Part 168

CAUSES.--Sclerosis of the liver is, conspicuously, a disease of adult life and onward. Except the congenital example mentioned below, the earliest age at which the disease has occurred, so far as I am able to ascertain, is four years--a case reported by Wettergreen of hypertrophic sclerosis, in which neither a syphilitic nor paludal cause could be ascertained. Cayley reports a case in a child of six; Murchison, Frerichs, Griffith, one each at ten. After this period the increase relatively to age is rapid. The majority of cases occur between thirty {991} and fifty years. Yet Virchow has given the details of a congenital example. According to Förster, of 31 cases of cirrhosis, 16 were between forty and sixty years. The preponderance of cases in the male sex is very decided. Of Bamberger's 51 cases, 39 were men, 12 were women; of Frerichs' 36 cases, 20 occurred in men and 16 in women--a larger proportion of women than any other author records; of 12 cases observed by myself, only 1 was a woman. Nationality does not affect the production of cirrhosis, except as regards the personal habits of the people. This disease is comparatively uncommon in wine- and beer-drinking countries, and frequent amongst a spirit-drinking people. The great etiological factor is the abuse, the habitual use, of spirits, and hence the number of cases observed in North Germany, England, Scotland, and the United States. Murchison affirms that he has never seen a case produced in any other way. Even in children of tender years the abuse of spirits can usually be traced. Nevertheless, there are instances of the disease the origin of which cannot be referred to alcoholic excess. The congenital cases, as that narrated by Virchow, and the instances occurring in children and adults not given to spirits in any form, indicate that there are other pathogenetic influences which may bring about a sclerosis of the liver. Virchow was one of the first to illuminate the subject of visceral syphilis and to demonstrate the occurrence of sclerosis of the liver from syphilitic infection. Very often the syphilitic cachexia coincides with alcoholic excess. There can be no doubt that chronic malarial poisoning causes, or powerfully predisposes to, cirrhosis. I have submitted elsewhere pathological evidence on this point, and the Italian physicians, who have the opportunity to obtain accurate data, maintain that malarial toxæmia does bring about this state. It is probable that the overgrowth of connective tissue is induced by the repeated congestions of the malarial attacks, and by the obstruction due to catarrh of the bile-ducts which so often occurs in the febrile paroxysms.

J. Wickham Legg and Charcot nearly simultaneously discovered that obstruction of the bile-ducts, if continued a sufficient length of time, sets up a hyperplasia of the connective tissue of the liver. The evidence is pathological and experimental. Thus, Legg has seen a liver markedly cirrhotic in a case where a small cancer of the duodenum completely obstructed the flow of bile into the intestine. By tying the common duct in dogs it was found that a hyperplasia of the connective tissue very soon occurred, and this was followed, of course, by contraction of the new tissue and atrophy of the hepatic cells. Closure of the hepatic vein has the same effect, and also, as Solowieff has asserted, closure of the portal vein; on the other hand, by Frerichs and others the closure of the portal is attributed to the sclerosis.

Certain poisons, as antimony, arsenic, notably phosphorus, have the power to set up an irritative hyperplasia of the connective tissue of the {992} liver. These metals accumulate in the liver in preparation for excretion. Wegner, in the study of the action of phosphorus on dogs, rabbits, and other animals, has induced a marked degree of sclerosis, but such results have not been observed in cases of poisoning by phosphorus in man, except in an instance reported by Küssner.

Finally, a condition of the liver corresponding in all respects to cirrhosis has been induced by perihepatitis, by the organization of the exudation and its subsequent contraction, and by the extension of the morbid process from the capsule to the interlobular connective tissue (Poulin).

