Health Questions and Answers

Chronic Pancreatitis

What classification system is used for chronic pancreatitis (CP)?
CP is an inflammatory condition that leads to progressive and irreversible changes in the pancreas, which ultimately results in impairment of exocrine and endocrine function. This differs from acute pancreatitis, which is a nonprogressive event with pancreatic function returning to normal after the attack. The modified Marseilles-Rome classification classifies CP into four groups based on morphology, molecular biology, and epidemiology:

  • Lithogenic CP (calcifying CP) is characterized by irregular fibrosis of the pancreas with intraductal protein plugs, intraductal stones, and ductal injury. Most cases of CP belong to this group, and the leading cause is alcohol abuse.
  • Obstructive CP demonstrates glandular changes, including uniform fibrosis, ductal changes with dilation, and acinar atrophy, all of which may improve when obstruction of the pancreatic duct is removed. Common causes of obstruction include intraductal tumor or benign ductal stricture.
  • Inflammatory CP is characterized histologically by mononuclear cell infiltration with exocrine parenchymal destruction, diffuse fibrosis, and atrophy. Associated disorders include auto-immune diseases, such as Sjögren’s syndrome, primary sclerosing cholangitis, and auto-immune pancreatitis.
  • Asymptomatic pancreatic fibrosis is characterized by silent, diffuse perilobular fibrosis as seen in so-called idiopathic senile CP.

What is the most common cause of chronic pancreatitis in adults?
Chronic alcohol abuse is the most common cause of CP in Western societies. It accounts for 70-80% of all cases. The risk of developing CP appears to be related to the duration and amount of alcohol consumed and not to the type of alcohol or pattern of drinking. Although there is variation in individual sensitivity to alcohol, published reports suggest that at least 5 years of alcohol intake exceeding 150 gm/day is needed prior to developing CP. Because only 5-10% of alcoholics develop CP, other cofactors may be involved. Proposed cofactors include a diet high in fat and protein, deficiency of antioxidants or trace elements, smoking, and, possibly, genetic predisposition.

What are the other causes of chronic pancreatitis?

  • Genetic (including hereditary pancreatitis and cystic fibrosis)
  • Obstructive (from a benign stricture resulting from trauma or previous episodes of acute pancreatitis or malignant pancreatic duct obstruction)
  • Tropical/nutritional
  • Metabolic (resulting from hypercalcemia or hypertriglyceridemia)
  • Autoimmune
  • Idiopathic

What is hereditary pancreatitis?
Hereditary pancreatitis is an autosomal dominant disorder with 80% penetrance and variable expression. It accounts for approximately 1% of all cases of CP and has been described in families throughout the world. Hereditary pancreatitis affects both sexes equally and presents typically as episodes of acute pancreatitis in childhood by ages 10-12. Recurrent episodes of acute pancreatitis lead to the development of CP. They have a predisposition for development of pancreatic carcinoma, with a 40% incidence by age 70. Genetic testing for trypsinogen gene mutations are specific for hereditary pancreatitis and should be offered to young patients with recurrent pancreatitis and a positive family history of pancreatic disease. The diagnosis is suspected when several family members have pancreatic disease, especially CP without other identifiable causes.

How is cystic fibrosis associated with chronic pancreatitis?
Cystic fibrosis is the most common autosomal recessive defect in Caucasians and is due to mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Approximately 85% of patients with cystic fibrosis develop exocrine pancreatic insufficiency. The CFTR mutation causes reduced and defective ductular and acinar pancreatic secretions, ultimately resulting in pancreatic duct obstruction and acinar cell destruction with fibrosis. It should be suspected in all young persons with acute pancreatitis in whom another cause is not readily apparent. A clue to its presence is difficulty conceiving in a male.

What is obstructive chronic pancreatitis?
Benign or malignant obstruction of the pancreatic duct can lead to CP. Causes include strictures from trauma, pseudocysts, calcific stones, papillary stenosis, pancreas divisum, and malignant tumors. Relief of the obstruction can reverse some of the pancreatic damage and preserve pancreatic function.

