Overview and Risk Factors
Pancreatitis is an inflammation of the pancreas caused by inappropriate activation of pancreatic enzymes (proteases, lipase, amylase) within and surrounding the pancreas, resulting in autodigestion of pancreatic tissue, necrosis, edema, and possibly hemorrhage.
About 80% of acute pancreatitis cases result from excessive intake of alcohol, which is directly toxic to pancreatic tissue, or from gallstones, which block the flow of pancreatic digestive enzymes. Less common etiologies include hypertriglyceridemia, hypercalcemia, mumps, abdominal trauma, and medications such as azathioprine, ACE inhibitors, valproic acid, thiazides, diuretics, and steroids. Rarely, pancreatitis occurs as a complication of endoscopic retrograde cholangiopancreatography (ERCP). About 10% of cases are idiopathic.
Acute pancreatitis varies from a mild, self-limited condition to a severe pathological process with hemorrhagic necrosis leading to systemic multi-organ failure and death. Clinical presentation includes steady, severe epigastric pain and tenderness that generally follow a large meal or alcohol intake. The pain often persists for hours, radiates to the back, and may be relieved by leaning forward. Further symptoms include abdominal distention, nausea, vomiting, fever, tachycardia, diaphoresis, and jaundice. Severe cases may present with signs of peritonitis (guarding, rebound tenderness, fever), dehydration, and shock.
Chronic pancreatitis is a slowly progressive destruction of pancreatic tissue that occurs over several years due to persistent inflammation and fibrosis. As many as 80% to 90% of cases result from long-standing alcohol abuse, but the condition can also be caused by cystic fibrosis, severe malnutrition, and hyperparathyroidism. Presentation may be similar to acute pancreatitis, with epigastric pain that often radiates to the back, nausea, vomiting, food intolerance, steatorrhea, jaundice, and glucose intolerance. However, chronic pancreatitis may be asymptomatic.
The annual incidence of pancreatitis in the United States is 4 per 100,000 in Native Americans, 5.7 per 100,000 in Caucasians, and 20.7 per 100,000 in African Americans. The risk among African Americans aged 35 to 64 is 10 times greater than for any other demographic group. Whether the increased incidence is related to genetics or to environmental and lifestyle factors is unclear.
Alcohol use. About 10% of chronic alcoholics will develop acute pancreatitis. From 70% to 80% of heavy alcohol users will develop chronic pancreatitis.
Gender. Acute pancreatitis due to gallstones is more common in women, reflecting the greater prevalence of gallstones in women.
Initial laboratory studies include complete blood count (CBC), liver function tests, blood alcohol level, amylase, lipase, and lipid panel. Radiographic scans also play an important role.
Lipase and amylase are generally elevated in acute pancreatitis, although the degrees of elevation do not correlate with disease severity. In chronic pancreatitis, lipase and amylase are usually not elevated.
Hypokalemia, hypocalcemia, and leukocytosis are often present in acute disease.
Elevated liver enzymes, bilirubin, and LDH may be present, especially if biliary disease is the etiology of pancreatitis. Liver enzymes may also be elevated due to compression of the common bile duct by an edematous pancreatic head.
Hypertriglyceridemia (>1000) may be the cause of pancreatitis in a small number of cases.
Patients are often hypoxemic, especially in severe disease.
Abdominal films, CT scan, and ultrasound evaluate for gallstone-related blockages, pancreatic necrosis or edema, and abscess or pseudocyst formation, and rule out nonpancreatic etiologies of abdominal pain.
Endoscopic retrograde cholangiopancreatography (ERCP) reveals the structure of the common bile duct and pancreatic duct and can be used to repair strictures and remove gallstones. However, many specialists are now using magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound more commonly than ERCP.
Supportive care is the mainstay of treatment. This includes aggressive IV fluid administration to maintain blood pressure; bowel rest (no oral intake, insert nasogastric tube if patient is vomiting); IV medications for pain control; antiemetics to relieve nausea or vomiting; insulin administration for glucose intolerance; and monitoring and correcting electrolyte abnormalities, especially calcium. In advanced cases, admission to an intensive care unit (ICU) may be indicated.