PATHOLOGICAL ANATOMY.--Several forms of cirrhosis are recognized by the modern French school of pathologists. According to Sabourin, there is an annular, a monolobular, and a multilobular form. These differ merely in regard to the arrangement of the new connective tissue. At the outset of the disease the liver is increased in size and hyperæmic. Its consistence is also greater than normal. The outer surface is at this period smooth, but on section the islets of the parenchymatous tissue, yellowish in color, are distinctly visible between the grayish or pale-rose tint of the intervening or proliferating tissue. This reddish-gray material consists of fine connective-tissue elements containing spindle-shaped cells. The development of this material is such as to even exceed in quantity the proper glandular structure. The bands of newly-formed connective tissue extend between individual lobules (monolobular cirrhosis) or between groups of lobules (multilobular cirrhosis). A portion of the spindle-shaped cells form new vessels communicating with the branches of the hepatic artery. Coincidently with the formation of the new connective tissue ensues its contraction. The enlarged organ diminishes in size from a slight degree to one-half its original volume; especially in the left lobe is the diminution of size most marked. On the surface it exhibits a knobbed or nodular aspect (hobnail liver), and these knobs present through the capsule a yellow appearance. The granulations, so called, consist of small prominences corresponding to lobules or groups of lobules, and hence vary in size from that of a pinhead to that of a pea. Between these are the sharply-defined masses of connective tissue. On section the organ is found to be of firm almost cartilaginous hardness, and between the interlacing bundles of connective tissue are the small islands of parenchymatous tissue projecting above the cut surface and having a yellowish or brownish-yellow color. As the terminal branches of the portal are compressed in the process of shrinking undergone by the new connective tissue, they are destroyed. The result of this obliteration of the portal radicles is the impaired nutrition of the lobules and atrophy of the cells. Formerly it was held that the atrophy of the hepatic cells was due to the compression exercised by the contracting connective tissue, and Beale even maintained that the change began in {993} the cells, the connective tissue contracting as the cells receded before them. This view has been reaffirmed by Ackermann in a paper read last year before the Congress of German Naturalists and Physicians, but without any acknowledgment, so far as I can ascertain, of Beale's long-before expressed opinions. In the discussion which followed the reading of Ackermann's paper the position of its author was supported by Aufrecht, Küssner, and others, but controverted by Rindfleisch. It has been demonstrated by Cohnheim and Litten that the lobule is nourished not only by the portal radicles, but by the branches of the hepatic artery, which enter, by the interlobular vein, the capillaries of the lobule, and hence the nutrition of the cells suffers in consequence of the lessened blood-supply; but it is probable also that more or less compression is exercised. When the cells are destroyed, their remains may be discerned in the mass of connective tissue as fine fat-granules or masses of pigment yellowish or brownish in color. The peculiar appearance to which the name cirrhosis is applied is due to the lobules or groups of lobules which project on section above the divided surface, and are colored yellowish by the bile-pigment, which here exists in an exaggerated quantity. The cells themselves are not normal: they are enlarged by compensatory hypertrophy, and they contain much bile-pigment and a considerable quantity of fat. The compression of the capillaries, especially their obliteration, leads to stasis of the blood and its consequences in the whole chylopoietic system.

SYMPTOMS.--The development of sclerosis is usually very insidious. After some years' indulgence in spirit-drinking or affected for a length of time with the other causes of the malady, a gradual decline of vigor occurs. The complexion takes on a fawn color, stigmata slowly form on the face, there is more or less yellowness of the conjunctiva, and attacks of headache, giddiness, and even severe vertigo, are experienced. An increasing indisposition to mental effort, some hebetude of mind, and a gradually deepening despondency are felt. The appetite gradually fails, becomes capricious, and only highly-seasoned, rather odd, or unusual articles of food can be taken. Such subjects acquire a taste for condiments, for such uncooked vegetables as onions, celery, raw cabbage, etc., for fruits, and get a distaste for plainly-cooked meats and vegetables, for sweets, etc. The digestion is as capricious as the appetite: at first there are times of appetite, again of indifference, then of disgust; some heaviness is felt after meals; gaseous eructations, acidity, pyrosis, nausea, occur day after day as the case advances; and ultimately morning vomiting is regularly experienced. Nausea is felt on rising; then with much straining and distress a little glairy mucus and a teaspoonful of bile are brought up; after which, it may be, a little food can be taken. It is only after the case is fully declared that these troubles of stomach digestion become constant; previously they occur now and then in a paroxysmal way, whilst between there is only labored digestion.

