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complete bile stasis rarely occurs in common duct obstruction, infection must exert a positive influence in the production of the cirrhosis. I can therefore agree with Ford' in his conclusions "that the damming back of bile caused by the obliteration of the ducts does not always lead to the cirrhosis, per se, but may lead to it as well by causing a certain amount of inflammation of the bile channels," by adding, because of the infectious nature of the retained bile.

In urging the possibility of biliary cirrhosis resulting from neglected gallstone cases I am not unmindful of the criticism that jaundice is conspicuous by its absence in the majority of gallstone cases and that most of the instances reported of biliary cirrhosis have followed a long continued obstruction of the ducts with persistent jaundice. But as Weber' aptly expresses it, "to say that because bile passes into the duodenum, chronic obstruction in the common bile duct cannot be a cause of the hepatic cirrhosis, is like saying that because a man with urethral stricture or enlarged prostate has been able to pass urine, obstruction in the urethra cannot have been the cause of his dilated ureters and chronic interstitial nephritis."

Following the obstruction, the biliary ducts become greatly distended with bile, and the entire liver generally enlarged and tense. It is greenish in color, with more rounded edges, and presenting a peculiar streaked appearance. In a patient I have recently operated upon, the anterior border of the liver was obliterated to such a degree as to equal the posterior border. “The surface of the organ may present a granular or slightly puckered appearance from the contraction of the connective tissue, but little or none of the coarse hobnail irregularity often seen in ordinary cirrhosis.”

(Weber®). Microscopically such a liver reveals dilated bile channels and bloodvessels and some pathologists have observed a reduplication of the bile ducts supposed to have arisen from chronically inflamed liver cells, which have degenerated and become connected with the. former bile passages. Others claim that they are simply elongations and enlargements of the previously existing channels. About these channels is an increase of fibrous tissue and the cells of the lobules are frequently atrophic.

The spleen is usually enlarged, probably from hyperplasia of the splenic pulp due to infection by the blood or a condition of autointoxication caused by the diseased liver.

The symptoms of biliary cirrhosis vary greatly. There may be a failing in the general health, emaciation and loss of weight with anorexia, often vomiting. Jaundice is always present, though sometimes slight in degree.

In the more severe cases the obstruction to the duct is followed by the rapid onset of autointoxication or cholemia, emaciation is rapid, jaundice is deep and accompanied by a bile-stained urine and clay-colored stools. The liver is enlarged and hard on palpation. There is itching with petechias, headache, vomiting and then delirium and death. If the case is protracted, ascites, and edema of the lower extremities may be observed.

Adhesion of the gallbladder or ducts to surrounding viscera will follow nearly all severe inflammations of the gallbladder from a pericholecystitis and embarrass the functions of the contiguous organs involved by the adhesions. In the suppurative form of cholecystitis such adhesions are apt to become more extensive from the extension of the infection to the surrounding viscera and peritoneum. The anatomic relations of the gallbladder to the hepatic flexure of the colon, to the duodenum, to the pylorus, pancreas and great omentum are so intimate that these structures are rendered very liable to involvement in this adhesive peritonitis.

Intestinal obstruction has frequently been diagnosed in a case of suppurative cholecystitis with a local peritonitis involving and paralyzing the large bowel. After the subsidence of the acute symptoms severe pain may persist from the perisaltic action of an adherent duodenum or great omentum, or dilation of the stomach may ensue from the obstruction, by constricting bands, involving the pylorus or duodenum.

The influnce of adhesions is well illustrated in the following case recently observed, especially when we recall the oft-quoted statement that jaundice preceded by colic is nearly always due to stone.

CASE II.—Mrs. C., aged 36, a laundress. Gave family history of father having died from cirrhosis of the liver, her mother of carcinoma of the breast.

The patient's right breast was removed two years ago for carcinoma and shortly afterward a complete vaginal hysterectomy performed, but she is totally ignorant of the cause for the latter operation. She has had six children, four of whom are living.

Her menstrual flow ceased after the hysterectomy, but at her periods she suffered intense pelvic cramp-like pain up to a year ago when the pain changed in location to the upper abdomen and was referred to the right shoulder and back. Recently the pain became more intense, was always accompanied by a chill, fever and vomiting followed by slight jaundice, lasting for three days. The bowels are usually constipated and the stools always dark.

