runs downwards and forwards along the cystic duct and usually behind it, dividing into two branches. Its close relationship to the cystic duct explains the occlusion of the artery by an obstructing stone in the duct and accounts for gangrene of the gall-bladder when an infection already exists. The cystic duct, one and one-half inches in length, runs downwards and to the left between the layers of the lesser omentum, where it joins the common hepatic duct to form the common bile duct. The angle of union is very oblique, the hepatic duct forming a nearly direct continuation with the common duct. The hepatic duct is about two inches in length and widens as it descends to the right and in front of the portal vein to become continuous with the common bile duct. The latter, about three inches in length, empties at a papilla in the lower part of the perpendicular portion of the duodenum. As a rule the pancreatic duct also empties into the duodenum, through this papilla; the common duct may be divided into three portions. the supra-duodenal portion, extending to the upper portion of the duodenum. It is contained within the free edge of the lesser omentum, the hepatic artery lying to the left and the portal vein behind. In this part of its course the common duct can easily be palpated between the thumb and index finger of the left hand; the index finger being introduced into the foramen of Winslow, the back of the operator being turned to the edge of the table. The second portion, retro-duodenal, lies behind the duodenum, and between it and the head of the pancreas or in a groove or within a tunnel of the latter. Munger found in fifty-five out of fifty-eight cases, this part of the duct surrounded by pancreatic tissue. The third or interstitial part of the duct runs obliquely through the wall of the duodenum for a distance of about three-quarters of an inch. At its termination there is a slight widening-the diverticulum or Ampulla of Vater, in which stones are liable to lodge. Surrounding the outlet of the common duct there is a circular muscle; the sphincter of Oddi and the longitudinal fibres within the duct wall are continuous with those of the gall-bladder.

FUNCTION.

The function of the gall-bladder is not definitely known. That it is not essential is evident in studies of comparative anatomy and from the fact that it is not missed after removal.

As seen in the larger fowl, it presents a rhythmic contraction. Okada found that during digestion contractions occur about two to five times per minute in order that a certain quantity may be poured into the duodenum as soon as this receives the chyme discharged from the stomach. That some

storage function seems desirable to the human being is proved by the fact that a secondary gall-bladder (though of small size) not infrequently forms after the gall-bladder has been removed. Bile, while in the gall-bladder becomes darker in color and thickens (solid matter increasing from 1 to 400 per cent.).

Pain in the right shoulder, so often complained of in gallstone colic and diseases of the liver, is due to the partial origin of the phrenic nerve from the fourth cervical, which also sends branches to the shoulder. Pain in the region of the scapula in diseases of the gall-bladder is probably a reflex and accounted for through irritation of the intercostal filaments to the diaphragm from which the pain is reflected to the posterior dorsal cutaneous.

Anomalies: It may be anomalous in being inside the liver, left-sided or entirely floating.

WOUNDS OR PERFORATION OF THE GALL-BLADDER.

Rupture of a distended gall-bladder has been occasionally met with as the result of direct violence, such as being caught between bumpers or being run over. In the same way perforating wounds of the gall-bladder have been recorded. Most perforations in the gall-bladder and the bile ducts, however, are the result of diseased conditions which cause either great distention with thinning of the gall-bladder wall or have been associated with perforation of stones.

SYMPTOMS.

Perforation usually develops slowly, ushered in with a pericystitis and often the formation of an extra-cystic abscess. As a rule there are premonitory symptoms, indicating that there is something wrong. In other cases rupture takes place without a warning signal and at once gives the patient the ap-pearance of suffering a grave abdominal disaster. When rupture occurs in a discased gall-bladder, it is often associated with occlusion of the cystic duct and only a relatively small amount of bile or muco-pus escapes into the peritoneal cavity, which probably has already been shut off by adhesions. If adhesions are absent it is likely to be poured into the general peritoneal cavity. As a sign of this, one may see localized jaundice strictly limited to the umbilicus and the skin immediately surrounding it. The result of rupture of the biliary passages will depend upon the condition of the bile. If it contains pathogenic organisms, a general septic peritonitis or a localized peritonitis resulting in abscess formation will follow. However, it rarely has the rapidly fatal ending that is seen after perforation of the appendix. If the bile is sterile,

or nearly so, a sub-acute peritonitis with a plastic exudate occurs, as a result of which encapsulation of the escaped bile takes place. When the patient has recovered from the shock, · jaundice develops in about sixty-five per cent. of cases.

ETIOLOGY OF GALL-BLADDER DISEASE AND GALL-STONES.

Identical: Both rare in young children, although small stones have been found in the new born. In 409 cases Walton found no stones under the twentieth year. Usually found between fourth and fifth decades of life. Ninety per cent. of gall-stone cases operated upon occur in women.

