Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 90

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

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In the congenital lesions the tissue reaction often does te e55: go beyond this stage. In the primary and tertiary lesico, die however, the reaction is more intense. As a result there rar ] added to this proliferation of fibroblasts an inflammatory = filtration consisting chiefly of lymphocytes including plaz, cells, often also of numerous eosinophiles. Under certain (is ditions giant cells are formed from the endothelium lining à smaller blood vessels and also perhaps the lymph rase These giant cells may occur in chancres, in gummata, ca especially in tertiary lesions of the skin. They are due : the presence of the treponemata within the blood and lyn; vessels and to their action on the endothelial cells. The ?- sulting giant cells often contain treponemata in large noE- bers.

The same lesion of proliferation of fibroblasts taking place in the walls of veins and arteries, especially in the intima leads to narrowing and more or less complete occlusion de many of the smaller vessels. The areas thus deprived of nutz- tion gradually undergo necrosis (gumma formation) which results in an active inflammatory exudate of serum and of e :- dothelial leucocytes (caseation) ; less often of polymorpheaz- clear leucocytes (suppuration). With the occurrence of từ necrosis and of the acute inflammatory exudate the trepid- mata as a rule rapidly disappear from the lesion and the sma affected tends in time to heal, owing to a local immunity being apparently produced by the leucocytosis. In this respect !! focal lesions in syphilis differ materially from those in tube". culosis which tend to spread indefinitely.

Reverting now to the liver we find that in congenita syphilis the treponemata injure primarily the connective te- sue cells, especially those lying between the liver cells and the walls of the sinusoids. As the result of the active and ori-

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watoff Of the woroblasts due to efforts at regen- 1, the connective tissue increases greatly in amount. 3 shown by the fact that where the treponemata are most ous (Fig. 15) the connective tissue is most abundant 16). Later as the collagen fibrils contract the liver re compressed and more or less atrophy accordingly re- This diffuse type of lesion, due to primary increase of tive tissue and secondary atrophy of liver cells, is per- well recognized as characteristic of congenital syphilis. ot infrequently complicated with focal lesions (miliary rger gummata) due to occlusion of the sinusoids, necro- the liver and other cells in the area affected, and in- atory infiltration with serum and polymorphonuclear or elial leucocytes.

Acquired syphilis the early lesion in the liver is diffuse 17) and similar to that in congenital syphilis but occurs jer and smaller foci only and usually leads to necrosis flammatory infiltration, forming the characteristic gum- of this type of infection, which later may heal and et, resulting in deep scars and more or less lobulation liver.

lis reading of the lesions occurring in syphilis is correct, Ithough the gross manifestations are many and varied, llular reaction caused by the treponema pallidum is ally the same in all of them and varies only in degree, varying conditions of injury and reaction and of local neral immunity.

V. ALCOHOLIC CIRRHOSIS.

the chronic, progressive, so-called alcoholic, type of is there occurs a peculiar form of necrosis of the liver which seem to be characteristic of it. The cytoplasm of s first undergoes a degenerative change in consequence h an irregular, coarse, hyaline meshwork (Fig. 18) ap- it. This meshwork stains deeply with eosin and with tungstic acid hematoxylin after fixation in Zenker's This degenerative change may attack single cells o! : large groups (Fig. 19) of them : it may occur focally diffusely. The affected cells may be situated in any the lobule, but lie most commonly, perhaps, in the f the portal vessels, and sometimes are sharply limited location.

ffected cells and the nuclei within them are usually

After the hyaline change has reached a certain de- intensity the cells are surrounded and invaded by s polymorphonuclear (Fig. 20) or endothelial (Fig. pocytes (sometimes the one, sometimes the other), ssolve the cells, the hyaline material last, and thus jut their disappearance.

with this hyaline change and destruction of the liver te occurs active regeneration as evidenced by occa- totic figures in adjoining liver cells. There is also less proliferative activity on the part of the fibro- alting in increase of connective tissue.

different processes of hyaline degeneration ending

in necrosis, of leucocytic infiltration, of regeneration of liver cells, and of increase in the amount of connective tissue, when extensive, diffuse, and acute, lead to considerable increase in the size and weight of the liver (2400 grams in one instance). The surface of such a liver is smooth and on section the cut surface is uniformly even, the lobulation indistinct, and the consistence much increased so that the liver tissue tears with difficulty. In other cases the various changes are much less extensive and hence more chronic because they do not cause death so quickly.