A physical examination revealed slight jaundice of the skin and mucous membranes, slight rigidity of the abdominal walls and a localized area of tenderness over the gallbladder region. There was no anemia, the leukocytes numbered 7,000 and the stools were negative in an examination for free fat. Her temperature varied from ninety-eight to ninety-nine degrees. The pulse from seventy-five to ninetyfive.

At operation, February 23, 1904, numerous adhesions were encountered between the gallbladder and neighboring viscera (stomach and duodenum) and the omentum. The gallbladder was not enlarged, contained no stones, and was filled with thick, dark bile, which upon subsequent culture, upon bouillon only, proved to be sterile. The ducts were clear, but the liver was somewhat enlarged and presented that peculiar streaked greenish appearance which I have learned to regard as an indication of biliary cirrhosis. Cholecystostomy was followed by an uninterrupted recovery.

The absence of a known primary attack of cholecystitis, the pain, fever and vomiting followed by jaundice and the operative findings of adhesions only, were extremely interesting. The diagnosis was regarded as a certain one of

cholelithiasis, probably in the common duct, pancreatitis having been excluded by the absence of anemia, wasting and epigastric pain.

Case III.- In another patient symptoms of "stomach trouble” were experienced three years prior to the time I first saw her. There was pain at night in the epigastrium and over the gallbladder, a feeling of distress after eating, and constipation. During the past year these attacks recurred every two or three weeks with increasing severity in the pain. One week ago the pain became distinctly cramplike over the region of the gallbladder. There were vomiting, jaundice, biliuria, and a feeling of distress in the epigastrium after eating. The pain did not radiate to the right shoulder. Blood count showed a slight anemia, and 11,330 leukocytes.

At operation the gallbladder was found to be surrounded by adhesions attaching it to the omentum, duodenum, and pylorus. It was filled with thick, dark, ropy-like bile, but no stones. Bile revealed B. coli communis in pure culture.

Cholecystostomy was followed by uninterrupted recovery.

Carcinoma of the biliary passages, when primary, is frequently a result of gallstone irritation, especially with an hereditary predisposition to malignant disease. The malignant growth occurs most commonly in the gallbladder, infiltrating the walls and spreading to the neighboring hepatic tissue.

In the bile ducts the growth may be primary, or as a result of extension from the gallbladder, the walls of the duct becoming infiltrated and occluded.

The diagnosis is difficult to make in the early stages, because, with the probable history of previous gallstone attacks, the resulting pericholecystitis with adherent and tangled omentum will give a resistance to palpation just as the beginning tumor will. There are digestive disturbances with gradual loss of weight or strength; jaundice is absent, unless the portal lymphatics become enlarged and cause pressure, or the infiltration of the duct walls occludes the lumen. It then increases slowly, becoming intense and permanent. Fever and rigors are rarely present. Later in the disease

the wellmarked cachexia develops, and there is ascites from disturbance of the portal circulation. The appearance of a hard nodular tumor tender to palpation, moving with respiration and increasing rapidly, decides the diagnosis. It is well to remember that in cases of chronic obstruction of the common duct by a stone, of long standing, a cachexia may be present, very closely resembling that of malignant disease.

When the gallbladder is infiltrated by a growth from neighboring organs, the condition is beyond surgical help, and needs no description.

The indications of the methods of treatment in disease of the biliary tract can be discussed briefly, so firm is my belief in the efficacy of surgical interference only. I have seen so many disasters overtake all endeavors at temporizing with cholagogues and local applications that I am not only in accord with Robson's statement, “as soon as gallstones give serious trouble, their removal by operation is the most radical method of treatment, since it is only from the complications, which in many cases of cholelithiasis arise sooner or later, that any danger after operation may be apprehended;" but will go a step further in advising operation when gallstones are believed to be present.

In certain patients, usually women, obese and dyspneic, with a fat and flabby abdomen, past the middle period of life, with usually a tendency to varicose veins and a weak heart, operation is attended with considerable danger. Such patients also may have small amounts of sugar from pancreatic involvment, and I would hesitate to operate in the absence of an absolute indication that such operation was necessary to save life. These patients are better kept at absolute rest without food for twenty-four to forty-eight hours, with gentle catharsis and diuresis and the use of heat or cold to the gallbladder region for the relief of pain. After recovery from the attack, the tendency to lithiasis must be combated by sending them to Carlsbad or by directing like treatment at home, and inflammatory conditions in the duodenum prevented by a careful avoidance of heavy and indigestible food. In acute gallstone obstruction of the com

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