CIRRHOSIS DUE TO MALARIA.

This form of cirrhosis is rare. Osler says that in a large number of malarial cases observed in the Johns Hopkins Hospital during the last nine years not a single case of cirrhosis complicating this disease was noted. It is said that the melanin which lodges in the liver produces the chronic inflammation, fibrous connective tissue developing in large amounts. Jaundice accompanies the cirrhotic condition. Iron pigmentation is noticed in the liver-cells nearest the central and peripheral zones. In this form of cirrhosis there are pain upon pressure, vomiting of bile, and biliary diarrhea, which is often due to biliary pigments and hemoglobin. This occurs particularly in the black water fevers, and in other forms of tropical malaria. This form of cirrhosis is particularly well marked in malarial cachexia, the liver being extremely large, weighing from 2000 to 3000 grams, revealing perihepatitis and marked pigmentation.

SYPHILITIC CIRRHOSIS.

This may be due either to congenital or acquired syphilis. The liver becomes enlarged, tough, and resistant, being as hard as sole-leather, in a measure resembling amyloid liver.

Upon microscopic examination it will be observed that there is a great increase in the connective tissue between the lobules, many areas revealing numerous round and spindle cells. Gummata may also be found in this condition. These may vary from the size of a millet-seed to that of a walnut, and sometimes even larger. These gummata vary from a reddishgreen to a creamy white color. They are often surrounded by a zone of fibrous connective tissue, and when contraction of this newly formed tissue occurs, marked distortion of the organ results. The gummata may occur in the liver without extensive cirrhosis during the course of acquired or congenital syphilis.

Symptoms. The symptoms are those of atrophic cirrhosis ascites, loss of weight, gastric derangements, anemia, and, late in the course, slight jaundice.

Diagnosis. The diagnosis depends upon the history of infection, with enlargement of the organ.

Treatment.-Antisyphilitic treatment should be instituted

early.

HYPERTROPHIC CIRRHOSIS.

Synonyms. Hanot's cirrhosis; biliary cirrhosis; enlarged cirrhotic liver.

Etiology. This is a comparatively rare affection, occurring in the male sex, most frequently between the ages of twenty and thirty-five. Very little is known about the etiology. It has been said that malaria, syphilis, enteric fever, and cholera are predisposing factors. Alcohol has also been mentioned as a predisposing factor. The disease appears to be much more frequent in France than in other parts of the world. Lately the hypothesis has been advocated that it is due to a primary parasitic disease of the biliary passages. It is possible that protozoa and bacteria may have some share in the process.

Pathology.-The organ is greatly increased in size, in some instances weighing as much as 4000 grams. The surface is granular. The portion of the peritoneal coat which lines the liver is frequently adherent to the organ, and is thickened. The liver is tough, cuts with much resistance, and is bile-stained, giving the organ a yellowish-green color. Microscopic examination reveals large masses of fibrous connective tissue between the lobules, and it is said that this connective tissue does not show the marked tendency to contraction that is so characteristic of the atrophic form. Aufrecht called attention to the fact that all the liver-cells are enlarged, and contain more than one nucleus. In the interlobular portions of the organ large numbers of round cells are frequently noted, as well as a number of fibroblasts and some fully developed connective tissue. The biliary passages show catarrhal change, and there is also a great increase in the number of ducts. The spleen is greatly enlarged, and the various tissues of the body are usually deeply bile-stained. Leukocytosis may be present.

Symptoms. The early symptoms of the disease are not characteristic. They may consist of irregular gastric phenomena, such as nausea, loss of appetite, and a sensation of pressure in the epigastrium. It is only when the liver enlarges and becomes painful, and jaundice develops, that the symptoms of the disease become characteristic. At the height of the affection the liver is greatly enlarged, and may encroach upon the normal thoracic area. The liver is tender upon palpation. The jaundice is pronounced. The spleen is greatly enlarged, being easily determined by palpa

tion. If pain occurs in the splenic area, it is due to a perisplenitis. Ascites does not occur. If fluid be found in the peritoneal cavity, its presence is due to complicating peritonitis. At some time in the course of the disease the appetite, which is at first lost, returns; bulimia may even be a symptom. The general nutrition of the patient, however, suffers considerably, and he rapidly loses flesh and strength. The urine is diminished in amount, is concentrated, and of a high specific gravity, containing bile pigment. Polyuria is sometimes associated with marked improvement in the condition of the patient.

