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By JOHN B. Deaver, M. D.,
of Philadelphia,

Surgeon-in-Chief, German Hospital, Philadelphia, Pa.

In discussing the surgery of the biliary tract I am mindful of the great amount of literature which has been written upon the subject during recent years, and must acknowledge that this paper will offer nothing new in the way of diagnosis or treatment. The views of every individual surgeon, diverse as they must be from others, in some points, are often of value in pointing out better ways of approaching a correct diagnosis or of performing a successful operation. This is particularly true of gallstone surgery, because infection of the biliary tract leads to so many varied lesions, with either easily recognized or obscure symptoms.

The patient may never have had jaundice, may have but little pain and at no time suffer from the agonizing and classic picture of acute duct obstruction, and yet may have a mass of adhesions in the gallbladder region, a stone in either of the ducts and even a fistulous communication with some adjacent portion of the gastrointestinal canal. The gallbladder is often found packed with calculi or distended with pus (empyema) and the evidence so slight as to require all the judgment and experience of a skilled observer to detect the lesion.

Chronic gallstone disease is often extremely difficult to diagnose, the dragging effect of adhesions upon the gastrointestinal tract, hindering the peristalic movements of the same, obstructing the free action of the pylorus with consequent duodenal catarrh or dilation or ptosis of the stomach, may cause symptoms entirely referable to the gastrointestinal canal.

A small, shrunken, distorted gallbladder, impossible to palpate, may be filled with stones and pus, with no jaundice, no colic, and yet cause a decline in health and strength without apparent cause.

When we review the previous life of an individual supposedly suffering from some infection of the biliary tract, no cause stands out so prominently as a previous attack of enteric fever. The typhoid bacillus is a most fertile factor in the production of acute or chronic biliary tract disease or in the causation of gallstones.

The literature affords full confirmation of this statement. The names of Welch and Blackstein,' Cushing,' and Flexner are well known in this connection.

The following case is interesting:

CASE I.-Mrs. W., aged 36, suffered from an attack of typhoid fever when 16; several years after this attack she began to suffer from indigestion with eructations of gas, and a feeling of distress in the epigastrium. This condition was followed by attacks of colicky pain in the epigastrium, radiating to the right shoulder and through to the back. The attacks of colic were followed by vomiting, which would give relief. There was never any jaundice.

In June, 1903, the attacks of colic became very severe, always with vomiting, accompanied by marked jaundice. Four months ago the patient noticed a swelling over the region of the gallbladder with extreme tenderness at this point upon palpation.

One week before admission to the German Hospital, patient had suffered an attack of pain, which was only relieved by a hypodermic of morphin. The following day

jaundice occurred. Urine was intensely colored; there was tenderness in the epigastrium and over the region of the gallbladder, with pain radiating to the right shoulder; nausea, anorexia, and loss of weight.

When admitted on January 21, jaundice had disappeared, there was no anemia, and no mass could be felt in the gallbladder region, though there was considerable tenderness on palpation. The area of liver dulness was somewhat lower than normal. Blood count showed slight anemia; leukocytes, 4,500.

At operation the gallbladder was found contracted and distended with calculi about 7 mm. to 10 mm. in diameter. The common duct contained three large gallstones about 12 mm. in diameter; the hepatic duct was clear. The opening in the common duct was drained by a tube passing up to the liver and the gallbladder was drained. The patient made an uneventful recovery.

In this case it is reasonable to suppose that the typhoid bacillus infected the gallbladder, and was followed by a catarrhal condition of the gallbladder and ducts, the formation of stones, and finally their expulsion into the common duct.

While to the omnipresent colon bacillus the first place must be credited in the rôle of gallstone producer, the influence of its relative, the typhoid organism, must always be kept in mind. The entrance of bacteria into the biliary tract is possible by three ways: Either they ascend the bile ducts from the duodenum, are deposited by the general circulation, or reach the ducts and gallbladder by means of the portal vein.