Even in the latest stages of alcoholic cirrhosis, however, it is usually possible to find liver cells undergoing the peculiar hyaline change which seems to be characteristic of this process. Still it is not possible to deny that this destructive hyaline change may cease entirely and leave nothing but the sclerosis as evidence of what has taken place.

The increase in the amount of connective tissue causes trouble later when it contracts by occluding bile ducts and blood vessels here and there throughout the liver. Obstruc- tion of the bile ducts results in focal bile stasis so that scat- tered areas appear dark green. In these areas the bile capil- laries are often greatly distended and in places ruptured so that masses of inspissated bile have escaped into the lymph spaces between the liver trabecula and the walls of the sinusoids. Here the masses are taken up by endothelial leuco- cytes and dissolved just as in the ordinary generalized bile stasis due to obstruction of the common duct.

It is not at all uncommon to find all these different pro- cesses (hyaline degeneration, leucocytic infiltration, regenera- tion, proliferation of connective tissue, and focal bile stasis) present in one and the same liver section.

The obstruction to the general flow of blood through the vessels resulting in portal stasis and ascites needs no mention here.

This type of cirrhosis is very commonly complicated by fatty infiltration (Fig. 21) which leads to marked increase in the weight of the liver (3315 and 3580 grams in two in- stances, and greater weights are on record). As a rule the clinician's diagnosis of hypertrophic cirrhosis proves to be of this nature. So far as can be determined from histological observation, the presence of the fat interferes in no way with the degenerative process. Cells filled with one or more fat vacuoles undergo hyaline change like the others.

The cause of the increase of the connective tissue in this type of cirrhosis is not perfectly obvious. The primary injury affects the liver cells and is followed by more or less regenera- tion of them. We have seen perfectly clearly in the first type of cirrhosis (that following extensive central necrosis), that injury to the liver cells does not result in proliferation of fibroblasts. On the other hand we have, in alcoholic cirrhosis, around and invading each necrotic cell, an acute inflamma- tory exudate of leucocytes which must cause more or less stretching of the connective tissue. The injury which results in proliferation of fibroblasts seems, therefore, as in pigment cirrhosis to be mechanical in origin, not toxic.

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JOHNS HOPKINS HOSPITAL BULLETIN.

If we leave tumors out of the question, the only other com- mon cause, besides direct toxic or mechanical injury to fibro- blasts, which stimulates them to proliferate is the presence of fibrin and that plays no part in this form of cirrhosis.

It has long been a much disputed point, chiefly with refer- ence to the alcoholic type of cirrhosis, whether the number of bile ducts in certain cases is greatly increased or whether many of them are not compressed columns of liver cells. The type of necrosis following central necrosis shows that bile ducts may grow out to a considerable distance towards the hepatic vein. In infectious cirrhosis a similar prolongation of bile ducts may occur. On the other hand the diffuse form of syphilitic cirrhosis shows that liver cell trabecula may be greatly compressed so as to resemble to some extent bile ducts. Therefore, it is theoretically possible that both true and ap- parent bile duct formations may occur in alcoholic cirrhosis. As a matter of fact both probably do. If these so-called bile ducts are carefully studied after proper staining it will often be found that in some of the epithelial cells composing them hyaline material similar to that in the degenerating liver cells is present (Figs. 23 and 24). Likewise in alcoholic cirrhosis complicated with fatty infiltration fat vacuoles will occasion- ally be found in the cells (Fig. 24) which look like bile duct epithelium. The presence of the fat vacuoles and of the hyaline material proves beyond question, it seems to me, that the cells containing them are compressed liver cells and not bile duct epithelium.

The terms hypertrophic and atrophic cirrhosis cause the student and the clinician much trouble. This analysis of these five types of lesions shows that we may get a large, hypertrophied, smooth liver in at least three of them, in in- fectious, pigment, and alcoholic cirrhosis. It is due in each instance to an extensive, diffuse, acute process. If the acute lesion ceases and healing takes place, or if the process is of moderate intensity and long duration so that healing and scar tissue are more prominent than degeneration and exudation, the liver will diminish in size below the normal. The cir- rhotic liver following central necrosis is necessarily at all stages below the normal in weight.

Atrophic cirrhosis simply means a liver in which a large proportion of the liver cells have been destroyed and have dis- appeared, while the existing and new-formed connective tissue have been rendered unduly prominent.

