CHROMIC PANCREATITIS
Definition. Chronic pancreatitis and chronic relapsing pancreatitis can be considered together, since both represent a slowly progressive destrucÂtion of pancreatic acini, varying amounts of inÂflammation, fibrosis, and dilatation and distortion of the pancreatic ducts. In chronic relapsing panÂcreatitis there are associated episodes of acute inÂflammation. The end result is that of varying deÂgrees of pancreatic destruction and exocrine insufficiency.
Etiology and Pathogenesis. By and large the same conditions listed in as being asÂsociated with acute pancreatitis may also lead to chronic pancreatitis. Biliary tract disease, howÂever, is rarely associated with chronic pancreaÂtitis. In the United States the major associated conditions are alcoholism in adults and cystic fiÂbrosis in children; in the developing countries the most common cause seems to be protein-calorie malnutrition. The cause is unknown in many cases. Injury is presumed to be secondary to au-todigestion, as in acute pancreatitis (Fig. 42-4), but this has not been established.
Clinical Manifestations. The most important symptoms and signs of chronic pancreatitis are summarized in Table 42-5. In general, severe, inÂtractable abdominal pain is the cardinal sympÂtom, although pain may be mild or even absent in a minority of patients or episodic with relapsÂing pancreatitis. The pain may go through to the back, be partially relieved by sitting up and leanÂing forward, be exacerbated by eating or drinking alcohol, or exhibit none of these features. Patients usually lose weight because of anorexia and/or an associated malabsorption (steatorrhea and azotor-rhea). Encasement of the common bile duct in fiÂbrous tissue may produce obstructive jaundice. The islets of Langerhans often become sufficiently destroyed to produce diabetes mellitus. GastroinÂtestinal bleeding may rarely result from thromÂbosis of the splenic vein, leading to gastric varices, or more commonly from gastritis, resulting from the associated excessive use of ethanol or aspirin (in an attempt to relieve pain). Rarely, an abdomÂinal mass representing a pseudocyst may be palÂpated.
Diagnosis. The diagnosis of chronic panÂcreatitis as a cause of pain is usually easy in the presence of the classic triad of pancreatic calÂcification, pancreatic exocrine deficiency (malabÂsorption], and diabetes mellitus, especially if any of the known risk factors are present. However, only a minority of patients present with this comÂplete clinical picture. The differential diagnosis usually includes abdominal malignancy, espeÂcially carcinoma of the pancreas or of the stomach or colon. Biliary tract disease, peptic ulcer disÂease, mesenteric vascular disease, and functional abdominal complaints may occasionally simulate the pain of chronic pancreatitis.
Measurement of serum amylase is of no help in the diagnosis of chronic pancreatitis, since it is usually elevated only during acute exacerbations of chronic, relapsing pancreatitis. Three structural features may be of help: (1) the demonstration of pancreatic calcification by a plain abdominal raÂdiograph or, with greater sensitivity, by CT; (2) the demonstration of dilated, distorted ducts, best shown by ERCP (Fig. 42-5); (3) the demonstration of pseudocysts by ultrasonography and/or CT.
Malabsorption can be demonstrated by fecal analysis for fat, and its pancreatic origin can be deduced by the tests described in Chapter 36C. In chronic pancreatitis pancreatic stimulation tests characteristically show reductions in pancreatic juice volume, bicarbonate content, amylase outÂput, and tryptic activity.
Treatment and Prognosis. The treatment of chronic pancreatitis is directed toward (1J preÂvention of further injury, (2J relief of pain, and (3] replacement of lost exocrine function. Prevention of further injury usually depends upon attempting to reverse one or more of the factors listed in , especially alcoholism. The replacement of lost exocrine function is described in Chapter 36C on Malabsorption. The treatment of pain is usuÂally the most difficult and important challenge. There are three general approaches:
Analgesics. Attempts should be made to begin with nonaddictive analgesics before resorting to narcotics. Many patients unfortunately become addicted because of the severity and duration of the pain.
“Putting the Pancreas at Rest.” The ingestion of large amounts of pancreatic enzymes may reduce pain, presumably by diminishing stimuli to its exÂocrine secretion. Avoiding large meals and alcoÂhol also may help.
Surgical Therapy. Surgery to relieve a ductal obÂstruction or drainage of a pseudocyst may be efÂfective in selected cases of intractable pain, alÂthough the results are often unsatisfactory. Fortunately, the pain of chronic pancreatitis tends to diminish over time, presumably because of the destruction of most of the residual functioning exÂocrine cells. Patients seldom die of uncompliÂcated chronic pancreatitis.
Complications. The complications that may be associated with chronic pancreatitis are listed in . An increased incidence of carcinoma of the pancreas probably occurs only in rare forms of hereditary pancreatitis.