As the compression of the portal radicles maintains, by reason of the obstruction, a constant hyperæmia of the intestinal mucous membrane, a catarrhal state, with fermentation of the fatty, starchy, and saccharine constituents of the food, and hence complicated products of an irritating kind, must result therefrom. Hemorrhoids, varying in size according to {994} the degree of obstruction, form, sometimes bleeding more or less profusely, again being merely troublesome or painful. Fissures of the anus and fistula in ano not unfrequently complicate the case. The bowels are necessarily rather relaxed than confined, but at the onset of the malady they may be confined, afterward assuming more or less of the characteristics of diarrhoea. The stools may be offensive with the products of decomposition, rather clay-colored or golden, or brownish and almost black from the presence of blood. In some cases the stools are parti-colored--clay-colored in part, brownish in part--and in exceptional examples continue normal or nearly so until near the end. As the transudations from the portal vessels increase, the mucous membrane of the intestinal canal becomes oedematous, and, the normal secretions being arrested, the discharges finally consist of a watery fluid, whitish or grayish, dark-brown or blackish, and very offensive. The decomposition of foods instead of their proper digestion and solution, and especially the fermentation of the starchy and saccharine constituents of the aliment taken, produce a great quantity of gas; hence meteorism comes to be an ordinary symptom. The accumulation of gas is greatly promoted by the paretic state of the muscular layer and by the relaxation of the abdominal walls consequent on the oedema of the muscular tissue. A high degree of distress is sometimes caused by the great accumulation of flatus; the abdomen is greatly distended and the diaphragm is pushed up against the heart and lungs, compelling the patient at length to sit up to breathe with ease. Of course the accumulation of fluid may be greater, and the gas only add to the discomfort.

A very common symptom is hemorrhage. Sometimes it happens, indeed, that this is the only evidence of the portal obstruction at first observed. Hæmatemesis is more common than intestinal hemorrhage. Now the blood may be large in quantity, appear little changed from its usual coagulated state, and be brought up promptly with slight effort of vomiting; now it is passed by stool, is in coffee-colored, granular masses or in a tar-like, semifluid state; and again it appears in coffee-grounds mixed with the contents of the stomach. These variations are due to the character, seat, and extent of the hemorrhage and to the condition of the mucous membrane. Merely-distended capillaries, yielding, may furnish a little blood, which, acted on by the gastric juice, forms coffee-grounds, or, if not acted on in consequence of the failure of the gastric glands to functionate, appears as bloody streaks mixed with mucus. Enlarged veins, giving way, may furnish a large quantity of partly-coagulated venous blood, charred or not as the state of the juices will determine. In some cases hemorrhages into the submucous tissue or thromboses of the submucous veins lead to solution of the membrane thus deprived of its nutritional supply, and ulcers form. Two admirable examples of this kind have been seen by the writer in which large hæmatemesis occurred from ulcers near the pylorus. They were round, smooth ulcers, containing coagula, and the eroded vessels (veins) were readily seen opening into the cavity of each.

The obstruction to the portal circulation results also in an enlargement of the spleen. There may be a simple enlargement due to the hyperæmia merely; there may be an enlargement due to the hyperæmia and to a resulting hyperplasia of the connective tissue; there may be also, in {995} addition to the second form of enlargement, amyloid degeneration, syphilitic hyperplasia, etc. The increased dimensions of the spleen are by no means always made out, and authorities differ greatly as to the proportion of cases in which the enlargement can be detected. The organ may indeed be considerably enlarged whilst pushed upward into the left hypochondrium by the effusion, and yet the attempt to measure and define its dimensions may be fruitless. From a slight increase due to the hyperæmia up to the enormous dimensions acquired by the added amyloid material there are all possible variations in size.

