosis is very extensive so thr in some lobules every liver cell is killed. If the patient su: vives, the necrotic liver cells are invaded and, so quickly moved by the action of leucocytes (Figs. 2 and 3) that in fre or six days the liver will diminish in weight from 1500 griz: to 600 or 500 grams or even less. The liver will be perfecter uniformly lessened in size, and flabby to the touch. This ? the early stage of so-called acute yellow and red atrophy the liver. If the patient still survives, active regenerati: takes place, the liver cells giving rise to new liver cella, blå duct epithelium producing bile duct epithelium. As a Ns .: of this active regeneration those parts of the liver where liv .: cells persist rapidly enlarge and the lobules assume more e: less completely their former shape, or perhaps undergo cez- pensatory hypertrophy. These are the yellow bile-staite! areas of acute yellow atrophy of several weeks' duration. i: those parts of the liver where all the liver cells were killed, de bile ducts (Figs. 4 and 5) grow a third or half the way ?- wards the hepatic vein and then stop. They do not produse liver cells. The lobules are much diminished in size, tx leucocytes disappear from the trabecular spaces, the sinusoid: are dilated. These are the red parts of a case of acute yellow atrophy of two to several weeks' standing.

This type of lesion teaches two things that are of important: in considering the other types of lesions which result in cirrhosis. First, that simple necrosis of liver cells withes: injury to blood vessels and connective tissue stroma, does Mi result in proliferation of connective tissue. The connective tissue which is there shrinks together and thickens, leading # an apparent but not real increase of it. Second, that lite" cells regenerate only from liver cells. The bile ducts length: owing to proliferation of bile epithelium but they cannot forz liver cells.

Various degrees of this series of lesions known under thre different names, central necrosis, acute yellow and red atropty. and cirrhosis, are not, I believe, so infrequent as is gener :: supposed. It ought to be possible to recognize the resultic: type of cirrhosis long after the acute lesion is over even with- out a clinical history to help. Two points are of diagnostie- value: the very irregular distribution of the connective tisce as seen on gross examination: and the preservation of the shape of the lobules, much shrunken, in the sclerosed para. Whether or not continued contraction of the connective tisz may in time lead to obstruction of bile ducts and blood res- sels resulting in jaundice and ascites, I am at present unab- to say.

It is of interest that this type of cirrhosis is of acute origin: therein it differs from the four other varieties which are all of a more or less chronic nature.

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II. INFECTIOUS CIRRHOSIS.

e second type of cirrhosis I shall term infectious cirrhosis se it is due to the presence of bacteria in the lesions. In xperience it is comparatively rare. Bacteria may and do access to the liver by direct continuity and through the ic artery, the portal vein, and the bile ducts. It is only ection through the bile ducts that I shall speak here, as eems to be the only form of bacterial infection which to a dictinct form of cirrhosis.

'ection through the bile ducts, when there is bile stasis gall stone or other obstruction, not infrequently leads to ion with various bacteria and to necrosis (Fig. 9), ss-formation, and death. A rarer form of invasion some- takes place along apparently normal bile ducts and leads ery characteristic type of cirrhosis. It is to this variety ection that I wish to call your attention.

experience of the early stages of the process is limited 'o livers which agree very closely in their gross and scopic appearances although the infection is of longer du- i in one than in the other. Both were from children, a of twelve and a boy ' of three. At post mortem examina- the livers were two to three times the normal size and increased in consistence. The surface and cut section smooth. Clinically jaundice and enlargement of the were prominent symptoms.

at the infecting organism is I do not know as infection .ot suspected and no cultures were taken. The bacteria at in the acutest lesions in the girl are slender bacilli 7). In many ways the lesions in the liver may be said respond to the chronic process produced in the kidney by lon bacillus.

ection is spread chiefly through the bile ducts but the or- ns have also invaded the surrounding connective tissue re spreading through it. The pathological changes are ed almost entirely to the region around the portal ves- d are extending quite uniformly toward the hepatic vein 1 lobule. The lesion is by nature chronic. It is active preading in many places; quiescent and healing in

bile ducts (Fig. 8) frequently show more or less dila- and in some places are filled with polymorphonuclear tes (Fig. 10), in other places with endothelial leuco- Fig. 8). Here and there where the process is active duct epithelium is necrotic or gone and the exudation ding into the surrounding tissue (Fig. 10). Here the , lead to necrosis of the liver cells, of the blood vessel lium and of the fibroblasts, and to an acute inflamma- date consisting of polymorphonuclear leucocytes and Where the process is less active and the bacteria have # the exudation consists chiefly of endothelial leuco- my of which are phagocytic and contain fragments of litotic figures in endothelial leucocytes are found occa- Lymphocytes are present in relatively small num-

By by Dr. O. R. Mabee.

ty by Dr. H. A. Christian.

bers. The lymphatics (Fig. 6) in the capsule of the liver are in places distended and filled with endothelial leucocytes and a little fibrin.

Proliferative activity on the part of the fibroblasts is well marked and evidently follows the direct injury done the con- nective tissue cells by the toxins from the bacteria; in other words it is simple regeneration.

As a result of the exudation around the portal vessels, of the encroachment of the process on the liver cells, and of the proliferative activity on the part of the fibroblasts, the portal tissues show up as broad bands running very regularly be- tween the lobules of the liver cells (Fig. 11).

In those parts of the liver where the lesion is older and the exudation is less active the bile ducts are more or less dilated and often appear considerably increased in number as though a diffuse bile duct adenoma were present. This appearance is probably due to contraction following marked dilatation and stretching of the ducts when the lesion was more acute. In those parts of the liver where complete repair has taken place this same apparent increase in the size and number of the bile ducts in the midst of abundant scar tissue is still no- ticeable, at least in the early cases.

