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exists as trypsinogen until it comes in contact with the intestinal secretion, when the full proteolytic power is exerted.
Starling,' therefore, suggests that "it seems possible that the accidental entry of the succus entericus into the gland through an abnormally dilated duct might account for the production of certain cases of pancreatitis.”
In addition, the influence of other agents as causative factors in obstructing the pancreatic ducts must be considered, and particularly the influence of microorganisms. Bacteria may not only infect the retained secretion, but may also by direct continuity ascend from an existing gastrointestinal catarrh.
That gallstones do not always induce acute pancreatitis is also explained from the anatomic standpoint, when we consider that in two-thirds of subjects an accessory pancreatic duct exists, and that in about 10 per cent. the common bile duct and the duct of Wirsung open by separate orifices into the duodenum. In addition, the gallstones may remain in the gallbladder, become impacted in the common duct at a point where no pressure is exerted upon the pancreas, or escape into the bowel without becoming checked in the ampulla.
Chronic pancreatitis is also frequently due to some obstruction of the duct of the pancreas by gallstones. This is particularly apparent when the biliary calculus is large and so situated that the duct of Wirsung is occluded without the entrance of the bile into the pancreas. When obstruction occurs the secretion is gradually dammed back upon the gland, infection is favored and the pancreas becomes damaged. The gland, especially at the head, enlarges, and to the palpating hand is hard, frequently nodular. The surface is granular and compact with the replacement of the loose interlobular tissue of the normal gland by that of a dense and scar-like hardness. In more advanced cases, areas of fat are observed to have encroached upon the parenchyma, and finally nothing may remain of the pancreas but a mass of fat held together by strands of fibrous tissue.
The diagnosis of pancreatitis is often exceedingly difficult, and the chronic form is very frequently confused with carcinoma involving the head of the organ. In one of my cases with intense jaundice, the condition was believed to be carcinoma, even at the operating table, though at necropsy a marked condition of interlobular pancreatitis was found; no malignancy. Mikulicz had an exactly similar experience. The complexity of the symptomatology in chronic pancreatitis depends upon the associated lesions in the stomach, intestine and liver, where such conditions as gastrointestinal and biliary tract inflammation, arteriosclerosis, alcohol, etc., have been the causal factors in the production of the chronic pancreatitis.
In general, it may be stated that when an individual, from whom the history of a previous gallstone colic may or may not be elicited, is suddenly seized with severe epigastric pain, nausea, vomiting, rapid pulse, dyspnea and cyanosis, followed by a rapid loss of strength, the diagnosis is acute pancreatitis. The early symptoms strongly resemble those of intestinal obstruction, and the exhaustion and collapse are frequently so severe as to induce death within fortyeight hours. The pain is colicky in character and there are either intervals of relief or else continued pain with exacerbations of severe colicky attacks. This is explainable from the obstruction of the ampulla, as inflammation without obstruction does not tend to excite pain of a colicky character. Bilateral and nearly board-like rigidity of the overlying abdominal walls is present from the onset.
Tympany develops in the epigastrium from paresis of the stomach and intestines, but not to the extent of obscuring liver dullness, unless suppuration and peritonitis occur. Tenderness to pressure is an early symptom. If the patient survives, jaundice may develop, if not already present from the previous gallstone disease; pain in the epigastrium continues and fever is observed.
If secondary infection occurs the epigastrium is distended and tympanitic, and palpation may detect distinct tenderness over the pancreas or a sense of resistance. - The actual
abscess can rarely be felt in the early stages, though it may appear as a tumor mass above the umbilicus.
Chronic pancreatitis, due to gallstones, is often difficult to recognize. This can be easily understood from the etiology of the disease. Long before the disease of the pancreas can give rise to symptoms, the gastrointestinal disorders, the gallstones, arteriosclerosis, etc., will have shown some manifestations of their presence, and the later symptoms, in nearly the same locality, will be supposed to be a continuation of the primary lesion. Furthermore, it is probable that disturbances in the functions of the stomach, intestines, and liver must take place when the causes mentioned induce a lesion of the pancreas, so that the symptomatology observed is very complex. There may be a history of colicky pain in the gallbladder region, associated with jaundice, and often with fever intermittent in type, or pain referred to the left costovertebral angle, where there may also be tenderness. The epigastrium is tender, often distended, and during the attack the recti muscles become rigid, and a point of tenderness may be detected over the head of the pancreas, one inch above and one inch to the right of the umbilicus. In a few cases the stools may appear greasy and lighter in color, and may contain muscle fibers.