The terms monolobular and multilobular cirrhosis are also extremely confusing. They state only a relation between masses of liver cells which rarely correspond to liver lobules and strands of connective tissue. They do not in the least ex- plain the nature of the process. In infectious cirrhosis the lesion is confined quite uniformly to the portal vessels : the same is true to a less degree of pigment cirrhosis. If, after old custom, the hepatic vein is taken as the center of the lobule, then these two types of cirrhosis may be said, perhaps, to deserve the term monolobular.

In syphilitic cirrhosis of the diffuse type the sclerosis spreads quite evenly throughout every lobule.

In cirrhosis following central necrosis, large groups bules are completely sclerosed, while other large groups tas perfectly normal. The lesion is most irregular in dis" tion.

In alcoholic cirrhosis the distribution and intensity # ! degenerative process vary greatly in different cases, at. increase of the connective tissue follows in the same lite. often cuts into lobules in every direction. At other tir - is fairly regular in its distribution. As a rule, however .: lobular arrangement is quickly distorted. Hepatic veine hard to find. Sometimes the more normal areas are sms: other times large so that on gross examination either mono- or multilobular, might be appropriate. It must be borne in mind that regeneration of liver cells plays a: : portant rôle in alcoholic cirrhosis and may lead to cocor. tively large areas of newly formed liver cells, showing t lobular arrangement, containing no bile ducts, and someta regarded as adenomata.

It would seem much wiser to discard these terms which not explain and serve only to confuse. They emphasize wrong end of a pathological process and represent only : result of two forces acting against each other, the expand efforts of regenerating liver cells, the contracting force ef : proliferated fibroblasts which tend to squeeze the surrour. liver cells into the narrowest compass, namely, into sphere masses.

Granting that cirrhosis may arise in the ways descri from at least five different types of lesions, is it possible, ir : case of a given sclerosed liver, to determine what the Datos of the acute process was to which it owed its origin? I am 3 clined to think that in most cases, perhaps in all, it is poresta to do so, if the characteristics of each type are clearly o prehended and if the sclerosed liver is carefully examina'.

CONCLUSIONS.

At least five different types of lesions may terminate cirrhosis (sclerosis) of the liver; one is acute, the other foc more or less chronic in character.

Toxic cirrhosis (following extensive central neeres demonstrates clearly three facts :

1. That when all the liver cells of a lobule are destrete. the bile ducts grow out a certain distance towards the heps. vein, but that they do not produce liver cells.

2. That liver cells regenerate only from liver cells, mint from bile duct epithelium.

3. That fibroblasts (connective tissue cells) do not por liferate when liver cells alone are destroyed.

The other four types of lesions terminating in cirrhose show that fibroblasts multiply (regenerate) only when fibre blasts themselves have been injured or destroyed and tt> lead to increase of the connective tissue.

The so-called alcoholic type of cirrhosis is characterized t: a peculiar hyaline degeneration of the cytoplasm of the live: cells preceding necrosis. In this same type of cirrhosis the contraction of the connective tissue frequently compresses groups of liver cells so that they may resemble bile ducts: i:

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21 1

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FIG. 1 .- First stage of toxic cirrhosis. Necrosis of liver cells around hepatic vein (central necrosis) : invasion by polymorphonuclear leucocytes which lie mostly between the necrotic liver cells and the walls of the sinusoids.

FIG. 2 .- Second stage of toxic cirrhosis.

Acute yellow atrophy following exten- sive central necrosis. Liver cells all destroyed and removed; place occupied by large numbers of endothelial leucocytes.

FIG. 3 .- From same case as Fig. 2 showing a small group of liver cells from which regeneration may take place.

FIG. 4. - Late stage of toxic cirrhosis. Lobule of liver from acute yellow atrophy after repair has taken place No regeneration of liver cells; sinusoids filled with blood; bile ducts have extended part way towards the hepatic vein and then stopped: contraction and thickening but no increase of connective tissue.

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THE JOHNS HOPKINS HOSPITAL BULLETIN, MARCH, 1911.

PLATE VI.

Fig. 5 .- Late atage of toxic cirrhosis. Sclerosis of liver following extensive central necrosis and acute yellow atrophy. Lobular arrangement preserved but shrunken; bile ducts prominent.

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FIG. 7 .- Early stage of infectious cirrhosis. Bacilli present just outside of a distended bile duct filled with leucocytes.

FIG. 6 .- Early stage of infectious cinhas Lymphatic in capsule of liver dilated and file! chiefly with endothelial leucocytes.