Partly in consequence of the increased blood-pressure in the vessels of the peritoneum, and partly in consequence of the watery condition of the blood itself, effusion takes place into the sac of the peritoneum. Such an accumulation is known as ascites, or dropsy of the abdomen. The time at which the effusion begins, the amount of it, and the degree of contraction of the liver necessary to produce it, vary in each case. Ascites may be the first symptom to announce the onset of cirrhosis; it is more frequently amongst the later symptoms, and is the evidence of much interference in the portal circulation. However, it is not due wholly to hepatic disease. The blood in cirrhosis is much reduced and watery, hence slight causes suffice to induce an outward diffusion. Given a certain obstacle to the passage of the blood through the liver, transudation will be the more prompt to appear the greater the anæmia. In some cases an enormous quantity of fluid collects: from ten to thirty pounds may be regarded as usual, and forty to sixty pounds as exceptional, although the highest amount just given is not rare. The fluid of ascites nearly represents the serum of the blood. It has a straw color and is clear, but it may have a reddish tint from the presence of blood, a greenish-yellow or brown from bile-pigment. The solids of the serum are in the proportion of from 1 to 3 per cent., and consist of albumen chiefly and salts, of which sodium chloride is the principal. Hoppe's analysis gives this result: 1.55 to 1.75 solids, of which 0.62 to 0.77 is albumen. According to Frerichs, the amounts of solids ranges from 2.04 to 2.48, and of these albumen constitutes 1.01 to 1.34.

Oedema of the inferior extremities comes on after, usually--rarely with--the ascites. If the mechanism of this oedematous swelling be as supposed, the effusion into the areolar tissue necessarily succeeds to the abdominal effusion. The pressure of the fluid in the cavity on the ascending vena cava and iliac veins seems to be the principal factor; but to this must also be added the intestinal gas, which in some instances exerts a powerful force. The ankles have in rather rare cases appeared swollen before the abdomen, but the detection of fluid in the peritoneal cavity when in small quantity is not always easy. Obese women, with much accumulation of fat in the omentum and flatus in the intestines, have swollen feet and legs if erect for some time, the effusion being due to pressure on the vena cava. The legs may become enormously distended. The scrotum and penis in the male, the vulva in the female, the buttocks and the abdominal wall, also become oedematous, sometimes immensely. Walking grows increasingly difficult. Warmth and moisture and the friction of the sensitive surfaces excite vesicular and pustular eruptions where the {996} scrotum and labiæ come in contact with the thighs. Urination may be impeded by the oedema of the prepuce.

An attempt at compensation for these evils growing out of the obstruction in the portal system is made by the natural powers. Anastomoses of veins through minute branches are made use of to convey the blood of the obstructed portal circulation into the general venous system, and to this end become greatly enlarged. The interlobular veins being obliterated by the contracting connective tissue, the pressure in the branches and trunk of the portal vein is much increased. Hence an outlet is sought for in the veins which communicate between the portal and the ascending vena cava. One of the most important of these is a vein in the round ligament, at one time supposed to be the closed umbilical vein, but proved by Sappey to be an accessory portal vein. Bamberger, however, has found the umbilical vein pervious, and since, Hoffmann has demonstrated the same fact. It is probable, indeed, that Sappey's observation is correct for some cases. In either event, the veins of the abdominal wall about the umbilicus communicating with the epigastric become enormously distended, and in some advanced cases of cirrhosis form a circle known as the caput Medusæ. Further communication between the portal and the veins of the diaphragm takes place by means of the veins in the coronary and suspensory ligaments. In some instances a new route is established between the veins of the diaphragm and the portal by means of new vessels formed in the organized connective tissue resulting from perihepatitis. Still another channel of communication exists between the inferior oesophageal veins, the azygos, and the coronary, and finally between the inferior hemorrhoidal and the hypogastric. The more completely can communication be established between these anastomosing veins the less severe the results of portal obstruction.

Besides these indirect evidences of portal obstruction and a contracting organ, there are direct means of ascertaining the condition of the liver. By the methods of physical diagnosis we may acquire much information. On auscultation, as our Jackson was the first to show, a grating or creaking like leather, or friction sound, is audible over the right hypochondrium synchronously with the respiratory movements or when produced by moving with the fingers the abdominal wall on the liver. This sound is caused by the bands of false membrane which extend between the two surfaces, and hence indicates a secondary perihepatitis.