The course of the disease is protracted. From the onset of the icteroid symptoms the disease may last from four to twelve years. In the later stages of the disease the jaundice becomes more marked, hemorrhages develop, and an intermittent fever shows itself, death being due to asthenia or to complications. It occasionally happens that toward the close of the affection the liver begins to shrink in size. Arthropathies affecting the fingers and toes, and even some of the larger bones of the extremities, have been noted in the later stages of the disease.

Complications.-These consist in peritonitis, myocarditis, and such changes in the heart as dilatation and hypertrophy. Anemia occasionally occurs, and there is some slight degree of leukocytosis, from 9000 to 20,000 per cubic millimeter. Urinary disease and albuminuria are rarer than in atrophic cirrhosis. Occasionally in the later stages of the discase the hemorrhagic diathesis develops. There may be epistaxis, hemorrhages into the skin, from the gums, and from the intestinal tract. Diagnosis.

Prognosis. The prognosis is always unfavorable. Treatment. The treatment consists in directing attention to the catarrhal condition of the stomach and intestinal tract. The diet should be a bland, unirritating one, and alcohol should be avoided. Iodid of potassium and calomel in continuous small doses have been highly recommended. Arsenic occasionally is of use.

ACUTE YELLOW ATROPHY OF THE LIVER.

Definition. An acute disease of the liver characterized by severe nervous symptoms, vomiting, and hemorrhages, with an associated diminution in the size of the organ, due to parenchymatous and fatty changes.

Synonyms. Acute parenchymatous hepatitis; icterus gravis.

Etiology. This is an exceedingly rare disease, and there have been but 250 cases recorded in medical literature up to the year 1894. It most frequently occurs between the ages of twenty and thirty, no age, however, being exempt. One case has been recorded four days after birth. Females are more frequently affected. Pregnancy appears to play a predisposing part. Season is without influence. No relation has been traced between syphilis and acute yellow atrophy; the same is true of alcohol. Toxic elements appear to have a very close association, and the changes occurring in this condition resemble poisoning by phosphorus; in fact, many symptoms are common to both conditions. It has been claimed by some authorities that mental emotion appears to predispose; there is, however, no proof of this.

Pathology. The organ is flabby, greatly reduced in size, weighing as little as from 90 to 120 grams, being so greatly reduced that on opening the abdomen it is hidden under the diaphragm. The surface is smooth, the capsule is wrinkled, and the color a yellow or dull red, the gall-bladder usually being empty. The consistency of the organ is quite firm, this being due to the fact that the connective tissue and the blood

vessels are more or less well preserved, while the secreting or essential portion is atrophied.

Upon viewing the organ microscopically, a fine granular mass represents the greater portion of the hepatic cells. In many portions fatty degeneration has followed the cloudy swelling, and leucin and tyrosin crystals are often observed. The interstitial parts of the organ—that is, the fibrous connective tissue and the blood-vessels are quite distinct. The spleen is commonly enlarged. It has been suggested that the disease is caused by a micro-organism.

Symptoms. The disease begins as an ordinary attack of catarrhal jaundice. There is loss of appetite, nausea, vomiting, and epigastric distress, and this is followed in a day or two by the appearance of jaundice. One symptom is, however, of importance, and that is the occurrence of some rise in the temperature early in the course of the attack. This stage may last from five days to a week, but may vary considerably. The bowels are constipated; the tongue is coated, and the pulse ranges from 60 to 70 per minute. The usual signs of jaundice in the skin are apparent. As a rule, about this time a sudden change occurs in the clinical picture; there is marked, repeated, and severe vomiting, the patient rapidly becoming drowsy, semiconscious, and often delirious; the delirium may be maniacal, and the jaundice becomes intensified and of a greenish hue. The tongue is dry and brown; the pulse is rapid—from 120 to 140 per minute; and the respiration is quickened. The temperature falls, becoming subnormal. The vomiting has been almost continuous; the vomited matter now shows traces of blood. Enterorrhagia may

occur, the stools being dark and offensive. There may be epistaxis and bleeding from the mouth, and petechiæ may occur. In women metrorrhagia, and in pregnant women abortion or premature birth, occurs. Associated with these symptoms, marked changes occur in the liver.

Upon physical examination it will be noted that dullness in the hepatic area is markedly diminished; in severe cases it may disappear altogether.

In the urine characteristic changes are noted, and the amount of urine is diminished. Leucin, tyrosin, and albumin are present. Bile pigments are increased in amount. The second stage is of extremely short duration, lasting only two or three days, the patient dying with symptoms of delirium, and in convulsions.