The first is, of course, the more probable, and presumably should follow some disturbance in the biliary outflow or a preliminary infection or catarrh of the walls of the duodenum.

I have been unable to determine accurately this previous attack in many of my cases, because all patients have been subject at some time during their previous life to more or less numerous attacks of abdominal colic, usually ascribed

to an error in diet, and forgotten or made little of. Many patients, however, will give the history of one or more attacks of catarrhal jaundice, bilious fever, etc., which have subsided rapidly under treatment, and for many years a period of perfect health has been enjoyed. During these years the slow precipitation of cholesterin and bilirubinate of calcium upon a clump of bacteria, a ball of mucus, or a shred of epithelium may accumulate into a gallstone. Such calculi frequently remain quiescent, and are only ascertained at a chance postmortem when death has occurred from some other disease. Kehr states that not more than one in twenty of those having gallstones suffer any inconvenience from their presence. But tissue which has once been the subject of inflammation, however mild, and in which there is the additional trauma of the presence of gallstones, will furnish a fertile soil for the culture of bacteria. In other cases, the calculi, small and numerous, suddenly give rise to intense symptoms and become propelled through the cystic and common ducts by some force arising from an inflammatory reaction in the walls of the biliary tract from an infection. The distention of the gallbladder by the outpouring of mucus and serum, the dragging upon delicate nerve endings by the stretching of the swollen muscular walls are sufficient to produce the attack of biliary colic with pain referred to the right shoulder, so familiar to us all.

The passage of the stone along the common duct is of great moment to the patient, not alone from the intense and agonizing colic which it engenders, but also from the possible occurrence of complications. Ulceration, perforation, or stricture of the ducts may become immediate sequels, and biliary cirrhosis or pancreatitis the more remote result.

In other cases there is no passage of stones into the cystic duct, and in the mild infections the inflammatory symptoms may subside into a period of latency, the bile once more flow in and out of the gallbladder, and the stones resting quietly, give no symptoms. Frequently during attacks of cholecystitis the inflammatory process extends through the coats of the gallbladder and gives rise to adhesions to the

liver, colon, stomach, duodenum, or omentum, which cause vague pains and gastrointestinal disturbances after the attack has passed.

Recurring attacks of inflammation in the gallbladder will gradually thicken its walls and lead to shrinkage of the organ, with perhaps strictures or contortions. The mucosa shows signs of chronic degeneration, with round-celled infiltration giving place to connective-tissue proliferation and hypertrophy of the muscular coat.

I have scarcely considered the complications of infection of the biliary tract, but have referred to three, of great im-portance and upon which I wish to dwell more particularly: Pancreatitis, biliary cirrhosis, and adhesions of the gallbladder to various of the surrounding viscera.

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The relation of gallbladder disease to inflammation of the pancreas has been so well studied here in Baltimore by Opie that what few remarks I wish to make may doubtless have a familiar sound to all of you. Opie collected fortyone cases of acute pancreatitis associated with cholelithiasis. From one well-studied case which came to autopsy, and from numerous experiments upon animals, he was able to demonstrate definitely "the possibility of reproducing in animals by means of bile, the hemorrhagic lesion which occurs in human patients, and the evidence that the bile diverted into the pancreatic duct by a biliary calculus is capable of producing the lesion of acute hemorrhagic pancreatitis.'

Opie has also collected from the recent literature thirteen cases of acute pancreatitis in which gallstones were present in ten. To these I might add my own reported cases, four in number, one of which was associated with biliary calculi.

This makes seventeen cases, in eleven (65 per cent.) the pancreatic disease being accompanied by calculi in the biliary tract. A considerable number of cases do occur, however, in which gallstones are absent, and should be carefully studied in the endeavor to throw some light upon this interesting disease. Pawlow and his pupils have called attention to the fact that most of the trypsin (the proteid digestant)

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