To ascertain the dimensions of the liver--to mark out the area of hepatic dulness--with accuracy is a most necessary procedure. The period of the disease is an important element in the problem. When the new material is deposited and the congestion of the portal system first occurs, an increase in the dimensions of the organ is observed. This enlargement, of brief duration, must not be confounded with the hypertrophic sclerosis, another form of the malady. So considerable is the increase in the size of the liver that there is an evident enlargement of the right hypochondrium, and the whole abdomen seems fuller. The organ may be felt, on palpation, projecting one, two, or even three fingers' breadths below the margin of the ribs, and the left lobe extends well across the epigastrium, increasing the sense of resistance and the area {997} of dulness in this direction. The enlarged liver, as felt below the ribs, appears firmer than is natural, is yet smooth, and the margin is sharply defined. The duration of this period of enlargement is indefinite, but it is rather brief, and is followed by the contracting and atrophic stage. It is not often, indeed, that the patient presents himself during the period of enlargement. Sometimes a perihepatitis or an unwonted tenderness in the right side compels attention during this stage, but more frequently it escapes notice. If perihepatitis occur, there will be fever, pain, and tenderness, a slight icterode hue of the skin, and possibly Jackson's friction sound. These symptoms, taken in conjunction with the history of the case and the obvious enlargement of the organ, will indicate the existence of the first stage of sclerosis.

The contraction of the liver, or, as it may be expressed, the atrophy of the hepatic cells and the consequent shrinking of the interlobular connective tissue, goes on slowly. Several months may be occupied in an amount of atrophy distinct enough to be recognized by the narrowing of the area of hepatic dulness. Especially difficult is the recognition of the contraction when ascites has fully distended the abdomen. It may be necessary under such circumstances to postpone a decision until tapping has removed the fluid. If the organ can be felt by depressing the walls of the abdomen, more or less unevenness of surface may be detected, and the inferior margin may give the impression of hardness and sharpness of outline. At the same time, the increased dulness of the epigastric region observed during the hypertrophic stage will have gradually ceased because of the shrinking of the left lobe. The liver may be undergoing the atrophic degeneration to a marked extent and yet remain large--larger even than normal. Such a state of things may be due to conjoint amyloid or fatty degeneration of the organ, and, indeed, more or less fatty change occurs in all cases of cirrhosis. The shrinking of the liver persists until the area of dulness is not greater in area than two or three ribs.

The disturbances of function in sclerosis of the liver are not limited to the chylopoietic system. As the secreting structure of the liver is continually lessened in extent by the atrophy, symptoms result from the necessary interference in the hepatic functions. These symptoms are concerned with the liver, with the nutrition of the tissues of the body, and with the kidneys. As regards the biliary function of the liver, the quantity of bile acids and pigment is reduced below the normal in proportion to the damage done to the organ. As a rule, there is little jaundice in sclerosis, and very little bile-pigment present in the urine. Hence there must be little produced. Instead of a jaundiced hue of the skin, it has a fawn color--an earthy, sallow tint eminently characteristic of a chronic affection in which the power to produce bile is much impaired. Occasionally it happens, particularly in the early stages of cirrhosis, that a well-marked jaundice appears in the face and body, but this probably is due to a catarrh of the bile-ducts. In most cases the integument presents the earthy and sallow hue above mentioned. Graves appears to have been the first to interpret aright the greater significance of this appearance of the skin than the purely jaundiced tint. The glycogenic {998} function of the liver must be impaired in the same ratio as the biliary. The nutrition of the body suffers; the skin becomes dry and harsh; the fat disappears; the temperature of the body, unless the conditions for producing fever are present, is barely up to normal, if not somewhat below; a marked degree of anæmia supervenes; and the action of the heart becomes feeble and rapid after a period of slowness. The blood is altered in quality, and hence hemorrhages--epistaxis especially--occur, petechiæ and ecchymoses appear in the skin, and stigmata are numerous about the face and nose.