What is tropical pancreatitis?
Tropical or nutritional pancreatitis is seen commonly in residents of Southern India, Indonesia, and sub-Saharan Africa. It presents in young adults who manifest with abdominal pain, severe malnutrition, and exocrine or endocrine insufficiency with diabetes and large pancreatic duct calculi. The cause of tropical pancreatitis is unknown. Proposed theories include tropical pancreatitis being the sequela of prolonged severe protein-calorie malnutrition and, possibly, oxidative injury from consumption of the cassava fruit.

What is autoimmune pancreatitis?
Autoimmune pancreatitis, also known as sclerosing pancreatitis or lymphoplasmacytic pancreatitis, is the most recently described form of CP. It is characterized by the presence of autoantibodies, increased levels of serum immunoglobulins, elevated serum IgG4 levels, and response to steroid therapy. Anatomically, there is diffuse or focal enlargement of the pancreas with pancreatic duct strictures. Histologic findings are characterized by a dense lymphoplasmacytic infiltrate. In 60% of cases, autoimmune pancreatitis is associated with other autoimmune disorders, such as primary sclerosing cholangitis, primary biliary cirrhosis, autoimmune hepatitis, Sjögren’s syndrome, and scleroderma. The serologic and histologic findings are useful in diagnosing autoimmune pancreatitis and in distinguishing it from other forms of CP. It presents most commonly with jaundice secondary to intrapancreatic common bile duct obstruction, and patients respond with amelioration of symptoms to corticosteroids.

What is idiopathic chronic pancreatitis?
Idiopathic CP remains a wastepaper basket of the unknown causes of CP. It accounts for 10-30% of all cases of CP. Misdiagnosis may occur if there is concealed alcohol use, or if genetic studies are not done to rule out cystic fibrosis or trypsinogen gene mutations. There appears to be a bimodal age distribution with two forms: early-onset juvenile form and late-onset senile form. Early-onset juvenile form has a median age of 18 years and is characterized by severe pain with delayed development of pancreatic calcifications, exocrine insufficiency, and endocrine insufficiency. Conversely, the late-onset senile form has a median age of 56 years and is characterized by exocrine and endocrine insufficiency, albeit in the absence of pain.

What is the most common presenting symptom of chronic pancreatitis?
Abdominal pain is the most common presenting symptom, occurring in 50-100% of patients with CP. Although the pain associated with CP is highly variable, it is described usually as being epigastric, dull, constant, radiating to the back, improvement with sitting or leaning forward, and worsening after meals. Frequently, there is associated nausea and vomiting. Over time, the pain of CP may persist, diminish, or resolve completely.

What are the causes of weight loss in patients with chronic pancreatitis?

  • Decreased caloric intake as a result of fear of aggravating pain (sitophobia)
  • Malassimilation due to pancreatic exocrine insufficiencyUncontrolled diabetes
  • Early satiety secondary to delayed gastric emptying or duodenal obstruction

Is steatorrhea an early symptom of chronic pancreatitis?
No. Steatorrhea occurs when pancreatic exocrine secretion is insufficient to maintain normal digestion and absorption of lipids. Because 90% of exocrine function must be lost before steatorrhea develops, it signifies advanced disease. 

Is diabetes mellitus an early manifestation of chronic pancreatitis?
Similar to steatorrhea secondary to exocrine insufficiency, diabetes mellitus with endocrine insufficiency occurs late in the course of CP. Up to 70% of patients with CP will eventually develop diabetes, which is caused by the destruction of insulin-producing beta cells. In contrast to type 1 diabetes, CP also destroys glucagon-producing alpha cells, which results in a brittle type of diabetes subject to frequent episodes of hypoglycemia. Diabetic ketoacidosis and nephropathy are uncommon in diabetes caused by CP; however, retinopathy and neuropathy occur at similar frequencies to other forms of diabetes. 

Are measurements of serum pancreatic enzymes helpful in the diagnosis of chronic pancreatitis?