Addressing the underlying etiology is another treatment priority. For example, the patient should avoid alcohol and fatty foods. Cholecystectomy for gallstone pancreatitis should be delayed until the acute event resolves. Endoscopic or surgical intervention may be necessary in select cases.
Alcohol use, smoking, body weight, diet, genetic factors, and medications all affect the risk of developing pancreatitis. Diet may also have an important role after diagnosis. Dietary recommendations differ, depending on whether the condition is acute or chronic.
Maintain a healthy body weight. Obesity appears to be a risk factor for the development of pancreatitis1 and for an increased severity when it occurs.2 Gallstones are a risk factor for acute pancreatitis, one that occurs more frequently in obese persons. Diets low in fat and high in fiber are helpful for gallstone prevention and for obesity prevention and management (See chapters on gallstones and obesity).
Control triglyceride levels. To reduce triglycerides, a fat-restricted diet is advised3 (See Hyperlipidemia chapter). The only exception may be the therapeutic use of high doses of omega-3 fatty acids, which may reduce triglycerides by 30% to 50%.4 Foods with a high glycemic index, particularly sucrose (table sugar) and high fructose corn syrup, also tend to raise triglycerides.5,6 Patients with triglyceridemia-related pancreatitis may be well-advised to choose carbohydrates that do not raise triglyceride levels; ie, ones that are fiber-rich and have a low glycemic index.7
Oxidative stress, defined as a disturbance in the balance between pro-oxidants and antioxidants leading to cellular damage, is a frequent finding in patients with chronic pancreatitis. A known source of this imbalance is the metabolism of xenobiotics, resulting in glutathione depletion and subsequent damage to pancreatic acinar cells.8 Patients with chronic pancreatitis have demonstrably low tissue levels of antioxidant enzymes.9 These patients also have lower blood concentrations of several antioxidants, including selenium (a glutathione precursor), vitamin A, vitamin E, and several carotenoids, compared with patients who have acute pancreatitis and with controls.10 Some studies have suggested that antioxidant supplements (combinations of either selenium, beta carotene, and vitamins C and E, or methionine, vitamin C, and selenium) ameliorate the pain associated with chronic (not acute) pancreatitis, diminish the frequency of acute exacerbations, and reduce the need for pancreatic surgery.8,11
Avoidance of alcohol reduces the risk of both acute and chronic pancreatitis.12 The risk for chronic pancreatitis in particular is exacerbated by the combination of smoking and alcohol intake.13
See Basic Diet Orders and Obesity chapter for general recommendations.
What to Tell the Family
Acute pancreatitis is usually preventable. To avoid the disease, alcohol must be eliminated and dietary steps taken to prevent gallstones and hypertriglyceridemia. A low-fat, high-fiber diet can help prevent gallstones and lower triglycerides, but medication may be necessary to lower triglycerides enough to prevent pancreatitis. Chronic pancreatitis may be a result of oxidative stress in persons with low concentrations of antioxidant enzymes, low antioxidant intake, or both, and may respond to a therapeutic diet and antioxidant supplements. Avoidance of medications known to elevate risk for this condition may be necessary. These drugs include atypical antipsychotics (clozapine, olanzapine, and risperidone)14; protease inhibitors15; and hormone replacement therapy.16
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11. Bowrey DJ, Morris-Stiff GJ, Puntis MC. Selenium deficiency and chronic pancreatitis: disease mechanism and potential for therapy. HPB Surg. 1999;11:207-216.
12. Corrao G, Bagnardi V, Zambon A, et al. A meta-analysis of alcohol consumption and the risk of 15 diseases. Prev Med. 2004;38:613-619.
13. Morton C, Klatsky AL, Udaltsova N. Smoking, coffee, and pancreatitis. Am J Gastroenterol. 2004;99:731-738.
14. Koller EA, Cross JT, Doraiswamy PM, et al. Pancreatitis associated with atypical antipsychotics: from the Food and Drug Administration's MedWatch surveillance system and published reports. Pharmacotherapy. 2003;23:1123-1130.
15. Mantel-Teeuwisse AK, Kloosterman JM, Maitland-van der Zee AH, et al. Drug-Induced lipid changes: a review of the unintended effects of some commonly used drugs on serum lipid levels. Drug Safety. 2001;24:443-456.
16. Barrett-Connor E. Postmenopausal estrogen therapy and selected (less-often-considered) disease