The urine in cirrhosis is high-colored because of the abundance of pigment, and in the early stages of the disease is increased in amount, although of lower specific gravity. When much effusion takes place into the peritoneal sac, the compression of the renal veins by the fluid lessens the activity of the kidneys and diminishes the urinary flow. Much discussion has taken place over the quantity of urea present in the urine in cases of cirrhosis, but it has been established that the relative quantity of urea lessens in proportion to the damage suffered by the liver. The urates are in excess.

COURSE, DURATION, AND TERMINATION.--There are enormous variations in the course of the disease as respects the rate of its progress. In general, it may be said that the whole duration is from three months to six years. The onset is often insidious, and little distress is occasioned until effusion begins in the abdomen. In other cases there is considerable pain in the right hypochondrium, severe disorders of digestion and intestinal derangements, rapid emaciation, ascites, and some intercurrent malady which terminates them, often quite unexpectedly. The usual course is as follows: After the protracted use of alcoholic stimulants the symptoms of gastro-intestinal catarrh appear; there occur acidity, pyrosis, morning vomiting, and distress after meals; the bowels are irregular, the stools rather dark and offensive; the bodily vigor declines and the mental condition is depressed and hypochondriacal; emaciation progresses; the skin becomes dry, harsh, and fawn-colored; stigmata appear on the face; some uneasiness is felt in the abdomen, through the right hypochondrium, and about the umbilicus; presently the abdomen enlarges and the feet and legs swell; after a time the abdominal enlargement is extreme and the walls become thin, the genitals and thighs are greatly distended, and the prepuce is so swollen that urination grows more and more difficult, the penis almost disappearing in the surrounding oedema; notwithstanding the immense size of the abdomen and lower extremities, the chest, face, and upper extremities are wasted away; to lie down is impossible, and only snatches of disturbed sleep are procured in the upright sitting posture; breathing grows more and more difficult, and a sense of suffocation is imminent; and, thus worn out by suffering and want of sleep, the patient at last sinks into a soporose state and dies comatose, if not cut off before by some acute serous inflammation--pleuritis, peritonitis, peri- or endocarditis, pneumonia, etc.

{999} The course of any case of cirrhosis is much influenced by the amount of damage to the hepatic cells and by the extent of the compensatory changes in the circulation. Ulcers of the stomach or intestine, opening vessels, or hemorrhages from the mucous membranes may have a pronounced effect on the progress of any case. A fatal result was determined in a case under the writer's charge by hemorrhage from ulcers near the pylorus, which were caused by thromboses of the stomach veins at that point. Occasionally, the occurrence of thrombosis of the portal vein adds an embarrassing and dangerous complication. The liver, besides the change due to cirrhosis, may be affected by amyloid or fatty degeneration, or by both combined. It should not be forgotten that more or less fatty change takes place in the hepatic cells undergoing atrophy, whence the appearance called cirrhosis. Sclerosis may be a general condition in which several organs participate, the kidneys notably. These organs are changed by a hyperplasia of the connective tissue, and especially by fatty degeneration of the epithelium. In the brain the sclerosis consists in chronic pachymeningitis, adhesions of the dura, etc., and with these connective-tissue changes are often associated extravasations of blood. These lesions are probably due to chronic alcoholism rather than to the cirrhosis--are simultaneous lesions, instead of consecutive.

The duration of cirrhosis must necessarily depend largely on the occurrence of the complications above mentioned and on the appearance of intercurrent diseases. The most usual intercurrent maladies are peritonitis, pleuritis, and other serous inflammations. An attack of cerebral (meningeal) hemorrhage may occur. Failure of the heart may be due to fatty degeneration of its muscular tissue. Stupor, coma, and insensibility may come on toward the close in consequence of the retention of excrementitious matters. By Flint, Jr., these cerebral symptoms were referred to the retained cholesterin, and hence he designated this state cholesteræmia. Numerous experimentalists (Pagès, Chomjakow, Von Krusenstern, Koloman Müller) have studied this question, and only Müller has been able to confirm Flint's theory. The condition is more suitably designated cholæmia, which signifies blood-poisoning from the excrementitious biliary matters retained in the system.