What do elevated levels of bilirubin and alkaline phosphatase suggest in the patient with chronic pancreatitis?
Elevations in bilirubin and alkaline phosphatase suggest biliary obstruction secondary to compression of the intrapancreatic portion of the bile duct by edema, fibrosis, or pancreatic carcinoma. Elevations can also occur in patients from toxic effects of alcohol intake or other hepatotoxins (i.e., medications). Attempts to document biliary obstruction must be a priority because biliary cirrhosis can result. 

What specialized test directly measures pancreatic exocrine function?
The secretin stimulation test, with or without concomitant cholecystokinin (CCK) administration, measures the volume of secretion and the concentration of bicarbonate output (via aspiration of duodenal contents) in response to injection of secretin. Bicarbonate levels <50 mEq/L are consistent with CP; levels >50 mEq/L but below 75 mEq/L, are indeterminate; levels >75 mEq/L are normal. The test is invasive, requiring duodenal catheter (Dreiling tube) insertion for collection of secretions, but has a reported sensitivity of 75-95%. 

What conditions may be associated with a false-positive secretin stimulation test?
Primary diabetes mellitus, Billroth II gastrectomy, celiac sprue, cirrhosis, and the recovery phase after an attack of acute pancreatitis. 

What indirect tests of pancreatic exocrine function are used?
The bentiromide and pancreolauryl tests are noninvasive methods of assessing pancreatic exocrine function but are no longer available in the United States. Most indirect tests of pancreatic function measure the absorption of a compound that first requires digestion by pancreatic enzymes, thereby assessing indirectly pancreatic function. The bentiromide test exploits the lack of the digestive enzyme chymotrypsin, which occurs in patients with CP. This test involves the ingestion of bentiromide, a tripeptide digested by pancreatic chymotrypsin with subsequent release of para-aminobenzoic acid (PABA). Free PABA is absorbed in the small intestine, conjugated in the liver, and is then excreted in the urine. Recovery of ≥50% of the administered dosage in a 6-hour urine collection is considered normal. False-positive results may occur in patients with diabetes mellitus, renal insufficiency, liver disease, or malabsorptive states other than CP. The pancreolauryl test exploits the reduced secretion of arylesterases from the pancreas. After ingestion of fluorescein dilaurate (with a standard breakfast), arylesterases release fluorescein from the dilaurate. Free fluorescein is absorbed in the small intestine, conjugated in the liver, then excreted in the urine. False-positive results may be seen in patients with chronic inflammatory bowel disease, severe biliary diseases, and Billroth II gastrectomy. Both tests have sensitivities of 80-100% in patients with advanced CP with steatorrhea. 

Another test to indirectly assess pancreatic exocrine function is the measurement of serum trypsinogen, which is very low (<20 ng/mL) in patients with CP. Serum trypsinogen levels tend to be low in patients with advanced CP and steatorrhea and are usually normal in patients with less advanced disease. Other causes of low trypsinogen levels include pancreatic ductal obstruction.

Additional indirect tests of pancreatic exocrine function include the fecal chymotrypsin and fecal elastase, [14C] olein test, and 72-hour quantitative fecal fat determination. The limitation of most of these tests is their lack of sensitivity, except in patients with advanced CP, characterized by malassimilation and steatorrhea. Unfortunately, we do not have a serologic or noninvasive test for the diagnosis of mild or moderate CP not characterized by exocrine insufficiency of the magnitude to result in steatorrhea.

Are plain abdominal radiographs helpful in the diagnosis of chronic pancreatitis?
. The identification of focal or diffuse pancreatic calcifications on plain abdominal radiographs makes the diagnosis of advanced CP almost certain. It is seen in 30-40% of patients with CP. Because calcification is not found in early CP, plain abdominal films cannot be used to exclude the diagnosis. Of note, one must be certain that the calcifications are within the pancreas and do not simply represent vascular calcifications 

What other imaging modalities are used in the diagnosis of chronic pancreatitis?
Transabdominal ultrasound (US) findings of CP include pancreatic duct dilation, calcifications, pancreatic ductal stones, pseudocysts, and, in milder disease, reduction in parenchymal echogenicity or irregular gland contour. The sensitivity and specificity of US in the diagnosis of CP are 60-70% and 80-90%, respectively. The major limitation of US is that the pancreas cannot be adequately visualized in many patients secondary to overlying bowel gas. 

