Chronic pancreatitis is defined histologically as irreversible pancreatic gland destruction with fibrosis which can result in impaired exocrine and endocrine dysfunction. However, up to 90% of the pancreas gland needs to be affected before endocrine or exocrine dysfunction is clinically apparent.
Making the diagnosis of chronic pancreatitis clinically can be difficult in the absence clinical evidence of fat malabsorption or glucose intolerance, or the classic radiologic findings of pancreatic calcification, intraductal pancreatic stones or a dilated pancreatic duct. Often endoscopic ultrasound (EUS) examination is preferred to ERCP to make the diagnosis of early chronic pancreatitis; although this can be an overly sensitive. Pancreatic function testing is not widely available.
While the most common cause of chronic pancreatitis remains alcohol, other important causes include hereditary pancreatitis (CFTR gene, SPINK-1 gene, PRSS-1 gene) and autoimmune pancreatitis (AIP). Identifying a cause is important to lessen the development of repeat attacks and to risk-stratify the patient for cancer risk. Making the diagnosis of AIP ( elevated IgG4, hyperintense peripancreatic “halo” on CT scan) is important as some of these patients may respond to treatment with steroids.
Management of chronic pancreatitis is aimed at identifying and treating the complications including pain, exocrine insufficiency, endocrine insufficiency (glucose intolerance, diabetes mellitus), biliary obstruction, splenic vein occlusion, pseudocyst formation, bile duct or duodenal obstruction, and increased cancer risk. The management of pain associated with chronic pancreatitis is primarily medical (analgesia and a trial of pancreatic enzymes), with a limited role for celiac nerve block or endoscopic therapy. Surgical management for pain control (pancreatic resection, lateral pancreatojejunostomy) may be warranted and appears to be superior to endoscopic therapy long-term. Exocrine insufficiency is typically managed with pancreatic enzymes and restriction of fat intake titrated to correct fat malabsorption, resolve steatorrhea and maintain weight. Concomitant gastric acid inhibition is necessary to avoid acid inactivation of pancreatic enzymes. Long-term biliary obstruction is best managed through surgical biliary diversion or occasionally by endoscopic stenting to avoid the development of secondary biliary cirrhosis. The risk of cancer associated with chronic pancreatitis varies with the underlying etiology, with patients with hereditary pancreatitis having the highest risk. While routine screening for pancreatic cancer in patients with chronic pancreatitis is not recommended, the development of an acute change in a previously stable patient with chronic pancreatitis (weight loss, biliary obstruction, worsening pain, elevated CA19-9) should stimulate a search for an underlying malignancy.
At the Yale Pancreas Disease Program, we offer expert multidisciplinary evaluation, diagnosis, and treatment of patients with chronic pancreatitis.