Any fully-developed case of cirrhosis can only terminate in one way, for we possess no means of restoring the hepatic cells when once destroyed. At the outset of the disease, before any serious changes have taken place, it is probable it may be arrested. Proceeding to its natural termination without complications or intercurrent affections, death finally occurs from exhaustion. The emaciation becomes extreme, the stomach gets to be excessively irritable, and an exhausting diarrhoea consumes the last remains of strength. Then an oedema of the lungs or failure of the heart or a deep coma ends the scene.

DIAGNOSIS.--Cirrhosis in its first stage is to be distinguished from diseases which cause enlargement of the liver, and in its second or contracting stage from diseases that induce contraction of the organ. The history of alcoholic excess is an important means of differentiating this {1000} from other affections. The enlargement belonging to alcoholism is distinguished from that due to amyloid disease by the permanent character of the latter and by its history of chronic suppuration, in addition to, it may be, alcoholic excess; from cancer, by the character of the enlargement, by its permanence, by the secondary deposits in the mesentery and elsewhere, by the severe and persistent pain; from hydatids or echinococci cysts by the painless enlargement of the latter, by the absence, usually, of any interference with the hepatic functions, by the purring thrill, and by the presence of the characteristic hooklets in the fluid withdrawn. From the maladies characterized by the contraction of the organ it is distinguished by the rapidity with which the case is developed in acute yellow atrophy, and by the profound constitutional disturbance characteristic of this form of contraction. When the liver is lessened in size in consequence of the compression exercised by the contracting exudation of a local peritonitis, there is a history of pain and soreness of the right hypochondrium, followed by the symptoms of contraction--a very different history from that of cirrhosis, in which the local attacks of pain and distress succeed to or accompany the symptoms of contraction. Occlusion of the gall-ducts by a calculus may set up a slow atrophy having some points of resemblance to cirrhosis; but in this malady attacks of hepatic colic precede the signs of obstruction, the jaundice, and gray evacuations, and the evidences of contraction succeed to these very characteristic symptoms; whereas in cirrhosis paroxysms of pain followed by jaundice are not known. Occlusion of the portal vein may also be followed by atrophy, but this is usually due to some other affection of the abdominal organs, and the change in the condition of the liver occurs very promptly, there being neither the history nor the course of symptoms belonging to cirrhosis.

TREATMENT.--As the abuse of alcoholic liquors--even their habitual use in moderation--is the chief pathogenetic factor, they should be entirely given up. Condiments, coffee and tea, highly-seasoned animal foods, are of less importance as causes, but are sufficiently injurious to require them to be discontinued. The food of such subjects should not contain fat, because the bile is necessary to its right assimilation, and should have but a small proportion relatively of starch and sugar, since these articles readily ferment in the presence of an excess of mucus and in the absence of the bile. The succulent vegetables, as lettuce, celery, spinach, etc., should be substituted for the starchy and saccharine. A diet largely composed of skimmed milk renders an important service both as a nutrient and a diuretic and depurant. Lean meats, acid fruits, and the weak alkaline mineral waters should be the basis of a proper system of alimentation.

As malarial intoxication is a cause now distinctly recognized, patients should be removed from such influences. If this be impracticable, the effects of the poison should, as far as possible, be removed, especially the glandular complications. To this end, such remedies should be employed as will affect the overgrowth of the connective tissue, as the compound solution of iodine, the bichloride of mercury, and the chloride of gold (or gold and sodium). Quinine will be necessary, according to circumstances.