Computed tomography (CT) findings of CP include pancreatic duct dilation, intraductal filling defects, calcifications, cavitary, and cystic lesions. Other significant findings include heterogeneous density of the pancreatic gland with atrophy or enlargement. CT is 10-20% more sensitive than US, with a similar specificity.

Magnetic resonance imaging (MRI) gives more accurate pancreatic duct evaluation than CT. It may reveal enlargement, stenosis, and pancreatic duct filling defects.

What is the role of endoscopic retrograde cholangiopancreatography (ERCP) in the diagnosis of chronic pancreatitis?
Abnormalities of the pancreatic duct are visualized by ERCP in patients with moderate to advanced CP. Conversely, patients with early CP may have a normal pancreatogram. Findings on ERCP include characteristic “chain of lakes” beading of the main pancreatic duct, ectatic side branches, and intraductal filling defects. ERCP is considered the gold standard imaging procedure for the diagnosis of CP, with a 90% sensitivity and 100% specificity. 

In general, there is good correlation between the findings seen on ERCP and results of the secretin stimulation test in the diagnosis of CP. ERCP may also be useful in distinguishing CP from pancreatic carcinoma. The presence of a dominant stricture is highly suggestive of pancreatic carcinoma, whereas CP is characterized by ductular changes (with multiple areas of stenosis, dilation, irregular branching ducts, and intraductal calculi).

What is the role of magnetic resonance cholangiopancreatography (MRCP) in the diagnosis of chronic pancreatitis?

Preliminary studies have shown close correlation of the ductular findings seen on MRCP with ERCP in patients with CP, including the presence of pancreatic ductal dilation, ductal narrowing, and filling defects. Imaging by MRCP is limited in assessing areas where the pancreatic duct is small, for instance, pancreatic tail and side branches. The benefits of MRCP over ERCP include that of being noninvasive and being able to evaluate both pancreatic parenchyma and ducts at the same time. It can visualize the ductular anatomy not seen on ERCP when a stricture is present and visualize cystic lesions not in connection with the ductular system. Thus, it is an excellent initial study in patients with suspected CP. If negative, additional studies can be performed for further evaluation.

What is the role of endoscopic ultrasound (EUS) in the diagnosis of chronic pancreatitis?
EUS allows high-resolution imaging of the pancreas without interference by overlying bowel gas typically encountered with transabdominal ultrasound. The diagnosis of CP by EUS is based on the presence of abnormal pancreatic ductal and parenchymal findings. The diagnosis requires the presence of at least three criteria. CP is unlikely in the absence of any criteria and highly likely if there are ≥5 criteria. A prospective evaluation comparing EUS with ERCP and secretin stimulation test in the diagnosis of CP showed good correlation, especially in patients with advanced CP. In mild CP, EUS may show findings not detected by ERCP or functional testing, and it remains controversial whether a diagnosis of CP can be made by EUS findings alone.

What are the endoscopic ultrasound criteria for the diagnosis of chronic pancreatitis?
Ductal findings

  • Dilated main duct
  • Dilated side branches
  • Duct irregularities
  • Hyperechoic duct margins
  • Stones/calcification

Parenchymal findings

  • Hyperechoic foci
  • Hyperechoic strands
  • Gland lobularity
  • Cystic cavities

What is the role of magnetic resonance cholangiopancreatography (MRCP) in the diagnosis of chronic pancreatitis?
Preliminary studies have shown close correlation of the ductular findings seen on MRCP with ERCP in patients with CP, including the presence of pancreatic ductal dilation, ductal narrowing, and filling defects. Imaging by MRCP is limited in assessing areas where the pancreatic duct is small, for instance, pancreatic tail and side branches. The benefits of MRCP over ERCP include that of being noninvasive and being able to evaluate both pancreatic parenchyma and ducts at the same time. It can visualize the ductular anatomy not seen on ERCP when a stricture is present and visualize cystic lesions not in connection with the ductular system. Thus, it is an excellent initial study in patients with suspected CP. If negative, additional studies can be performed for further evaluation.