The causative primary infection most commonly occurs in young married women in connection with some parturient period. Mayo says that of all married women who have gallstones ninety per cent. identify the beginning with some particular pregnancy. Hemorrhoids, which are common in the last months of pregnancy may explain this relationship. Appendicitis, typhoid fever, ulcer of the stomach and duodenum and enterocolitis may be followed by cholecystitis and later gall-stones. The infection may reach the gall-bladder: (1) By direct extension of the infection through the duodenal papilla or its lymphatics. While organisms which are rare in the duodenum, may not ascend against a normal bile stream, they may grow in an obstructed bile duct. (2) Through the portal circulation and elimination with the bile. (3) Through the arterial circulation. It has been established that certain pathogenic organisms show a special affinity for some particular organ and tissue, and it is now believed that this is the principal route through which the gall-bladder is infected. Rosenow has shown that streptococci and colon bacilli from acute cholecystitis intravenously injected, give rise to a like disease in animals. This power may be lost by prolonged cultivation. In a considerable percentage of even chronic cases the deep layers of the gall-bladder show streptococci, and it is thought that this organism is the primal agent in most cases of infection of the viscus, and that the colon bacillus is secondary; but the latter as well as the typhoid bacillus may be the primary cause through the systemic circulation.

In 1886 Gallipe found germs in the gall-stones themselves. In more than seventy per cent. cultures will show organisms, so that Moynihan's epigram is largely true, viz.: "that every gall-stone is a tombstone to the memory of the dead germs that lie within it." In order of frequency the germs buried in gallstones and culturable after years are colon bacillus, typhoid bacillus and streptococcus.

PATHOGENESIS OF GALL-STONES.

Practically all are developed in the gall-bladder. Cholesterin, the principal constituent of most gall-stones, is not derived from the bile even when it is stagnant, but from the excessive function of the cells lining the gall-bladder, when this is the seat of infection. As there is no cholesterin bearing mucosa in the bile ducts, stones containing cholesterin cannot be developed in them, but stones made up mostly of coloring matter are sometimes formed in the ducts. The number, shape and size varies greatly, from one to one thousand or more. Single stones are usually globular or ovate, when multiple they are usually beautifully facetted and glistening.

CHEMICAL COMPOSITION.

1. Pure cholesterin: rare and then very small, round, translucent and very light.

2. Laminated cholesterin stones: ninety per cent. cholesterin with bilirubin, biliverdin and calcium.

3. The mixed cholesterin is the commonest type and they are usually found when there are many stones. They are much facetted, with brown, yellow or white surfaces.

4. Mixed bilirubin calcium with twenty-five per cent. cholesterin. Few and large.

5. Pure bilirubin calcium are usually very small, rarely larger than a pea, brown or black in appearance and occasionally conglomerate.

6. Rarely conglomerate due to welding together of a number of stones.

COMPLICATIONS OF CHOLECYSTITIS AND GALL-STONES.

In acute cases there is danger of ulceration, gangrene and perforation.

1. Abscess of the liver. Usually "multiple" from extension upwards of a cholangitis, or may rarely be "single" from ulceration of a gall-stone through the gall-bladder and into the liver.

2.

Fistula may occur between the gall-bladder and the duodenum, colon or stomach, the result of perforation. The rarest fistulae are into the urinary tract, the stones passing into the renal pelvis or into the urinary bladder through a patent urachus. Cutaneous fistula may have (1) a mucoid discharge, due to obstruction of the cystic duct from a stone or stones, or stenosis, or (2) a flow of bile, due to obstruction of the common duct usually from a stone.

3. Adhesions between the gall-bladder and bile ducts and contiguous structures are common, causing symptoms even after inflammation of the gall-bladder has subsided, or the gall-bladder and gall-stones have been removed. 4. Malignant disease of the gall-bladder may follow prolonged irritation from stones.

5. Acute intestinal obstruction may result from impaction of a large gall-stone, which has ulcerated into the duodenum.

6.

Another important complication of gall-stone disease is acute and especially chronic pancreatitis, due to the anatomical relationship of the ducts on entering the duodenum, usually by a common opening.

SYMPTOMS OF ACUTE CHOLECYSTITIS.

This usually begins with nausea and vomiting of short duration, elevation of temperature; pain in the epigastrium and in the back, accompanied by tenderness in the region of the gall-bladder with rigidity of the overlying muscles. The pain varies much and in typhoid fever may be absent. It is spasmodic in character with periods of great exacerbation probably due to over-distension. When the gall-bladder is much distended it can easily be felt. Respirations will be diminished or absent over this side. The gall-bladder usually enlarges towards the umbilicus. In rare cases it may extend backwards to the costo-iliac angle. If acute cholecystitis of the catarrhal type is accompanied by jaundice, it will be painless. The disease is usually not associated with jaundice, unless there is obstruction of the common duct. Usually not accompanied by high fever until empyema or ulceration have resulted. The pulse remains nearly normal as it does in many infections of the liver.

Polynuclear leukocytosis rarely exceeds 12,000 unless there is extension to the small bile ducts or pericystic suppuration. The diagnosis is easy. Palpation reveals a tender and enlarged gall-bladder. The symptoms of chronic cholecystitis resemble those of gall-stones because the two conditions are usually associated.

TREATMENT OF ACUTE CHOLECYSTITIS.

A few cases may recover spontaneously by restoration of the natural drainage into the intestine, but where the symptoms persist and increase in severity, with the impending danger of empyema, ulceration and perforation, immediate surgical intervention is indicated. As a rule drainage of the gall