FIG. 8 .- Early stage of infectious cirrhosis. Bile ducts dilated and filled with endothelial leucocytes.

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Fio. 9 .- Bile stasis complicated by infection along bile ducts. Area of necrosis ifiltrated by polymorphonuclear leucocytes.

FIG. 10 .- Early stage of infectious cirrhosis. Bile duct distended and filled with polymorphonuclear leucocytes: in adjoining area of softening chiefly endothelial leucocytes containing bile and fat.

11 .- Early stage of infectious cirrhosis showing lesion situated around the vessels.

Fin. 12 .- Late stage of infectious cirrhosis after repair has taken place.

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THE JOHNS HOPKINS HOSPITAL BULLETIN, MARCH, 1911.

PLAT:

FIG. 13 .- Pigment cirrhosis from a case of hæmochromatosis showing masses of endothelial leucocytes filled with blood pigment crowding the lymph spaces around the portal vessels and mechanically causing sclerosis.

Fig. 14 .- Pigment cirrhosis from a severer case of hæmochromatosis showing Mi! pigment and sclerosis.

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FIG. 15 .- Syphilitic cirrhosis. From a case of congenital syphilis showing masses of treponemata situated in the connective tissue between the liver cells and the walls of the sinusoids.

FIG. 16 .- From the same liver as Fig. 15 to show the great increase el connective tissue between the liver cells and the walls of the sinusnids, st ... by contraction leads to compression and atrophy of the liver cells.

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IG. 17 .- Syphilitic cirrhosis. Liver from a case of acquired syphilis in the adult wing marked diffuse increase of the connective tissue around the liver cells sing compression and atrophy of them.

19 .- Alcoholic cirrhosis showing numerous liver cells undergoing culiar form of hyaline degeneration.

FIG. 18 .- Alcoholic cirrhosis. Liver cells undergoing a peculiar hyaline degenera- tion before necrosis. .

FIG. 20 .- Alcoholic cirrhosis. The cells which have undergone necrosis following hyaline degeneration are being invaded by polymorphonuclear leucocytes.

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PLATE

THE JOHNS HOPKINS HOSPITAL BULLETIN, MARCH, 1911.

FIG. 21 .- Alcoholic cirrhosis complicated with fatty infiltration.

FIG. 23 .-- Alcoholic cirrhosis. Compressed column of liver cells resembling a bile duct; two of the cells show the type of hyaline degeneration peculiar to the liver cells in this type of cirrhosis.

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FIG. 22 .- Alcoholic cirrhosis. The necrotic liver cells are being removed by t: action of endothelial leucocytes.

FIG. 24 .- Alcoholic cirrhosis. Compressed columns of liver cells; one liver cell shows hyaline degeneration: two others contain fat vacuoles.

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LỊCH WALIS ILIS Orteur possible to demonstrate vacuoles or hyaline material due to degeneration in lasm, neither of which occurs in true bile duct n.

c cirrhosis the connective tissue thickens from con- but does not increase in amount because the fibro- 'e not been injured.

:ctious cirrhosis the fibroblasts are destroyed along liver cells: hence there is active regeneration and duction of connective tissue.

hilitic infection of the liver the primary injury is ibroblasts; in consequence they proliferate (regene- en in excess: the contraction later of the collagen

fibrils produced by them results in compression and more or less atrophy of the included liver cells.

In pigment and alcoholic cirrhosis the proliferation of the fibroblasts is apparently due to injury caused mechanically by cells of exudative origin stretching the connective tissue : the reaction is similar to that produced in the lungs and peri- bronchial lymph nodes by endothelial leucocytes filled with carbon packing themselves in the finer lymph spaces.

For the drawings I am indebted to Miss Etta R. Piotti; for the photomicrographs numbered 7, 13, and 18 to Dr. S. B. Wolbach; for the others to Mr. L. S. Brown, of the Massa- chusetts General Hospital.

HOID SPINE; WITH THE REPORT OF TWO ADDITIONAL CASES WITH BONY CHANGES IN THE VERTEBRAE.

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

Associate Professor of Medicine and Clinical Therapeutics, the Johns Hopkins University.

sential character of the condition termed " typhoid as been the subject of much controversy but the find- cent years have settled the question in favor of defi- nic changes-a spondylitis-as against a neurosis. In writer 1 reported two cases of typhoid spine in which rence of bony changes in the vertebra was proved by rams. At that time, while the occurrence of bony n the form of kyphosis, etc., had been noted, there been any report of bony changes as shown by 3. Since then several such cases have been reported e present paper two additional ones are described.