What is the most common complication of chronic pancreatitis?
The most common complication of CP is pseudocyst formation, occurring in up to 25% of patients. Pseudocysts should be suspected in any patient with stable CP who has worsening abdominal or back pain. Other less common presentations of pseudocysts include a palpable mass on physical exam when they are very large, nausea, vomiting, jaundice, and gastrointestinal (GI) bleeding. In contrast to acute pseudocysts (defined as being present for <6 weeks), chronic pseudocysts, especially those >6 cm, almost never resolve spontaneously. Although most pseudocysts are asymptomatic, problems like pseudoaneurysm and abscess formation can occur. Of note, cystic collections in the pancreas are most often due to pseudocysts, accounting for 70-90% of cases.

How are pseudocysts treated?
In general, asymptomatic pseudocysts do not require treatment regardless of size. Initially, they may be followed by abdominal ultrasound at 3 and 6 months. If asymptomatic, there is no need in most patients for further routine evaluation. Indications for pseudocyst treatment include presence of symptoms, progressive enlargement, presence of complications (i.e., infection, hemorrhage, intraperitoneal rupture, intestinal obstruction), and suspicion of malignancy. Effective treatment includes surgical excision for pseudocysts localized to the tail of the pancreas, and internal or external drainage (performed by surgical, endoscopic, or percutaneous means). Surgical or endoscopic internal drainage is usually the treatment of choice, especially for mature pseudocysts (i.e., present for longer than 6 weeks with a formed cyst wall). Surgical options include cyst-gastrostomy, cyst-duodenostomy, or cyst-jejunostomy. Endoscopic cyst-gastrostomy or cyst-duodenostomy requires abutment of the pseudocyst onto adjacent viscera. EUS can determine the distance of a pseudocyst from the GI lumen, while assessing cyst contents and avoiding adjacent vasculature during performance of endoscopic drainage. External drainage is necessary for immature or infected pseudocysts, and this can be achieved surgically or percutaneously under radiologic guidance. Complications of external drainage include higher recurrence rates, drain track superinfection, and formation of pancreatic-cutaneous fistulas.

What are other complications of chronic pancreatitis?
Distal common bile duct (CBD) obstruction occurs in 5-10% of patients with CP. Compression of the intrapancreatic portion of the CBD by edema, fibrosis, or pseudocyst in the pancreatic head can lead to cholestasis, jaundice, biliary pain, and, potentially, cholangitis. If left untreated, secondary biliary cirrhosis can occur. Duodenal obstruction may occur secondary to external compression by edema or fibrosis of the pancreatic head. It affects up to 5% of patients with CP. Presenting symptoms include nausea, vomiting, weight loss, postprandial abdominal pain, and early satiety. External pancreatic fistulas are rare, and occur most frequently after surgical or percutaneous drainage of a pseudocyst. Internal pancreatic fistulas occur usually spontaneously from main pancreatic duct rupture or pseudocyst leakage, typically in patients with CP secondary to alcohol. This can lead to a collection of pancreatic fluid in the peritoneal cavity or into the pleural space, resulting in pancreatic ascites or pleural effusion, respectively. Pseudoaneurysms result from pseudocyst erosion into the splenic vein. If the pseudocyst is in communication with the main pancreatic duct, GI bleeding may occur. Gastric varices result from splenic vein thrombosis and may also cause GI bleeding. Patients with CP are also predisposed to developing pancreatic adenocarcinoma, with a lifetime risk of approximately 4%.

How is distal common bile duct obstruction diagnosed and treated?
Imaging by ERCP or MRCP may demonstrate narrowing of the distal CBD in the form of gradual tapering, bird’s beak stenosis, or “hourglass” stricture. Complications of biliary obstruction include jaundice, abdominal pain, ascending cholangitis, and secondary biliary cirrhosis. Other causes of jaundice, such as intrinsic liver disease, should be ruled out. Treatment options include close observation for a short period of time (<2 months), with serial liver function tests (LFTs) or endoscopic or surgical decompression procedures. If abnormal LFTs persist secondary to obstruction, decompression is advised to prevent secondary biliary cirrhosis. Endoscopic biliary stent placement may provide temporary benefit, especially in the acute setting, but long-term success is low due to the need for multiple=”multiple” stent exchanges, stent blockage, and stent migration. Particularly for younger patients, surgical biliary bypass with cholecystojejunostomy or choledochojejunostomy is preferred. When associated with concomitant pseudocyst or dilated pancreatic duct, surgical biliary decompression may be combined with lateral pancreaticojejunostomy.