In many places the inflammatory exudation in the smaller bile ducts has led to occlusion of them and to obstruction to the outflow of bile which appears in the ducts and bile capil- laries above the point of obstruction in the form of yellow- ish green inspissated masses. The obstruction is focal only, not general and complete; therefore, the resulting jaundice is not intense.

The characteristics of this type of cirrhosis, while the in- fectious process is still active, are apparently the following :

The lesion spreads very uniformly from the portal vessels toward the hepatic veins, rarely cutting into a lobule. As a result the true lobular arrangement is more or less perfectly preserved. The bile ducts are often dilated and tortuous, so that they appear increased in number. The injury done the fibroblasts leads to active regeneration on their part and to the production of abundant connective tissue. As the result of the extensive inflammatory exudation and of the regenera- tion of the connective tissue the liver is much increased in size. The surface and cut section are comparatively smooth, perhaps owing to the even distribution of the inflammatory process.

Two cases of congenital jaundice with a uniformly dis-

? tributed cirrhotic process and obliteration of the common bile duct show microscopically a marked increase of connective tissue around the portal vessels and are undoubtedly due to intrauterine infection extending along the bile ducts (Fig. 12).

III. PIGMENT CIRRHOSIS.

A third form of cirrhosis which deserves mention is that known as pigment cirrhosis, occurring in cases of hemo- chromatosis. It appears to be due entirely to mechanical causes. Endothelial leucocytes filled with blood pigment col- lect often in great numbers in the lymphatic spaces and vessels

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JOHNS HOPKINS HOSPITAL BULLETIN.

of the liver, chiefly around the portal vessels (Figs. 13 and 14) but to some extent around the hepatic vein and irregularly throughout the lobule between the liver cells and the walls of the sinusoids. Whether they emigrate from the sinusoids after becoming filled with pigment, or absorb it like the liver cells and bile epithelium from the hemoglobin dissolved in the serum and lymph cannot be determined. But after they are filled with pigment they unquestionably are able to migrate. Wherever they collect in numbers they seem to injure the connective tissue mechanically by stretching it. In conse- quence there is a certain amount of regeneration on the part of the fibroblasts so that more or less sclerosis (Fig. 14) is produced."

A similar increase of connective tissue is caused in the same way under similar conditions in the pancreas, adrenals, and lymph nodes. In time more or less of the pigment is dis- solved by the action of the endothelial leucocytes, which then disappear, leaving the connective tissue behind as the only re- mains of the process.

This lesion, like infectious cirrhosis, may result in the acute stage in a large, smooth liver weighing in one instance, from a woman, 2500 grams. The primary injury seems to be done to the connective tissue. By contraction of this con- nective tissue later, more or less injury is probably caused to the liver cells.

The sclerosis which occurs in the liver and other organs in the pathological condition known as hemochromatosis is per- fectly analogous to that which takes place in the lungs and peribronchial lymph nodes as the result of the inhalation of large amounts of carbon. Endothelial leucocytes carry much of the pigment into the walls of the alveoli and from there to the lymph spaces and vessels around the bronchi and larger blood vessels. Many of the cells remain packed in these situa- tions and lead to considerable increase of the connective tissue.

Many of the cells in the lymphatics are carried to the peri- bronchial lymph nodes. At first they lie free in the lymph sinuses but soon migrate into the parenchyma when they lead to increase of connective tissue and secondarily to gradual dis- appearance of the lymphocytes. Some of the endothelial leucocytes filled with pigment migrate into the capsule of the lymph node and into the adjoining fat tissue.

This type of cirrhosis is characterized by pigmentation, by a very uniformly distributed increase of connective tissue, and by a smooth surface of the liver, externally and on section. It may attain a fairly large size. The increase of the connective tissue seems to be due to mechanical causes only.

IV. SYPHILITIC CIRRHOSIS.

Syphilitic infection of the liver is usually divided into two types, the congenital and the acquired. In the congenital type a diffuse lesion predominates, in the acquired a focal lesion ; but the two types of lesions are often combined in the con- genital form and may coexist to some extent in the acquired.

" See Cirrhosis Hepatis Anthracotica, by W. H. Welch, Johns Hopkins Bulletin, 1891, vol. II, 32, where I should interpret the origin of the sclerosis in the same way.

The primary, essential lesion produced by the trepor tir pallidum is best studied in chancres removed before neens eri has begun and in the liver and other organs of cases of es TŁ טות

genital syphilis. The so-called tertiary lesions would pra- bly be equally serviceable for study if they could more de ( F be obtained before the stage of necrosis.

cel In studying syphilitic lesions it is necessary at our presa stage of technical development, to prepare two parallel serias to sul I cor sections, the one stained by Levaditi's method after fixation afec formaldehyde so as to demonstrate the causative agent, 2 It other by various methods after fixation in Zenker's fluid n &ni show the tissue reaction. When this is done it is found to sis the treponemata, present often in great numbers in the z mary as well as in the congenital lesions, are situated in an en: minute lymph spaces between the cells and especially betre the fibrils. They occur most numerously in the connect (F: tissue between the collagen fibrils everywhere within the ax in invaded including that in the intima of arteries and want. The injurious action of the organisms is exerted chiefly if as exclusively on the fibroblasts which are thereby stimulstadion. ma active regeneration, as a result of which much fibrous tien of 1 is produced. This leads in part at least to the hardness of ti primary lesion and to the sclerosis of the liver and other cette. gans in congenital cases. the

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 89

Author: Jacob Anthony Kimmell Publication date: 1910 Publisher: Number of Pages: 1189

Author: Jacob Anthony Kimmell
Publication date: 1910
Publisher:
Number of Pages: 1189