Do we possess any means to check the overgrowth of connective tissue {1001} in cases of sclerosis? The writer believes that those remedies have this power to a less or greater extent which are separated by the liver from the blood. These are chiefly the salts of gold, silver, copper, arsenic, and mercury (chloride), and phosphorus. The most useful of these are the chloride of gold and sodium and the chloride of mercury, and some phosphates. The writer has had, he thinks, curative results in the commencement of the disease from the chloride of gold and sodium and the phosphate of sodium. German practitioners believe that the chloride of ammonium is a powerful alterant and deobstruent, and prescribe it in this affection to stop the overgrowth of connective tissue. That it does have this effect can hardly be disputed, but the daily quantity necessary is large, the taste very disagreeable, and the stomachal effect that of an irritant. Hence it is by no means so effective as the chlorides above mentioned. The chloride of gold and sodium (1/10 grain) can be given at the same time with chloride of mercury (1/20 grain) if it is desirable to combine their effects. The writer has seen what appeared to be cases of cirrhosis in the first stage yield to the persistent administration of phosphate of sodium--drachm j ter in die--and the chloride of gold and sodium.

When contraction of the liver has ensued, and hemorrhages, effusion into the cavity of the peritoneum, and a high degree of gastro-intestinal catarrh have occurred, the relief of the secondary symptoms takes the first place in importance. There are but three modes by which an effusion into the abdomen can be removed: by the skin, by the kidneys, by the intestinal canal. Each of these may be employed in turn. By the skin warm baths, vapor baths, digitalis stupes, and especially the subcutaneous injection of pilocarpin, may be employed. These alone may be sufficient in some cases--rather rarely, however. They may all be used simultaneously or in turn to effect the purpose. A digitalis stupe may be made to have the effect of a vapor bath: a large one is placed on the abdomen and the body is covered with blankets, which results in the production of abundant sweating. The vapor bath is applied in the ordinary way, so that no explanation is needed. If there be no contraindication in the state of the heart, pilocarpin salts can be injected in sufficient quantity to induce active diaphoresis. These measures proving inadequate, an attempt should be made to dispose of the fluid by acting on the kidneys and promoting diuresis. Amongst the diuretics in ascites, Wilks places the resin of copaiba first. The dose ranges from two to five grains, and it may be given in combination with gold or mercury chloride. When this remedy increases the flow of urine, it does good, but if the quantity of urine remains unchanged, it does no good, and should be discontinued.

As the effusion of fluid is due to the portal obstruction, it follows that depletion of the terminal radicles of this system will act most directly on the origin of the troubles. Hydragogue cathartics have, therefore, an important place in the treatment of ascites of hepatic origin. One of the most generally efficient of these remedies is the compound jalap powder, for whilst it produces free watery evacuations, it also stimulates the kidneys somewhat. It is generally better to give a full dose--one or two teaspoonfuls--in the early morning, so that the disturbance caused by it will subside before the time for taking food. Several free watery evacuations should be produced by it. Sometimes the resin or extract of podophyllin is added to the compound jalap powder to increase its activity. {1002} Purgative combinations of colocynth, gamboge, and resin of podophyllin are also occasionally employed, but the most efficient hydragogue is elaterium. The last-mentioned may act very efficiently without causing any considerable depression, but the results obtained by it are usually fleeting. After even a very free discharge of fluid the effusion quickly increases, and further purgation is required. Tapping is a palliative expedient which must sometimes be considered. With the present improved aspirator and the antiseptic method the fluid may be withdrawn with ease and safety. It is not necessary in any case to remove all the fluid--merely that quantity which will relieve the pressure on the diaphragm and on the renal vessels. The author has seen general peritonitis result from tapping. As such a complication will increase all the difficulties of a case, it is very desirable to prevent it by careful application of the antiseptic method and sealing of the punctured orifice to prevent the entrance of germs.

In the protracted cases of cirrhosis there ensues, finally, a highly catarrhal state of the mucous membrane, the bowels become very irritable, and frequent offensive and watery discharges occur. If under these circumstances the abdominal effusion increases, the remedies must consist of diuretics and diaphoretics rather than purgatives. Indeed, an exhaustive colliquative diarrhoea may require bismuth, copper, and other astringents, combined with opium, to prevent the patient passing into the condition of collapse. Hemorrhage by vomiting or by stool will demand ice, subsulphate of iron, ipecac, ergotin in the form of subcutaneous injection especially, and other remedies which have been found useful in gastric or intestinal hemorrhage.