How is duodenal obstruction diagnosed and treated?
Duodenal obstruction is best diagnosed by upper GI series, given that endoscopy may under appreciate the degree of duodenal stenosis. Treatment includes supportive medical therapy initially, but with persistent stenosis, surgery is warranted. Usually, a gastrojejunostomy is done, and this can be combined with biliary drainage (if there is concomitant CBD obstruction) or with lateral pancreaticojejunostomy (if pain results from pancreatic duct obstruction). In nonoperative patients, endoscopic placement of metal stents may provide palliation.

How are pancreatic fistulas treated?
General treatment strategies for pancreatic fistulas include reducing pancreatic secretions with long-acting somatostatin analogs (octreotide 50-200 μg subcutaneously every 8 hours) and with total parenteral nutrition and nothing by mouth. Successful treatment may take weeks, and time is usually the healer. Endoscopic stenting of the main pancreatic duct may facilitate healing, if ERCP identifies the site of ductal disruption or leak. For internal pancreatic fistulas, additional treatment options include large volume paracentesis for pancreatic ascites, thoracentesis for pancreatic pleural effusion, and diuretics. Surgical decompression or resection may be required, if ERCP cannot visualize the source of ductal disruption or leak or there is persistence of the fistula after medical therapy.

How is pancreatic ascites or pancreatic pleural effusion diagnosed?
The diagnosis is made by examining the fluid obtained from paracentesis or thoracentesis, which has typically a very high amylase concentration (>1000 IU/L).

Why does the presence of gastric varices in the absence of esophageal varices suggest chronic pancreatitis?
Anatomically, the splenic vein is in close proximity to the pancreas, and chronic inflammation, as seen in CP, may lead to splenic vein thrombosis. Thrombosis of the splenic vein leads to intrasplenic venous hypertension, splenomegaly, and collateral formation through the short gastric veins, resulting in gastric varices. Isolated gastric varices occur in approximately 5% of patients with CP. Massive gastrointestinal hemorrhage may occur. Splenectomy is curative. Treatment is not required in the absence of bleeding.

Are signs of fat-soluble vitamin deficiencies highly suggestive of chronic pancreatitis?
No. Although absorption of fat-soluble vitamins (A, D, E, K) is decreased in CP, clinical manifestations of vitamin deficiencies, like easy bruisability, bone pain, and poor night vision, are uncommon.

Are patients with chronic pancreatitis predisposed to nephrolithiasis?
Yes. Steatorrhea from CP may lead to hyperoxaluria and subsequent oxalate kidney stone formation. Patients with untreated steatorrhea have high concentrations of long-chain fatty acids in the colon, which bind intraluminal calcium by formation of insoluble calcium soaps. With less calcium in the intestinal lumen to bind oxalate, more intestinal oxalate is absorbed, which results in hyperoxaluria and nephrolithiasis.

How should hyperoxaluria be treated in patients with chronic pancreatitis?
Treatment options include pancreatic enzyme replacement, low dietary oxalate intake, low dietary long-chain triglyceride intake, and increased intake of calcium (3 g/day) or aluminum in the form of antacids (3.5 gm/day).

Can patients with chronic pancreatitis develop vitamin B12 malabsorption?
Yes. Vitamin B12 (cobalamin) malabsorption occurs in up to 40% of patients with advanced CP. The probable mechanism is competitive binding of cobalamin by cobalamin-binding proteins instead of by intrinsic factor. Cobalamin-binding proteins are destroyed usually by pancreatic proteases, and treatment with pancreatic enzyme replacement may correct the condition.