Glycosuria, especially in an alcoholic subject, with a cirrhotic liver is a valuable sign of the interacinar form of pancreatitis.
As the disease advances, gastrointestinal disorders become constant, with emaciation, loss of strength, jaundice, and recurring attacks of epigastric pain, often extending around the left side or through to the back as just referred to.
In thin subjects a tumor may be made out, and if malignant disease can be excluded, the diagnosis becomes clear; but such a differentiation is extremely difficult, the indurated pancreas frequently producing a permanent jaundice, with enlarged gallbladder. In advanced stages with destruction of the parenchyma of the gland and involvment of the islands of Langerhans, glycosuria is more common,
and the patient finally dies of exhaustion, or perhaps some terminal infection.
In cases associated with syphilis, arteriosclerosis or tuberulosis, the onset is much slower, more general, and more indefinite. Sensations of pressure in the epigastrium, gastrointestinal disorders, epigastric tenderness may be complained of and emaciation observed.
Some patients undoubtedly recover after having lost much weight, and with a history of gallstone colic, jaundice, and anemia. The duct of the pancreas having become patulous, the secretion is no longer retained, and sufficient healthy parenchyma remains to perform the pancreatic functions.
In all cases careful attention must be paid to the minute points in the previous history of the patient. The stools should always be searched for fat and muscle fibers, the urine for sugar, phenol (salol test), and the fat-splitting ferment. If gastric complications are suspected, the testmeal is invaluable and the blood count will show the qualitative changes in the red and white cells. The clinician, by careful palpation and percussion, can ascertain the point of greatest tenderness and resistance with the possible finding of a tumor mass. A röntgen ray examination may show a mass in the region of the head of the pancreas not moving with respiration. Such a finding is valuable, as the shadow cast by the pancreas is not readily movable with the motion of the diaphragm. It is only by grouping both the clinical and the laboratory findings that the disease of the pancreas may be accurately and satisfactorily studied.
Biliary cirrhosis in cases of obstructive cholelithiasis results from the irritant effects of retained accumulating bile, which, from the backward pressure, passes out of the bile ducts, and causes atrophy of the lobules. As long ago as 1873 Legg tied the common bile duct in animals and produced jaundice, a well-marked emaciation, and finally death. At autopsy he found enlargement of the liver and an increase of the interlobular connective tissue.
Charcot and Gombault, in 1876, published their monograph on diseases of the pancreas, and reported four cases of cirrhosis of the liver following obstruction of the bile ducts, the obstruction having been caused by calculi in the gallbladder, calculi in the ampulla, carcinoma of the pancreas, and a cholangitis of the larger bile ducts.
The literature contains many references to cases of obstructive biliary cirrhosis, most of which have been the result of a congenital deficiency of the bile ducts, but many instances are directly traceable to gallstones. The calculi may cause the obstruction by pressure upon the hepatic, by a stone in the cystic duct, by direct occlusion of the common duct by a stone, by the contracting influence of a stricture following ulceration of the common duct, or by an enlarged head of the pancreas.
The resulting liver cirrhosis has been compared to that in the pancreas as the result of long continued obstruction to its ducts, and to the chronic intestitial nephritis, which accompanies obstruction to the outflow of urine by a calculus.
The occurrence of a biliary cirrhosis from obstruction and retained bile, per se, has been denied by many writers, who believe that there must always occur an inflammation of the bile ducts, a cholangitis, subsequent to the stasis.
While many experiments upon animals have demonstrated the possibility of a cirrhosis of the liver solely dependent upon the damming back of the bile and not to any inflammation of the walls of the smaller bile channels, the latter is probably invariably present in man.
This leads us to consider the influence of infection upon the inflammatory origin of the cirrhosis, and which from the purely clinical standpoint seems to be one of great import
In the great majority of common duct obstruction cases for which I have operated, a bacteriological investigation of the bile has revealed the presence of some microorganisms, the colon bacillus, the typhoid bacillus, the staphylococcus, or the streptococcus. It has, therefore, been apparent, in my experience, that with the knowledge that