Typhoid fever in Nov., 1908; tetany (?); recovery; : Jan. 8, 1909. Symptoms of typhoid spine, March 15, ond admission Apr. 17, 1909. Second attack (relapse!) fever Apr. 26, 1909; recovery.

ent was a white male, aged 45 years, by occupation a His family history was negative and in his personal : only illness was an attack of mataria in July, 1908. rmerly been a very heavy drinker but had taken no six months before admission. First admission, Nov. The present -illness ,began with headache, weakness, nd general malaise. Apparently at times he had been lirious as there was a history of his wandering about n an aimless way. He was admitted on the sixth day ase. On admission the tongue was coated; some râles [ over both lungs; the heart was clear. There were erous rose spots on the chest and abdomen and the palpable. A blood culture gave typhoid bacilli, and the fon was positive on the day of admission and again on y. The patient showed signs of marked toxæmia, but sture of special interest was the occurrence of a condi- Ike tetany during the course of the disease. There was ion of the toes and the hand was held in the position ny, this becoming much more marked when the cuff of jessure apparatus was applied to the upper arm. The became normal on the 37th day of the attack and the discharged in good condition on Jan. 8, 1909. During cence there was no complaint of any pain or discom- back and he felt well on leaving the hospital.

Second Admission-April 17, 1909 .- After discharge from the hospital he did not return to work until Jan. 30, when he resumed his occupation in the blacksmith department of the works where he was employed. This involved some heavy lifting but he was quite sure that there had not been any injury or strain. He felt perfectly well until March 15, when he began to have pain in the lower part of the back; there was no other symptom. The onset was gradual and he was able to continue at work for one week but then had to give up on account of the severity of the pain. This was not constant but came on in paroxysms which lasted from 15 to 20 minutes. The patient commented on the effect on his general condition, remarking that the pain had made him " weak and discouraged." He emphasized the fact that the pain was much worse in the night than during the day and attributed his feeling so badly to loss of sleep rather than to the pain.

Examination .- The patient's general condition was good. The lungs were clear throughout except for a few rales at the bases. The heart was slightly increased in size, the impulse being feeble; the sounds were rather distant and the first had a slight mur- murish quality at the apex. The pulse was of fair volume and the blood pressure 110 mm. Hg. The abdomen was negative; no rose spots were seen and the spleen was not felt. The abdomi. .. walls were soft; there was no contraction of the muscles. hæmoglobin was 86 per cent, red cells 5,100,000 and_16 5700 per cmm. When the patient stood up there

well marked scoliosis in the lumbar region and the :: was held higher than the left. The usual lu-

almost obliterated. There was very little mov ...

Lower

spine when the patient bent forward and to the left : ight and

there was practically no movement in the lower . 'de when he bent backward. The spine showed very litt ~ uvement below the tenth thoracic vertebra. On palpation there was some ten- derness on both sides of the lumbar spine but no tenderness on pressure over the spinous processes of the vertebra. The muscles on both sides were contracted and stood out prominently, this be- ing more marked on the right side. The knee jerks and tendo Achillis reflexes were rather more active than normal and equal on the two sides, but the arm reflexes showed much the same in- crease. There was a normal response to plantar stimulation. At this time the patient had slight fever, about 100º F., which dis- appeared in the next three or four days. For the next five days the condition was practically the same. There was slight tender- ness on pressure over the lower spines, especially about the fourth

jed. Sc., 1906, CXXXII, 878.

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JOHNS HOPKINS HOSPITAL BULLETIN.

[No. 19

lumbar vertebra, and distinct tenderness on either side especially to the left of the fourth and fifth lumbar vertebrae. As long as the patient made no movement he was fairly comfortable but when asked to stand on his toes and come down forcibly on the heels he did this very slowly and carefully. When he walked the back was held very stiffly and when he tried to get out of bed he had great difficulty in doing it, the back being held rigidly and the patient bracing himself as much as possible by the arms. The abdominal muscles at times were held very rigidly. When the patient was flat in bed the lumbar lordosis seemed to be obliter- ated and there was marked rigidity of the muscles on both sides of the spine in this region. The X-ray plate on April 22d showed marked ossification of both lateral ligaments in the lumbar region and also a suggestion of this in the anterior ligament (Dr. Baetjer).

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Twentieth Century History of Findlay and Hancock County, Ohio, and Representative Citizens, Part 90

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

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