How is steatorrhea in chronic pancreatitis treated?
The primary therapeutic modality for patients with steatorrhea is pancreatic enzyme replacement. These consist of lipase, which is necessary to prevent fat malabsorption that occurs when lipase secretion is <10% of normal levels. The usual dose of lipase is at least 30,000 units with each meal, given as 10,000 units before eating and 20,000 units during the meal to ensure adequate mixing. Pancreatic enzymes are available in enteric and nonenteric-coated formulations. The major advantage of enteric-coated compounds is that they do not dissolve in the stomach and thus are less susceptible to acid pepsin inactivation of pancreatic enzymes, which limits effectiveness of therapy. With nonenteric-coated pancreatic enzymes, the addition of an H2-receptor antagonist or proton pump inhibitor is suggested to prevent acid inactivation of lipase and improve efficacy. Pancreatic enzyme replacements differ in their dissolution qualities and therefore their effectiveness. This decreased physiologic availability is most often found with generic substitutions. In patients with weight loss and poor response to pancreatic enzyme replacement, medium chain triglycerides (MCT) may provide much needed nutritional support given that they are more easily degraded and absorbed. Restricting fat intake, usually to <20 gm/day, may also help with steatorrhea. However, this is inappropriate in cachectic patients who need optimal caloric intake for support of nutritional status.

What are nonsurgical modalities of pain control in chronic pancreatitis?
Abdominal pain is the most common symptom of CP that requires medical care. Alcohol cessation, small low-fat meals, and nonnarcotic analgesics may provide some initial relief.
If abdominal pain persists, other nonsurgical therapeutic options include pancreatic enzyme supplements, narcotic analgesics, somatostatin, and celiac plexus block. Pancreatic enzyme supplements should be the first measure used in patients with persistent, severe abdominal pain. They may decrease pain by reducing the abdominal distention and diarrhea associated with malassimilation, as well as by possibly limiting pancreatic stimulation. Treatment of chronic pain in CP is usually facilitated by pancreatic enzyme supplements with high protease content and nonenteric-coating, which differ from the high lipase, enteric-coated supplements preferred in the treatment of steatorrhea. Somatostatin at a dose of 200 μg subcutaneously every 8 hours may also reduce the pain of CP. In patients with inadequate pain control from these measures, narcotic analgesics may be needed, realizing that secondary addiction is a significant risk if pain persists. Antidepressants may be added as an adjunctive agent. Celiac plexus block, with alcohol or steroids, has limited results in alleviating pain due to CP because of its short benefits. The occasional benefits last usually between 2 and 6 months, with less effective pain relief with repeat sessions. Other potential medical therapies that are being studied for pain control in CP include the use of antioxidants.

Does endoscopy have a role in pain control in chronic pancreatitis?
The role of endoscopy in the management of pain in patients with CP is evolving, especially in patients with a dominant stricture. Numerous reports suggest that endoscopic sphincterotomy with pancreatic stricture dilation and pancreatic duct stent placement relieves recurrent or persistent pain associated with CP. Several studies have also reported marked improvement in pain after endoscopic removal of intraductal pancreatic stones with extracorporeal lithotripsy and pancreatic duct sphincterotomy with stone extraction. Although endoscopic techniques show promise for pain management in CP, substantiation is needed in the form of randomized, blinded, prospective studies.

What is the role of surgery in pain control in chronic pancreatitis?
Surgery is reserved generally for patients who have continued, persistent pain, despite the aforementioned medical therapies. They are difficult technically but may provide longer-lasting pain control. Surgical treatments include ductal decompression with a lateral pancreaticojejunostomy (modified Puestow’s procedure) or partial resection of the pancreas. Lateral pancreaticojejunostomy is preferred in patients with ductal obstruction in the head of the pancreas and distal duct obstruction, whereas partial pancreatic resection is most appropriate in patients without ductal dilation, so-called small duct disease, or localized distal (tail) disease. Pain relief can be achieved with surgery in up to 80% of patients with CP. Other surgical techniques for the treatment of chronic pain in CP include total pancreatectomy followed by autologous islet cell transplantation, which is presently experimental and being studied.




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